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Pathology of the Kidney

Congenital Diseases


10% of population

20% of chronic renal failure in children due to renal dysplasia/ hypoplasia

6% due to polycystic kidney

Renal Agenesis

Lack of metanephric primordium; failure of ureteral bud dev.; failure of contact of ureteral bud & metanephros


Rare. Male: female = 2.5:1. A/w with other congenital malformation. Most stillborn. flat nose, wide-set eyes, prominent epicanthal folds, large flabby & low-set ears, receding chin. Disease incompatible with life.


Male:female = 2:1.

Renal Hypoplasia

Renal Hypoplasia with Oligomeganephronia. Reduced number of lobules & calyces (<5). Histology. Small kidney. Hypertrophied glomaruli. Normal should be >10. Kidney is small. Primitive glomeruli & tubules in dense fibrous/ fatty interstitium. True hypoplastic kidney shows no scars.

Ectopic kidneys

kidney above pelvic rim. Complication. kinking/ tortuosity of ureters. obstructs urinary flow. Predispose to UTI.

Horseshoe Kidney

Fusion of upper/ lower(90%) of kidneys. leads to renal calculi.


Cystic Kidney Diseases

Simple Cyst


single/ multiple cysts of renal cortex

usually 2-5 cm diameter.

smooth wall

lined by low cuboidal epithelium.

filled with clear serous fluid

occasionally hemorrhagic.


hemorrhage. stromal reaction. can cause flank pain & irregular contours. may mimick RCC.

Cystic Renal Dysplasia

sporadic, nonfamilial disease due to abnormal metanephric differentiation. kidneys enlarged & multicystic. associated with obstructive abnormalities of ureter & lower urinary tract. immature ducts surrounded by undifferentiated mesenchyme. focal cartilage formation. may be unilateral or bilateral.

Polycystic Kidney Disease

Adult Polycystic Kidney Disease. Infantile Polycystic Kidney Disease. Medullary Sponge Kidney. Nephronophthisis - Medullary Cystic Disease Complex. Autosomal Dominant. Impairment of tubular epithelial growth & differentiation. Morphology. Clinical Course. Autosomal Recessive. Rapidly progress to renal failure. Kidneys enlarged by multiple cylindrically dilated collecting ducts. Largely associated with polycystic liver & proliferating bile ducts. mulitple cystic dilation in collecting ducts of medulla. innocuous. progressive renal disorders. onset in childhood. small medullary cysts. Clinical Features. PKD1 gene. PKD2 gene. Can present from early childhood or as late as 80 years old. mutations alter cell-cell & cell-matrix interactions. kidneys enlarged. composed almost totally of cysts. Interstitial inflammation & fibrosis in late disease. Symptoms. Association. Complications. Ducts at right angle to cortex and fills both cortex & medulla. congenital hepatic fibrosis. but may predispose to renal calculi. corticomedullary area. a/w cortico tubular atrophy & interstitial fibrosis. polyuria, sodium wasting, tubular acidosis. progression to renal failure. should be considered in children presenting with chronic renal failure + amilyr history + tubulointerstitial nephritis on biopsy. Always bilateral. 3-4cm in diameter. anywhere along nephron. compresses adjacent parenchyma. Flank Pain. hematuria. proteinuria. Bilateral Abdominal Mass inducing dragging sensation. Polycystic Liver Disease. Cerebral Berry Aneurysm. Mitral Valve Prolapse. Hypertension. Progressive Renal Failure. due to hemorrhage into cyst. 40%. 5 - 10 %. 20 - 25%. coronary heart disease. hypertensive brain hemorrhage. Worsened in hypertension.

