Renal pathology (dr magdy ismail) copy

Pathology of the kidney and its
collecting system
Pr.Dr.Magdy Ismaeil Ahmed

 Normal structure of the kidneyNormal structure of the kidney :-:-
 Kidney consists of glomeruli ,tubules ,interstitium and bloodKidney consists of glomeruli ,tubules ,interstitium and blood
vessels .All are anatomically linked .Damage to one componentvessels .All are anatomically linked .Damage to one component
affects the others . Whatever ,different renal diseases leading toaffects the others . Whatever ,different renal diseases leading to
destruction all kidney componentsdestruction all kidney components  End stage kidney.End stage kidney.
 Normal kidney functionNormal kidney function :-:-
1-Excretion of waste products1-Excretion of waste products
2-Secretion of hormones ( renin ,eryropoietin )2-Secretion of hormones ( renin ,eryropoietin )
3-Maintain acid-base balance3-Maintain acid-base balance
4-Regulation of body salts and water.4-Regulation of body salts and water.

Congenital anomaliesCongenital anomalies
10% of newborns develop significant malformation10% of newborns develop significant malformation
Mostly arises from maldevelopment rather than inherited genes.Mostly arises from maldevelopment rather than inherited genes.
1-Renal agenesis1-Renal agenesis:-:- Failure of kidney developmentFailure of kidney development
a-Bilaterala-Bilateral  incompatible with life .incompatible with life .
b-Unilateralb-Unilateral Compensatory hypertrophy of the other kidneyCompensatory hypertrophy of the other kidney  ProgressiveProgressive
glomeruloscelrosis.glomeruloscelrosis.
2-Hypoplasia :-2-Hypoplasia :- Incomplete development.Usually unilateral,and posses a reducedIncomplete development.Usually unilateral,and posses a reduced
number of renal lobes and pyramides (<6). D.D from atrophynumber of renal lobes and pyramides (<6). D.D from atrophy
3-Ectopic kidney3-Ectopic kidney (out of place) ;-(out of place) ;- Presence of the kidney in an ectopic site (in pelvis orPresence of the kidney in an ectopic site (in pelvis or
above pelvic brim ).It complicated by kinking or tortuousity of uretersabove pelvic brim ).It complicated by kinking or tortuousity of ureters  UrinaryUrinary
retention and frequent infection.retention and frequent infection.
4-Horse4-Horse ––shoe kidney:-shoe kidney:- Both kidneys are fused together :- Fusion of upper polesBoth kidneys are fused together :- Fusion of upper poles
(10%) or lower poles (90%) in front the great vessels(10%) or lower poles (90%) in front the great vessels  may cause renal failure.may cause renal failure.
5-Aberrant renal artery5-Aberrant renal artery ;-;- It passes in front renal pelvisIt passes in front renal pelvis  hydronephrosishydronephrosis
6-Congenital double ureters and double pelvis6-Congenital double ureters and double pelvis
7-Supernumerary kidney :-7-Supernumerary kidney :- More than 2 kidneys.More than 2 kidneys.

Cystic diseases of the kidneyCystic diseases of the kidney
1-Simple cyst1-Simple cyst
2-Cyst renal dysplasia2-Cyst renal dysplasia
3-Polycystic kidney diseases3-Polycystic kidney diseases (adulthood)(A.D)(adulthood)(A.D)
(PKD)(PKD) (childhood)(A.R)(childhood)(A.R)
4-Medullary sponge kidney4-Medullary sponge kidney
5-Nephronophthisis-uremic medullary cystic complex5-Nephronophthisis-uremic medullary cystic complex
(UMCD)(UMCD)
6-Acquired (dialysis-associated ) cystic disease.6-Acquired (dialysis-associated ) cystic disease.

1-Simple cyst1-Simple cyst :-:-
-Non inherited-Non inherited
-Single or multiple cysts-Single or multiple cysts
-Cortical rarely medullary-Cortical rarely medullary
-2-10 cm in diameter lined by low cubical epithelium ,filled with clear-2-10 cm in diameter lined by low cubical epithelium ,filled with clear
serous fluidserous fluid
-Complicated by hemorrhage-Complicated by hemorrhage flank painflank pain
2-Cystic renal dysplasia:-2-Cystic renal dysplasia:-
-Sporadic (Non familial) either unilateral or bilateral-Sporadic (Non familial) either unilateral or bilateral
-It results from abnormal metanephric differentiation-It results from abnormal metanephric differentiation
-Associated with urinary tract obstruction-Associated with urinary tract obstruction
GrosslyGrossly :- Affected kidney is multicystic:- Affected kidney is multicystic
HistologyHistology :- immature ducts surrounded by undifferentiated mesenchyme:- immature ducts surrounded by undifferentiated mesenchyme
+Focal cartilage formation+Focal cartilage formation

3-Adult PKD (A.D.)3-Adult PKD (A.D.)
-1/1000 persons-1/1000 persons
-PKD gene is on-PKD gene is on Ch 16Ch 16
-Always bilateral (arises in children till 50--Always bilateral (arises in children till 50-
60 years of age.60 years of age.
Clinical presentation :-Clinical presentation :-
1-Abdominal pain and abdominal masses1-Abdominal pain and abdominal masses
2-Hematuria and H.P2-Hematuria and H.P
3-proteinuria3-proteinuria Renal failureRenal failure
Grossly :-Grossly :- Massively enlarged kidneyMassively enlarged kidney
Multiple cysts (3-4 cm ) along nephronsMultiple cysts (3-4 cm ) along nephrons
and compress renal parenchyma ,not conne-and compress renal parenchyma ,not conne-
cted with renal pelvis (D.D hydronephrosis)cted with renal pelvis (D.D hydronephrosis)
Microscopically :Microscopically :- variable sized cystic- variable sized cystic
structures lined by variable epitheliumstructures lined by variable epithelium
filled by clear ,bloody or turbid fluid.filled by clear ,bloody or turbid fluid.
Pathogenesis :-Pathogenesis :-
1-Partial intratubular obstrction1-Partial intratubular obstrction
3-Increased compliance of tubular B.M3-Increased compliance of tubular B.M
3-Focal epithelial hyperplasia3-Focal epithelial hyperplasia
Associations:-Associations:-
-40% of cases (polycystic liver disease)-40% of cases (polycystic liver disease)
-10-30% (cerebral berry aneurysm)-10-30% (cerebral berry aneurysm)
Cause of deathCause of death :- Brain hemorrhage,:- Brain hemorrhage,
H.P or infection ,R.FH.P or infection ,R.F
Childhood PKD (A.R)Childhood PKD (A.R)
-Rarely bilateral anomaly-Rarely bilateral anomaly
-Mostly at perinatal or neonatal or-Mostly at perinatal or neonatal or
juvenile periodsjuvenile periods Rapid R.FRapid R.F
GrosslyGrossly :- Multicystic enlarged kidney:- Multicystic enlarged kidney
Cylindrically dilated collecting tubulesCylindrically dilated collecting tubules
lie at right angles to the cortex fillinglie at right angles to the cortex filling
both cortex and medullaboth cortex and medulla
Microscopic :Microscopic :- dilated collecting tubules- dilated collecting tubules
lined by uniform cubical cellslined by uniform cubical cells
Association :-Association :-
1- Polycystic liver disease and prolifer-1- Polycystic liver disease and prolifer-
ated bile ductsated bile ducts  Congenital hepaticCongenital hepatic
fibrosisfibrosis
2-In adults2-In adults  Hepatosplenomegaly andHepatosplenomegaly and
Portal hypertensionPortal hypertension

Medullary cystic diseasesMedullary cystic diseases
4-Medullary sponge kidney4-Medullary sponge kidney
-Usually in adults-Usually in adults
-Characterized by Multiple cystic-Characterized by Multiple cystic
Dilatation of the collecting ducts of theDilatation of the collecting ducts of the
MedullaMedulla
-It is discovered radiologically-It is discovered radiologically
-It may predispose to renal infection or renal-It may predispose to renal infection or renal
calculi and hematuriacalculi and hematuria
6-Acquired (dialysis associated) cystic6-Acquired (dialysis associated) cystic
diseasedisease
Multiple cortical and medullary cysts inMultiple cortical and medullary cysts in
patients with prolonged renal dialysis.patients with prolonged renal dialysis.
The cysts are lined by atypical hyperplasticThe cysts are lined by atypical hyperplastic
epitheliumepithelium  predisposes to adenoma orpredisposes to adenoma or
carcinoma .carcinoma .
5-Nephronophisis-(UMCD) complex5-Nephronophisis-(UMCD) complex
-A family of progressive renal disorders-A family of progressive renal disorders
-It begins in childhood-It begins in childhood
-It characterized by small cysts in the-It characterized by small cysts in the
medulla (at cortico-medullary junction )medulla (at cortico-medullary junction )
associated with cortical tubular atrophyassociated with cortical tubular atrophy
and interstitial fibrosis.and interstitial fibrosis.
4 variants:-4 variants:-
1-sporadic (20%)1-sporadic (20%)
2-Familial (A.R) juvnile nephronophisis2-Familial (A.R) juvnile nephronophisis
(50%)(50%)
3-Renal retinal (recessive) dysplasia (15%)3-Renal retinal (recessive) dysplasia (15%)
4-Adult onset (dominant) MCD (15%)4-Adult onset (dominant) MCD (15%)
Diagnosis :-Diagnosis :-
1- in children or adolescent1- in children or adolescent  unexplainedunexplained
R.FR.F
2-Positive family history +Chronic tubulo-2-Positive family history +Chronic tubulo-
interstitial nephritis .interstitial nephritis .

RENAL PATHOLOGYRENAL PATHOLOGY
Diseases can affect the following renal structures :-
A- Glomeruli (often immunological) B- Tubules (toxic, infectious)
C-Interstitium (toxic, infectious) D-Vascular (metabolic)
GLOMERULIGLOMERULI
Network of capillaries
a) lined by fenestrated endothelium
b) basement membrane
c) podocytes (“foot processes”)
Glomerular capillary wall
a) lined with fenestrated endothelium ( 70-100 nm)
b) glomerular basement membrane(GBM) consists of :-
1-Collagen (type IV) forms network to which glycoproteins attach
2-Heparan sulfate, laminin, glycoproteins.
c) visceral epithelial cells (podocytes; “foot processes”) composed of :-
i) Interdigitating foot processes embedded to basement membrane
ii) Foot processes are separated by 20-30 nm filtration slits bridged by
thin diaphragm (nephrin)

D-Entire glomerulus is supported by mesangial cells, modified smooth
muscle cells and lying between capillaries ,they function as :-
i-Phagocytic, contractile, supportive ,proliferative.
ii-Can secrete biologically active mediators (hormones & collagen)
Functions of glomeruliFunctions of glomeruli
a) very permeable to H2O and small solutes
b) impermeable to large M.W proteins (~ 70 k.D or larger; i.e., albumin)
c) “glomerular barrier function”
i) Its selective permeability based on:-1-Size (M.W) :-large molecules
can`t cross GBM  Lead to no harm – 2-Charge: cationic (+) more
permeablesubepithelial deposits.Neutral mesangial deposits
,while anionic (-)  subendothelial or do not deposits(no harm)
ii) podocytes important in maintaining this “function”:-slit diaphragm
maintain size-selectivity by specific proteins

1- NEPHRIN: extend towards each other from neighb-
oring podocytes comprising the slit diaphragm
2- PODOCIN: intracellular (podocyte) protein where
nephrin attaches - mutations in genes encoding
these proteins give rise to nephrotic syndrome
(glomerular disease)

Clinical ManifestationsClinical Manifestations
TerminologyTerminology
A)-Azotemia: ↑ BUN and ↑ creatinine related to ↓ GFR due to :-
-Renal causes:- Parenchymal diseases
-Pre-renal azotemia: ↓ RBF, hypoperfusion w/ou parenchymal damage
- Postr-enal azotemia: obstruction of urine flow below level of kidney
b) Uremia :- Azotemia associated with clinical S & S .
C-Asymptomatic hematuria and/or proteinuria:- Glomerular hematuria and
subnephrotic proteinuria ,due mild glomerular disease.
D-Acute renal failure :- Oliguria or anuria and recent azotemia
E-Chronic renal failure :- Prolonged signs & symptoms of uremia

5-Chronic renal failure: 4 stages
1- ↓ Renal reserve:
GFR 35-50% normal,
Patient asymptomatic,
More susceptible to develop azotemia
2- Renal insufficiency:
GFR 20-35% of normal,
Azotemia, anemia, ↑ BP, polyuria/nocturia ( ↓ concentrating ability)
3-Renal failure:
GFR 5-20% of normal
kidneys cannot regulate volume & ions: edema, hypocalcemia,metabolic
acidosis, uremia with neurological, CV and GI complications
4-End stage renal disease:
GFR < 5% of normal, terminal stage of uremia

Glomerular DiseasesGlomerular Diseases
Glomerulonephr/ itisGlomerulonephr/ itis
DefinitionDefinition :-:- Inflammation of the kidney glomeruli . It is a major
cause of renal diseases.
Types :-Types :-
1-Primary GNitis1-Primary GNitis :- The kidney is the principle organ involved.
2-Secondary GNitis :-2-Secondary GNitis :-
-The kidney is one of many organs can damaged by systemic diseases.
-It is the most common cause of CRF in humans.

