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Abnormalities of the kidney and urinary tract
Lecture 15
Functions of the Kidney
 Excretion of metabolic wastes
 Regulation of mineral and water balance
 Release of renin that is important in regulation of blood pressure and blood volume
 Release of erythropoietin in response to hypoxia; erythropoietin stimulates the production
of red blood cells in the bone marrow
 Hydroxylates 25-OH-cholecalciferol (vitamin D metabolite), to promote bone resorption
(the process by which osteoclasts break down bone and release the minerals, resulting in
a transfer of calcium from bone fluid to the blood) and calcium and phosphorus
absorption from the gut

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Disorders of the kidney
• In order for the kidneys to function normally three things must occur.
 First, there must be adequate blood flow through the glomerular capillaries.
 Second, the glomerular capillaries, which selectively filter blood, must be intact.
Normal glomeruli allow fluids and small solutes to be filtered into the renal tubules
but not proteins or blood cells.
 Third, the tubules of the kidney must be able to reabsorb essential substances
selectively from the filtrate while excreting other substances into the filtrate to be
eliminated in the final urine.
Renin & Erythropoietin
• The juxtaglomerular apparatus consists of three cells:
 The macula densa, a part of the distal convoluted tubule of the same nephron
 Juxtaglomerular cells, which secrete Renin
 Extraglomerular mesangial cells
• Erythropoietin (EPO) is produced by interstitial fibroblasts in the kidney in close
association with peritubular capillary and proximal convoluted tubule.
• It is also produced in perisinusoidal cells in the liver.
• While liver production predominates in the fetal and perinatal period, renal production is
predominant during adulthood

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RAAS
Nephron Structure 1) Glomerulus
• Basic structural and functional unit of the kidney
• About 1 million nephrons in each kidney
• Consists of glomerulus and renal tubule

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1) Glomerulus
• Tuft(‫،ﺣﺰﻣﺔ‬ ‫)ﺑﺎﻗﺔ‬of capillaries supplied by an afferent glomerular arteriole that
recombine into an efferent glomerular.
• These capillaries are unusual in having a high blood pressure which is necessary
for maintaining an effective glomerular filtration rate (GFR) to produce the
plasma filtrate from which urine will be made.
• Material is filtered by a 3-layered glomerular filter
• Inner: fenestrated capillary endothelium
• Middle: basement membrane
• Outer: capillary endothelial cells (with foot processes{Podocytes} and
filtration slits)
• Mesangial cells: contractile phagocytic cells that hold the capillary tuft together;
regulate caliber of capillaries affecting filtration rate
Glomerulus Structure
• glomerulus - The network or tuft of fenestrated capillary endothelial cells covered by a
layer of specialized epithelial cells (the visceral layer of the renal corpuscle), the
podocytes, through which water and small dissolved solutes pass to enter the capsular
space of the renal corpuscle of the nephron of the kidney;

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2) Renal Tubules
• Renal tubule: reabsorbs most of filtrate; secretes unwanted components into tubular
fluid; regulates H2O balance
• Proximal end: Bowman’s capsule
• Distal end: empties into collecting tubules
• Requirements for normal renal function
• Free flow of blood through the glomerular capillaries
• Normally functioning glomerular filter that restricts passage of blood cells and
protein
• Normal outflow of urine
Nephron Structure

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Nephron Function
Assessment of Kidney Function
 Urinalysis
 Proteinuria - indicates glomerular damage
 Glycosuria - indicates tubular damage
 Urine volume and osmolarity
 pH
 Enzymes - indicates tubular damage
 Microscopic examination - casts, crystals, bacteria, etc.
PH & Specific gravity
• PH: 6.5
• aciduria: acidosis
• alkaluria : alkalosis , renal tubular acidosis
• Specific gravity: 1.015-1.025
• lower SG: chronic renal failure, diabetes insipidus

