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Renal
Dr T Jenyon
Plan
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Background
Symptoms and Signs
Renal medicine
Renal failure
Rare renal
UTI and calculi
Surgical renal
Background
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Kidney is retroperitoneal
11-14cm in length
Has a high proportion of cardiac output
Central role in fluid and electrolyte balance
Background
• Other roles:
– Erythropoetin
– Vitamin D metabolism
– Caltabolism of small proteins (insulin)
– Drug excretion
Background - Fluid and electrolytes
• ADH (posterior pituitary) controls Osmolality
• Renin-angiotensin-aldosterone controls
Extracellular volume (via Na)
Background – Urea and creatinine
• Urea – nitrogenous waste due to breakdown of
amino acids
• Raised in
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Renal failure
High protein intake
GI bleed (acts as high protein meal)
Dehydration

• Creatinine
• Raised in
• Renal failure
• Large muscle mass
• Acute muscle damage
Notes
• Alcoholics tend to have a very low urea as poor diet
and knackered liver
• Sudden increase in Urea but not creatinine think
dehydration or GI bleed
• Ratio should be around 1:20
• Altered ratio (1:5) suggests acute renal failure, GI bleed etc

• Low Hb, high urea, think GI bleed
Renal anatomy
Symptoms and signs
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Frequency/Polyuria
Oliguria
Dysuria/pain
Incontinence
Palpable kidneys
Glycosuria
Haematuria
Proteinuria
Frequency / Polyuria
• Frequency implies increaed frequency voiding –
different from polyuria (increased volume)
• Frequency – Think UTI
• Polyuria
• Excess intake
• Osmotic diuresis (DM)
• Defective concentrating ability of kidney
• Diuretics
• CRF
• Diabetes insipidus
Oliguria
• Urine output <0.5ml/kg/hr or less than 400mls per
day
• Causes (basically causes of ARF)
– Pre-renal - Decreased perfusion of kidneys
• shock/hypovolaemia

– Renal
• ATN/GN

– Post renal - Obstruction of urine flow
• Intra-lumen – stone
• In the wall – stricture/tumour
• Compressing wall – prostate/tumour/AAA
• Remember blocked catheter if catherised
Dysuria/Pain
• Dysuria – pain on urination
– Think of UTI/STI
– Can get sterile urethritis

• Renal stones classically cause ‘renal colic’
– loin to groin pain coming in waves, makes patient
roll around
Incontinence
• Involuntary voiding of urine
• If new onset suspect UTI, in men suspect protatism and overflow – check
for bladder
• Types:
– Functional, i.e. caught short
– Stress, weak pelvic floor, small amounts leak when coughing or laughing
• Do pelvic floor exercises, can try Duloxeteine, TFVT or colposuspension is surgical
option

– Urge, uncontrolled emptying of bladder, e.g. brain damage.
• Find cause, try timed voiding, oxybutynin/tolterodine can help
Palpable kidneys
• Bilateral palpable kidneys
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ADPKD
Bilateral hydronephrosis
Amyloid
Bilateral RCC
Tuberous sclerosis

• Unilateral palpable kidneys

– RCC
– Hydronephrosis
– Bilateral cause with only one palpable

• (In chronic renal failure kidneys tend to be small
and shrunken)
Kidney Vs Spleen
• Kidney
– Moves late on
inspiration
– Possible to get above
– Smooth shape
– Resonant to percussion

• Spleen
– Moves early on
inspiration
– Can’t get above
– Notched leading edge
– Dull to percussion
– Enlarges towards RIF
Glycosuira
• Blood glucose of >10mmol will spill over into
urine
• Think DM
• Can have congenital low renal threshold for
glucose
Haematuria
• Is it Blood?
– Rifampicin, beetroot, myoglobinuria
(rhabdomyolysis)

• Is it from urological tract
– DD Vagina/rectum

• Is it from kidney
– Look for red cell casts

• Is it painless
– Think cancer
Haematuria
• Generalised disorder
– IBE, coagulopathy, sickle cell, vasculitis

• Specific disorder
– Kidneys or Ureter/bladder/Urethra
• Medical
– GN – IgA or thin BM disease
– Infection - UTI/prostatitis/schistosomiasis

• Surgical
– Stone, tumour, trauma
Proteinuria
• Urine Dipstix react to albumin but not Bence Jones Protein (myeloma)
• ‘microalbuminuria’ is proteinuria in the range of 30-300mg/L (e.g. DM)
• Quantify proteinuria with 24hr urine of protein/creatinine ratio (PCR) or
albumin creatinine ratio (ACR)
• >3.5g/day suggests nephrotic syndrome this may make the urine frothy
• Proteinuria and heamaturia with red cell casts suggests Nephritic
syndrome
Proteinuria
• Benign
– Orthostatic proteinuria
– Exercise/febrile illness

• Excess circulating protein
– Myeloma

• Renal damage
– DM/GN/nephritic/nephrotic syndrome

• UTI
Renal Medicine
Nephrotic syndrome
Nephritic syndrome
GN
TIN
Renal Medicine
• Appears complex no definitive relationship
between syndromes/symptoms and
pathology/biopsy
• But

– Some patterns are present
– Results from biopsy can help guide treatment

• E.g. kid presents with nephrotic syndrome:

– They are assumed to have minimal change GN.
– Treat with Steroids.
– If they do not respond to steroids they will have a
biopsy that might reveal a different cause that might
need a different treatment
Nephrotic Syndrome
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Massive proteinuria (>3.5g/day)
Hypoalbuminaemia (<30g/L)
Oedema
Hyperlipdaema

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Increased thrombotic tendency (loose antithrombin III and protein S)
Increased susceptibility to infection (loose immunoglobulins)
Nephrotic syndrome
• Commonest cause in kids:
– Minimal change glomerulonephritis
• Not much to see on microscopy (minimal change), get fusion of
podocytes on electron microscopy
• Benign (only 1% progress to ESRF), treat high dose (60mg)
Prednisolone, only biopsy if not responding

• Commonest in adults
– Membranous nephropathy
• Thickened BM with spikes on silver staining (IgG)
• 1/3 better,1/3 same, 1/3 ESRF
• Idiopathic, or assoc Malignancy, drugs, SLE (V), Hep B
Nephrotic syndrome
• Other causes of Nephrotic syndrome:
– Focal Segmental Glomerulosclerosis
• Only some (focal) glomeruli have some (segmental)
sclerosis. Idiopathic or assoc HIV
• High recurrence in transplant

– DM
– Amyloid
– SLE
Nephritic Syndrome
• Symptomatic haematuria and proteinuria
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Haematuria with red cell casts
Proteinuria (<3.5g/day)
Oliguria
Hypertension
Oedema

– (remember UTI can give you haematuria and proteinuria)
Nephritic Syndrome
• Commonest cause:
– IgA nephropathy (Bergers disease)
• 3-4 days post infection – usually URTI
• 16-35 yr olds with episodic macroscopic haematuria
• IgA and C3 on biopsy with mesangial hypercellularity

• 2nd commonest:
– Proliferative GN / Post Strep GN
– 1-3 weeks post strep infection
• IgG and C3 on biopsy
• ASOT (anti streptolysin-O-Titre)
Nephritic syndrome
• Other causes:
– HSP (Henoch Schonlein Purpura)
• Systemic variant of IgA nephropathy
• Usually 3-10yrs old
– Plus fever, rash (purpura on legs and buttocks), joint pain,
abdo pain

– SLE
– Cryoglobulinaemia
– Infective endocarditis
– Tubulointerstitial nephritis
Asymptomatic haematuria and proteinuria
• Alports syndrome
– (inherited renal failure and deafness)

• Thin basement membrane disease
– (inherited AD, BP and renal function normal)

• Remember UTI
– But often plus frequency, dysuria, temperature
Parts of Kidney
• Simplified
– Glomerulus
– Blood vessels
– Tubules
– Interstitium
Glomerulonephritis
• Inflammation of glomerulus
• Usually present with:
– Haematuria with red cell casts
– +/- Proteinuria
– May present as ARF, nephritic or nephrotic
syndrome
GN
• IgA (bergers disease)
– IgA, young girl, 3-4 days post URTI

• Minimal change
– Commonest cause of nephrotic syndrome in kids, fusion of podocytes, treat
high dose Prednisolone, excellent prognosis

• Membranous
– Commonest cause of nephrotic syndrome in adults, thickened BM with spikes
(IgG), idiopathic, or malignancy, SLE, Drugs or Hep B

• Proliferative (post strep)
– Post Strep, 1-3 weeks post infection, IgG on biopsy, ASOT and low C3

• Focal Segmental Glomerulosclerosis
– Only some glomeruli have segmental sclerosis, assoc HIV, high recurrence in
transplants

• Thin BM disease
– AD – family history, heamaturia without renal failure or hypertension
GN
• Membranoproliferative/mesangiocapillary
– Mesangial proliferation with double BM
– Two types
• I - assoc Cryoglobulinaemia/Hepatitis C
• II - assoc Partial lipodystophy

• Rapidly progressive GN

– ESRF in weeks
– Focal necrotising GN with cresentic changes
– Assoc:
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Vasculitis – Wegners/Churg-Strauss
Goodpastures
SLE/ RA
Other GN (eg IgA)
Parts of kidney
– Glomerulus
– Blood vessels
– Tubules
– Interstitium

Act as one
Tubulointerstitial Nephritis
• A cause of a Nephritic type picture due to damage to
the tubules or interstitium
• Almost all due to hypersensitivity reactions to drugs
– Penicillins or NSAIDS

– Also Cadmodium, mercury, reflux, sickle cell or urate nephropathy

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Often get Eosinophilia
May have fever, arthralgia and rash
‘Non-oliguric renal failure’
(No red cell casts – signifies glomerular
damage)
Renal Failure
Acute Renal Failure
Chronic renal failure
Acute renal failure
• Suddenly and usually reversible loss in renal
function occurring over hours or days.
• Usually associated with a reduced urine
volume
Causes ARF
– Pre-renal - Decreased perfusion of kidneys
• shock/hypovolaemia
• (usually reversible but may progress to ATN)