I-Pry glomerulonephritisI-Pry glomerulonephritis
1-Acute diffuse proliferative GN1-Acute diffuse proliferative GN
2-Rapidly progressive GN2-Rapidly progressive GN
3-Membranous GN3-Membranous GN
4-Membranoproliferative GN4-Membranoproliferative GN
5-Lipoid nephrosis (minimal change5-Lipoid nephrosis (minimal change
disease)disease)
6-Focal segmental glomerulosclerosis6-Focal segmental glomerulosclerosis
7-IgA Nephropathy7-IgA Nephropathy
8-Chronic GN8-Chronic GN
II-2nd glomerulonephritisII-2nd glomerulonephritis
1-SLE1-SLE
2-D.M2-D.M
3-Amyloidosis3-Amyloidosis
4-Goodpasture’s syndrome4-Goodpasture’s syndrome
5-Polyarteritis nodosa5-Polyarteritis nodosa
6-Wagener’s granulomatosis6-Wagener’s granulomatosis
7-Henoch-Schonlein purpura7-Henoch-Schonlein purpura
8-Bacterial endocarditis8-Bacterial endocarditis
Hereditary disordersHereditary disorders
-Alport`s syndrome-Alport`s syndrome
-Fabry`s disease-Fabry`s disease

Glomerular diseases presented by :-Glomerular diseases presented by :-
1-Nephritic syndrome1-Nephritic syndrome
2-Nephrotic syndrome2-Nephrotic syndrome
3-Mixture of both3-Mixture of both
Glomerular diseases should be studied in terms ofGlomerular diseases should be studied in terms of
1-Pathogenesis 2-Morphology 3-Clinical presentation1-Pathogenesis 2-Morphology 3-Clinical presentation
Pathogenesis of Glomerular injuryPathogenesis of Glomerular injury
Two basic mechanisms :-Two basic mechanisms :-
1-Immune mechanisms ( pry or secondary ).1-Immune mechanisms ( pry or secondary ).
2-Non -immune mechanisms .2-Non -immune mechanisms .
I-The immune mechanismsI-The immune mechanisms
Three mechanisms:-Three mechanisms:-
1-Antibody mediated1-Antibody mediated
2-Cell mediated2-Cell mediated
3-Activation of alternate complement pathway3-Activation of alternate complement pathway

I-Anti-body mediated injuryI-Anti-body mediated injury
1-In situ immune complex deposition :-1-In situ immune complex deposition :-Antibodies react directly with tissueAntibodies react directly with tissue
antigenantigen
a-Fixed intrinsic tissue Ag (anti-tissue Aba-Fixed intrinsic tissue Ag (anti-tissue Ab ––mediated GN)mediated GN)
i-Anti-GBM nephritis (e.g Good- pasture syndrome)i-Anti-GBM nephritis (e.g Good- pasture syndrome)
ii-Heyman nephritis ( Heyman Ag of epithelial cells)ii-Heyman nephritis ( Heyman Ag of epithelial cells)
iii-Idiopathic human membranous GNiii-Idiopathic human membranous GN
b-Antibodies against Planted non-glomerular antigensb-Antibodies against Planted non-glomerular antigens
i-Exogenous Ag (drugs &infectious agent)i-Exogenous Ag (drugs &infectious agent)
ii-Endogenous (DNA,Igs, I.complexes)ii-Endogenous (DNA,Igs, I.complexes)
2-Circulating I.C deposition (get trapped within glomeruli )(type III reaction)2-Circulating I.C deposition (get trapped within glomeruli )(type III reaction)
i-Endogenous Ag (SLE )i-Endogenous Ag (SLE )
ii-Exogenous Ag (infectious products )ii-Exogenous Ag (infectious products )

 II-Cell mediated injuryII-Cell mediated injury :-:- sensitized T cells can cause glomerular
injury, in absence of immune deposits . It may occur in some forms of
RP GN
Mediators of immune glomerular injury.
Oxidants Proteases Eicosanoids
Cytokines Growth Factors Nitric Oxide
Others

III-Activation of alternate complement pathway:-III-Activation of alternate complement pathway:- Circulating Ag-Circulating Ag-
Abs complex trapped in glomeruliAbs complex trapped in glomeruli bind to and activate the complementbind to and activate the complement 
Releasing mediatorsReleasing mediators  glomerular injuryglomerular injury
I.F .microscopes :- It appears asI.F .microscopes :- It appears as aa linear pattern in anti-GBM nephritislinear pattern in anti-GBM nephritis or in aor in a
granular patterngranular pattern in all other types.in all other types.
Mediators of immune injuryMediators of immune injury :- Mediated either by antibodies:- Mediated either by antibodies
deposition or T-cell immune reactiondeposition or T-cell immune reaction
A-Antibody depositionA-Antibody deposition:-:- causes release ofcauses release of
1-Neutrophils :1-Neutrophils :-- Release proteases (damage BM),archidonic acid metabolitesRelease proteases (damage BM),archidonic acid metabolites
(decrease GFR) and oxygen free radicals (damage the cells)(decrease GFR) and oxygen free radicals (damage the cells)
2-C5b-92-C5b-9 :-Terminal membrane attack complex:-Terminal membrane attack complex  cell lysis & stimulate mesangialcell lysis & stimulate mesangial
cellscells  protease,oxygen free radicals ,IL-1 and PGprotease,oxygen free radicals ,IL-1 and PG
3-Monocytes and macrophages3-Monocytes and macrophages :- Release cytokines ,and GFs:- Release cytokines ,and GFs
4-Platelet4-Plateletss :-Release archidonic acid metabolites and GFs:-Release archidonic acid metabolites and GFs
5-Coagulation proteins5-Coagulation proteins :-Fibrin:-Fibrin  stimulate cresentic GN.stimulate cresentic GN.
B-T-cell reactionB-T-cell reaction :- stimulate:- stimulate macrophagesmacrophages && mesangial cellsmesangial cells GlomerularGlomerular
injuryinjury

Fate :-Fate :-
1-One attack of streptococcal infection1-One attack of streptococcal infection  I.Cs ,degraded by mesangialI.Cs ,degraded by mesangial
cellscells  ↓↓ inflammation and a limited courseinflammation and a limited course
2-Showers of antigens (SLE or HBV)2-Showers of antigens (SLE or HBV) Repeated cycles of I.C,sRepeated cycles of I.C,s
depositiondeposition  Progressive glomerular injury.Progressive glomerular injury.
II-Non immune mechanismsII-Non immune mechanisms
1-Most of glomeruli1-Most of glomeruli destroyed by different renal diseasesdestroyed by different renal diseases ↓↓ GFR (30-GFR (30-
50% )50% ) progressing to end stage glomerulosclerosis andprogressing to end stage glomerulosclerosis and RF.RF.
2-Other glomeruli2-Other glomeruli hypertrophied to increase workloadhypertrophied to increase workload  glomerularglomerular
capillary hypertensioncapillary hypertension  systemic hypertensionsystemic hypertension  epithelial andepithelial and
endoth . injuryendoth . injury  proteinuria .proteinuria .
3-Mesangial response3-Mesangial response occurs in form of mesangial cell proliferationoccurs in form of mesangial cell proliferation
and matrix deposition and Intra-glomerular coagulationand matrix deposition and Intra-glomerular coagulation  Glomerulo-Glomerulo-
sclerosissclerosis further loss of renal function and vicious circle.further loss of renal function and vicious circle.

Destruction of some Gl
Compansatory hypertrophy of
unaffected Gl
Capillary hypertension
Systemic hypertension
Epithelial &endothelial
damage
Leakage of proteins into
mesangium
Fibrin deposition & proliferation of
mesangial cellsMore sclerosis

Pathological features occur in GN.Pathological features occur in GN.
a) Hypercellularitya) Hypercellularity:
ii) Cell proliferation) Cell proliferation (endothelial ,epithelial and mesangial cells)(endothelial ,epithelial and mesangial cells)
ii) Leukocytes infiltrationii) Leukocytes infiltration (neutrophils, monocytes and lymphocytes)(neutrophils, monocytes and lymphocytes)
iii) Crescents formationiii) Crescents formation of glomeruli from proliferated parietal epithelial cell andof glomeruli from proliferated parietal epithelial cell and
monocytes (TNF, IL-1, IFN-monocytes (TNF, IL-1, IFN-γγ) as well as , fibrin .) as well as , fibrin .
b) Basement membrane thickeningb) Basement membrane thickening:- Either due to :-
i-Thickening of GBM proper as with diabetic glomerulosclerosis Or
ii-Deposition of immune complexes on subendothelial or subepithelial side of GBM or
within GBM itself .
c) Hyalinosis & sclerosisc) Hyalinosis & sclerosis :- Accumulation of plasma proteins Obliterates
capillary lumen of glomerulous (sclerotic feature) and increased mesangial matrix (
hyalinosis) .
d)-Others alterationsd)-Others alterations :- Thrombosis, fibrin deposition or lipid accumulation
Different terminology of glomerlar affection
1-Diffuse (all glomeruli are affected)
2- Focal (Some glomeruli are affected )
b) Global ( Entire glomerulus is affected )
d) Segmental (Part or a segment of each glomerulous is affected )
e) Mesangial (affecting mesangial region)

Proliferation of Gl cells + Leukocytic infiltration
Swollen endo.cells+
Closed epith slits
Decrease GFR
Oliguria
Fluid retention Hypertension
Focal damage of cells & BM
Escape of
RBC,s Proteins
Hematuria Proteinuria
Nephritic syndrome :-
*Definition : Acut clinical syndrome manifested by Oliguria, Hematuria (red
cell casts) some Proteinuria ,little Edema ± Hypertension
Mechanism :-
Diseases presenting with nephritic syndrome :- ADPGN,RPGN,G.P syndrome
GN with vasculitis.

Nephrotic syndrome :-Nephrotic syndrome :-
Definition ;Definition ;-- A clinical syndrome characterized by :-A clinical syndrome characterized by :-
1-Heavy proteinuria >3.5 gm/day 2-Hypoalbuinemia1-Heavy proteinuria >3.5 gm/day 2-Hypoalbuinemia
3-Massive edema(salt &water retention) 4-Hyperlipidemia &lipiduria3-Massive edema(salt &water retention) 4-Hyperlipidemia &lipiduria
5-Increased liability to infection and thrombotic complications .5-Increased liability to infection and thrombotic complications .
CausesCauses
Pry glomerular diseases
1-Membranous GN (commonest in
adults 30%)
2-Membrano-proliferative GN
3-Lipoid nephrosis (commonest in
childrens 65%)
4-Focal segmental glomerulosclerosis
5-IgA nephropathy & others
2nd
glomerular diseases (systemic)
1-D.M 2-Amyloidosis 3-SLE
4-Drugs (gold,pencillamine ,heroin)
5-Infections (malaria ,syphilis,HBV,AIDS )
6-Malignancy (melanoma ,carcinoma )
7-Miscellanous ( bee sting allergy and
hereditary nephritis )

Pathogenesis :-
1-Initially GBM destroyed→  capillary permeability and
progressive loss of plasma proteins → hypoalbuminemia
2-Hypoalbuminemia plasma colloid os.pr. → edema
3-Edema → ↓plasma volume →↑ aldosterone↑ water and solute
retention by kidney → exacerbation of edema (anasarca; massive
amounts of edema fluid);
4-Hypoalbuminemia → ↑ lipoprotein production by the liver 
Hyperlipidemia &lipiduria
Epidemiology :-
In children < 15 yrs, nephrotic syndromeprimary renal disease
(~ 98 %)
In adults nephrotic syndrome associated with 2nd
renal disease

Mixed nephritic & nephrotic syndromes :-
MGN , IgA nephropathy, lupus nephritis, Henӧch - schonlein
purpura.
1-Acute diffuse proliferative glomerulonephritis
It is common renal disease , mostly affect children
Causes :- An immune complex disease ,the antigen either
2-Exogenous antigen ( post-infection ) :-
a- Bacterial group A β-hemolytic streptococci or S. pyogenes
b- Viral (HBV, HCV,mumps) or parasitic (malaria ,toxoplasma)
3-Endogenous antigen :- SLE
Pathogenesis:-
*Post-streptococcal pharyngitis (1-4 weeks) anti-Streptococcal
Abs raise .
*The circulating Ag-Ab complex trapped within glomeruli 
activating, complement  glomerular injury .