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• high SG: acute nephritis, diabetes mellitus, heart failure
 Diabetes Insipidus: occurs when the kidneys cannot concentrate the urine normally, and a
large amount of dilute urine is excreted. It is caused by a failure of the kidneys to respond
to ADH
Microscopic examination of the urine
Assessment of Kidney Function
Blood Chemistries
 Blood urea nitrogen (BUN)
 Creatinine
 Electrolytes - Ca, Mg, K, P
 Glomerular filtration rate - determines the clearance of inulin, creatinine and BUN
 Renal clearance - measures the clearance of p-aminohippuric acid by filtration and
secretion

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NPN (Non - Protein Nitrogen)
 NPN (Non - Protein Nitrogen) is a “funky” ( ‫ﺗﻘﻠﻴﺪﻱ‬ ‫)ﻏﻴﺮ‬ term that can be used for a bunch
of different substances that have the element nitrogen in them, but are not proteins.
 This is a little unusual, because most of the body’s nitrogen is associated with proteins.
 There are many different unrelated NPNs, but we are only interested in 4 of them:
 Creatinine , Blood Urea Nitrogen ( BUN ) , Uric Acid and Ammonia
 In general, plasma NPNs are increased in renal failure and are commonly ordered as
blood tests to check renal function
BUN (Blood Urea Nitrogen)
 Blood Urea Nitrogen = BUN = Urea
 50% of the NPNs
 Product of protein catabolism which produces ammonia
 Ammonia is very toxic.
 Liver converts ammonia and CO2 to Urea
 Filtered by the glomerulus but also reabsorbed by renal tubules ( 40 % )
o Some is lost through the skin and the GI tract ( < 10 % )
o Plasma BUN is affected by
 Renal function
 Dietary protein
 Protein catabolism
 Reference range:10 – 20 mg / dl
 To convert BUN to Urea : BUN x 2.14 = Urea (mg / dl)
BUN disease correlations
Azotemia = Elevated plasma BUN
 Prerenal  BUN ( Not related to renal function )
o Low Blood Pressure( CHF, Shock, hemorrhage, dehydration)
o Decreased blood flow to kidney = No filtration
o Increased dietary protein or protein catabolism

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 Prerenal  BUN ( Not related to renal function )
o Decreased dietary protein
o Increased protein synthesis ( Pregnant women , children )
 Renal causes of  BUN
o Renal disease with decreased glomerular filtration
o Glomerular nephritis
o Renal failure form Diabetes Mellitus
 Post renal causes of  BUN ( not related to renal function )
o Obstruction of urine flow
o Kidney stones
o Bladder or prostate tumors
o UTIs
CREATININE
 Creatinine is a by-product of skeletal muscle metabolism and is present in the plasma at
relatively constant levels. The main drawback to the use of “creatinine clearance” to
measure renal function is that any condition that increases skeletal muscle breakdown
(sepsis, muscle injury or muscle disease, for example) will elevate levels of serum
creatinine and invalidate the measure.
 Liver : Amino Acids -----------Creatine
 Muscles : Creatine -----------------Phosphocreatine
 Muscles : Phosphocreatine-------- Creatinine
 Creatinine is formed from creatine and creatine phosphate in muscle
 Creatinine formed at a constant rate by the muscles as a function of muscle mass
 Creatinine is removed from the plasma by glomerular filtration
 Creatinine is not secreted or absorbed by the renal tubules
 Therefore :
o Plasma creatinine is a function of glomerular filtration
o It’s a very good test to evaluate renal function

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Creatinine disease correlations
 Increased plasma creatinine associated with decreased glomerular filtration ( renal
function )
 Glomerular filtration may be 50 % of normal before plasma creatinine is elevated
 Plasma creatinine is influenced by dietary protein intake to variable degrees; this rise
may be even more exaggerated in patients with renal disease. For this it should be
measured in the fasting state in all patients.
 Plasma creatinine concentrations are very stable from day to day - If there is a delta
check , its very suspicious and must be investigated
 Reference range: 0.5 - 1.2 mg / dl
BUN / Creatinine Ratio
Uric acid
 Breakdown product of purines ( nucleic acid / DNA )
 Purines from cellular breakdown are converted to uric acid by the liver
 Uric acid is filtered by the glomerulus ( but 98 – 100 % reabsorbed )
 Elevated plasma uric acid can promote formation of solid uric acid crystals in
joints and urine