Glomerular Diseases

Pathogenesis. Nephritic Syndrome. Membranoproliferative GN (mesangiocapillary GN). Nephrotic Syndrom. Immune Complex. Cell-mediated. Epithelial Cell Injury. Renal Ablation Glomerulopathy. inflammation of glomeruli. Clinical Presentation. morphology. Acute. Chronic GN. thickened capillary loops & glomerular cell proliferation. cause of 20% of nephrotic syndrome in children & adults. Clinical. Type I MPGN. Type II MPGN. pathology of glomerular capillary walls causing massive protein leakage. Clinical Features. Minimal Change Disease (Lipoid Nephrosis). Focal Segmental Sclerosis. Membranous Nephropathy. glomerular deposition of Ag-Ab complexes. Trapped Circulating Immune Complex. Immune Complex Formed In-Situ. T cells become sensitized and induce cytotoxic damage to kidneys. Gross hematuria. Proteinuria. Decr GFR. enlarged hypercellular glomeruli. fibrin deposit within capillary lumen & mesangium. interstitial edema & inflammation. immune complexes deposited in glomeruli. Acute Proliferative (post-strep/infx). Rapidly Progressive Glomerulonephritis (Cresentic). IgA Nephropathy. Hereditary Syndromes. common end-stage of many glomerulonephropathies. glomeruli completed effaced by hyalinosis. Insidious onset. proteinuria, hypertension, uremia. may also have nephrotic/ nephritic syndrome. Progress to uremia and death. No treatment. Presentation. poor prognosis. Type I MPGN may present with other autoimmune disorders. Caused by circulating immune complexes. a/w Hep B & C antigenemia, SLE, infected AV shunts & seconfary infx with persistent antigenemia. Morphology. Autoimmune disease. genetic predisposition to Type II MPGN. Morphology. massive proteinuria. hypoalbuminemia. systemic edema. sodium & water retention. hyperlipidemia & lipiduria. susceptibility to infection. thromoembolism. major cause of nephrotic syndrome in children. Morphology. Etiology & Pathogenesis Unknown. Clinical. Sclerosis of some glomeruli. focal involvement. segmental involvement. Pathogenesis. Morphology. Clinical. Major cause of nephrotic syndrome in adults. diffuse glomerular capillary wall thickening. Pathogenesis. Morphology. Clinical. deposited subendothelialy/ in mesangium. reaction not incited by glomerulus. activation of alternative complement pathway. Resolution. Ag originates from glomerulus. Anti-GBM nephritis. Heymann Nephritis. Planted circulating immune complexes. smoky brown (rather than bright red). often with RBC casts & dysmorphic rbc. mild to moderate. Azotemia/ Uremia. Hypertension. Oliguria. WBC infiltration. endothelial, mesangial & epithelial cell proliferation. all glomerular lobules involved. granular ("lumpy bumpy") immunofluroscent pattern. nephritic syndrome. 1-4 weeks AFTER pharyngeal or skin strep (grpA, beta hemolytic, nephritogenic strains) infx. immune complexes formed either in situ or circulating, deposited in glomeruli. clinical course. Complication. clinical syndrome characterised by rapid & progressive loss of renal function w oliguria. Treatment. Morphology. Type I RPGN. Type II RPGN. Type III RPGN. mesangial proliferation & IgA deposition. Due to abnormal IgA production & clearance. Morphology. Clinical. Alport Syndrome. Thin Membrane Disease. impossible to identify antecedental lesion. often discovered only after incidence of renal insufficiency. hypertension very common & may dominate clinical picture. progressively less nephrotic syndrome as glomeruli become obliterated, reducing proteinuria. requires renal dialysis & transplant. non-nephrotic. combined nephritic-nephrotic. Prinicipally presents as nephrotic syndrome. Most progress to renal insufficiency/ end-stage renal failure. Type II MPGN worse prognosis. similar to chronic serum sickness. large glomeruli. hypercellularity. EM. Immunofluorescence. C3 Nephritic factor. activates alternative complement pathway. large glomeruli. hypercellularity. EM. immunofluorescence. >3.5 g/day. excessive permeability of glomerular capillary wall to proteins. highly selective. non-selective. decreased oncotic pressure. compensatory synthesis of proteins (including lipoproteins) by liver. decreased plasma vol. decreased GFR. Normal glomeruli in light microscopy. EM. Immunofluorescence shows no immune deposits. Immune defect of T cells suspected. T cells secrete cytokine which cause loss of epithelial foot processes. may be linked to nephrin gene. insidious development of nephrotic syndrome. no hypertension. Renal function normal. Low molecular weight proteinuria. Good prognosis. only some glomeruli affected. only a portion of capillary tuft is involved in affected glomeruli. Idiopathic. Secondary. Both causs visceral epithelial damage. focal & segmental involvement of glomeruli. LM. EM. Immunofluorescence. non-selective proteinuria. Need to differentiate from Minimal Change Disease in children. Poor prognosis. Collapsing FSGS variant. due to electron-dense deposits along subepithelial side of GBM. Idiopathic (85%). 15% Due to underlying malignancy, SLE, exposure to gold/ mercury, drug-induced. LM. EM. as disease progress. Insidious development of Nephrotic Syndrome. Persistent proteinuria may be present w/o other symptoms of nephrotic syndrome. does not respond to steroids. Variable course. granular immunofluorescent pattern. EM shows clumps of electodense deposits. Ag not of glomerular origin. but may be exogenous or endogenous. leucocytic infiltration. endothelial, mesangal & parietal epithelial proliferation. Immune complexes removed by phagocytes. autoimmune disease to Glomerular Basement Membrane type IV collagen. linear immunoflourescent pattern. salt/water overload. other infections can also give same picture. serum anti-streptolysin O (ASTO) levels high. exogenous Ag from streptococci, pneumococci, staphylocci viruses eg. mumps, measles, chicken pox, HepB/C. endogenous Ag from SLE (can also cause other nephropathies). EM electron-dense deposits in sub-endo, sub-epith (most common) mesangium, or intra-membranous. granular immunofluroscent pattern. hypo-complementemia. 