Pathology :-
Gross picture :-
1-Bilateral renal affection .
2-Enlarged kidneys with tense capsule and subcapsular
small petechae.
3-Cut section Goodly differentiated cortex and medulla
Microscopically :-
A-Light microscopy ;-
1-Glomeruli :- Enlarged & hypercellular (proliferated epithelial
,endothelial and mesangial cells  obstructing capillary lumen
+ fibrin deposition +PNL,s & monocytes infiltration of glomer.
2-Tubules :- Red cell casts.
3-Interstitial tissue ;-Edema +PNL,s infiltration
4-Blood vessels :-Dilated & congested
B-Immunofluorescence:-Diffuse granular deposits of IgG , IgM
& complement C3 along GBM

C-E/M :- Subepithelial electron dense deposits “humps” in case of post-strept
ococcal GN.
*Clinically:- manifested as nephritic syndrome
i->95% recover in childrens :- (1%) proceed to RPGN or 1% chronic GN
ii-In adults 60% recovery rate , the rest proceed to RPGN or chronic renal
failure.
Lab.findings :-
Blood1-hypocomplementemia (C3) 2-increased ASOT
Urine :- Proteinuria ,hyaline casts and red cell casts .

Acute GNAcute GN
(post infectious GN)(post infectious GN)

Crescentic (rapidly progressive GN) (big white man)Crescentic (rapidly progressive GN) (big white man)
DefinitionDefinition :-:-
1-Clinico-pathologic syndrome1-Clinico-pathologic syndrome FormingForming crescentscrescents ( in most( in most
glomeruli).glomeruli).
2-Accompanied by2-Accompanied by a rapid progressive loss of renal functiona rapid progressive loss of renal function
3-Presenting with R.F3-Presenting with R.F  death (within weeks to months).death (within weeks to months).
Etiology :-Etiology :-
1-Primary (idiopathic)1-Primary (idiopathic) (RPGN)(RPGN)
2-Secondary :-2-Secondary :-
a-Post-infectiousa-Post-infectious (RPGN) complicating acute GN.(RPGN) complicating acute GN.
b-Systemic diseasesb-Systemic diseases (SLE ,G.P, vasculitis ,W.G., H. Sch. Purpura ,(SLE ,G.P, vasculitis ,W.G., H. Sch. Purpura ,
Essential cryoglobulinemia)Essential cryoglobulinemia)

type Example
1-Type I (12%) ( Linear deposits (anti-
GBM ab)
2-Type II (44%) ( circulating I.C.)
3-Type III (44%) (pauci-immune)
- Idiopathic
- G.P syndrome
- Idiopathic
- SLE,
- Post-strept. Infection
- H.Sc purpura
- W.G or
- Microscopic poly- angiitis.
Types

Idiopathic RPGN (12%):-Idiopathic RPGN (12%):-
-No history of previous infection or systemic disease-No history of previous infection or systemic disease
-About 1/3 of patients show linear fluorescence-About 1/3 of patients show linear fluorescence  denoting anti-GBMdenoting anti-GBM
diseasedisease
-1/4 have granular I.F-1/4 have granular I.F denoting immunocomplex etiology.denoting immunocomplex etiology.
-1/2 have no Igs and/or immuno-complement deposition.-1/2 have no Igs and/or immuno-complement deposition.
PrognosisPrognosis :- Mostly going to:- Mostly going to CRFCRF
TreatmentTreatment :-:-
1-Plasma exchange Or1-Plasma exchange Or
2-Corticosteroides if oligouria is less severe2-Corticosteroides if oligouria is less severe

Types:
1-Type I – anti-GBM antibody disease :-Idiopathic or G.pasture
syndrome in which anti-GBM antibodies cross react with alveolar BM
 alveolar damage and presenting with pulmonary hemorrhage
Good pasture`s syndromeood pasture`s syndrome
-Autoimmune disease consists of-Autoimmune disease consists of pulmonary hemorrhage and RPGNpulmonary hemorrhage and RPGN..
-It characterized by linear deposition of-It characterized by linear deposition of IgGIgG andand C3C3 on the GBMon the GBM
Morphological features :-
1-Most glomeruli show Crescent formation in Bowman’s space
(proliferated parietal epithelial cells and monocytes ) Glom. damage
healed by scarring
2-Fibrin in Bowman’s capsule  Crescent formation .(treated with
anticoagulants
3- Areas of segmental necrosis within glomeruli
4-patients with substantial (~ 80%) crescents  Progress to R.F

Plasmapheresis :- is helpful to remove circulating anti-GBM Abs in this type of
RPGN
PathologyPathology
GrosslyGrossly ;- Bilateral enlarged ,pale kidneys with surface petechae;- Bilateral enlarged ,pale kidneys with surface petechae
Light microscopicallyLight microscopically :-:-
GlomeruliGlomeruli :-:- Involved glomeruliInvolved glomeruli :-show segmental necrosis , GBM breaks and:-show segmental necrosis , GBM breaks and
CrescentsCrescents  compress glomerulicompress glomeruli
..Uninvolved portionUninvolved portion of the glomerulousof the glomerulous No proliferationNo proliferation
Mechanism of crescents formation :-Mechanism of crescents formation :-
1-Damaged capillaries1-Damaged capillaries  Leak fibrin +migrated mononuclear cells in Bowman`sLeak fibrin +migrated mononuclear cells in Bowman`s
spacespace  stimulate proliferation of parietal epithelial cells .stimulate proliferation of parietal epithelial cells .
2-Deposited fibrin and the Proliferated epithelial cells2-Deposited fibrin and the Proliferated epithelial cells  CrescentsCrescents
3- Fibrosis follow later on .3- Fibrosis follow later on .
E/ ME/ M :- Ruptured GBM ± sub-epithelial deposits.:- Ruptured GBM ± sub-epithelial deposits.
I.F :I.F :- Linear staining of deposited- Linear staining of deposited IgGIgG andand C3C3 along GBM.along GBM.
Lab findings :-Lab findings :- As nephritic syndromeAs nephritic syndrome OOligourialigouria andand azotemiaazotemia
-Blood & urine :- As ADGN-Blood & urine :- As ADGN
FateFate :- Fairly good prognosis , 50% recover . Renal dialysis or transplantation is a:- Fairly good prognosis , 50% recover . Renal dialysis or transplantation is a

2-Type II – immune-complex mediated disease:-
-Can be a complication of any of the immune -complex nephritides
SLE, post –streptococcal , IgA nephropathy,
H.S Purpura
Or idiopathic
-All these show immune- complex granular (lumpy-bumpy) pattern .
-It show characteristic lesion of the underlying diseases (D.D. from type I)
e.g.Diffuse proliferation and leukocytes infiltration  post-infection GN or SLE
Mesangial proliferation  IgA nepropathy and H.S purpura.
plasmapheresis  ineffective ?
3-Type III – pauci-immune type:- No anti-GBM Ab or immune- complexes .
Patients do have ANCA (~90%) . Either c or p patterns , have a role in some vascul-
itides (i.e.,Wegener Granulomatosis or microscopic poly- angiitis )
Clinical:
i) Hematuria Red cell casts in urine
ii) Transplant or chronic dialysis  Most patients

Glomeruli:-
1-Segmental necrosis
2-Focal GBM breaks
3-Focal loss of epith. foot processes
4-Subepithelial lumpy I.C deposits
5-Crescents (prolif.parietal cells
+fibrin(
6-Mesangial cells hyperplasia

Membranous GNMembranous GN
-The commonest cause of-The commonest cause of nephrotic syndrome in adultsnephrotic syndrome in adults ..
-It characterized by-It characterized by diffuse thickening of G.B.M.diffuse thickening of G.B.M.
-It is classified as non-inflammatory-It is classified as non-inflammatory  NO cellular proliferationNO cellular proliferation
1-Idiopathic (85%):-1-Idiopathic (85%):-May be auto-immune disease ( imbalance between Th &Ts cells)May be auto-immune disease ( imbalance between Th &Ts cells)
2- Secondary ,associated with :-2- Secondary ,associated with :-
-- CarcinomaCarcinoma !! (i.e., melanoma, carcinoma of lung and colon ) Or!! (i.e., melanoma, carcinoma of lung and colon ) Or
--Systemic infectionsSystemic infections (HBV, malaria ,Bilh. ) Or(HBV, malaria ,Bilh. ) Or
--DrugsDrugs (Gold , penicillamine , Hg , NSAID).(Gold , penicillamine , Hg , NSAID).
Pathogenesis:-Pathogenesis:-
1-Idiopathic MGN1-Idiopathic MGN :-Auto-immune disease ,the antibodies directed against renal auto-:-Auto-immune disease ,the antibodies directed against renal auto-
antigen subepithelial siteantigen subepithelial site In situ immun-complex activate complementIn situ immun-complex activate complement ProteasesProteases
and oxidantsand oxidants Injury of capillary wallInjury of capillary wall  Leakage of proteinLeakage of protein
2-Secondary MGN2-Secondary MGN :- Initiated through a circulating Ag-Ab complex:- Initiated through a circulating Ag-Ab complex

Morphology :-Morphology :-
Grossly:-Grossly:- Both kidneys areBoth kidneys are enlarged and paleenlarged and pale
A-Light microscopy :-A-Light microscopy :-
1-Glomeruli :1-Glomeruli :- Early- Early lesionlesion  Normal glomeruli .Normal glomeruli . Later onLater on  diffusely thickened GBMdiffusely thickened GBM
2-Tubules :-2-Tubules :- Hyaline droplets .Hyaline droplets .
3-Interstitial tissue :-3-Interstitial tissue :- MNC,s infiltrationMNC,s infiltration
B-I.F:B-I.F:-- Diffuse granular deposits ofDiffuse granular deposits of IgsIgs andand complementcomplement Marked thickening of GBMMarked thickening of GBM 
obliteration of capillary lumen & mesangial sclerosis.obliteration of capillary lumen & mesangial sclerosis.
C-E/M :C-E/M :- Irregular sub-epithelial deposits with loss of epithelial foot processes.- Irregular sub-epithelial deposits with loss of epithelial foot processes.
Clinical :-Clinical :-
a)-Presents mainly by nephrotic syndrome (non-selective proteinuria .No response to steroids) .
b)- 15% Hematuria (Non-nephritic ) .
c) 15-35% hematuria and hypertension .
Fate :-Fate :- It persists in 60% of the cases May end by R.F or R. insufficiency.
Progression of diseaseProgression of disease
1- stage I: Subepithelial deposits (small and granular)
2- stage II: “spikes” of BM protrude between deposits of electron dense material (e.g., IgG, C3)
3-Stage III: Incorporated deposits into GBM .
4-Stage IV : GBM very distorted and damaged

Stage I Stage II
Stage III Stage VI
Spike

a) GBM thickening (i.e.,“membrano”) + Mesangial cell proliferation (“proliferative
”) .It accounts 5-10% of Nephrotic Syndrome in children and adults.
a) Sub-nephrotic stage :- Some patients have hematuria or proteinuria and others
demonstrate a combined nephritic – nephrotic picture.
Types .
i-Type I: mainly idiopathic. Or chronic immune-complex reaction initiated
by ( HBV, HCV, SLE .bacterial endocarditis, Bilharziasis ,α -1 -ATD
,strep.infections )
.with granular deposits of Igs (IgG, IgM) and complement (C3 & C1q and C4), in
subepithelial, sub-endothelial and mesangial positions .It occurs due to activation of
classic complement pathway .
ii) Type II & III) :- “Dense deposit disease”. GBM contain ribbon like deposits
and sub-epithelial humps . Most patients of type II have C3 nephritic factor in their
sera  acts as properdin stabilize C3 convertase activity  It enhances C3
breakdown and causes hypo-complementemia .
pathology
Grossly :- Bilateral kidney enlargement
L/M :- Glomeruli :-  Mesangial cells proliferation and accentuation of glomeular
lobules .PAS stain show capillary wall doubling (double –contour or tram -track
appearance) due to interposition of the mesangial cell inside the capillary loop
Membrano-proliferative GN:-Membrano-proliferative GN:- It characterized byIt characterized by:-:-

PLS & TOXINS
+
IgA
C3
B,D,Mg+
C3bBb (alternate path.C3 convertase)
Properdin
Degrade
C3 C3b
Stabilize
Feed back
C3 Nef
I.H

E/M &I.F.:- It categorized into two types
Type1:- sub-endothelial deposits (complement &Igs)
Type II (dense deposit disease) :- Dense deposits within lamina densa of BM
(only C3 , no antibodies) It reflects alternate complement pathway.
Clinical:
i) It occurs primarily in older children and young adults
ii) It manifested by nephritic or nephrotic syndrome
iii) It reveals low levels of C3 (hypo-complementemia),due to
increased consumption of C3
iv) Do not have post-infectious GN
v) No systemic inflammatory condition
vi) Most progress to end-stage renal failure, regardless of treatment !!
Within 10 Ys
Prognosis :- Type II has a worse prognosis ,being autoimmune in nature
(the patient has nephritic factor in his serum) ,it recurs after transplan.