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Uric acid diseases
o Gout
o Increased plasma uric acid
o Painful uric acid crystals in joints
o Usually in older males ( > 30 years-old )
o Associated with alcohol consumption
o Uric acid may also form kidney stones
o Other causes of increased uric acid
o Leukemias and lymphomas ( DNA catabolism)
o Megaloblastic anemias (  DNA catabolism )
o Renal disease ( but not very specific )
• Reference range: 3.5 - 7.2 mg/dl (males)
2.6 - 6.0 mg/dl (females)
• Let’s remember 3.0 - 7.0 mg/dl
Ammonia
 Produced from the deamaination of amino acids in the muscle and from bacteria
in the GI tract
 Ammonia is very toxic - The liver converts ammonia into urea
 Urea is less toxic and can be removed from the plasma by the kidneys
 In severe hepatic disease, the liver fails to convert ammonia into urea, resulting in
increased plasma ammonia levels
 Increased plasma ammonia concentrations in :
 Liver failure
 Reye’s Syndrome :(Skin rash, vomiting, hypoglycemia and liver damage
associated with aspirin consumption by children with viral illness, it also
occurs in the absence of aspirin use).
 Reference range: 20 – 60 µg / dl

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Creatinine Clearance
 Calculated measurement of the rate at which creatinine is removed from the plasma by
the kidneys
 Measurement of glomerular filtration (renal function )
 A good test of glomerular filtration because
 Creatinine is an endogenous substance.
 Creatinine is filtered by the glomerulus, but not secreted or re-absorbed by the
renal tubules
 24 Hour Urine collection
 Reference range = 90 - 130 ml / min
NPN TOP 10
1) Increased Creatinine associated with renal failure
2) Increased BUN associated with renal failure and protein catabolism
3) Increased Uric Acid associated with Gout
4) Increased Ammonia is associated with liver disease
5) Creatinine derived from cellular creatine …
6) Delta checks on plasma Creatinine must be investigated!!!
7) BUN ( Urea ) is derived from protein catabolism
8) Protein Ammonia Urea
9) Uric Acid is derived from purine ( a component of DNA ) catabolism
10) Decreased Creatinine Clearance associated with decreased Glomerular Filtration
Delta checks: A comparison of consecutive values for a given test in a patient's laboratory file
used to detect abrupt changes, usually generated as a part of computer-based quality control
programs.

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Overview of Renal Diseases
Glomerular disease
 Glomerular disease reduces the ability of the kidneys to maintain a balance of certain
substances in bloodstream.
 Normally, the kidneys should filter toxins out of the bloodstream and excrete them in the
urine, but should keep red blood cells and protein in the bloodstream.
 In people with glomerular disease, red blood cells and protein may be excreted into the
urine, while toxins may be retained.
 Glomerular disease can occur by itself (eg, affecting only the kidney), or may be
associated with an underlying medical condition that affects other organ systems, such as
lupus, diabetes, or certain infections.
 Glomerular disease can develop suddenly (acute), or develop slowly over a period of
years (chronic).
 Treatment of glomerular disease depends upon its cause and type.