1-2 weeks after recovery from sore throat. Majority recover fully with conservative Rx. RPGN (rapidly progressive glomerulonephritis). Chr renal disease. hematuria. moderate proteinuria. hypertension & edema. Progressive renal impairment within weeks. Intensive plasma exchange. steroids & cytotoxic agents. Crescents. Ruptures in GBM. subepithelial deposits seen in EM. anti-GBM disease. linear IgG deposits in GBM. anti-GBM Ab may cross react with pulmonary alveolar basment membrane. Immune-complex mediated. Complication of any immune complex mediated glomerulonephritis. Immunofluorescence shows granular pattern. pauci-immune type. may be part of systemic vasculitis. majority of cases are isolated & idiopathic. due to genetic or acquire defecrs in immune regulation. deposition of IgA on mesangium. A/w. Glomeruli may be normal with subtle hypercellularity. Or may show focal proliferative/ sclerotic lesions. Immunofluorescence. affects children & young adults. Presents with gross hematuria within 1-2 days of non-specific URTI/GI/GU infx. A/w Henoch-Scholein Syndrome. Variable course. glomerulopathy + nerve deafness. also a/w lens dislocation, cataracts, corneal dystrophy. segmental glomerular proliferation or sclerosis. Foam cells. EM. only hematuria & proteinuria. 50%. but may also present as nephritic syndrome/ mild proteinuria. no complete recovery. lobular appearance. proliferation of mesangial cells. infiltration of leukocytes. subendothelial electron-dense deposits. C3 deposited in granular pattern. Presence of IgG, C1q & C4. Autoantibody. reduced complement levels. lobular appearance. proliferation of mesangial cells. infiltration of leukocytes. deposition of material of unknown composition. mesangial rings. IgG, C1q & C4 absent. only low molecular weight proteins. milder injury. loss of high molecular weight proteins. more severe injury. increased aldosterone. uniform & diffuse effacement of foot processes of visceral epithelial cells. leads to proteinuria. mainly albumin. 90% response rate to short corticosteroid therapy. proteinuria may recur after steroid withdrawal. Low tendency to chronic renal failure. prior glomerular disease (eg IgA nephropathy). loss of renal mass (renal ablation FSGS). Presence IgM & C3. segmental hyalinosis involving capillary walls & lumens. starting with juxtamedullary glomeruli. progressing to all levels of cortex. Sampling Errors. increased mesangial matrix. collapsed basement membrane. hyalinosis. lipid droplet deposition. global sclerosis. collapsing variant of FSGS. Similar to lipoid nephrosis. Ig & complement deposits in areas of hyalinosis (segmental trapping). more likely to exhibit. Idiopathic FSGS responds poorly to steroid. commonly progress to chronic renal failure. recurs in 50% of transplants. more severe disease with poor prognosis. a/w HIV. a form of chronic immune complex nephritis. may be due to autoantibodies. Diffuse thickening of GBM. subepithelial deposits in GBM. separated from each other by small, spikelike protrusions of GBM matrix. spikes close over deposits. podocytes lose foot processes. GBM become sclerosed & fully hyalinised. Non-selective proteinuria. spontaneous remission. progressive renal failure in 1-15 years. prognosis better in children than adults. immune complexes. complement. malaise, fever, nausea. oliguria, hematuria (smoky urine). maintain Na & water balance. Complication more common in adults. urinary RBC casts. variable. resulting in severe oliguria. to remove antibodies. immunosuppression. due to parietal cell proliferation & macrophage migration into Bowman space. tend to undergo sclerosis. Ab to type IV collagen of GBM. Pulmonary hemorrhage (Goodpasture Syndrome). lack of Anti-GBM or immune complexes. Most have anti-neutrophil cytoplasmic Ab (ANCA). Wegener granulomatosis. microscopic polyarteritis. activate alternative complement pathway. celiac disease. liver disease. mesangial deposition of IgA, C3, properdin. absence of C1q, C4. lasting several days before subsiding. recurs every few months. systemic syndrome due to IgA deposition in mesangium. purpuric rash. abdominal pain. joint arthritis. kidney involvement. Most maintain normal function for decades. Slow progression to chronic renal failure. interstitial cells with foamy appearance due to accumulation of fats & mucopolysaccharides. GBM appears thin & attenuated. irregular foci of thickening or atenuation with splitting of lamina densa. GBM thickened. Glomerular capillary wall shows double contour/ tram track appearance. suggests immune complex pathogenesis. GBM thickened. Glomerular capillary wall shows double contour/ tram track appearance. lamina densa & subendothelial space transformed into irregular, ribbon-like, electron dense structure. "dense deposit disease". granular-linear deposit of C3 in GBM. albumin. complete remission within 8 wks of steroid therapy. 50%. chronic reflux. analgesic abuse. unilateral renal agensis. if 10% have lesion & biopsy shows 10 glomeruli. if 10% have lesion & biopsy shows 20 glomeruli. deposition of hyaline masses. sclerosis of whole glomerulus. only in some affected glomeruli. pronouced tubular atrophy & interstitial fibrosis. collapse & sclerosis of entire glomerular tuft. Loss of foot processes in of visceral epithelial cells. but greater degree of epithelial cell detachment. esp IgM. hematuria. reduced GFR. Hypertension. "spike & dome patten). incorporates them into GBM. later catabolised & removed. recurrent hemoptysis. defects in intestinal mucosa. defective hepatobillary clearance of IgA. basket-weave appearance. due to splitting of GBM by cell processes extending peripheral capillary loops. due to splitting of GBM by cell processes extending peripheral capillary loops. 35% chance of missing lesion. 12% chance of missing lesion. w denudation of underlying GBM. leaving cavitis in GBM.