– Renal
• ATN(85%)
• GN/interstitial disease

– Post renal - Obstruction of urine flow
• Intra-lumen – stone
• In the wall – stricture/tumour
• Compressing wall – prostate/tumour/AAA
• Remember blocked catheter if catherised
Acute tubular necrosis - ATN
• Tubular cells have a very high oxygen
requirement.
• If deprived of oxygen they die
• Take 7-21 days to regenerate
• If insult is prolonged the damage may be
irreversible
• Oliguria – polyuria - normal
Uraemia
• (a term loosely applied to describe the symptoms that accompany renal
failure, presumably due to build up of toxic products)

• Anorexia, nausea, vomiting
• Pruritis, hiccups
• Encephalopathy, fits, coma

• Pulmonary oedema, hyperkalaemia, acidosis
Approach to ARF
• Rule out or treat hypovolaemia
• Insert catheter (rules out obstruction and allows
close monitoring of fluid balance)
• Urine dip
• Bloods (U&Es, FBC, ABG, ECG, CRP (+/-ANA, anti GBM, ANCA))
• USS urinary tract
• Early nephrological advice
• Treat complication – e.g. hyperkalaemia, adjust drug
doses e.g. gentamicin
Dialysis in ARF
• 4 main indications
– Hyperkalaemia not responding to medical
treatment
– Pulmonary oedema not responding to medical
treatment
– Severe acidosis
– Complications of uraemia – pericarditis or
encephalopathy
Chronic Renal Failure
• Substantial and irreversible deterioration of
renal function, classically develops over a
period of years
• Commonest causes
– DM
– HTN
– Glomerulonephritis
– ADPKD
Chronic renal failure - Problems
• Fluid retention
• Anaemia (Burr cell)
• Metabolic bone disease
– (low Ca, high phosphate)
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Hyperparathyroidism (2 and 3rd), osteomalacia, osteoporosis

Infection
Hypertension, increased CVS risk
Pericarditis (uraemic)
Acidosis, hyperkalemia
Approach to CRF
• Identify cause
• Prevent further progression if possible
• Once creatinine hits 300 there is usually
progressive deterioration regardless of the
cause
Dialysis in CRF
• This should be started when patient has
advanced renal failure, but before they
develop complications
• Usually creatinine around 600-800
• Usually haemodialysis 4 hours 3x a week
Dialysis
• 2 main types
• Intermittent haemodialysis
– AV fistula
– Better filtration

• Continuous peritoneal dialysis

– ‘Tenckhoff’ catheter
– Better kids (growth) and elderly (less haemodynamic
fluctuations)

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(Haemofiltration – ITU, continuous)
Transplant
• Refer to transplant team early
• Transplant nurse, transplant coordinator etc
• Needs ABO and HLA compatibility
• 90%1 year graft survival
• 50% 10 year graft survival
• Best with living related donor
Transplant drugs
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Steriods
Azathioprine
Ciclosporin
Tacrolimus/Sirolimus
Mycophenolate
Complication of transplant
• Graft failure
– Acute – usually preventable with
immunosuppressant's
– Chronic – Slow decline in function – irreversible

• Infection
• Malignancy – skin (SCC), lymphoma
• Side effects of drugs – e.g. gum hypertrophy
with ciclosporin
Diseases which can reoccur in a graft
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IgA Nephropathy
Goodpastures
Focal Segmental Glomerulosclerosis
Metabolic diseases (DM)
Rare Renal
Goodpastures
• Autoantibodies against type IV collagen in
lung and kidney basement membrane (anti –
GBM)
– Haemoptysis
– Haematuira

• Immunosuppression and plasma exchange
(recurs in transplant)
Wegners
• A vasculitis with granulomas
• Get sinusitis, nose bleeds, nasal deformities,
arthritis, cavitating lung lesions, haemoptysis
and renal failure

• Circulating C-ANCA against PR3
SLE and Scleroderma
• Kidneys often involved
• No renal involvement in drug induced SLE
• SLE renal involvement graded I-V, V being
nephrotic syndrome due to membranous GN

• Scleroderma can get renal crisis – ACEi and
dialysis can be lifesaving
DM
• Diabetics often have kidney damage
• It is a microvascular complication
– (due to ischemia, glycosilation)

• Get Kimmelstiel-Wilson nodules in kidneys
• Microalbuminuria (30-300) is one of the first
signs – is screened for
• ACEi is renoprotective
Tumour Lysis Syndrome
• When cells die they release contents into
blood
• When large number of cells die all at once,
often in cancer on starting treatment urate
levels begin to cause issues
• Urate causes ARF
• Oncologists often start allopurinol (or
Rasburicase) prior to chemotherapy
ADPKD
• Autosomal dominant polycystic renal disease
• PKD1 (chromo 16) PKD2 (chromo 4)
• Multiple cysts in kidneys cause:
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Enlargement
Pain
Haematuria
Renal failure
At risk of SAH

• Screen with USS
Multiple Myeloma
• ARF is common in myeloma
– Immunoglobulins can block tubules – get
‘fractured casts with giant cell reaction’
– At risk of infection
– High calcium damages kidney
Renal Tubular Acidosis
• Rare cause of metabolic acidosis due to renal
issues
• “If patient is acidotic and urine is not the
suspect”
RTA
• Type I
– Don’t get rid of H+ in distal tubule
– Assoc stones and hypokalaemia