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Post-Streptococcal (Acute) glomerulonephritis (PSGN)
 May develop 1 - 2 weeks after an untreated throat infection, or 3 - 4 weeks after a skin
infection (impetigo) infection with group A ((beta-haemolytic) streptococcus. . .
 It may occur in any age (in adults after age 60), but it most often occurs in children ages
5- 12. Trapping of antibody–antigen complexes in glomerular capillaries causes
inflammation of the glomerulus and alters its selective permeability, allowing plasma
proteins and blood cells to enter the kidney filtrate.
 (Proteinuria & Hematuria) , associated with fluid retention, hypertension and edema. This
disorder is uncommon in prosperous countries, common elsewhere.
IgA nephropathy-IgN- (Berger’s disease)
 It is the most common GN in the world with extremely varied presentation usually
including hematuria, mild proteinuria and hypertension.
 Often slowly evolving over decades, may lead to ESRF.
 In young, often acute exacerbations with similarities to post-streptococcal
glomerulonephritis; or occurs with Henoch-Schonlein purpura and vasculitic changes in
glomeruli, skin and bowel (usually self-limiting).
 IgA is deposited in mesangium of glomeruli.
Small vessel vasculitis
 Usually associated with antibodies to neutrophil granule enzymes (ANCA); may cause
aggressive but treatable nephritis, can be associated with severe vasculitis affecting lungs
and other organs.
 Anti-neutrophil cytoplasmic antibodies (ANCAs) are a group of autoantibodies.
Glomerulonephritis
 Glomerulonephritis, also known as glomerular nephritis, is a renal disease (usually of
both kidneys) characterized by inflammation of the glomeruli, or capillaries in the
kidneys.
 Majority of the glomerular diseases are caused by antigen-antibody reaction within the
glomeruli.
1) Immune-complex glomerulonephritis
• Usually follows a beta-streptococcal infection
• Circulating antigen and antibody complexes are filtered by glomeruli and incite
inflammation
• Leukocytes release lysosomal enzymes that cause injury to the glomeruli
• Occurs in SLE; immune complexes trapped in glomeruli
• Occurs in IgA nephropathy

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2) Anti-glomerular basement membrane (anti-GBM) glomerulonephritis:
 autoantibodies attack glomerular basement membrane
 They are categorized into several different pathological patterns, which are broadly
grouped into non-proliferative or proliferative types.
 Diagnosing the pattern of GN is important because the outcome and treatment differs in
different types.
 Primary causes are ones which are intrinsic to the kidney, whilst secondary causes are
associated with certain infections (bacterial, viral or parasitic pathogens), drugs, systemic
disorders (SLE, vasculitis) or diabetes.
Pathogenesis of Acute glomerulonephritis

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Rapidly progressing glomerulonephritis
 Occurs most commonly in individuals in their 50s and 60s.
 It describes an extreme inflammatory nephritis which causes rapid loss of renal
function over days to weeks.
 Renal biopsy shows crescentic lesions often associated with necrotising lesions within
the glomerulus (focal segmental (necrotising) glomerulonephritis).
 May be idiopathic in origin
 It is typically seen in Goodpasture’s disease, where there are specific anti-GBM
antibodies.

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Nephrotic Syndrome
 Proteinuria (>3.5g in 24hrs)
o ++++ Protein
o Urine looks frothy
o Tip: Nephrotic & Protein both have an “O” which may help you remember!
 Hypoalbuminemia
o Albumin is lost in the urine
o Due to gaps in Podocytes allowing proteins to escape
 Edema
o Swelling around ankles & eyes
o Due to loss of albumin
o Intravascular oncotic pressure ↓
o Fluid moves out of vessels
 Hyperlipidemia
o Not really understood why this happens
o Just a case of remembering it does!

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Nephritic Syndrome
 Hematuria
o +++ Blood – May be microscopic or macroscopic haematuria
o Red cell casts – distinguishing feature, form in nephrons & indicate
glomerular damage
o Podocytes develop large pores which allow blood & protein through
 Proteinuria
o ++ Protein (small amount)
 Hypertension
o Usually only mild
 Oliguria (Low urine volume <300ml/day)
o Due to renal function been poor
Nephrotic Syndrome - associated diseases
 Primary causes
o Minimal change Glomerulonephritis
o Focal Segmental Glomerulosclerosis
o Membranous Glomerulonephritis.
 Secondary causes
o SLE
o Hep B & C
o HIV
o Diabetes Mellitus
o Malignancy
o & lots of others
Nephritic Syndrome – associated diseases
 Post streptococcal Glomerulonephritis – appears weeks after URTI
 IgA Nephropathy – appears within a day or two after URTI
 Rapidly progressive Glomerulonephritis (crescentic glomerulonephritis)