Diabetic Nephropathy

Most common cause of chronic renal failure. Glomerular Lesion. Hyaline Arteriosclerosis. Pyelonephritis. GBM thickening. Diffuse glomerulosclerosis. Nodular glomerulosclerosis. amorphous hyaline thickening of wall of arterioles. affects both afferent & efferent arterioles. related to duration of disease & level of blood pressure. a/w hypertension. inflammation of kidneys. DM predisposes to pyelonephritis. necrotizing papilitis. glomerular capillary basement membrane thickened throughout entire length of glomerulus. basal lamina is widened and sometimes replaced by concenric layers of hyaline material (mainly type IV collagen). Thickened GBM is more permeable to plasma protein. But may not be seen with associated change in renal function. diffuse increase in mesangial matrix. mesangial cell proliferation. a/w GBM thickening. leads to nephrotic syndrome. ball-like deposits of laminated matrix in mesangial core of lobule. Occurs irregularly throughout kidney. Deposits. Advanced disease. Management. narrowing of lumen. plasma proteins penetrate into the abnormally permeable walls of arterioles and get trapped. but can present w/o hypertension in diabetics. usually begins in interstitial tissue. spread to tubules and glomeruli. ischemia from microangiopathy. increased susceptibility to bacterial infections. acute necrosis of renal papillae. ie. Kimmelstiel- Wilson lesion. random glomeruli. positive on periodic acid-Schiff stain. contain mucopoysaccharide, lipid, fibrils, collagen fibres. Nodular nephrosclerosis major cause of morbidity & mortality in diabetics. multiple nodules in 1 glomerulus. tubular ischemia. interstitial fibrosis. Anti-hypertensives. Strict blood sugar control. Dietary protein restriction. Renal/ Pancreas Transplantation. ball-like deposits of laminated matrix within mesangial core of lobule. tend to develop at periphery of glomerulus. push glomerular capillary further periphery. related to duration of disease. genetic predisposition. induces sufficient ischemia to cause fine scarring of kidneys. finely granular cortical surface. ACE-Inhibitors. Angiotensin II Receptor blocker. forms halos around the nodules.