Minimal change disease (Lipoid nephrosis ,epithelial cell dise.)Minimal change disease (Lipoid nephrosis ,epithelial cell dise.)
Most common cause of Nephrotic syndrome in children < 15 yrs (65%) peak 2-6Ys.
Also in adults (~ 20 %). Associated with Hereditary disease . Or NSAIDs
Etiology :-
1-Idiopathic or
2-Predisposed by R.T.I 25% or routine immunization 10% or atopy
Clinically :- 1-Presented mainly by selective proteinuria (albuminuria )
2-Dramatically respond to corticosteroids with possible recurrence (steroid
Dependence or resistance . 3-High cure rate at puberty.
Pathogenesis:-Immune dysfunction Elaboration of cytokine-like substances 
damaging visceral epithelial cells  Proteinuria.
Morphology :-
Grossly :- Within normal kidney appearance
Light microscopy :- Minimal change in glomeruli .The tubules show lipid laden
epithelial cells (lipoid -nephrosis)
E/M :- Uniform diffuse effacement of “foot” processes of visceral epithelial cells
I/F:- No immune deposition .

Focal / segmental proliferative GNFocal / segmental proliferative GN
a) Only some of the glomeruli and /or segments of individual glomeruli are involved
.Others are normal .
b) It differs from focal segmental glomerulosclerosis .It may be an immune-complex
disease rather than an inflammatory disease
c) Glomeruli are essentially normo-cellular
Pathogenesis:-
Many conditions produce this defect:-
1-Primary (idiopathic) renal disease.
2-Secondary to a systemic disease :-As:- IgA nephropathy,H.Schönlein GN
or W. granulomatosis. –PAN , SBE , Good-pasture`s syndrome
Pathology :-
L/M:- Focal & segmental endothelial cells & mesangial cells proliferation
I.F.:-Mesangial deposits of IgA ± IgG & C3 and fibrin in most cases.
Clinically :-
1-Hematuria (Recurrent)
2-Non nephrotic proteinuria  Nephrotic syndrome .

Focal segmental glomerulosclerosis (epithelial cell and B.M disease)
Some glomeruli (focal) exhibit (segmental) areas of sclerosis whereas others are
normal (Focal segmental)
Occurs in the following setting:
1-Primary (idiopathic) disease (e.g., idiopathic focal segmental glomerulosclerosis)
2-Secondary disease :- due to other conditions ( HIV, heroin addiction, sickle cell
disease , morbid obesity and IgA nephropathy)
3-Adaptive process :- due to nephrectomy or advanced stages of hypertension.
FSGSclerosis differes from MCD by having :-FSGSclerosis differes from MCD by having :-
1-↑ Incidence of hematuria and H.P
2- Proteinuria (non- selective) and Steroids
(poor or no response)
3- 50% of Pts develop CRF (Within 10 years)
5-IgM and C3 are present in selective area.

Pathogenesis :-Pathogenesis :-
1-Idiopathic FSG1-Idiopathic FSG :- It is considered as an accentuation of MCD:- It is considered as an accentuation of MCD marketed bymarketed by
epithelial damageepithelial damage Trapping of plasma proteins in hyperpermeabil fociTrapping of plasma proteins in hyperpermeabil foci HyalinosisHyalinosis
And sclerosis and mesangial cell reaction to protein and fibrin.And sclerosis and mesangial cell reaction to protein and fibrin.
2-Secondary FSG:-2-Secondary FSG:- It occurs as a complication of other diseases (heroin and AIDS)It occurs as a complication of other diseases (heroin and AIDS) 
 Renal functionRenal function Progressive glomerulosclrosis and R.FProgressive glomerulosclrosis and R.F
.Presence of AIDS virus in epithelial cells.Presence of AIDS virus in epithelial cells  augment the epithelial damage .augment the epithelial damage .
Pathology :-Pathology :-
Light microscopyLight microscopy :- The lesion starts in glomeruli at J.G zone ,then spreads outward:- The lesion starts in glomeruli at J.G zone ,then spreads outward
EarlyEarly Focal segmental glomerulosclerosis .Focal segmental glomerulosclerosis .
Later onLater on  Diffuse glomerulosclerolosis + tubular atrophy + Interstitial fibrosis.Diffuse glomerulosclerolosis + tubular atrophy + Interstitial fibrosis.
E/ME/M :- Diffuse effacement of epithelial foot processes and detached cells .Denuded:- Diffuse effacement of epithelial foot processes and detached cells .Denuded
BM . Hypertrophied mesangial cells .BM . Hypertrophied mesangial cells .
I.FI.F.:- Deposition of.:- Deposition of IgMIgM andand C3C3 in hyaline massesin hyaline masses
ClinicallyClinically :- Nephrotic syndrome .Hematuria and:- Nephrotic syndrome .Hematuria and  GFR and H.P are commonGFR and H.P are common
findings.findings.
Fate :-Fate :- Progression to CRF in 50% of cases after (10 Ys).Progression to CRF in 50% of cases after (10 Ys).

IgA nephropathy (Berger`s Disease)
- A major cause of recurrent hematuria .
- It is associated with chronic liver disease (unable to remove circulating I.C )
- IgA and fibronectin found in > 70 % of these patients.
Pathogenesis :-
Ab IgA :- Defective synthesis ,secretion or clearance  IgA nephropathy .
Ag :- Either bacterial, viral or dietary .Hematuria following upper RTI
,GIT or UTI due to increased surface secretion of IgA!!(surface epithelium)
- C1q and C4 (classic pathway activation) are typically absent in serum
- C3 and properdin and IgA are usually present in mesangium and absent in serum
( indicate activation of alternate pathway)
Lab findings
L/M :- It varies includes FPGN , FSGS , MPGN and rarely RPGN
I.F :-Mesangial deposits of IgA+C3 and properdin ,± IgG .
E/M:- Finely granular electron dense deposits in mesangium.
clinical
- Common in young men (15-30 Y)
- Presents with recurrent attacks of hematuria post infections (respiratory,urinary
tract or GIT)

- Mild proteinuria
- Crescent
- Hypertension
- Vascular sclerosis
 poor prognosis  passes to end stage
renal failure (40%) .
Mesangial deposits
IgA+C3 and properdin ,± IgG

Chronic Diffuse Glomerulonephritis:-Chronic Diffuse Glomerulonephritis:-
An end pool of many different renal diseasesAn end pool of many different renal diseases..
Causes:-Causes:-
A -Idiopathic (20%)A -Idiopathic (20%)
B-Secondary to :B-Secondary to :
1-Post-streptococcal GN (1-2%)1-Post-streptococcal GN (1-2%)
2-RPGN (90%)2-RPGN (90%)
3-Membranous GN (50%)3-Membranous GN (50%)
4-Membrano-proliferative GN ( 50%)4-Membrano-proliferative GN ( 50%)
5-Focal glomerulosclerosis (50%)5-Focal glomerulosclerosis (50%)
6-IgA nephropathy ( 40%)6-IgA nephropathy ( 40%)
Diagnosis :-Diagnosis :-
1-In early lesions1-In early lesions :- The primary disease can be recognized:- The primary disease can be recognized
2-In late lesions2-In late lesions :-:- GlomeruliGlomeruli :- hyalinosed .:- hyalinosed . TubulesTubules:-Atrophic .:-Atrophic .Bl.VsBl.Vs :- sclerosed:- sclerosed
that harden the recognition of the initiating diseasethat harden the recognition of the initiating disease

Pathology :-Pathology :-
Grossly :-Grossly :-
-Small and contracted kidneys (< 50gm)-Small and contracted kidneys (< 50gm)
-The capsule :- Thickened ,irregular and adherent to the cortex-The capsule :- Thickened ,irregular and adherent to the cortex
-The cortical surface :- Is diffusely granular & increased peri-pelvic fat-The cortical surface :- Is diffusely granular & increased peri-pelvic fat
-Cut section :- Cortex is thin and atrophic with unremarkable medulla.-Cut section :- Cortex is thin and atrophic with unremarkable medulla.
Microscopically :-Microscopically :-
1-Glomeruli1-Glomeruli :-:- At an early stage it reveals the primary disease ,later on the glomeruli becomeAt an early stage it reveals the primary disease ,later on the glomeruli become
few in numbers , atrophic & acellular and hyalinized .few in numbers , atrophic & acellular and hyalinized .
2-Tubules :2-Tubules :- Tubules related to atrophic glomeruli- Tubules related to atrophic glomeruli Small and atrophic .Degenerated tubularSmall and atrophic .Degenerated tubular
cells with hyaline droplets .and containing eosinophilic casts.cells with hyaline droplets .and containing eosinophilic casts.
3-Interstitium3-Interstitium :- Fibrosis and lymphocytic infiltration:- Fibrosis and lymphocytic infiltration
4-Vessels :-4-Vessels :- arterial and arteriolosclerosis secondary to hypertension .arterial and arteriolosclerosis secondary to hypertension .
5-Patient on5-Patient on long term dialysislong term dialysis show :- 1- Acquired cystic changes 2-Deposition of calciumshow :- 1- Acquired cystic changes 2-Deposition of calcium
oxalate crystals in tubules 3-Calcification of tufts. 4-Adenoma or carcinoma of the kidneyoxalate crystals in tubules 3-Calcification of tufts. 4-Adenoma or carcinoma of the kidney
Clinical courseClinical course :-:-
1-Insidious course1-Insidious course
2-Proteinuria , hypertension and azotemia2-Proteinuria , hypertension and azotemia
3-Episodes of nephritic or nephrotic syndrome3-Episodes of nephritic or nephrotic syndrome

Glomerular lesions associated with systemic diseasesGlomerular lesions associated with systemic diseases
Diabetic glomerulo/sclerosisDiabetic glomerulo/sclerosis (Kimmelstiel-Wilson Disease)(Kimmelstiel-Wilson Disease)
-It produces Nephrotic proteinuria (55% of JDM&30% of ADM , 12-22Y of
diabetes )
-It characterized by diabetic micro-angiopathy (small arteries,arterioles .capillaries)
-Hyaline arteriosclerosis involves both afferent and efferent arterioles , which occur by
progressive accumulation of GBM material .
-It depends upon severity and duration of hyperglycemia !! ??
Etiology :- Origin proteinuria not known (non-nephrotic or nephrotic )
1) EarlyThickening of GBM
2) Lately :-Glomerular enlargement
3) “Diffuse Glomerulosclerosis” refers to enlarged glomeruli with expanded
Mesangium and diffusely thickened GBM
4- Nodular glomerulosclerosis (i.e.,Kimmelstiel-Wilson Disease) – highly specific for
diabetes
5) one of leading causes  CRF in USA
6) Two processes play role in diabetic glomerular lesions
1- Metabolic defect (i.e glycosylation end products that ↑ GBM thickening and ↑
mesangial matrix
2-Hemodynamic effects: - glomerular hypertrophy  development of glomerulo-

Clinical features:-
i) Usually mild proteinuria .
ii) Nephrotic syndrome present → renal failure within 6 yrs. severe proteinuria
usually associated with other signs of advanced diabetes (i.e.,retinopathy)

AmyloidosisAmyloidosis
- Amyloid deposits in 1-B.M of glomerular capillaries 2- Walls of afferent and
efferent arterioles 3-Basement membrane of the collecting tubules .
- Either pry or 2nd
forms
- Congo red (amyloid ) deposits mainly in mesangium and capillaries
ClinicalClinical
i) Proteinuria nephrotic syndrome
ii) progressive glomerular destruction
 death from uremia

Henoch-SchHenoch-Schöönlein Purpuranlein Purpura
Usually occurs in children 2-8 Y , and becomes severe in adults ,oftenly following RTI.
Clinically :-
1- Skin lesions :-Purpura on legs, arms and buttock (leukocyto-clastic vasculitis )
2- Abdominal symptoms :-Pain, vomiting, intestinal bleeding and arthralagia
3-Renal abnormalities:-hematuria , nephrotic syndrome (proteinuria ).Not all these S
& S need to be present.
Pathologically :-
Glomerular lesion :-1-Focal mesangial proliferation 2-Crescentic GN 3- Always
associated with IgA deposition
Course :-
-Resolution is the role (in children )
-CRF  in cases of diffuse lesion or
Nephrotic Syndrome or
crescents.