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 Goodpastures - anti GBM antibodies against basal membrane antigens
 Vaculitic disorder – Wegners granulomatosis, Microscopic Polyangitis, Churg
Strauss disease
 Membranoproliferative Glomerulonephritis - primary or secondary to SLE,
Hepatitis B/C etc
 Henoch-Schönlein purpura - systemic vasculitis – deposition of IgA in the skin &
kidneys

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Chronic glomerulonephritis
 Chronic inflammation of the glomeruli.
 Etiology may be diverse; many patients with chronic glomerulonephritis may have no
history of acute renal disease.
 May be associated with chronic hypertension, diabetes mellitus.
 May remain asymptomatic for a number of years before symptoms of proteinuria,
hematuria occur.
 Progressive loss of renal function occurs over a number of years leading to renal
insufficiency and renal failure.
 Glomerulonephritis Treatment
o Antibiotic therapy if caused by bacterial infection
o Immunosuppressive drugs if autoimmune destruction of glomeruli is occurring
o Management of resulting edema, mineral imbalance and possible hypertension
 Manifestations
o Proteinuria (appearance of protein in the urine, primarily albumin)
o Hematuria (appearance of blood in the urine)
o With chronic forms of glomerulonephritis, decreased urine volume and fluid
retention may occur as renal insufficiency and renal failure develops.
o Hypertension is a possible consequence of reduced renal blood flow and
activation of renin–angiotensin system.
Urinary Tract Infection (UTI)
 Classifications:
1. Upper UTIs are known as Pyelonephritis.
2. Lower UTIs:
a. Ureteritis.
b. Cystitis.
c. Urethritis.
o Women develop UTI more than men because their shorter urethras

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 Predisposing Factors:
1. Sexual intercourse.
2. Indwelling catheter.
3. Urine stasis.
4. Urinary tract instrumentation.
5. Metabolic disorders
 UTI Clinical Manifestations
1. Upper UTIs:
a. Chills, fever.
b. Malaise.
c. Pain below the ribs.
d. Nausea, Vomiting.
2. Lower UTIs:
a. Back pain .
b. Hematuria.
c. Cloudy urine.
d. Inability to urinate despite the urge.
e. Fever.
f. Frequent need to urinate.
g. General discomfort (malaise).
h. Painful urination (dysuria)
 Diagnostic tests:
1. Urine analysis.
2. Urine culture.
3. WBCs.
 Treatment
o Appropriate antibiotics
o Surgical correction of obstruction or structural abnormality that might be
causing urine retention
o Urinary Tract Infection (cont’d)

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 Prevention:
1. Avoid products that may irritate the urethra (e.g., bubble bath, scented feminine products).
2. Cleanse the genital area before sexual intercourse.
3. Change soiled diapers in infants and toddlers promptly.
4. Drink plenty of water to remove bacteria from the urinary tract.
5. Do not routinely resist the urge to urinate
6. Take showers instead of baths.
7. Urinate after sexual intercourse.
8. Women and girls should wipe from front to back after voiding to prevent contaminating
the urethra with bacteria from the anal area.
Urolithiasis (Kidney Stones)
 Urolithiasis: The process of forming stones in the kidney, bladder, and/or urethra (urinary
tract).
 Etiology:
1. Immobility.
2. Hypercalcemia.
3. UTIs.
4. Urine stasis.
5. Fractures.
 Clinical Manifestations:
1. Renal colic.
2. Nausea and vomiting accompanying severe pain.
3. Fever and chills.
4. Hematuria.
5. Rarely, oliguria or anuria.
6. Bladder distension (urine retention)
 Diagnostic tests:
1. KUB radiograph reveals visible calculi.
2. IVP (Intravenous Pyelogram) determines size and location of calculi.
3. Renal Ultrasonography reveals obstructive changes.