• Type II
– Leak bicarbonate
– No stones, usually assoc fanconi’s syndrome

• Type IV
– Get Hyperkalaemia
– Usually in diabetics with mild renal failure
Fanconi syndrome
• Generalised disturbance of renal function
• Can be inherited or acquired
• A cause of RTA II
Hepatorenal Failure
• Renal failure as a consequence of liver failure
• Very poor prognosis unless liver sorted out
Amyloid
• ‘Extracellular deposition of protein which form
B-pleated sheets’
• Tissues/organs become larger and firmer
• On microscopy get ‘apple green birefringence
in polarized light after staining with congo-red’
• Often due to myeloma (AL) or chronic
inlammatory diseases (AA)
• Can cause renal failure
Renal artery stenosis
• A cause of hypertension
• Narrowing in artery to kidney (e.g.
athersclerosis, NF) decreases perfusion
pressure
• That kidney begins to increase blood pressure
(renin-angiotensin-aldosterone)
• Get asymetrical kidneys on USS
• ACEi are contraindicated
UTI
UTI
• Mostly E-Coli (70% E-coli)
– Can use
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Trimethoprium
Nitrofurantoin
Amoxicillin
(Cefalexin a favourite if pregnant)

– Three day course if uncomplicated

• If developed pyelonephritis – needs i.v antibiotics
(renal angle tenderness, rigors)
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•
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Staph Saprophiticus – UTI only
Proteus – staghorn calculi
Pseudomonas – long term catheter, green
UTI
• Remember STIs as a cause of dysuria
• Can get sterile urethritis
• Can get asymptomatic Bacteriuria – treat if
pregnant
• If suspect TB do three EMU
• Prostate can be infected perianal pain and
tender prostate, difficult to treat, long course
of Abx
Pyelonephritis
• Infection of the kidney
• Usually due to ascending infection
• Fever/Rigors
• Loin pain
• Needs admisison, treat often with gentamicin,
cephalosporin or ciprofloxacin
Renal stones (nephrolithiasis)
• Pain – loin to groin, can’t get comfortable, rolling
around
• 95% have haematuria on dipstix
• Commonest cause: Calcium oxalate,
• Others: triple phosphate (staghorn calculi),
uric acid (radio lucent)

• Risk factors – dehydration, UTI, hypercalcaemia,
high dietary oxalate
Renal stones
• Treat:
– Diclofenac, esp PR is excellent
– May need antiemetic

• Check U&Es to ensure no renal failure from obstruction
• Do X-ray KUB, IVU or CT KUB
• Often pass on their own can do lithrotripsy, esp for
renal pelvis
• (Don’t forget AAA as a cause of ‘renal colic’)
BPH
• Benign prostatic hyperplasia
• Protate gets uniformly enlarged – smooth on
pr
• PSA may be slightly raised
• May get symptoms of Bladder outflow
obstruction
– Hesitancy, poor stream, terminal dribbling,
nocturia
BPH
• Treatment
– Drugs
• Tamsulosin – a-blocker relaxes smooth muscle
particular in urogenital tract and eases some of the
outflow obstruction
• Finasteride – 5a blocker, interfers with testosterone
conversion to potent DHT, helps provent progression

– Surgery
• TURP – Transurethral resection of the prostate
Prostate cancer
• 2nd commonest malignancy of men
• Adenocacinoma that arises in peripheral
prostate
• PSA tumour marker
• Likes metasisizing to bone (sclerotic lesions on
x-ray)
Prostate cancer
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•
•
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Craggy prostate on PR
Raised PSA (>4ug/l)
Do Transrectal ultrasound and biopsy
Bone scan/CT/MRI pelvis

• Gleason score – two scores 1-5
– Min score 2 max 10

• Treat
Prostatectomy/Radiotherapy/Brachytherapy/C
hemotherapy (Zolodex)Watch and wait
Torsion
• Urological emergency
– Testis twists and cuts off blood supply
– Will die in hours
– Sudden onset of pain
– Testis may lie high and transversely

– Needs surgery – untwist and if viable do
orchidoplexy, if not ochidectomy
Testicular lumps
• Can you get above it – ie is it a hernia
• Cold, hard, attached to testis – Cancer
• Whole testis swollen and tender – Epididymoorchitis
• Is it a lumpy ‘bag of worms’ ontop –
varicocele
• Is it cystic – above testis – epididymal cyst
• Is it cystic – surrounds testis - hydrocele
Testicular tumours
• Painless hard lump on testis
• Germ cell
– Teratomas, 20-30s, secrete BHCG and aFP
– Seminomas, 30-40s, secrete alk phos
• Treat Orchidectomy and chemo – esp cisplatin

• Non germ cell
– Leydig, sertoli and lymphoma
RCC
• Renal cell carcinoma, aka clear cell
• Classic triad of
– Pain
– Haematuria
– Renal mass

• Assoc smoking and von Hippel Lindau
• Can spread via direct extension, blood and lymph.
• Have a special ability to grow along vessels renal vein
to IVC
• Can secrete EPO
TCC
• Transitional cell carcinoma
• Can arise from Bladder, Ureter or renal pelvis
• Assoc smoking and analine dies
• Think in anyone >50 with painless haematuria
• Can do urine cytology, often do cystoscopy
•

Schistosomiasis can cause SCC of the bladder
Paeds Urology
• Phimosis – narrowing of opening of foreskin
• Paraphimosis – swelling of glans due to tight
foreskin being retracted and not replaced
• Hypospadias – abnormal opening of urethra
• Undescended testis – common in prems, try
to surgically correct, if intra-abdominal
remove due to risk of malignant change
• Balanitis – inflammation of the glans
Notes
•
•
•
•
•