Bacterial endocarditisBacterial endocarditis :-:-
Immune -complex mediated GN showing morphologic continuum fromImmune -complex mediated GN showing morphologic continuum from focalfocal
Necrotizing GN to diffuse GNNecrotizing GN to diffuse GN , sometimes with crescents (not embolic as, sometimes with crescents (not embolic as
previouslypreviously
thought)thought)
SLE (lupus nephritis) :SLE (lupus nephritis) :
The Kidneys are involved virtually in all cases of SLEThe Kidneys are involved virtually in all cases of SLE
5 Patterns of lupus nephritis5 Patterns of lupus nephritis
ClassClass PathologyPathology ClinicalClinical
II
IIII
(10%(10%((
III(33%III(33%((
NormalNormal By L/M , E/M and I.FBy L/M , E/M and I.F
““Mesangial lupus nephritisMesangial lupus nephritis”” ,slight,slight  inin
mesangial matrix &cells & mesangial Igsmesangial matrix &cells & mesangial Igs
& complement deposits.& complement deposits.
““Focal proliferative GNFocal proliferative GN”” Focal andFocal and
segmental glomerularsegmental glomerular swellingswelling withwith
endothelial and mesangial proliferationendothelial and mesangial proliferation
,PNL,s infiltration +fibrinoid deposits and,PNL,s infiltration +fibrinoid deposits and
capillar y thrombi +subendoth IC deposits.capillar y thrombi +subendoth IC deposits.
10% of patients10% of patients minimalminimal
hematuria or proteinuriahematuria or proteinuria
1-Recurrent1-Recurrent hemturiahemturia
2-Moderate2-Moderate proteinuriaproteinuria
3-Mild3-Mild renal insufficiencyrenal insufficiency

ClassClass PathologyPathology ClinicalClinical
IVIV
(50%)(50%)
V(10%)V(10%)
““Diffuse proliferative GNDiffuse proliferative GN””
-Proliferated (endo. Mesa.epithel.)-Proliferated (endo. Mesa.epithel.)
-Subendothelial deposits (wire--Subendothelial deposits (wire-
looploop”” ..
-Tubular changes ,BM and I.T ,I.C.-Tubular changes ,BM and I.T ,I.C.
deposits .deposits .
““Membranous GN”Membranous GN” diffuselydiffusely
thickened capillay walls andthickened capillay walls and
subepithelial IC deposits.subepithelial IC deposits.
-Either asymptomatic-Either asymptomatic
-Hematuria ,proteinuria ,HP,-Hematuria ,proteinuria ,HP,
-- GFRGFR
--Most severe form with worstMost severe form with worst
prognosis.prognosis.
-Severe proteinuria-Severe proteinuria
-Nephrotic syndrome-Nephrotic syndrome
Hereditary nephritis (Alport syndromeHereditary nephritis (Alport syndrome((
A group of hereditary renal diseases causing primarily GNA group of hereditary renal diseases causing primarily GN..
Clinically :-Clinically :- Commonly affecting males (40Y) .The patient is presented with :- 1-EarCommonly affecting males (40Y) .The patient is presented with :- 1-Ear
Nerve deafness 2-EyeNerve deafness 2-Eye lens (dislocation ,cataract) & corneal dystrophy 3-lens (dislocation ,cataract) & corneal dystrophy 3-
KidneyKidney hematuriahematuria..
PathologicallyPathologically :- The GBM shows :-1-Irregular thickening:- The GBM shows :-1-Irregular thickening
2-lamination and foci of rarefaction (defect in2-lamination and foci of rarefaction (defect in collagen type IVcollagen type IV necessary of BMnecessary of BM

Systemic lupus erythematosis kidney
Thin arrow point to Wire-loop appearance
Thick arrow point to hematoxyphil bodies in B.space

Acute renal failure (ARF) and acute tubular necrosis(ATN)Acute renal failure (ARF) and acute tubular necrosis(ATN)
Acute tubular necrosis (ATN):-Acute tubular necrosis (ATN):- Major cause of ARF. It is reversible .Major cause of ARF. It is reversible .
Acute renal failure:-Acute renal failure:- is a syndrome characterized by acute suppressionis a syndrome characterized by acute suppression
of renal function and presented byof renal function and presented by oliguria ,rarely anuria or polyuriaoliguria ,rarely anuria or polyuria..
Causes of acute renal failure :-Causes of acute renal failure :-
I-Pre-renal :-I-Pre-renal :-
1-Shock1-Shock
2-Vascular obstruction (thrombus ,embolism,atheroscl., PAN )2-Vascular obstruction (thrombus ,embolism,atheroscl., PAN )
3-Hypertension3-Hypertension
II-Renal :-II-Renal :-
1-RPGN 2-Acute pyelonephritis 3-DIC with cortical necrosis 4-ATN1-RPGN 2-Acute pyelonephritis 3-DIC with cortical necrosis 4-ATN
5-Papillary necrosis.5-Papillary necrosis.
III-Post-renal :III-Post-renal :-- Obstructive uropathy.Obstructive uropathy.

Tubulo-interstitial diseases :-Most tubular diseases involve the interstitium
1-Tubular diseases (ATN) :-2 distinct types of tubular diseases.
-Ischemic - or nephrotoxic tubular injury :-
ATN:- It is a clinical entity, characterized by destruction of tubular epithelial cells
and presented clinically by oliguria or anuria . It is caused by ischemia or toxins .
Ischemic ATN :- After shock (sepsis,burns,crush imjury or acute pancreatitis)
.Uncommon after hemorrhagic shock “shock kidney”
Nephrotoxic ATN :-
1-It is caused by drugs (gentamycin,cephalosporine. contrast media, cyclosporine , Hg
,lead, arsenic ,methyl alcohol) and certain toxins as (muschroome ,insecticides and
herbiticides)
2-Massive hemoglobinuria or myoglobinuria (hemolysis)
3-Dehydration and hypoxia
Pathology
Grossly :- Kidneys are enlarged with pale necrotic cortex and congested medulla

Ischemic ATNIschemic ATN :-:-
1-Patchy tubular necrosis1-Patchy tubular necrosis in proximal & distal convoluted tubules and ascendingin proximal & distal convoluted tubules and ascending
Limbs of Henle`s with large skip areas in-betweenLimbs of Henle`s with large skip areas in-between
2-Foci of ruptured BM2-Foci of ruptured BM
Nephrotoxic ATNNephrotoxic ATN :-:- Extensive tubular necrosisExtensive tubular necrosis in whole length of proximal CTin whole length of proximal CT
withwith preserved tubular basement membranepreserved tubular basement membrane .. In both types the distal tubules andIn both types the distal tubules and
collecting ducts containcollecting ducts contain castscasts. +interstitial edema and vascular infiltration by PNL,s. +interstitial edema and vascular infiltration by PNL,s
The recovery phase showThe recovery phase show epithelial regenerationepithelial regeneration (flat tubular cells and mitotic(flat tubular cells and mitotic
Figures , except in areas with BM rupture .Figures , except in areas with BM rupture .
Hg clHg cl  Acidophil inclusions in cellsAcidophil inclusions in cells Lately necrosis & calcification .Lately necrosis & calcification .
CCl4CCl4Fatty changes + necrosis.Fatty changes + necrosis.
Ethyl alcoholEthyl alcohol vacuolar degeneration + Ca oxalate crystals.vacuolar degeneration + Ca oxalate crystals.
Mechanism of oliguria due to ATN:-Mechanism of oliguria due to ATN:- BothBoth ischemia and toxins causeischemia and toxins cause tubulartubular
andand glomerularglomerular damagedamage
1-Tubular damage1-Tubular damage :-:-
a-Arterial V.Ca-Arterial V.C  RA systemRA system GFRGFROliguriaOliguria
b-Cast formation +tubular obstruction and increase intra-tubular prb-Cast formation +tubular obstruction and increase intra-tubular pr
GFRGFROilguriaOilguria
c-Back leak of tubular fluidsc-Back leak of tubular fluids  Press on glomeruli and tubulesPress on glomeruli and tubules  OliguriaOliguria
2-Damaged glomeruli2-Damaged glomeruli  GFRGFR OliguriaOliguria

Ischemia or
Toxins
Direct Gl damage
V.C
Tubular damage
Tubular
back
leak
Oliguria
Obstruction
by casts
intratubular
pressure
GFR
Ischemia or
Toxins
V.C

Treatment protocol
1) Initial phase
2) Maintenance phase
3) Recovery phase
Initial phase :- About 36 hours. It incited by medical , surgical, obstetric
events and characterized by slight oliguria and azotemia
Maintenance phase:- 1-3 weeks and dominated by persistent R.F&hyperkalemia.
It charcterized by :-
a) Marked oliguria (50-400 ml/day)
b) Edema, hyperkalemia and uremia
- Treatment by dialysis ,the patient may die from poor management
Recovery phase :- It characterized by :-
-Polyuria (up to 3 L/day)
-Electrolyte imbalances .
-Increased infection
-About 25% of patients die in this phase
Finally:- The patient recovers with some impairment of renal function

Feature Ischemic ATN Nephrotoxic ATN
1-Synonymus
2-Frequency
3-major causes
3-Gross picture
4-Microscopic
5-Prognosis
Lower(distal)nephron nephrosis,
anoxic nephrosis,shock kidney
More common (80%)
Shock,crush injures,mismatched blood
transfusion
Enlarged kidney,swollen ,cut section
pale cortex ,dark medulla.
1-Distal damage more prominent
2-Focal tubular necrosis
3-Regenerating epithelium
4-casts,hayline,pigment,myoglobin
5-BM disrupted
Worse
Upper( proximal) nephron
nephrosis,toxic ATN
Less common
Poisons ,heavy metals ,certain
drugs
Similar to ischemic ATN
1-Proximal tubular damage
more prominent
2-More diffuse necrosis
3-Regenerating epithelium
4-Luminal dystrophic
calcification
5-BM intact
Good

2- Interstitial diseases (nephritis):-2- Interstitial diseases (nephritis):-
A-Infective :-A-Infective :-
1-Acute &chronic pyelonephritis1-Acute &chronic pyelonephritis
2-T.B pyelonephritis2-T.B pyelonephritis
3-Pyonephrosis3-Pyonephrosis
4-Pyemic abscesses of the kidney4-Pyemic abscesses of the kidney
5-Other infections (viruses,parasitic)5-Other infections (viruses,parasitic)
B-Non-infective :-B-Non-infective :-
1-Acute hypersensitivity interstitial nephritis1-Acute hypersensitivity interstitial nephritis
2-Analgesic abuse (phenacetin) nephropathy2-Analgesic abuse (phenacetin) nephropathy
3-Balkan nephropathy3-Balkan nephropathy
4-Urate & gout nephropathy4-Urate & gout nephropathy
5-Radiation nephritis5-Radiation nephritis
6-Transplant rejection6-Transplant rejection
7-Nephrocalcinosis7-Nephrocalcinosis
8-Idiopathic interstitial nephritis .8-Idiopathic interstitial nephritis .

Urinary tract infection (UTI) and pyelonephritis(PN)Urinary tract infection (UTI) and pyelonephritis(PN)
Definitions :-Definitions :-
Cystitis :-Cystitis :- Inflammation of urinary bladderInflammation of urinary bladder
PyelitisPyelitis :-Inflammation of renal pelvis:-Inflammation of renal pelvis
NephritisNephritis :-Inflammation of interstitial tissue of the kidney:-Inflammation of interstitial tissue of the kidney
PyelonephritisPyelonephritis :- Inflammation of interstitial tissue of the kidney and renal pelvis:- Inflammation of interstitial tissue of the kidney and renal pelvis
NephrosisNephrosis:- Renal tubules diseases .:- Renal tubules diseases .
PyonephrosisPyonephrosis:-:- Severe suppurative inflammation of the kidney (sac of pus)Severe suppurative inflammation of the kidney (sac of pus)
Predisposing factors of UTIPredisposing factors of UTI:-The normal kidney is resistant to organisms except under:-The normal kidney is resistant to organisms except under
certain pathological conditionscertain pathological conditions  Infection can occur.Infection can occur.
1-Obstructive uropathy & Neurogenic bladder1-Obstructive uropathy & Neurogenic bladder
2-Catheterization &instrumentations of the urinary tract.2-Catheterization &instrumentations of the urinary tract.
3-Vesico-ureteral reflex3-Vesico-ureteral reflex
4-Pregnancy4-Pregnancy
5-Congenital anomalies of UT5-Congenital anomalies of UT
6-D.M. & Immunosuppression6-D.M. & Immunosuppression
7-It is common in females (15-45Ys)(short wide urethera , wetted perineum, absence of7-It is common in females (15-45Ys)(short wide urethera , wetted perineum, absence of
antibacterial prostatic secretion , hormonal effect of estrogen and pregnancy)antibacterial prostatic secretion , hormonal effect of estrogen and pregnancy)

Causative organisms :-Causative organisms :-
1-Normal fecal flora (85%) of UTI1-Normal fecal flora (85%) of UTI
2-E.coli , Proteus, Klebsiella , enterobacter , streptococcal fecalis , staphylococci.2-E.coli , Proteus, Klebsiella , enterobacter , streptococcal fecalis , staphylococci.
Routes of infection :-Routes of infection :-
1-Hematogenous spread1-Hematogenous spread :- S:- Septicemia &infective endocarditis (staph.&E.coliepticemia &infective endocarditis (staph.&E.coli.).) reachreach
the kidney by blood streamthe kidney by blood stream  infectioninfection
2-Ascending infection2-Ascending infection :-:- Through urethera,bladder ,vesico-ureteral reflux or Intra-Through urethera,bladder ,vesico-ureteral reflux or Intra-
renalrenal
reflux (through blunted or concave renal papille) (E.coli , proteus or enterobacter),passreflux (through blunted or concave renal papille) (E.coli , proteus or enterobacter),pass
through patent renal tubules at the papillae (commonly at upper and lower poles of thethrough patent renal tubules at the papillae (commonly at upper and lower poles of the
kidney)kidney)
3-Descending infection3-Descending infection :-:-Through peri-ureteral lymphatic or through urineThrough peri-ureteral lymphatic or through urine
Manifestaions of UTI:-Manifestaions of UTI:-
1-Asymptomatic bacteruria ( High bacterial count in urine )1-Asymptomatic bacteruria ( High bacterial count in urine )
2-Urgency and frequency and dysuria2-Urgency and frequency and dysuria
3-Flank pain ,fever and chills.3-Flank pain ,fever and chills.
4-Pus casts in urine4-Pus casts in urine  pyelonephritispyelonephritis
5-Number of bacteria > 103 to 105 indicate infection rather than contamination5-Number of bacteria > 103 to 105 indicate infection rather than contamination