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 Treatment
1. Preventative measures include increased fluid intake, acidification of the urine
and reduction of serum uric acid levels.
2. Surgical removal of stones.
3. Lithotripsy— Ultrasonic destruction of stones. Fragmented stones may then pass
naturally with the urine.
Renal tumors
 Tumors of the kidney may be either :
 rare benign Adenomas or, more commonly, malignant renal cell carcinomas
 If benign adenomas arise, they tend to be small and usually not clinically significant.
 The prognosis for renal cell carcinomas depends upon the morphology of the cells
involved and the extent of spread outside the kidney.
 Renal carcinomas may metastasize to the lymphatic system, liver, lungs and bone
marrow.
 Wilm’s tumor (nephroblastoma)
o Rare malignant tumor that arises in infants and children.
o The tumor presents with unique histology that may resemble embryonic kidney.
o Tumor can metastasize rapidly.
 Manifestations
o Hematuria
o Flank pain
o Weight loss
o Many renal tumors asymptomatic until the tumor is of advanced size and begins
to disrupt renal structures
o Metastatic tumors that can occur with advanced disease
 Treatment
o Chemotherapy, radiation therapy
o Surgical removal of tumors
Polycystic kidney disease
 Hereditary disease characterized by cyst formation and massive kidney enlargement.
 It can be Autosomal dominant (adult form) or autosomal recessive (childhood form)

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 Pathophysiology:
 Renal cysts are fluid-filled sacs affecting nephrons; cysts fill, enlarge, multiply
thus compressing and obstructing kidney tissue; renal parenchyma atrophies,
becomes fibrotic and there is a progressive loss of renal function that may
culminate in renal failure.
 Cysts occur elsewhere in body including liver, spleen
 Cysts develop in both kidneys and gradually increase in size. As normal kidney tissue is
destroyed by the enlarging cysts The recessive form of the disease may cause renal
failure in childhood while the dominant form progresses more slowly and generally does
not lead to renal failure until patients enter their 60s or 70s.
 Adult form accounts for 10% of persons in End Stage Renal Disease (ESRD)
 Manifestations
o Grossly enlarged kidneys
o Hypertension from activation of the renin–angiotensin system
o Renal insufficiency leading to renal failure
o Pain in the flanks
o Frequent infections
 Treatment
o Management of renal insufficiency and renal failure with dialysis
o Management of hypertension; patients may be at particular risk for aneurysms and
cerebral hemorrhage
o Renal transplantation
o Antibiotics for frequent infections

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Renal failure
 Renal failure refers to a significant loss of renal function in both kidneys to the point
where less than 10 to 20% of normal GFR remains.
 Renal failure may occur as an acute and rapidly progressing process or may present as a
chronic form in which there is a progressive loss of renal function over a number of
years.
Acute renal failure
 Abrupt decrease in renal function.
 Regarding the causes of acute renal failure may be prerenal, intrarenal or
postrenal in nature.
 Acute renal failure is often reversible so long as permanent injury to the kidney
has not occurred.
 Causes of Acute Renal Failure
Prerenal failure
o Caused by impaired or reduced blood flow to the kidney Possible causes: shock,
hypotension, anaphylaxis, sepsis Unless blood flow and oxygen delivery are restored
permanent damage to the kidney will result
Intrarenal failure
o Results from acute damage to renal structures
o Possible causes: acute glomerulonephritis, pyelonephritis, may also result from acute
tubular necrosis (ATN), which is damage of kidney structure from exposure to
toxins, solvents, drugs and heavy metals; ATN is the most common cause of acute
renal failure, it accounts 50% of cases of acute renal failure
o Antibiotics & NSAIDs.
Postrenal failure
o Results from conditions that block urine outflow Possible causes: obstruction of urine
outflow by calculi, tumors, prostatic hypertrophy
 Manifestations
o Oliguria (reduced urine output)
o Possible edema and fluid retention
o Elevated blood urea nitrogen levels (BUN) and serum creatinine
o Alterations in serum electrolytes

