URINARY SYSTEM REVIEW

DR. PRASANNA N KUMAR OMC

DISEASES OF THE KIDNEY

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Glomerular - glomerulonephritis Tubular tubulo interstitial nephritis, pyelonephritis Interstitium Vascular diseases – nephrosclerosis, benign and malignant All forms of chronic renal disease ultimately to destroy all four components of the kidney CRF and end-stage kidneys

RENAL DISEASES CLINICAL MANIFESTATIONS

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Oliguria (< 500ml of urine/day), anuria (< 50 ml/day)

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Proteinuria (normal protein (Tamm-Horsfall proteins) excretion in urine - < 150 mg/day) Selective proteinuria – clearance of low molecular weight proteins - albumin.

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Non-selective proteinuria - clearance of high MW proteins – albumin, globulins, IgG, IgM Hematuria – macroscopic/microscopic Edema

OTHER RENAL DISEASES CLINICAL MANIFESTATIONS

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Renal tubular diseases polyuria, nocturia, electrolyte disorders Urinary tract infection – kidney (pyelonephritis), bladder (cystitis) symptomatic/asymptomatic bacteriuria, pyuria Nephrolithiasis (renal stones) renal colic, hematuria

NEPHROTIC SYNDROME

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Proteinuria? – disruption of glomerular basement membrane Hypoalbuminemia – due to proteinuria Edema – due to decreased plasma oncotic pressure due to ?

Hyperlipidemia and lipiduria – due to increased lipoprotein synthesis

NEPHRITIC SYNDROME

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Oliguria and azotemia – renal inflammation

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Hypertension – decreased clearance of sodium and water

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Hematuria – leakage of blood into Bowman’s capsule

GLOMERULAR DISEASES CLINICAL MANIFESTATIONS

Nephritic syndrome Nephrotic syndrome Mild to moderate proteinuria Heavy proteinuria Visible hematuria Microscopic hematuria ± Edema Oliguria Severe edema Hyperlipidemia, lipiduria, hypoalbuminemia Hypertension, azotemia Thrombosis

RENAL FAILURE

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Acute renal failure – rapid deterioration of renal function - oliguria/anuria + azotemia Chronic renal failure - end result of all chronic renal diseases. GFR < 20-25% of normal edema, hyperkalemia prolonged uremia, ↑BUN anemia (?), chronic bone disease (?) GIT bleeding End stage renal disease - GFR < 5% of normal, terminal stage of uremia

UREMIA SOME CLINICAL FEATURES

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Hematologic Cardiac – anemia, bleeding tendency – hypertension, CCF, pericarditis

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Respiratory- pulmonary edema GIT – nausea, vomiting, gastritis Neuromuscular – myopathy, neuropathy Dermatologic – pruritus Bone – secondary hyperparathyroidism, hypocalcemia, hyperphosphatemia Fluid & electrolytes – edema, hyperkalemia

GLOMERULAR DISEASES

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Primary Glomerulonephritis

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Diffuse proliferative glomerulonephritis √

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Crescentic GN Membranous GN √

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Lipoid nephrosis (minimal change disease) √

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Focal segmental glomerulosclerosis

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Membranoproliferative GN IgA nephropathy Chronic GN √

GLOMERULAR DISEASES

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Secondary (Systemic) Diseases

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Systemic lupus erythematosus √ Diabetes mellitus √ Amyloidosis Goodpasture syndrome √ Polyarteritis nodosa Wegener granulomatosis Henoch Schönlein purpura

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Bacterial endocarditis

GLOMERULAR INJURY IMMUNE PATHOGENESIS

ANTIBODY MEDIATED INJURY 1.

2.

circulating immune complex deposition – major etiologic factor – granular deposits by IF antibodies against fixed glomerular antigens – linear deposits by IF 3 . antibodies against planted glomerular antigens – granular deposits by IF microscopy

Goodpasture antigen Antibody to Goodpasture antigen IMMUNOLOGICAL MECHANISMS OF GLOMERULONEPHRITIS 2 1 3

ENDOGENOUS ANTIGENS eg: SLE EXOGENOUS ANTIGENS eg: streptococci, Hepatitis B,C, Plasmodium falciparum , 1.