Hypertensive Nephropathy

Benign Nephrosclerosis. Malignant Nephrosclerosis. Renal disease in benign hypertension. similar changes also found in many renal diseases. pathogenesis due to hyaline arteriosclerosis. Morphology. Renal changes in accelerated hypertension. Pathogenesis. Morphology. Clinical Course. renal disease cause hypertension. homogenous pink hyaline thickening of arteriole wall. lumin narrowing. loss of underlying cellular detail. Gross. Decreased blood flow. often superimposed on poorly controlled essential hypertension. vascular damage to kidneys. hyperplastic aerteriosclerosis. Renal ischemia. pin-point hemorrhage on cortical surface. Small vessels. Large vessels. Diastolic blood pressure >120mmHg. Raised intracranial pressure. encephalopathy. cardiovascular abnormality. renal failure. leads to nephrosclerosis. Kidneys are symmetrically atrophied. ischemic atrophy. glomerular changes. diffuse tubular atrophy. interstitial fibrosis. from long-standing benign hypertension. increased permeability to fibrinogen, plasma proteins, endothelial injury & platelet deposition. causes release of platelet derived growth fx. intimal smooth hyperplasia of vessels. further narrowing of lumina. Stimulation of Renin-angiotensin system. rupture of arterioles/ glomerular capillaries. fibriod necrosis. necrotizing arteriolitis. Hyperplastic arteriolosclerosis. marked narrowing of arterioles & small arteries. papilledema. headache, nausea, vomitting, visual impairment. capsule strips with difficulty. surface of diffuse, fine granularity. pale. tiny retention cysts. narrowed cortex. GBM thickening. tufts get obliterated by homogenous hyalinization. wrinkling of capillary BM. collapse & retraction. fibrinoid necrosis of arterioles. intravascular thrombosis. vicious cycle. vessel walls take on homogeneous granular eosinophilic appearance. loss of underlying cellular detail. inflammation secondary to vascular damage. onion-skin appearance. obliterates lumina. malignant arteriolosclerosis & malignant nephrosclerosis. proliferation of intimal cells. concentric arrangement of intimal smooth muscle cells.