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 Treatment
o Prevention of acute renal failure through support of blood pressure and blood volume
o Correction of fluid and electrolyte imbalances
o Dialysis, which may be employed while the kidneys are in the recovery phase
o Low protein, high carbohydrate diet to minimize the formation of nitrogenous wastes
Chronic renal failure
 Chronic renal failure is the end result of progressive kidney damage and loss of function.
 Some of the possible causes of chronic renal failure:
o Chronic glomerulonephritis
o Chronic infections
o Renal obstruction
o Exposure to toxic chemicals, toxins or drugs (aminoglycoside antibiotics)
o Diabetes
o Hypertension
o Nephrosclerosis (atherosclerosis of the renal artery)
o Aminoglycoside antibiotics and nephrotoxicity
 The aminoglycoside antibiotics are a widely used group of drugs that include
agents such as streptomycin, gentamicin and kanamycin.
 The aminoglycosides can be nephrotoxic under certain conditions.
Aminoglycoside toxicity is most likely to occur in elderly people, those with renal
insufficiency or with chronic use.
 Concurrent use of loop diuretics may also compound the adverse renal effects of
the aminoglycosides.

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 Chronic renal failure is often classified into four progressive stages based on the loss of
GFR
1) Diminished renal reserve — GFR decreased to 35 to 50% of normal
2) Renal insufficiency — GFR decreased to 20 to 35% of normal
3) Renal failure — GFR reduced to less than 20% of normal
4) End-Stage Renal Disease (ESRD) — GFR is less than 5% of normal
 Because the kidneys play such an essential role in a number of physiologic processes,
renal failure is a multisystem disease.
 The kidneys have a tremendous reserve capacity for function and as a result overt
symptoms generally do occur until renal insufficiency is present.
 Vicious cycle of chronic renal failure
There are several physiologic adaptations that occur in the kidneys in response to chronic
renal failure:
o Increased renal blood flow and GFR in functional nephrons
o Hypertrophy of functional nephrons
o In the short term these adaptations may be beneficial, but in the long term the
increased pressure in the kidneys and increased oxygen demand can further
damage the nephrons and worsen renal failure.
 Clinical Manifestations:
1. Decreased appetite and energy level
2. Increased urinary output and fluid intake
3. Bone or joint pain
4. Delayed or absent sexual maturation
5. Growth retardation
6. Dryness and itching of skin
7. Anemia
8. Markedly elevated BUN and creatinine
 Diagnostic Evaluation:
o Determine extent of disease; monitor progression.
1. Serum studies
a. Decreased hematocrit, hemoglobin, Na+, Ca++; increased K+, phosphorous
b. As renal function declines, BUN, uric acid, and creatinine values continue to climb.

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2. Urine studies:
a. Specific gravity—increased or decreased
b. 24-hour urine for creatinine clearance is decreased (increased creatinine in urine)
reflecting decreased GFR.
c. Changes in total output
3. Many other tests may be ordered to evaluate other systems and extent of disease (ie, chest x-
ray, electrocardiogram)
 Chronic renal failure Complications
 Chronic Renal Failure Treatment
1. Correction of calcium phosphorous imbalance. Administer activated vitamin D to increase
calcium absorption and calcium phosphate binders with meals to bind phosphate in the
gastrointestinal tract.
2. Correction of acidosis with buffers such as Bicitra
3. Diets should meet caloric needs of the child containing adequate protein for development
(1.0–1.5 g/kg per day).
4. Correction of anemia through the use of erythropoietin (Epogen) administered
subcutaneously at home
5. Growth retardation should be evaluated for possible use of growth hormone.
6. Treatment options for end-stage renal disease (ESRD) are hemodialysis, peritoneal
dialysis, or transplantation.
7. Institute dialysis therapy while transplant work-up is in progress.

