URINARY SYSTEM

Renal Diseases - Classification

 Glomeruli – Glomerulonephritis
 Tubules and interstitium –
Tubulointerstitial diseases
 Blood vessels – Renovascular
diseases
 Tumours of kidney
Glomerular diseases
Classification
Primary – Unknown etiology
Secondary – to existing disease like DM, SLE
 Pathogenesis
− Immunological
 AgAb reaction at the glomerular basement membrane – intrinsic or
planted antigens
 Entrapment of circulating AgAb complex formed elsewhere
 Activation of complement system or cytotoxic lymphocytes
− Deposition of immune complexes – infiltration of inflammatory
cells due to cytokine release – chemical mediators of inflammation
– damage to glomeruli
Pathologic features
• Hypercellularity – Proliferation of
endothelial, epithelial, mesangial cells
• Basement membrane thickening –
deposition of immune complexes
• Leucocytic infiltration – Acute and
chronic
• Crescents – Hemispherical –
proliferation of parietal epithelial cells,
hyalinisation and sclerosis - ESRD
Primary GN
Acute post streptococcal proliferative GN
• Children
• Streptococcal skin infections –
deposition of anti streptococcal
AgAb
• Gross – Flea Bitten kidney -
hemorrhages
Acute post streptococcal proliferative GN
• Microscopy
• Hypercellular glomeruli –
neutrophils
• Immunoflorescent granular immune
complexes in mesangium
• Clinical features
• Fever, malaise, oliguria
• Complete recovery in 95%
Membranous GN
• Common cause of Nephrotic
syndrome in adults
• Antibodies against glomerular
antigens
• Thickening of glomerular basement
membrane – granular deposits of
immune complexes
Minimal change disease (Lipoid Nephrosis)
• Common cause of Nephrotic
syndrome in children
• Loss of polyanionic proteoglycans
and damage to footprocesses of
visceral epithelial cells
• No immune deposits
• Features of nephrotic syndrome
Rapidly progressive glomerulonephritis
• Immune mediated
• Microscopy –
• Glomeruli enlarged and pale
• proliferation of endothelial and
mesangial cells
• Crescents
• Immune deposits
• Clinical profile
• Moderate proteinuria, hematuria,
hypertension, edema and acute
renal failure
• Hemoptysis – damage to alveolar
basement membrane of lung –
Goodpasteur syndrome
Membranoproliferative GN
• Immune mediated
• Microscopy
• Large glomeruli hypercellular
• Thickening of GBM – double contour
– “Tram track GBM”
• Features of nephrotic syndrome
IgA Nephropathy (Bergers disease)
• Deposition of IgA in mesangium
• Widening of mesangium with mesangial cells proliferation
• Gross hematuria
Chronic GN
• Chronic ESRD following acute GN
• Gross
• Kidneys symmetrically contracted with fine
granularity in surface
• Cortex is thinned
Chronic GN
• Microscopy
• Primary GN with hyaline degeneration
and obliteration of glomeruli
• Interstitial fibrosis
Secondary GN
Diabetic Nephropathy
• Type I DM (Insulin dependant)
• Pathology
• Thickening progressive widening of GBM –
diabetic microangiopathy
• Nodular glomerulosclerosis – Kimmelstein
Wilson lesion
• Diffuse glomerulosclerosis – complete
obliteration of glomeruli
• Fibrin cap and capsular drop – Bowmans
space
• Accumulation of glycogen in tubules
• Recurrent UTI
• Clinical features
• Proteinuria, chronic renal failure
Lupus Nephritis
• Deposition of circulating immune complexes
• Pathology
• Mesangial lupus nephritis
• Focal proliferative GN
• Diffuse proliferative GN
• Membranous GN
• Clinical features
• Proteinuria
TubuloInterstitial diseases
Pyelonephritis
• Inflammatory
• Acute & Chronic
• Etiology – gram negative bacilli – E coli from fecal flora
• Ascending infection from renal pelvis
• Predisposing factors
• Catheterisation
• Females – short urethra, increased risk of urethral trauma, absence of
antibacterial prostatic secretions, increased adherence of bacteria to distal
urethra
• Defects in bladder function
• Vesico ureteric reflux – incomptetence of vesicoureteral valve
• Pathology
• Acute pyelonephritis – suppurative abscess
• Complications
• renal papillary necrosis
• Pyonephrosis – severe suppuration