Tubular & Intersitial Diseases

Acute Tubular Necrosis. Acute Pyelonephritis. Xanthogranulomatous Pyelonephritis. Chronic Pyelonephritis. Renal TB. renal tubular cell destruction & renal impairment. Etiology. Pathogenesis. Morphology. Clinical features. Suppurative condition of kidney caused by bacterial infection. often due to infection of lower urinary tract. pathogenesis. morphology. Clinical Course. Caused by Proteus infx a/w urinary obstruction. Enlarged kidney filled with yellow nodules with grey-white tissue. Macrophages with vacuolated cytoplasm (foam cells), giant cells, lymphocytic infiltrate. Interstitial inflammation & scarring of renal parenchyma a/w gross scarring & deformity of pelvis & calyces. Inportant cause of chronic renal failure. Chronic Obstructive Pyelonephritis. Reflux Nephropathy. Morphology. Due to hematogenous spread from pulmonary TB. Starts as lesion in a papilla in the medulla. spreads with caseous necrosis within medulla and cortex to the whole kidney. Complication. most common cause of acute renal failure. ischemic. Nephrotoxic. arteriolar vasoconstriction. tubular obstruction by cell debris. back-leak of tubular fluid. altered glomerular ultrafiltration. Interstitial Inflammation. Protein casts in collecting ducts. Recovery phase shows epithelial regeneration. Ischemic. Nephrotoxic. initiating stage. maintainence stage. recovery stage. prognosis usually good unless there is overwhelming sepsis. mainly gram negative rods. urinary tract injury/ structural anomalies predispose. hematogenous infection. ascending infection. discrete yellow raised abscesses. suppurative necrosis/ abscess formation within renal parenchyma. Neutrophil infiltration. glomeruli appears resistant to infection. pyonephrosis. Necrotizing papillitis. lumbar pain. chills, fever, malaise. pyuria, bacteriuria. benign & self-limiting. complication. resembles renal carcinoma. Chronic diffused or localised Obstruction. Bilateral. Unilateral. UTI on pre-existing congenital viscero-ureteral reflux & intrarenal reflux. Results in scarring & atrophy of kidney. Gross. Microscopic. Complications. 5% of PTB cases. forms foci of caseous necrosis. tuberculous granulomas. renal destruction. ureter spread. reversible. due to period of inadequate blood flow to kidney causing hypoxia. toxic poisoning. increased endothelin. decreased nitric oxide & prostaglandin. edema. leuckcyte infiltration. Tamm-Horsfall protein. hemoglobin. plasma proteins. tubular cells with hyperchromatic nuclei & mitotic figures. Patchy tubular necrosis. involvement of proximal tubule straight segment & thick ascending loop of Henle. variable degrees of tubular injury & necrosis. 36 hr. persistent renal failure. severe oliguria. signs & symptoms of uremia & fluid overload. hyperkalemia. rising urine volumes. hpokalemia. E. coli. stasis of urine flow. bacteria seeding in septicemia/ infective endocarditis. more common. adhesion of bacteria to mucosal surfaces. colonisation of distal urethra. bacteria grows and expands against flow of urine. cystitis. infection of ureter and kidneys. widely scattered or limited to 1 region of kidney. begins in interstitium. ruptures & spreads into tubules. WBC casts found in urine. obstruction to drainage of pus. collection of suppurative exudate in renal pelvis, calyces & ureters. esp in diabetics, chronic analgesic abuse. sharply defined gray-white to yellow necrosis of apical 2/3 of pyramids. papillary tips show coagulative necrosis with neutophilic infiltrate. chronic pyelonephritis. Necrotizing Papillitis. Recurrent Infections. Recurrent inflammation & scarring. normally due to congenital anomalies of urinary system (esp urethra). can result in renal insufficiency. normally due to obstructive calculi. may be due to unilateral obstructive anomalies or ureter. unilateral reflux. bilateral reflux. Flat cortical scars. Papillary blunting. Calyceal dilation. Thick adherent renal capsule. Institial Inflammation & fibrosis. Disproportionate Tubular atrophy. Inflammation & fibrosis of calyceal mucosa & wall. Vascular changes. Associated Renal Ablation FSGS. chronic renal failure. hypertension. FSGS. fibrosis & obstruction. TB cystitis. TB epididymitis. shock, dehydration etc. drugs. toxin. lesser degree of tubular cell injury. involves short tubular segments. proximal tubules. dominated by inciting event. oliguria. predisposed by obstruction of urinary flow, instrumentation. more common in females. predisposed in viscero-ureteral reflux. diabetics. in patients with predisposing factors. a/w sepsis & renal failure. poor prognosis. posterior urethral valves. fatal. leads to renal insufficiency. pelvis & calyces. uneven scarring. uneven. atrophy of lining epithelium. tubules dilated or contracted. Dilated tubules contain colloid cast. hyaline arteriosclerosis. proteinuria. gentamicin, cephalosporin etc. mercury, lead, arsenic. a/w tubulorrhexis. esp in bilateral pyelonephritis. diffuse involvement. patches. pink to blue, glassy appearance, PAS-positive. thyroid-like appearance. due to associated hypertension. rupture of basement membrane.