Hyaline casts in normal individuals
Granular casts in renal damage
Dysmorphic RBCs indicate glomerular disease
Destruction of capillary loops – vasculitis
Tubular atrophy - CRF

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Renal revision

  • 2. Plan • • • • • • • Background Symptoms and Signs Renal medicine Renal failure Rare renal UTI and calculi Surgical renal
  • 3. Background • • • • Kidney is retroperitoneal 11-14cm in length Has a high proportion of cardiac output Central role in fluid and electrolyte balance
  • 4. Background • Other roles: – Erythropoetin – Vitamin D metabolism – Caltabolism of small proteins (insulin) – Drug excretion
  • 5. Background - Fluid and electrolytes • ADH (posterior pituitary) controls Osmolality • Renin-angiotensin-aldosterone controls Extracellular volume (via Na)
  • 6. Background – Urea and creatinine • Urea – nitrogenous waste due to breakdown of amino acids • Raised in • • • • Renal failure High protein intake GI bleed (acts as high protein meal) Dehydration • Creatinine • Raised in • Renal failure • Large muscle mass • Acute muscle damage
  • 7. Notes • Alcoholics tend to have a very low urea as poor diet and knackered liver • Sudden increase in Urea but not creatinine think dehydration or GI bleed • Ratio should be around 1:20 • Altered ratio (1:5) suggests acute renal failure, GI bleed etc • Low Hb, high urea, think GI bleed
  • 10. Frequency / Polyuria • Frequency implies increaed frequency voiding – different from polyuria (increased volume) • Frequency – Think UTI • Polyuria • Excess intake • Osmotic diuresis (DM) • Defective concentrating ability of kidney • Diuretics • CRF • Diabetes insipidus
  • 11. Oliguria • Urine output <0.5ml/kg/hr or less than 400mls per day • Causes (basically causes of ARF) – Pre-renal - Decreased perfusion of kidneys • shock/hypovolaemia – Renal • ATN/GN – Post renal - Obstruction of urine flow • Intra-lumen – stone • In the wall – stricture/tumour • Compressing wall – prostate/tumour/AAA • Remember blocked catheter if catherised
  • 12. Dysuria/Pain • Dysuria – pain on urination – Think of UTI/STI – Can get sterile urethritis • Renal stones classically cause ‘renal colic’ – loin to groin pain coming in waves, makes patient roll around
  • 13. Incontinence • Involuntary voiding of urine • If new onset suspect UTI, in men suspect protatism and overflow – check for bladder • Types: – Functional, i.e. caught short – Stress, weak pelvic floor, small amounts leak when coughing or laughing • Do pelvic floor exercises, can try Duloxeteine, TFVT or colposuspension is surgical option – Urge, uncontrolled emptying of bladder, e.g. brain damage. • Find cause, try timed voiding, oxybutynin/tolterodine can help
  • 14. Palpable kidneys • Bilateral palpable kidneys – – – – – ADPKD Bilateral hydronephrosis Amyloid Bilateral RCC Tuberous sclerosis • Unilateral palpable kidneys – RCC – Hydronephrosis – Bilateral cause with only one palpable • (In chronic renal failure kidneys tend to be small and shrunken)
  • 15. Kidney Vs Spleen • Kidney – Moves late on inspiration – Possible to get above – Smooth shape – Resonant to percussion • Spleen – Moves early on inspiration – Can’t get above – Notched leading edge – Dull to percussion – Enlarges towards RIF
  • 16. Glycosuira • Blood glucose of >10mmol will spill over into urine • Think DM • Can have congenital low renal threshold for glucose
  • 17. Haematuria • Is it Blood? – Rifampicin, beetroot, myoglobinuria (rhabdomyolysis) • Is it from urological tract – DD Vagina/rectum • Is it from kidney – Look for red cell casts • Is it painless – Think cancer
  • 18. Haematuria • Generalised disorder – IBE, coagulopathy, sickle cell, vasculitis • Specific disorder – Kidneys or Ureter/bladder/Urethra • Medical – GN – IgA or thin BM disease – Infection - UTI/prostatitis/schistosomiasis • Surgical – Stone, tumour, trauma
  • 19. Proteinuria • Urine Dipstix react to albumin but not Bence Jones Protein (myeloma) • ‘microalbuminuria’ is proteinuria in the range of 30-300mg/L (e.g. DM) • Quantify proteinuria with 24hr urine of protein/creatinine ratio (PCR) or albumin creatinine ratio (ACR) • >3.5g/day suggests nephrotic syndrome this may make the urine frothy • Proteinuria and heamaturia with red cell casts suggests Nephritic syndrome
  • 20. Proteinuria • Benign – Orthostatic proteinuria – Exercise/febrile illness • Excess circulating protein – Myeloma • Renal damage – DM/GN/nephritic/nephrotic syndrome • UTI
  • 22. Renal Medicine • Appears complex no definitive relationship between syndromes/symptoms and pathology/biopsy • But – Some patterns are present – Results from biopsy can help guide treatment • E.g. kid presents with nephrotic syndrome: – They are assumed to have minimal change GN. – Treat with Steroids. – If they do not respond to steroids they will have a biopsy that might reveal a different cause that might need a different treatment