• Perinephric abscess – spillover into perinephric tissues
• Clinical features
• Fever, pain in renal angle, frequency and urgency of urination, painful micturition
• Leucocyte casts in urine
• Diagnosis by urine culture
• Chronic pyelonephritis
• Gross
• kidneys symmetrically contracted – large
irregular pitted scars
• Pelvicalyceal system distorted
• Microscopy
• Tubulointerstitial inflammation
• Tubules filled with colloid cast material –
thyroidisation
• Periglomerular fibrosis
Clinical Profile
 Acute nephritic syndrome – Mild proteinuria, hematuria,
hypertension
 Nephrotic syndrome – Massive proteinuria, edema, hypolipidimia
 Asymptomatic proteinuria / hematuria
 Acute renal failure – oliguria
 Chronic renal failure – ESRD
 Others – Obstructive uropathy (calculi), UTI
• Acute renal failure
• Reversible
• Severe damage to tubular epithelium
• Ischemic acute tubular necrosis
• Severe ischemia to renal circulation – shock, haemorrhage, DIC
• Toxic acute tubular necrosis
• Toxins and drugs – mercury, sulphonamides, NSAIDs
• Clinical features
• Sudden reduction in urine output progresses to severe oliguria
• Rise of blood urea and nitrogen progresses to metabolic acidosis and hyperkalemia
• Chronic renal failure
• ESRD – elevation of urea and creatinine, reduction of GFR
• Multisystem disease
System Manifestations
Fluid electrolyte Dehydration, edema, hyperkalemia,
acidosis
Calcium metabolism Hypocalcemia, hyperphosphatemia
Skeletal system Renal osteodystrophy
CVS Congestive cardiac failure
RS Pulmonary edema
GIT Uremic gastroenteritis, ulcerations
Hematologic Anemia, bleeding disorders
Neuromuscular Myopathy, peripheral neuropathy
Dermatology dermatitis
Urolithiasis
• Major type – calcium phosphate and oxalate
• Etiology
• Hypercalciuria, hyperuricemia etc
• Highly concentrated urine
• Proteus infection
• Morphology
• Mostly Unilateral in renal calyces,
pelvis
• Usually small
• Triple phosphate stones – large in
shape of pelvicalyceal system – stag
horn calculi
• Clinical features
• Severe renal colic – small stones
• Hematuria – large stones
• Obstruction - UTI
Tumours of kidney
Classification
Epithelial Renal cell adenoma
Renal cell carcinoma
Oncocytoma
Nephroblastic tumours Nephroblastoma (wilms tumour)
Mesoblastic nephroma
Nonepithelial Angiomyolipoma
Fibroma
Hemangioma
Miscellaneous Reninoma
Clear cell sarcoma
Renomedullary interstitial tumour
Malignant rhabdoid tumour
Teratoma
Metastatic tumours Breast, lung
Renal cell carcinoma
• Men, 6-7th decade
• Etiology – smoking, obesity, HT, estrogen
therapy, asbestosis, chronic renal failure
etc
• Gross
• Solitary mass – upper pole
• Cut section – bright yellowish with
haemorrhage and cystic change
Renal cell carcinoma
• Microscopy
• Adenocarcinoma
• Cells with clear cytoplasm with irregular
nuclei
• Tubular, trabecular or solid pattern
• Clinical features
• Costovertebral pain, palpable mass, hematuria
• Paraneoplastic syndromes – polycythemia, hypercalcemia etc
• Direct spread to renal pelvis
• Hematogenous metastasis – lungs, bones etc.
Nephroblastoma (Wilms tumour)
• Pediatric
• Clinical features
• Large abdominal mass, pain, hematuria
• Spread to perineal tissue, adrenals, liver,
lung etc
• Gross – large irregular mass,
haemorrhage, fleshy in cut section
Nephroblastoma (Wilms tumour)
• Microsocopy
• Blastemal cells – primitive, scant
cytoplasm, round nucleus
• Stromal cells – myxoid areas,
heterogenous elements
• Epithelial cells – abortive tubules
Disorders of urinary tract
Cystitis
• Inflammatory degeneration of bladder
• Acute and chronic
• Etiology
• E coli, proteus
• Drugs – cyclophosphamide
• Special forms
• Ulcerative interstitial cystitis – Hunners ulcer – women – superficial ulcerations,
underlying fibrosis
• Emphysematous cystitis – Diabetic – Bullae
• Malakoplakia – chronic – yellowish raised lesions with pink mucosa
• E coli infection, immunocompromised patients
• Foamy macrophages (hansemans cells)
• Laminated mineralized concretions – Michaelis Gutmann bodies