Acute pyelonephritis :-Acute pyelonephritis :-
Definition :-Definition :- Acute kidney infectionAcute kidney infection
with patchy suppurative infl+tubularwith patchy suppurative infl+tubular
necrosis + pus castsnecrosis + pus casts
GrosslyGrossly :- Either normal or enlarged:- Either normal or enlarged
kidney.Small surface abscesseskidney.Small surface abscesses
or large sized abscess .or large sized abscess .
Microscopically ;Microscopically ;--
1-Early1-Early:-Diffuse interstitial infiltration:-Diffuse interstitial infiltration
by PNL,sby PNL,s
2-Later on2-Later on ,tubular infiltration by,tubular infiltration by
PNL,s and formation of manyPNL,s and formation of many
abscesses ,extension of polymorphs toabscesses ,extension of polymorphs to
collecting tubules forming pus casts.collecting tubules forming pus casts.
Glomeruli , resist this acute inflamma-Glomeruli , resist this acute inflamma-
tion till a large area of necrosis ortion till a large area of necrosis or
fungal infection can occurs.fungal infection can occurs.
ClinicallyClinically :- As UTI:- As UTI
Chronic pyelonephritis and refluxChronic pyelonephritis and reflux
nephropathynephropathy ..It is tubulo-interstitialIt is tubulo-interstitial
inflammationinflammation  cortico-medullary scarscortico-medullary scars
overlying dilated blunted and deformedoverlying dilated blunted and deformed
calyces.and CRF in 11-20% of casescalyces.and CRF in 11-20% of cases
Two forms :-Two forms :-
1-Obstructive CPN (enteric bact.)1-Obstructive CPN (enteric bact.)
Due to obstructive uropathyDue to obstructive uropathy  multiplemultiple
recurrences of infectionsrecurrences of infections CPNCPN
2-Reflux nephropathy2-Reflux nephropathy :-:- caused bycaused by
superadded infection over vesico-ureteralsuperadded infection over vesico-ureteral
reflux and intra-renal refluxreflux and intra-renal reflux
Pyelography :- asymmetrical contractedPyelography :- asymmetrical contracted
kidney with coarse scarkidney with coarse scar
PathologyPathology
Visible scarring and deformity of the pelvi-Visible scarring and deformity of the pelvi-
calyceal system.calyceal system.

Fate :-Fate :-
1-Renal abscess & Perinephric abscess1-Renal abscess & Perinephric abscess
2-Pyonephrosis (if obstruction occurs)2-Pyonephrosis (if obstruction occurs)
3-Renal scars and fibrosis.3-Renal scars and fibrosis.
4-Chronic pyelonephritis4-Chronic pyelonephritis
6-Necrotizing papillitis in diabetics6-Necrotizing papillitis in diabetics
Severe acute pyelonephritis +D.M.Severe acute pyelonephritis +D.M.
.Ischemic and supp.necrosis in tips of the.Ischemic and supp.necrosis in tips of the
renal papillaerenal papillae papillay necrosispapillay necrosis
(appears grayish white well demarcated(appears grayish white well demarcated
necrotic zones in form of coagulativenecrotic zones in form of coagulative
necrosis surrounded by PNL,s.necrosis surrounded by PNL,s.
Bilateral renal affectionBilateral renal affection  unequalunequal
contraction .contraction .
Diffuse or patchy fibrosis,scarring of theDiffuse or patchy fibrosis,scarring of the
Pelvicalcyseal systemPelvicalcyseal system  kidneykidney
deformity .Polar scar and blunt calyx indeformity .Polar scar and blunt calyx in
chronic reflux diseasechronic reflux disease
..
1-Tubules :1-Tubules :-- Dilated with atrophic lining andDilated with atrophic lining and
containing eosinophilic casts ( tubular thyr-containing eosinophilic casts ( tubular thyr-
oidization)oidization)
2-Interstitial tissue2-Interstitial tissue ;- fibrosis ,diffuse;- fibrosis ,diffuse
lymphocytic infiltrateslymphocytic infiltrates
3-Glomeruli :3-Glomeruli :- First- First normal .Then withnormal .Then with
increased periglomerular fibrosisincreased periglomerular fibrosisFocalFocal
segmental glomerulosclerosissegmental glomerulosclerosisproteinuria.proteinuria.
4-Blood vessels4-Blood vessels:- Arteriosclerotic changes due:- Arteriosclerotic changes due
to hypertension .to hypertension .

Non infectious – interstitial nephritis
Caused by:
i) Drugs
ii) Metabolic disorders (hypokalemia)
iii) Radiation injury
iv) Immune reactions
Acute Drug –Induced (Hypersensitivity) Interstitial Nephritis :-
It occurs 2-40 days after exposure to various drugs as (methicillin, ampicilline, rifam-
picin ,furosemide thiazides various NSAID ,phenin ,cimitidine).Withdrwal of the drug
 recovery in most patients.
C/P :-C/P :-
1-Fever
2-Transient eosinophilia
3-Skin rashes
4-Hematuria
5-Mild proteinuria
6-Sterile pyouria
7-Azotemia & ARF

Mechanism :-Mechanism :- Presence of latent period ,IgG,IgE ,MNC,s ,granulomatous infiltratePresence of latent period ,IgG,IgE ,MNC,s ,granulomatous infiltrate
,as well as,positive skin test denotes an immunological reaction .The drug acts as a,as well as,positive skin test denotes an immunological reaction .The drug acts as a
hapten that react with the tubular cell cytoplasm causing its injury byhapten that react with the tubular cell cytoplasm causing its injury by type Itype I and typeand type
IV hypersensitivityIV hypersensitivity reaction .reaction .
Analgesic NephropathyAnalgesic Nephropathy
large quantities of analgesics for long periodslarge quantities of analgesics for long periods  chronic tubulo-interstitial nephritis +chronic tubulo-interstitial nephritis +
renal papillary necrosis . ( e.g aspirin, caffeine, acetaminophen , codeine, phenacetin)renal papillary necrosis . ( e.g aspirin, caffeine, acetaminophen , codeine, phenacetin)
Mechanism :-Mechanism :-
The drugs act together causing firstly papillary necrosis and secondary tubulointer-The drugs act together causing firstly papillary necrosis and secondary tubulointer-
stitial nephritisstitial nephritis
C/P:-C/P:-
1-Polyuria 2-Headache 3-Anemia 4-GIT symptoms 5-Pyouria UTI 6-HP.1-Polyuria 2-Headache 3-Anemia 4-GIT symptoms 5-Pyouria UTI 6-HP.
7-CRF7-CRF
Fate :-Fate :-
Drug withdrawalDrug withdrawal stabilizes renalstabilizes renal
function . Increased risk of TCCfunction . Increased risk of TCC

MorphologyMorphology :-:-
GrosslyGrossly :-:-Normal or reduced kidney size with increased or decreasedNormal or reduced kidney size with increased or decreased
cortical thicknesscortical thickness..
MicroscopicallyMicroscopically :-:- Patchy necrosis of papillaePatchy necrosis of papillae  become complete ,lately ghosts ofbecome complete ,lately ghosts of
tubules and foci of dystrophic calcification with cortical atrophy of tubules and fibrosistubules and foci of dystrophic calcification with cortical atrophy of tubules and fibrosis
Miscellanous tubulointerstitial diseasesMiscellanous tubulointerstitial diseases
1-Urate nephropathy1-Urate nephropathy
2-Hypercalcimia2-Hypercalcimia
3-Multiple myeloma3-Multiple myeloma
4-Radiation nephritis4-Radiation nephritis
Multiple myeloma (myeloma nephrosis)Multiple myeloma (myeloma nephrosis)
Multiple myelomaMultiple myeloma  myeloma nephrosis,with casts in DCT and collecting ducts .myeloma nephrosis,with casts in DCT and collecting ducts .
Casts formed ofCasts formed of Bence-Jones proteinsBence-Jones proteins ,,Tamm-Horsfall poteinsTamm-Horsfall poteins andand albumin.albumin.
Multinucleated giant cellsMultinucleated giant cells are found around the casts.The epithelial cells lining theare found around the casts.The epithelial cells lining the
cast-filled tubules become necrotic or atrophic because of toxic action of the Bence-cast-filled tubules become necrotic or atrophic because of toxic action of the Bence-
jones proteins .Metastatic calcification may be encountered . Nodular glomerular lesionjones proteins .Metastatic calcification may be encountered . Nodular glomerular lesion
are present .are present .

 Pyelonephritis can also occur due to increased liability to infectionPyelonephritis can also occur due to increased liability to infection
.Interstitial infiltration by abnormal plasma cells..Interstitial infiltration by abnormal plasma cells.

Diseases of blood vesselsDiseases of blood vessels
Systemic Hypertension :-Systemic Hypertension :- elevated systemic blood pressure above 140/90 mmHgelevated systemic blood pressure above 140/90 mmHg
Types of hypertensionTypes of hypertension :-:-
Primary or idiopathicPrimary or idiopathic :- The commonest (90%):- The commonest (90%)
Secondary hypertensionSecondary hypertension :-:- caused bycaused by
Renal causesRenal causes EndocrineEndocrine vascularvascular NeurogenicNeurogenic
1-Acute GN1-Acute GN
2-CRF2-CRF
3-R.A.stenosis3-R.A.stenosis
4-Renal vasculitis4-Renal vasculitis
5-Renin producing5-Renin producing
TrTr
1-Cushing`s syndrome1-Cushing`s syndrome
2-Oral pills2-Oral pills
3-Pheochromocytoma3-Pheochromocytoma
4-Acromegaly4-Acromegaly
5-Grave`s disease5-Grave`s disease
1-Coarctation aorta1-Coarctation aorta
2-A.S2-A.S
3-PAN3-PAN
11--PsychogenicPsychogenic
22--I.C.PI.C.P
33--PolyneuritisPolyneuritis
..othersothers
Factors involved in regulation of Bl.Pr.
1- Vasoconstrictors :- Factors regulating peripheral resistance, include
angiotensin II , catecholamine, thromboxane, L.Ks and endothelin.

2-Vasodilators2-Vasodilators :- Kinines ,PGs , lactic acid , H+ and adenosine.:- Kinines ,PGs , lactic acid , H+ and adenosine.
3-Factors regulating C.O3-Factors regulating C.O. :- Blood volume ( which is regulated by Na. :- Blood volume ( which is regulated by Na
load, mineralo-corticoids , natriuretic factors).Heart rate , strock volumeload, mineralo-corticoids , natriuretic factors).Heart rate , strock volume
and contractility.and contractility.
4-Regional autoregulation4-Regional autoregulation :-:-blood volumeblood volume V.C and vice versa.V.C and vice versa.
Mechanism of renal hypertensionMechanism of renal hypertension
The kidney producesThe kidney produces reninrenin  angiotensin Iangiotensin Iangiotensin IIangiotensin II  on bl. Vson bl. Vs
V.CV.C and on adrenal cortex producingand on adrenal cortex producing aldosteronaldosteronsalt and water ret.salt and water ret.
Causes of increased renin secretionCauses of increased renin secretion :-:-
1-Unilateral renal artery stenosis (ischemia)1-Unilateral renal artery stenosis (ischemia)
2-Malignant hypertension2-Malignant hypertension
3-Vasculitis of renal blood vessels3-Vasculitis of renal blood vessels
4-Some cases of unilateral PN.or CRF4-Some cases of unilateral PN.or CRF
5-Renin secreting trs5-Renin secreting trs
6-RCC or Wilm`s Tr6-RCC or Wilm`s Tr

Kidney has important role in sodium homeostasisKidney has important role in sodium homeostasis:-:-
--Via its response to aldosteron,GFR and nutriuretic factors . Failure of these systemVia its response to aldosteron,GFR and nutriuretic factors . Failure of these system
Na retentionNa retention  H.P (e.g CRFH.P (e.g CRF((
--The loss of V.D substances of renal origin (PAF ,Kinins and PGI2)The loss of V.D substances of renal origin (PAF ,Kinins and PGI2)hypertensionhypertension
(renoprival H.P(renoprival H.P((
Mechanism of essential hypertensionMechanism of essential hypertension
No obvious cause butNo obvious cause but:-:-
11--Genetic predisposition and environmental factors are importantGenetic predisposition and environmental factors are important
22--Behviour patterns ,stress , obesity,oral pillsBehviour patterns ,stress , obesity,oral pills increase riskincrease risk
33--High sodium intake in genetically predisposed patientHigh sodium intake in genetically predisposed patient..