Renal cell carinoma. Wilms Tumour. Bladder CA. Prostate. neoplasm of renal tubular epithelium. incidence. risk factor. Clear cell carcinoma. Papillary cell carcinoma. Clinical course. 3rd most common cancer in children <10yo. derived from mesoderm. Risk factors. Clinical Features. types. Nodular hyperplasia (BPH). Prostate CA (adenocarcinoma). 2-3% of all cancer. 85% of renal tumours. male:female = 2:1. 60-70 year old. smoking. exposure to cadmium. acquired polycystic disease due to long term dialysis. Most common. associated with von Hippel Lindau disease. Morphology. papillary growth pattern. multifocal & bilateral tumour. clear or pink cytoplasm. painless hematuria. mass in flank. fever. paraneoplastic syndrome. metastasis. occupational exposure to 2-napthylamine/ 4-aminobiphenyl/ benzidene. smoking. schistosomiasis. cyclophosphamide. phenacetin. painless hematuria. frequency & urgency. chance of recurrence after excision. Transitional Cell Carcinoma. Squamous Cell Carcinoma. Adenocarcinoma. common in men over 50. Pathogenesis. morphology. common in men over 50. etiology. pathogenesis. morphology. Clinical features. yellow-orange to grey-white with areas of cystic softening/hemorrhage. invades renal vein, collecting system. solitary & large cells. cells with clear/ granular cytoplasm. papilla formation with fibrovascular core. due to necrosis. erythrocytemia. gynaecomastia. hypercalcemia. invades renal vein and spreads to. papillary. non-papillary. lack of cohesiveness. hyperplasia of stromal & epithelial cells. prostatic smooth muscle tension. Gross. Microscopy. hormonal influence. age. genetic. environmental influences. arise from peripheral zone of prostate. infiltrate seminal vesicle & bladder. hematogenous metastasis to bone. Gross. Microscopy. aymptomatic. urinary symptoms. back pain. PSA elevation. well-defined margins. sporadic. arise anywhere in the cortex. composed of lipid & glycogen. due to increased erythropoietin. rare. gonadotropin secretion. lung. bone. liver. Morphology. invasive. non-invasive. CIS. invasive carcinoma. massive shedding of malignant cells into urine. occurs in transitional & central zone. mediated by dihydrotestosterone. also a/w testosterone, estrogen. mediated by alpha 1 adrenergic receptors. enlarged prostate > 300g. nodular appearance. urethra compressed to slit-like appearance. hyperplasia may protrude into bladder lumen. composed of. epithelium heaped into numerous papillary buds & infolding. stroma is always presnt between glands. Corpora Amylacea. microscopic infarcts. retardation of cancer growth by anti-androgen therapy. familiar form. posterior region. rarely invades rectum. typically in the peripheral zone. poorly demarcated firm and yellow growth. infiltrates adjacent gland with ill-defined margins. may exhibit invasion & metastasis. adenocarcinoma. various degrees of differentiation. Prostatic Intraepithelial Neoplasia. normally stage T1a/T1b. good prognosis. advance disease. difficulty in initiation, dribbling. dysuria. frequency. hematuria. vertebral metastasis. red elevated lesions. multicentric origin. most arise from later/ posterior walls of bladder base. cytologically malignant cells within flat urothelium. area of mucosal reddening, granularity, thickening w/o evident intraluminal mass. compresses prostatic urethra. acts as growth factor in prostate. multiple well-circumscribed. cystic dilation of glandular elements. forms ball-valve type of urethral obstruction. glands. fibromuscular stroma. unlike in carcinomas. inspissated proteinaceous secretory material. palpable as hard, irregular mass on PR. less likely to obstruct urethra in early disease. invades seminal vesicles, periurethral zones, bladder. invasion posteriorly limited by Denonvilliers fascia. mets to bones causing osteoblastic lesions. cancerous glands small and closely spaced. lined by single layer of epithelial cells. well-differentiated. anaplastic. precursor to invasive carinoma. found at periphery of invasive cancer. contain foci of epithelial atypia. separate tumours. bladder distension, hypertrophy, infection. lined by basal layer of low cuboidal epithelium. covered by columnar secretory cells. squamous metaplasia. small glands infiltrating stroma in haphazard, irregular fashion. not surrounded by stromal cells. glands lie "back to back" and dissects stroma. lined by single layer of cuboidal cells + prominent nucleoli. absent basal cell layer. variable morphology and undifferentiated. tall,columnar epithelial surrounds glands. peripheral layer of flattened basal cells.