  • 23. Nephrotic Syndrome • • • • Massive proteinuria (>3.5g/day) Hypoalbuminaemia (<30g/L) Oedema Hyperlipdaema • • Increased thrombotic tendency (loose antithrombin III and protein S) Increased susceptibility to infection (loose immunoglobulins)
  • 24. Nephrotic syndrome • Commonest cause in kids: – Minimal change glomerulonephritis • Not much to see on microscopy (minimal change), get fusion of podocytes on electron microscopy • Benign (only 1% progress to ESRF), treat high dose (60mg) Prednisolone, only biopsy if not responding • Commonest in adults – Membranous nephropathy • Thickened BM with spikes on silver staining (IgG) • 1/3 better,1/3 same, 1/3 ESRF • Idiopathic, or assoc Malignancy, drugs, SLE (V), Hep B
  • 25. Nephrotic syndrome • Other causes of Nephrotic syndrome: – Focal Segmental Glomerulosclerosis • Only some (focal) glomeruli have some (segmental) sclerosis. Idiopathic or assoc HIV • High recurrence in transplant – DM – Amyloid – SLE
  • 26. Nephritic Syndrome • Symptomatic haematuria and proteinuria – – – – – Haematuria with red cell casts Proteinuria (<3.5g/day) Oliguria Hypertension Oedema – (remember UTI can give you haematuria and proteinuria)
  • 27. Nephritic Syndrome • Commonest cause: – IgA nephropathy (Bergers disease) • 3-4 days post infection – usually URTI • 16-35 yr olds with episodic macroscopic haematuria • IgA and C3 on biopsy with mesangial hypercellularity • 2nd commonest: – Proliferative GN / Post Strep GN – 1-3 weeks post strep infection • IgG and C3 on biopsy • ASOT (anti streptolysin-O-Titre)
  • 28. Nephritic syndrome • Other causes: – HSP (Henoch Schonlein Purpura) • Systemic variant of IgA nephropathy • Usually 3-10yrs old – Plus fever, rash (purpura on legs and buttocks), joint pain, abdo pain – SLE – Cryoglobulinaemia – Infective endocarditis – Tubulointerstitial nephritis
  • 29. Asymptomatic haematuria and proteinuria • Alports syndrome – (inherited renal failure and deafness) • Thin basement membrane disease – (inherited AD, BP and renal function normal) • Remember UTI – But often plus frequency, dysuria, temperature
  • 30. Parts of Kidney • Simplified – Glomerulus – Blood vessels – Tubules – Interstitium
  • 31. Glomerulonephritis • Inflammation of glomerulus • Usually present with: – Haematuria with red cell casts – +/- Proteinuria – May present as ARF, nephritic or nephrotic syndrome
  • 32. GN • IgA (bergers disease) – IgA, young girl, 3-4 days post URTI • Minimal change – Commonest cause of nephrotic syndrome in kids, fusion of podocytes, treat high dose Prednisolone, excellent prognosis • Membranous – Commonest cause of nephrotic syndrome in adults, thickened BM with spikes (IgG), idiopathic, or malignancy, SLE, Drugs or Hep B • Proliferative (post strep) – Post Strep, 1-3 weeks post infection, IgG on biopsy, ASOT and low C3 • Focal Segmental Glomerulosclerosis – Only some glomeruli have segmental sclerosis, assoc HIV, high recurrence in transplants • Thin BM disease – AD – family history, heamaturia without renal failure or hypertension
  • 33. GN • Membranoproliferative/mesangiocapillary – Mesangial proliferation with double BM – Two types • I - assoc Cryoglobulinaemia/Hepatitis C • II - assoc Partial lipodystophy • Rapidly progressive GN – ESRF in weeks – Focal necrotising GN with cresentic changes – Assoc: • • • • Vasculitis – Wegners/Churg-Strauss Goodpastures SLE/ RA Other GN (eg IgA)
  • 34. Parts of kidney – Glomerulus – Blood vessels – Tubules – Interstitium Act as one
  • 35. Tubulointerstitial Nephritis • A cause of a Nephritic type picture due to damage to the tubules or interstitium • Almost all due to hypersensitivity reactions to drugs – Penicillins or NSAIDS – Also Cadmodium, mercury, reflux, sickle cell or urate nephropathy • • • • Often get Eosinophilia May have fever, arthralgia and rash ‘Non-oliguric renal failure’ (No red cell casts – signifies glomerular damage)
  • 36. Renal Failure Acute Renal Failure Chronic renal failure
  • 37. Acute renal failure • Suddenly and usually reversible loss in renal function occurring over hours or days. • Usually associated with a reduced urine volume
  • 38. Causes ARF – Pre-renal - Decreased perfusion of kidneys • shock/hypovolaemia • (usually reversible but may progress to ATN) – Renal • ATN(85%) • GN/interstitial disease – Post renal - Obstruction of urine flow • Intra-lumen – stone • In the wall – stricture/tumour • Compressing wall – prostate/tumour/AAA • Remember blocked catheter if catherised
  • 39. Acute tubular necrosis - ATN • Tubular cells have a very high oxygen requirement. • If deprived of oxygen they die • Take 7-21 days to regenerate • If insult is prolonged the damage may be irreversible • Oliguria – polyuria - normal