Defect in renal Sod
excretion
+
Excess salt intake
Inadequate sod excretion
Salt &H2O retention
plasma &ECF vol.
C.O autoregulation
Hypertension
Neurohormonal release
+
Excess salt intake
vascular reactivity
 Naturitic hormone
Total P.R

Diseases of renal blood vesselsDiseases of renal blood vessels :-:-
Types:-Types:-
1-Atherosclerotic kidney 2-Arteriolosclerotic kidney 3-Polyarteritis nodosa1-Atherosclerotic kidney 2-Arteriolosclerotic kidney 3-Polyarteritis nodosa
4-Infarction kidney 5-Bilateral cortical necrosis 6-Necrosis of the renal papillae.4-Infarction kidney 5-Bilateral cortical necrosis 6-Necrosis of the renal papillae.
1-Atherosclerotic (senile) kidney :-1-Atherosclerotic (senile) kidney :-
This caused by atheroma of the renal arteryThis caused by atheroma of the renal artery Infarction ,ischemic atrophy and fibrosisInfarction ,ischemic atrophy and fibrosis
The kidney is contracted with an irregular outer surface due to depressed scars over theThe kidney is contracted with an irregular outer surface due to depressed scars over the
areas of healed infarction .areas of healed infarction .
2-Arteriolosclerotic kidney:-2-Arteriolosclerotic kidney:-
A-Benign nephrosclerosis:-A-Benign nephrosclerosis:- It refers to renal changes in cases of benign hypertensionIt refers to renal changes in cases of benign hypertension
Grossly :-Grossly :- Bilateral uniformly atrophic kidneys with finely granular outer surfacesBilateral uniformly atrophic kidneys with finely granular outer surfaces
11--Hyaline arteriolosclerosisHyaline arteriolosclerosis :-Hyaline thickening of arteriolar walls with obliterated:-Hyaline thickening of arteriolar walls with obliterated
lumenslumens
2-All kidney structures undergo2-All kidney structures undergo ischemic atrophyischemic atrophy :-:-
a-Tubular atrophic changes b-Diffuse glomerulosclerosis followed by hyalinosis ofa-Tubular atrophic changes b-Diffuse glomerulosclerosis followed by hyalinosis of
the tuft c-Interstitial tissue fibrosis and lymphocytic infiltratethe tuft c-Interstitial tissue fibrosis and lymphocytic infiltrate

Clinical picture :-
a) Mild oliguria
b) Slight loss of concentrating mechanism and  GFR
c) Mild degree of proteinuria is a constant finding
d)These patients usually die from hypertensive heart disease or cerebrovascular
disease rather than from renal disease
B-Malignant nephrosclerosis:-
Causes:-
1-Chronic benign hypertension  arteriolar wall injury 2-Arteritis .
In both conditions :-
A-Increased vascular permeability to fibrinogen along with endothelial injury and
platelets deposition fibrinoid necrosis.
B-Thrombosis with intimal hyperplasia narrowing of vascular lumens
C-Narrowed afferent vessels stimulate R-A system  More elevated blood pressure.
Grossly :- Kidney size either normal or slightly shrunken with surface hemorrhagic
petechiae (flea-bitten appearance)
Microscopically :-:- Necrotizing arteriolitisNecrotizing arteriolitis (arteriolar fibrinoid necrosis and infiltration(arteriolar fibrinoid necrosis and infiltration
by PNL,s .large arterioles show hyperplastic arteriolosclerosis (onion- skin).by PNL,s .large arterioles show hyperplastic arteriolosclerosis (onion- skin).

Arteriolosclerosis Malignant hyprtension Hypeplastic
arteriolosclerosis
Glomerulosclerosis Necrotizing arteriolitis
Hyaline arterioloscl.

Clinical picture (Diastolic bl. pressure > 130 mmHg,):-
1-Early symptoms due to ↑ I.C.P .Headache, nausea, vomiting and visual impairments
2-Hypertensive crisis(loss of consciousness, convulsions proteinuria and hematuria
(micro- or macro-)
3- Papilledema , encephalopathy, CV disorders, renal .F.
Fate :-
90% deaths due to uremia
10% deaths due to CV or cerebral hemorrhage

.Renal Artery StenosisRenal Artery Stenosis:-(Common in females 20-30Ys):-(Common in females 20-30Ys)
Causes:-Causes:-
1- ~ 70 % due to atheromatous plaque at origin of renal artery
2-Second leading cause is fibromuscular dysplasia of renal artery (hyperplasia of all
layers)
- Unilateral RAS is uncommon cause of hypertension (2-4% of renal hypertension )
Surgical treatment:- Cure rate :-Surgical treatment:- Cure rate :-
1-90% in fibromuscular dysplasia1-90% in fibromuscular dysplasia
2-60-75% in atherosclerotic stenosis.2-60-75% in atherosclerotic stenosis.
Renal cortical necrosisRenal cortical necrosis:-:-
CausesCauses:-It occurs due to thrombosis of small renal arteries &arterioles due to:-:-It occurs due to thrombosis of small renal arteries &arterioles due to:-
1-Toxemia of pregnancy1-Toxemia of pregnancy
2-Infections e.g pneumonia ,diphtheria ,scarlet fever2-Infections e.g pneumonia ,diphtheria ,scarlet fever
MorphologyMorphology :-Complete coagulative necrosis of the cortex of both kidneys.:-Complete coagulative necrosis of the cortex of both kidneys.
ClinicallyClinically :- Oliguria ,anuria:- Oliguria ,anuria  Acute renal failure.Acute renal failure.

Renal diseases associated with micro-angiopathic hemolytic anemiaRenal diseases associated with micro-angiopathic hemolytic anemia
A group of diseases with overlapping clinical manifestation :-A group of diseases with overlapping clinical manifestation :-
1-Microangiopathic hemolytic anemia1-Microangiopathic hemolytic anemia
2-Thrombocytopenia2-Thrombocytopenia
3-Renal failure3-Renal failure
4-Manifestations of DIC4-Manifestations of DIC  all are characterized by thrombosis of the interlobularall are characterized by thrombosis of the interlobular
arteries ,afferent arterioles and glomeruli , with necrosis and thickening of the vesselarteries ,afferent arterioles and glomeruli , with necrosis and thickening of the vessel
walls .The morphologic changes are similar to those of malignant hypertensionwalls .The morphologic changes are similar to those of malignant hypertension
,either preceds it or not associated with.,either preceds it or not associated with.
These diseases include :-These diseases include :-
1-Childhood and adulthood hemolytic uremic syndromes1-Childhood and adulthood hemolytic uremic syndromes
2-Thrombotic thrombocytopenic purpura.2-Thrombotic thrombocytopenic purpura.
3-Scleroderma3-Scleroderma..
All these diseases are caused by endothelial cell injury or intravascular coagulationAll these diseases are caused by endothelial cell injury or intravascular coagulation

Childhood hemolytic uremic sy.Childhood hemolytic uremic sy.
It produces ARF after GIT trouble & inf-It produces ARF after GIT trouble & inf-
Luenza .Up to 75% of patients are infectedLuenza .Up to 75% of patients are infected
with verocytotoxin producing E.coli.with verocytotoxin producing E.coli.
UndercookedUndercooked humburgerhumburger
ManifestaionsManifestaions :-:-
Sudden oliguria,hematuria,microagiop-Sudden oliguria,hematuria,microagiop-
athic hemolytic anemia and sometimesathic hemolytic anemia and sometimes
neurological signs.H.Pneurological signs.H.P
Pathogenesis:-Pathogenesis:-
Shigella toxins affects endotheliumShigella toxins affects endothelium
↑↑ adhesion of leukocytes.adhesion of leukocytes.↑↑ endothelinendothelin
andand ↓↓ NO. Endothelial lysis (in presenceNO. Endothelial lysis (in presence
of cytokines such as TNF).These changesof cytokines such as TNF).These changes
favour thrombosis and V.Cfavour thrombosis and V.C
. verocytotoxin can directly bind to Platletes. verocytotoxin can directly bind to Platletes
and cause activationand cause activation
-Renal cortical necrosis.-Renal cortical necrosis.
-Gl.capillary wall thickening-Gl.capillary wall thickening
(deposition of fibrin)(deposition of fibrin)
-Arteriolar fibrinoid necrosis, intimal Hyper--Arteriolar fibrinoid necrosis, intimal Hyper-
plasia and thrombi. most patients recover inplasia and thrombi. most patients recover in
few weeks, with proper care (i.e., dialysis,few weeks, with proper care (i.e., dialysis,
etc); < 5% lethalityetc); < 5% lethality
Adulthood HUSAdulthood HUS
Similar to that of children andSimilar to that of children and
arises in these sittingsarises in these sittings
1-In women with complicated pregnancy1-In women with complicated pregnancy
(retained placenta)(retained placenta)
2-In postpartum women(P.P RF)2-In postpartum women(P.P RF)
1-3 months after labour1-3 months after labour
3-As a complication of oral pills.3-As a complication of oral pills.
4-in Association with typhoid fever,E.coli4-in Association with typhoid fever,E.coli
,septicemia ,viral infection and,septicemia ,viral infection and
shigellosisshigellosis..
Familial HUSFamilial HUS
recurrent thromboses (~ 50%lethality)recurrent thromboses (~ 50%lethality)
deficiency of complement regulatorydeficiency of complement regulatory
protein e.g Factor Hprotein e.g Factor H

Idiopathic Thrombotic thrombocytopenic purpura.Idiopathic Thrombotic thrombocytopenic purpura.
It differes from HUS by itsIt differes from HUS by its CNS involvemenCNS involvement.Renal involvement in only 50% of casest.Renal involvement in only 50% of cases
.There is biochemical evidence of I.V coagulation . Exchange transfusion and steroid.There is biochemical evidence of I.V coagulation . Exchange transfusion and steroid
TxTx →→ mortality rate to < 50%mortality rate to < 50%
Atheroembolic renal disease:-Atheroembolic renal disease:-
Emboli of cholesterol crystals embolizes from aortic aneurysm or during cannulaizationEmboli of cholesterol crystals embolizes from aortic aneurysm or during cannulaization
.They lodge in intra-renal vessels.They lodge in intra-renal vessels arterial narrowing and ischemic injury .arterial narrowing and ischemic injury .
Renal infarctRenal infarct :-:-Kidney receive about 25% of C.OKidney receive about 25% of C.O
Causes of kidney infarctionCauses of kidney infarction
1-Atrial fibrillation1-Atrial fibrillation
2-Myocardial infarction complicated by mural thrombosis.2-Myocardial infarction complicated by mural thrombosis.
Manifestaions :-Manifestaions :-
1-Asymptomatic1-Asymptomatic
2-Pain &hematuria2-Pain &hematuria
3-Hypertension.3-Hypertension.

Urinary tract obstruction (Obstructive uropathy)Urinary tract obstruction (Obstructive uropathy)
Causes :-Causes :-
1-Urethral causes1-Urethral causes:-(congenital anomalies,phimosis,U.valve stricture,uretheritis and:-(congenital anomalies,phimosis,U.valve stricture,uretheritis and
rarely uretheral tumor )rarely uretheral tumor )
2-Prostatic causes2-Prostatic causes:- BPH,prostatic tumor,prostatitis:- BPH,prostatic tumor,prostatitis
3-U.bladder3-U.bladder:- bladder neck obstruction. bilharz. ,stone ,tumor, neurogenic bladder,:- bladder neck obstruction. bilharz. ,stone ,tumor, neurogenic bladder,
4-Ureters4-Ureters :- Ureteral stenosis ,stone ,sloughed papillae,clots , tumor,ureteritis.Kinking.:- Ureteral stenosis ,stone ,sloughed papillae,clots , tumor,ureteritis.Kinking.
5-Kidney5-Kidney :- Stone,tumor,abbarant renal artery,cong.stenosis.uretropelvic stricture:- Stone,tumor,abbarant renal artery,cong.stenosis.uretropelvic stricture
6-pressure by pregnant uterus ,retropreitoneal fibrosis6-pressure by pregnant uterus ,retropreitoneal fibrosis
Effects:-Effects:-ObstructionObstruction Infection and stone formation .Long term unrelievedInfection and stone formation .Long term unrelieved
obstructionobstruction HydronephrosisHydronephrosispyonephrosis and renal atrophypyonephrosis and renal atrophy
Hydronephrosis:-Hydronephrosis:- It is marked distension of the pelvi-calyceal system with urineIt is marked distension of the pelvi-calyceal system with urine
caused by partial and intermittent obstruction of the urinary tract ,followed by renalcaused by partial and intermittent obstruction of the urinary tract ,followed by renal
tissue atrophy .Unilateral ( partial or complete obstruction)tissue atrophy .Unilateral ( partial or complete obstruction) remain silent for longremain silent for long
period .Bilateral partial obstructionperiod .Bilateral partial obstruction  Polyuria, acquired distal tubular acidosisPolyuria, acquired distal tubular acidosis
+salt wasting +renal calculi +Tubulo-interstitial nephritis +atrophy and HP.+salt wasting +renal calculi +Tubulo-interstitial nephritis +atrophy and HP.
1-Hydronephrosis either unilateral or bilateral depending on the site of obstruction1-Hydronephrosis either unilateral or bilateral depending on the site of obstruction