Lupus Nephritis

most important feature of SLE. Glomerular pathology. Classification. most common cause of death in SLE. deposition of DNA/anti-DNA complexes within glomeruli. I. II. III. IV. V. inflammatory response. endothelial, mesangial & epithelial cell proliferation. glomerular necrosis. Normal glomeruli (by LM, EM, IF). rare. No treatment. Good prognosis. Purely Mesangial Lupus Nephritis. Focal Proliferative Glomerulonephritis. Diffuse Proliferative Glomerulonephritis. Membranous Glomerulonephritis. A. B. mild clinical symptoms. No treatment. Good prognosis. <50% of glomeruli involved. mesangial & endothelial cell swelling & proliferation. neutrophil infiltration. fibrinoid deposition with capillary thrombosis. a/w mild microscopic hematuria & proteinuria. Treatment: Steroids with cyclophosphamide. 5 year renal survival: 85-90%. most serious form. >50% of glomeruli involved. diffuse hypercellularity of glomeruli. "Wire Loops". IF shows immune complexes in granular pattern. EM shows subendothelial immune complex deposition. Clinical. Treatment: Steroid with cyclophosphamide. 5 year renal survival: 60-90%. widespread thickening of capillary wall. similar to idiopathic membranous glomerulonephritis. severe proteinuria & overt nephrotic syndrome. Controversial treatment. 5 year renal survival: 70-90%. Normal mesangium. IF, EM shows mesangial deposition. Mesangial hypercellularity. IF, EM shows mesangial deposition. endothelial and mesangial proliferation. producing epithelial crescents filling Bowman space. overall thickening of capillary wall. due to extensive immune complex deposition. hematuria. proteinuria. hypertension. renal insufficiency. increased deposition of GBM-like material. accumulation of immune complexes. 4-6 month trial of steroid therapy. withdraw if no response after 6 months. moderate to severe.

Urinary Outflow Obstruction

Urolithiasis. hydronephrosis. calculi forming in urinary collecting system, most commonly from kidney. Pathogenesis. Clinical Course. dilation of renal pelvis & calyces & parenchymal atrophy due to urine outflow obsruction. obstruction may be:. glomerular filtration continues even with outflow obstruction. irreversible damage occurs in 3 wks with complete obstruction & in 3 months in incomplete obstruction. Morphology. Clinical course. calcium oxalate stones. struvite stones. uric acid stones. cystine stones. lack of inhibitors to crystal formation in urine. Asymptomatic. ureteric colic. painful gross hematuria. predisposition to bacterial infection. urine outflow obstruction. congenital. acquired. filtrate dams up and diffuses into renal interstitium & perirenal space. build up of pressure in calyces & pelvis. kidney enlarged. pelvis & calyces dilated. renal cortex thinned and atrophied. dilated bowman spaces & tubules. tubular atrophy. minimal inflammation unless complicated by pyelonephritis. if obstruction is below bladder, there may be acute retention of urine. bilateral complete obstruction. bilateral incomplete obstruction. unilateral. urine supersaturation. magnesium ammonium phosphate. persistently alkaline urine. Vitamin A deficiency. hyperuricemia. genetic defect in amino acid transport. eg. pyrophosphate, mucopolysaccharide, diphosphonates. large stones trapped in renal pelvis. small stones passing into ureter & get trapped. paroxysms of flank pain radiating to groin. hydronephrosis. atresia of urethra. valve formation in ureter/urethra. compression by other stuctures. renal ptosis with torsion. kinking of ureter. foreign body. tumour. inflammation. neurogenic. pregnancy. drains into lymphatics & veins. dilation. compression of renal vasculature. impaired concentrating ability of tubules. tubular epithelium flattened. fibrosis. glomeruli disappear. anuria. polyuria. due to impaired tubular concentrating ability. asymptomatic. increased urine conc of calcium, urate, oxalate etc. hypercalciuria. excessive uric acid secretion. Proteus infectons. desquamation of squamous metaplastic epithelium also serves as nidus for stone formation. gout. diseases with rapid cell turnover. persistent acid (pH<5.5) urine. esp cystine. calculi. BPH, prostate ca, bladder ca. prostatitis, urethritis. bladder paralysis. mild & reversible. arterial insufficiency. venous stasis. concentration builds up to a level exceeding sloubility in urine. hyperabsorption from gut. renal hypercalciuria. hypercalcemia. urate provides nidus for calcium deposition. urease activity. bacteria also serves as nidus for stone formation. due to spinal cord lesion. primary renal defect of calcium reabsorption. hyperPTH, vit D intoxication, sarcoidosis.