  • 40. Uraemia • (a term loosely applied to describe the symptoms that accompany renal failure, presumably due to build up of toxic products) • Anorexia, nausea, vomiting • Pruritis, hiccups • Encephalopathy, fits, coma • Pulmonary oedema, hyperkalaemia, acidosis
  • 41. Approach to ARF • Rule out or treat hypovolaemia • Insert catheter (rules out obstruction and allows close monitoring of fluid balance) • Urine dip • Bloods (U&Es, FBC, ABG, ECG, CRP (+/-ANA, anti GBM, ANCA)) • USS urinary tract • Early nephrological advice • Treat complication – e.g. hyperkalaemia, adjust drug doses e.g. gentamicin
  • 42. Dialysis in ARF • 4 main indications – Hyperkalaemia not responding to medical treatment – Pulmonary oedema not responding to medical treatment – Severe acidosis – Complications of uraemia – pericarditis or encephalopathy
  • 43. Chronic Renal Failure • Substantial and irreversible deterioration of renal function, classically develops over a period of years • Commonest causes – DM – HTN – Glomerulonephritis – ADPKD
  • 44. Chronic renal failure - Problems • Fluid retention • Anaemia (Burr cell) • Metabolic bone disease – (low Ca, high phosphate) – • • • • Hyperparathyroidism (2 and 3rd), osteomalacia, osteoporosis Infection Hypertension, increased CVS risk Pericarditis (uraemic) Acidosis, hyperkalemia
  • 45. Approach to CRF • Identify cause • Prevent further progression if possible • Once creatinine hits 300 there is usually progressive deterioration regardless of the cause
  • 46. Dialysis in CRF • This should be started when patient has advanced renal failure, but before they develop complications • Usually creatinine around 600-800 • Usually haemodialysis 4 hours 3x a week
  • 47. Dialysis • 2 main types • Intermittent haemodialysis – AV fistula – Better filtration • Continuous peritoneal dialysis – ‘Tenckhoff’ catheter – Better kids (growth) and elderly (less haemodynamic fluctuations) • (Haemofiltration – ITU, continuous)
  • 48. Transplant • Refer to transplant team early • Transplant nurse, transplant coordinator etc • Needs ABO and HLA compatibility • 90%1 year graft survival • 50% 10 year graft survival • Best with living related donor
  • 50. Complication of transplant • Graft failure – Acute – usually preventable with immunosuppressant's – Chronic – Slow decline in function – irreversible • Infection • Malignancy – skin (SCC), lymphoma • Side effects of drugs – e.g. gum hypertrophy with ciclosporin
  • 51. Diseases which can reoccur in a graft • • • • IgA Nephropathy Goodpastures Focal Segmental Glomerulosclerosis Metabolic diseases (DM)
  • 53. Goodpastures • Autoantibodies against type IV collagen in lung and kidney basement membrane (anti – GBM) – Haemoptysis – Haematuira • Immunosuppression and plasma exchange (recurs in transplant)
  • 54. Wegners • A vasculitis with granulomas • Get sinusitis, nose bleeds, nasal deformities, arthritis, cavitating lung lesions, haemoptysis and renal failure • Circulating C-ANCA against PR3
  • 55. SLE and Scleroderma • Kidneys often involved • No renal involvement in drug induced SLE • SLE renal involvement graded I-V, V being nephrotic syndrome due to membranous GN • Scleroderma can get renal crisis – ACEi and dialysis can be lifesaving
  • 56. DM • Diabetics often have kidney damage • It is a microvascular complication – (due to ischemia, glycosilation) • Get Kimmelstiel-Wilson nodules in kidneys • Microalbuminuria (30-300) is one of the first signs – is screened for • ACEi is renoprotective
  • 57. Tumour Lysis Syndrome • When cells die they release contents into blood • When large number of cells die all at once, often in cancer on starting treatment urate levels begin to cause issues • Urate causes ARF • Oncologists often start allopurinol (or Rasburicase) prior to chemotherapy
  • 58. ADPKD • Autosomal dominant polycystic renal disease • PKD1 (chromo 16) PKD2 (chromo 4) • Multiple cysts in kidneys cause: – – – – – Enlargement Pain Haematuria Renal failure At risk of SAH • Screen with USS
  • 59. Multiple Myeloma • ARF is common in myeloma – Immunoglobulins can block tubules – get ‘fractured casts with giant cell reaction’ – At risk of infection – High calcium damages kidney
  • 60. Renal Tubular Acidosis • Rare cause of metabolic acidosis due to renal issues • “If patient is acidotic and urine is not the suspect”
  • 61. RTA • Type I – Don’t get rid of H+ in distal tubule – Assoc stones and hypokalaemia • Type II – Leak bicarbonate – No stones, usually assoc fanconi’s syndrome • Type IV – Get Hyperkalaemia – Usually in diabetics with mild renal failure
  • 62. Fanconi syndrome • Generalised disturbance of renal function • Can be inherited or acquired • A cause of RTA II
  • 63. Hepatorenal Failure • Renal failure as a consequence of liver failure • Very poor prognosis unless liver sorted out