2-Either intrarenal or extrarenal according to position of the renal pelvis2-Either intrarenal or extrarenal according to position of the renal pelvis
3-Above the site of obstruction the urinary tract is distended by urine3-Above the site of obstruction the urinary tract is distended by urine
4-When pelvis and calyces are distended ,pressure atrophy is exerted upon pyramids4-When pelvis and calyces are distended ,pressure atrophy is exerted upon pyramids
Flattened pyramids with progressive renal atrophy.Flattened pyramids with progressive renal atrophy.
A-Enlarged kidney with a nodular surfaceA-Enlarged kidney with a nodular surface
B-Cut sectionB-Cut section  multilocular sacs filled with urine,connected with each others and withmultilocular sacs filled with urine,connected with each others and with
Pelvi-calcyceal system (D.D polycystic kidney)Pelvi-calcyceal system (D.D polycystic kidney)
C-Thin and atrophic intervening renal tissueC-Thin and atrophic intervening renal tissue
1-Glomeruli :- Firstly spared ,later they undergo atrophy as well.1-Glomeruli :- Firstly spared ,later they undergo atrophy as well.
2-Tubules :- Early tubular dilatation ,followed by atrophy and replaced by fibrosis.2-Tubules :- Early tubular dilatation ,followed by atrophy and replaced by fibrosis.
3-Interstitial tissue :- Fibrosis with compression and obliterated blood vessels.3-Interstitial tissue :- Fibrosis with compression and obliterated blood vessels.
Clinical course :-Clinical course :-
1-Dull ache1-Dull ache painpain and sensation of heaviness in renal angleand sensation of heaviness in renal angle
2-Obstruction2-Obstruction  stasis and infectionstasis and infection  stonestone formationformation
3-Urinary tract infection3-Urinary tract infection pyonephrosis or pyelonephritispyonephrosis or pyelonephritis ..
4-Renal atrophy4-Renal atrophy  renal ischemiarenal ischemia  HypertensionHypertension ..
5-Bilateral hydronephrosis5-Bilateral hydronephrosisUremiaUremia
6-Obstruction below level of U.B.6-Obstruction below level of U.B. trabeculation of bladder wall and diverticulaetrabeculation of bladder wall and diverticulae

PyonephrosisPyonephrosis
DefinitionDefinition :-:- Distended pelvis and calyces by pus (kidneyDistended pelvis and calyces by pus (kidney  as a bag of pus) followedas a bag of pus) followed
by pressure atrophy and fibrosis of renal tissueby pressure atrophy and fibrosis of renal tissue..
1-Primary :- It starts de novo1-Primary :- It starts de novo
2-Secondary to chronic obstructive pyelonephritis or infected hydronephrosis2-Secondary to chronic obstructive pyelonephritis or infected hydronephrosis..
The kidney is enlarged with bossy outer surface .Pelvi-calyceal system is dilated as aThe kidney is enlarged with bossy outer surface .Pelvi-calyceal system is dilated as a
multilocular cysts filled with pus.Intervening renal tissue is atrophic and fibrosed .multilocular cysts filled with pus.Intervening renal tissue is atrophic and fibrosed .

Renal stones(urolithiasis)renal calculi
Urolithiasis: Calculus formation at any level in the urinary tract , most often arise
in renal pelvis or urinary bladder due to precipitation of crystalloids.
Causes:- Dysbalance between solvents and solutes
A-abnormal composition of urine
1-Increased concentration of urine
2-Increased urinary crystalloids (exceed solubility) e.g Ca ,oxalates ,urates &uric acid
and cysteine
B-Urinary stasis (obstruction)
1-Urinary obstruction  stasis and infection  creating a nidus for stone formation
2-Urinary obstruction  stasis and precipitation of crysalloids.
C-Urinary tract infection :-
1-Necrotic epithelial cells ,RBC,s,Bilh.ova and pus cells act as nuclei for stone
formation
2-Infection  a change of urinary pH  deposition of crystalloids (Acidic pH
formed by E.coli infection  forms oxalate and urates stones.Alkaline pH formed
by pyogenic infection  forms triple phosphate stone.)
D-Absence of solvents :- As absence of gylocoprotein (nephrocalcin) and some muco-
polysaccharides..

Type of stone % pH Character
Primary stones
1-Oxalate stones
2-Uric acid &urates stones
3-Cystine stone
Secondary stones
Triple phosphate (Mag
ammonium phosphate)
stones
60%
8%
2%
30%
Acidic
Acidic
Acidic
Alkaline
Hard,dark,spiny
Hard,yellowish brown ,smooth
Soft,yellowish ,granular
Single,large white ,friable
,smooth surface (stag –horn
stones) –Large branching stone
taking shape of pelvi-calcyeal
system.
Clinical presentation and complications:-
1-Migration of stones  Renal colic
2-Obstruction ,causes:-
a-Hydroureter &hydronephrosis
b-Stones formation
c-Infection:cystitis ,pyelonephritis
and pyonephrosis
3-Injury of bladder wall causes:-
Hematuria &squamous metaplasia

Tumors of the kidneyTumors of the kidney
1-Tumors of the renal pelvis :-1-Tumors of the renal pelvis :-
A-Benign tumorsA-Benign tumors :-T.C.(Villous) papilloma &hemangioma:-T.C.(Villous) papilloma &hemangioma
B-Malignant tumorsB-Malignant tumors :-:-
1-Primary tumors :-TCC and Sq.C.C1-Primary tumors :-TCC and Sq.C.C
2-Secondary:- Tumors from renal tissue directly infiltrate renal pelvis .2-Secondary:- Tumors from renal tissue directly infiltrate renal pelvis .
2-Tumors of the renal cells :-2-Tumors of the renal cells :-
A-Benign tumorsA-Benign tumors :- Oncocytoma ,papillary(chromophil)adenoma ,Metanephric:- Oncocytoma ,papillary(chromophil)adenoma ,Metanephric
(embryonal ) adenoma,nephrogenic adenofibroma.Medullary fibroma(embryonal ) adenoma,nephrogenic adenofibroma.Medullary fibroma
Malignant tumorsMalignant tumors :-:-
1-Conventional (clear cell) carcinoma,1-Conventional (clear cell) carcinoma,
2-papillary(chromophil)carcinoma ,2-papillary(chromophil)carcinoma ,
3-chromophobe carcinoma ,3-chromophobe carcinoma ,
4-collecting duct carcinoma ,4-collecting duct carcinoma ,
5-medullary carcinoma ,5-medullary carcinoma ,
6-renal cell carcinoma .6-renal cell carcinoma .

R.C.adenoma :-R.C.adenoma :-The cells are regular ,cuboidal or polygonal with regular central nucleiThe cells are regular ,cuboidal or polygonal with regular central nuclei
and cytoplasm containing lipid vacuoles .and cytoplasm containing lipid vacuoles .
D.D.:- from renal cell carcinoma by the tumor size (tumor size >3cm in diameter areD.D.:- from renal cell carcinoma by the tumor size (tumor size >3cm in diameter are
likely to metastasize.Tumor size(2-3 cm border line tumor is treated as an early cancer)likely to metastasize.Tumor size(2-3 cm border line tumor is treated as an early cancer)
Medullary fibromaMedullary fibroma :-:-
A tiny nodule in medulla composed ofA tiny nodule in medulla composed of fibroblast –like cellsfibroblast –like cells inin hyalinized stromahyalinized stroma ..
Juxtaglomerular tumor(reninoma):-Juxtaglomerular tumor(reninoma):-
A tumor of renal cortex consists of sheets of epithelioid cells with many small sizedA tumor of renal cortex consists of sheets of epithelioid cells with many small sized
blood vesselsblood vessels  produce excessive amounts of reninproduce excessive amounts of renin HypertensionHypertension
Malignant tumors :-Malignant tumors :-
1-Renal cell carcinoma (hypernephroma ,adenocarcinoma of kidney or Grawitz1-Renal cell carcinoma (hypernephroma ,adenocarcinoma of kidney or Grawitz
tumor)tumor)
NatureNature :- Adenocarcinoma originating from:- Adenocarcinoma originating from tubular epithelial cellstubular epithelial cells
It is common in old man (6It is common in old man (6thth
-7-7thth
decades).It sought to arise from adrenal rests (cleardecades).It sought to arise from adrenal rests (clear
cells) so called hypernephromacells) so called hypernephroma
Predisposing factors :-Predisposing factors :-
1-Environmental factors :- Carcinogens(chemical or viruses),Smoking .1-Environmental factors :- Carcinogens(chemical or viruses),Smoking .
3-Genetic factors (Von-Hipple lindau ) ot tr ch 3-8 and 3-11(familial) .3-Genetic factors (Von-Hipple lindau ) ot tr ch 3-8 and 3-11(familial) .

Three types of renal cell carcinoma are found:-Three types of renal cell carcinoma are found:-
11-Conventional (Clear cell ) carcinoma (60%):--Conventional (Clear cell ) carcinoma (60%):-
-Either sporadic or familial-Either sporadic or familial
-Del .of 3p .Common in males>females (34-90Y)-Del .of 3p .Common in males>females (34-90Y)
Gross picture :-Gross picture :-
ShapeShape:-:- a large well circumscribed mass with projecting processes or satellite nodulesa large well circumscribed mass with projecting processes or satellite nodules
Site of originSite of origin ;-Upper pole of kidney cortex.;-Upper pole of kidney cortex.SizeSize :- mean size about 8 Cm:- mean size about 8 Cm
Cut sectionCut section :-variegated ,golden yellow with areas of hemorrhage and necrosis.:-variegated ,golden yellow with areas of hemorrhage and necrosis.
The massThe mass early fungates through the renal pelvis and ureterearly fungates through the renal pelvis and ureter  painless hematuriapainless hematuria
.Capsular invasion occurs lately.Capsular invasion occurs lately  Late painLate pain
1-Pattern of growth1-Pattern of growth :-Either solid sheets of tumor cells separated by delicate richly:-Either solid sheets of tumor cells separated by delicate richly
vascularized fibrous stroma or well developed acinar growth pattern .Cystic,papillaryvascularized fibrous stroma or well developed acinar growth pattern .Cystic,papillary
/pseudopapillary ,tubular and sarcomatoid patterns are also seen .A rich vascular/pseudopapillary ,tubular and sarcomatoid patterns are also seen .A rich vascular
network is prominent in all .Others change as fibrosis ,hyalinosis , necrosis andnetwork is prominent in all .Others change as fibrosis ,hyalinosis , necrosis and
hemorrhages are common but desmoplasia is absent or minimalhemorrhages are common but desmoplasia is absent or minimal
2-Cell morphology2-Cell morphology :-the tumor cells are polygonal or cuboidal in shape or spindle cells:-the tumor cells are polygonal or cuboidal in shape or spindle cells
The tumor cells are clear cells (vegetable cells ) or granular cells or sarcomatoid orThe tumor cells are clear cells (vegetable cells ) or granular cells or sarcomatoid or

anaplastic with excessive mitosis and giant cells . The cell shape and cytoplasmicanaplastic with excessive mitosis and giant cells . The cell shape and cytoplasmic
content correlate with the grade ( spindle cellcontent correlate with the grade ( spindle cell  high grade, also clear cellhigh grade, also clear cell  gradegrade
1)1)
2-Papillary (chromophil) renal cell carcinoma2-Papillary (chromophil) renal cell carcinoma :- It is a minority of RCC .:- It is a minority of RCC . FamilialFamilial
(trisomy of ch 7) and sporadic (trisomy 7,16,17) as well as loss of ch Y .(trisomy of ch 7) and sporadic (trisomy 7,16,17) as well as loss of ch Y .
ClinicallyClinically :- It represents 7-14% of epithelial renal neoplasms . Common in males at:- It represents 7-14% of epithelial renal neoplasms . Common in males at
6-76-7thth
decades of life .decades of life .
Gross pictureGross picture :-:-SiteSite :At renal cortex .:At renal cortex .SizeSize Mean size 6.4 cm .Mean size 6.4 cm . CapsuleCapsule :- May be:- May be
..NumberNumber :- May be multifocal.:- May be multifocal.ConsistencyConsistency :- Varigated appearance with hemorrhage:- Varigated appearance with hemorrhage
and necrosis.and necrosis.
MicroscopicallyMicroscopically :- It may be papillary (the cores contain foamy macrophages and:- It may be papillary (the cores contain foamy macrophages and
hemosiderin laden macrophages . , papillary –trabecular (the papillae are compressedhemosiderin laden macrophages . , papillary –trabecular (the papillae are compressed
forming trabecular growth pattern. and papillary –solidforming trabecular growth pattern. and papillary –solid
OutcomeOutcome :- It is more favourable than conventional type:- It is more favourable than conventional type
D.D. :- CRRC with papillary or pseudopapillary growth patterns.D.D. :- CRRC with papillary or pseudopapillary growth patterns.
Papillary (chromophil )adenomaPapillary (chromophil )adenoma :- Is restricted to a papillary tumor that measure 1:- Is restricted to a papillary tumor that measure 1
cm or less and contain small ,regular nuclei( G I)cm or less and contain small ,regular nuclei( G I)

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