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Chronic Renal Failure Summary
Hemodialysis
 Hemodialysis is a procedure in which an “artificial kidney” machine takes the place of
the patient’s own failing kidneys. Using an indwelling catheter, blood is withdrawn from
the patient and passed through a chamber containing a dialysis membrane and clean
dialysate solution.
 Waste products that are in high concentration in the patient’s blood diffuse across the
dialysate membrane and into the dialysate solution.
 The cleaned blood is then returned to the patient via a second catheter.
 Complications to hemodialysis can include risk of infection, hypotension and electrolyte
imbalance.
 Patients receiving hemodialysis must undergo the procedure several times per week for 3
to 6 hours per treatment.
 Newer high flux dialysate membranes and improved dialysate solutions have reduced the
time of each dialysis session by 1 to 2 hours.

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Peritoneal dialysis
 An alternative to classic hemodialysis is a technique called peritoneal dialysis. With this
technique a “permanent” catheter is implanted into the peritoneal cavity.
 A clean dialysate solution is introduced through this catheter into the peritoneal cavity
and the patient’s own peritoneum (the membrane lining the abdominal cavity) is used as
the dialyzing membrane.
 After a fixed period of time, usually 8 to 48 hours depending on the system and the
frequency of dialysis, the used fluid is withdrawn.
 Complications of this technique may include infections from the catheter, hypotension,
edema and metabolic abnormalities.
 Peritoneal dialysis does, however, offer the advantage that it may be performed in a
patient’s own home and overnight when the patient sleeps.

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Kidney Transplantation
 The transplant surgery is performed under general anesthesia.
 The operation usually takes 2-4 hours.
 This type of operation is a heterotopic transplant meaning the kidney is placed in a
different location than the existing kidneys.
 (Liver and heart transplants are orthotopic transplants, in which the diseased organ is
removed and the transplanted organ is placed in the same location.)
 The kidney transplant is placed in the front (anterior) part of the lower abdomen, in the
pelvis.
 The original kidneys are not usually removed unless they are causing severe problems
such as uncontrollable high blood pressure, frequent kidney infections, or are greatly
enlarged.
 The artery that carries blood to the kidney and the vein that carries blood away is
surgically connected to the artery and vein already existing in the pelvis of the recipient.
The ureter is connected to the bladder.
 Recovery in the hospital is usually 3-7 days.
 Complications can occur with any surgery.
 The following complications do not occur often but can include:
o Bleeding, infection, or wound healing problems.
o Difficulty with blood circulation to the kidney or problem with flow of urine from
the kidney.
 These complications may require another operation to correct them.
 Rejection is an expected side effect of transplantation and up to 30% of people who
receive a kidney transplant will experience some degree of rejection.
 Most rejections occur within six months after transplantation, but can occur at any time,
even years later. Prompt treatment can reverse the rejection in most cases.
 Anti-Rejection Medications:
o Anti-rejection medications, also known as immunosuppressive agents, help to
prevent and treat rejection.
o They are necessary for the "lifetime" of the transplant. If these medications are
stopped, rejection may occur and the kidney transplant will fail.

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Disorders of the bladder and urethra
Urine reflux
 Urine reflux is the backward flow of urine from the bladder into the ureters and kidneys
(vesicoureteral reflux) or from the urethra into the bladder (urethrovesical reflux)
 Generally results from congenital abnormalities in the structure or location of the ureters
or urethra.
 Patients often present with urine retention and recurrent urinary tract infections.
 Treatment may include antibiotic therapy and possible surgical correction of the
structural abnormality.
Neurogenic bladder
 Bladder paralysis that occurs from interruption of nervous input to the muscles of the
bladder wall.
 Patients are unable to voluntarily or involuntarily empty their bladder.
 Causes may include spinal cord trauma, polio, multiple sclerosis and tumors affecting
spinal nerves.
 Manifestations include marked urine retention, frequent urinary tract infections and
possible deterioration of renal function (postrenal failure).
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