  • 64. Amyloid • ‘Extracellular deposition of protein which form B-pleated sheets’ • Tissues/organs become larger and firmer • On microscopy get ‘apple green birefringence in polarized light after staining with congo-red’ • Often due to myeloma (AL) or chronic inlammatory diseases (AA) • Can cause renal failure
  • 65. Renal artery stenosis • A cause of hypertension • Narrowing in artery to kidney (e.g. athersclerosis, NF) decreases perfusion pressure • That kidney begins to increase blood pressure (renin-angiotensin-aldosterone) • Get asymetrical kidneys on USS • ACEi are contraindicated
  • 66. UTI
  • 67. UTI • Mostly E-Coli (70% E-coli) – Can use • • • • Trimethoprium Nitrofurantoin Amoxicillin (Cefalexin a favourite if pregnant) – Three day course if uncomplicated • If developed pyelonephritis – needs i.v antibiotics (renal angle tenderness, rigors) • • • Staph Saprophiticus – UTI only Proteus – staghorn calculi Pseudomonas – long term catheter, green
  • 68. UTI • Remember STIs as a cause of dysuria • Can get sterile urethritis • Can get asymptomatic Bacteriuria – treat if pregnant • If suspect TB do three EMU • Prostate can be infected perianal pain and tender prostate, difficult to treat, long course of Abx
  • 69. Pyelonephritis • Infection of the kidney • Usually due to ascending infection • Fever/Rigors • Loin pain • Needs admisison, treat often with gentamicin, cephalosporin or ciprofloxacin
  • 70. Renal stones (nephrolithiasis) • Pain – loin to groin, can’t get comfortable, rolling around • 95% have haematuria on dipstix • Commonest cause: Calcium oxalate, • Others: triple phosphate (staghorn calculi), uric acid (radio lucent) • Risk factors – dehydration, UTI, hypercalcaemia, high dietary oxalate
  • 71. Renal stones • Treat: – Diclofenac, esp PR is excellent – May need antiemetic • Check U&Es to ensure no renal failure from obstruction • Do X-ray KUB, IVU or CT KUB • Often pass on their own can do lithrotripsy, esp for renal pelvis • (Don’t forget AAA as a cause of ‘renal colic’)
  • 72. BPH • Benign prostatic hyperplasia • Protate gets uniformly enlarged – smooth on pr • PSA may be slightly raised • May get symptoms of Bladder outflow obstruction – Hesitancy, poor stream, terminal dribbling, nocturia
  • 73. BPH • Treatment – Drugs • Tamsulosin – a-blocker relaxes smooth muscle particular in urogenital tract and eases some of the outflow obstruction • Finasteride – 5a blocker, interfers with testosterone conversion to potent DHT, helps provent progression – Surgery • TURP – Transurethral resection of the prostate
  • 74. Prostate cancer • 2nd commonest malignancy of men • Adenocacinoma that arises in peripheral prostate • PSA tumour marker • Likes metasisizing to bone (sclerotic lesions on x-ray)
  • 75. Prostate cancer • • • • Craggy prostate on PR Raised PSA (>4ug/l) Do Transrectal ultrasound and biopsy Bone scan/CT/MRI pelvis • Gleason score – two scores 1-5 – Min score 2 max 10 • Treat Prostatectomy/Radiotherapy/Brachytherapy/C hemotherapy (Zolodex)Watch and wait
  • 76. Torsion • Urological emergency – Testis twists and cuts off blood supply – Will die in hours – Sudden onset of pain – Testis may lie high and transversely – Needs surgery – untwist and if viable do orchidoplexy, if not ochidectomy
  • 77. Testicular lumps • Can you get above it – ie is it a hernia • Cold, hard, attached to testis – Cancer • Whole testis swollen and tender – Epididymoorchitis • Is it a lumpy ‘bag of worms’ ontop – varicocele • Is it cystic – above testis – epididymal cyst • Is it cystic – surrounds testis - hydrocele
  • 78. Testicular tumours • Painless hard lump on testis • Germ cell – Teratomas, 20-30s, secrete BHCG and aFP – Seminomas, 30-40s, secrete alk phos • Treat Orchidectomy and chemo – esp cisplatin • Non germ cell – Leydig, sertoli and lymphoma
  • 79. RCC • Renal cell carcinoma, aka clear cell • Classic triad of – Pain – Haematuria – Renal mass • Assoc smoking and von Hippel Lindau • Can spread via direct extension, blood and lymph. • Have a special ability to grow along vessels renal vein to IVC • Can secrete EPO
  • 80. TCC • Transitional cell carcinoma • Can arise from Bladder, Ureter or renal pelvis • Assoc smoking and analine dies • Think in anyone >50 with painless haematuria • Can do urine cytology, often do cystoscopy • Schistosomiasis can cause SCC of the bladder
  • 81. Paeds Urology • Phimosis – narrowing of opening of foreskin • Paraphimosis – swelling of glans due to tight foreskin being retracted and not replaced • Hypospadias – abnormal opening of urethra • Undescended testis – common in prems, try to surgically correct, if intra-abdominal remove due to risk of malignant change • Balanitis – inflammation of the glans
  • 82. Notes • • • • • Hyaline casts in normal individuals Granular casts in renal damage Dysmorphic RBCs indicate glomerular disease Destruction of capillary loops – vasculitis Tubular atrophy - CRF