IC MEDIATED GLOMERULAR INJURY Passive entrapment of IC in GBM Leukocyte infiltration on glomeruli, proliferation of mesangial & endothelial cells GLOMERULAR INJURY

NEPHROTIC SYNDROME

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If the history of massive proteinuria is in a child (< 15 years) – minimal change disease, lipoid nephrosis, foot process disease) If the history of massive proteinuria is in an adult, often associated with a systemic disease – DM, SLE, amyloidosis, primary - membranous GN

MINIMAL CHANGE DISEASE

Light Microscopy – nearly normal

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Cells of proximal convoluted tubules laden with lipids- Lipoid Nephrosis.

Electron Microscopy

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Uniform diffuse loss of foot processes Clinical course - Children, usually 2-3yrs – nephrotic syndrome post URI

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No hypertension, normal renal function.

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Prognosis- Good, >90% respond to a short course of corticosteroids

MEMBRANOUS GN

Chronic immune complex nephritis

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Secondary membranous GN - circulating immune complexes – SLE, hepatits B, syphilis, drugs,

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malignancy Idiopathic membranous GN - immune complexes in situ LM – diffuse capillary and basement membrane thickening IF – diffuse granular pattern (Ig & C’ deposits) EM – subepithelial deposits – “spike & dome” pattern Poor response to steroids

DIABETIC NEPHROPATHY

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Associated with long standing diabetes Diabetic kidney –

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Glomerular syndromes – nephrotic syndrome, chronic renal failure Recurrent & chronic pyelonephritis Papillary necrosis Arteriolosclerosis Non-nephrotic proteinuria, nephrotic syndrome, chronic renal failure in 4-5 years

Diabetic glomerulosclerosis – nodular lesions + capillary basement membrane thickening Kimmelstiel – Wilson lesion – nodular glomerulosclerosis – nodular accumulation of mesangial matrix material

DIABETIC NEPHROPATHY

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Hyaline arteriosclerosis arteriole.

of afferent and efferent Pyelonephritis – acute or chronic inflammation of the interstitial tissues and tubules. Necrotizing papillitis – acute necrosis of renal papillae due to acombination of ischemic injury and infection

SYSTEMIC LUPUS ERYTHEMATOSUS

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SLE – kidney involvement in 70% of cases, renal lesion severity and prognosis, most important cause of death in SLE

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Immune complex disease - deposition of DNA-anti DNA complexes within glomeruli – C’ activation – complement mediated damage (leukocytes, cytokines etc.)

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Necrosis of glomeruli in severe cases

Diffuse, proliferative GN “wire-loop” lesions

SLE – RENAL LESIONS

Focal, proliferative GN

ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS

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Acute diffuse glomerulonephritis, postinfectious GN

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Streptococci – group A β-hemolytic (most common) – nephritogenic strain – infection of the pharynx or skin – 1- 4 weeks later (?) - fever, oliguria, hematuria (smoky urine) hypertension (nephritic syndrome)

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Recovery in 95% of children (with conservative treatment), <1% - develop rapidly progressive GN or chronic GN

CLINICAL COURSE

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Recovery in 95% of children <1% - develop rapidly progressive GN or chronic GN RBCs in urine RBC casts in urine

RAPIDLY PROGRESSIVE GN (RPGN, CRESCENTIC GN)

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Manifestation of severe glomerular injury with

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crescents that compress the glomeruli Etiology – Idiopathic (50%), post-streptococcal

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(post infectious GN),SLE, Goodpasture syndrome Morphology – crescents Clinical – rapid deterioration, with loss of renal function Crescent-shaped mass of proliferating parietal cells & monocytes in the Bowman’s space

CHRONIC GN MORPHOLOGY

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GROSS – symmetrically contracted kidneys, finely

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granular subcapsular surface MIC.

– Glomeruli – hyalinized Remainder of nephron - ischemic atrophy of (lack of blood flow in glomerulus) Interstitium - chronic inflammatory cells & fibrosis, tubules - atrophy Blood vessels - thickening of walls (chronic ischemia ↑ blood pressure)

 Patient with dysuria, WBCs (pus cells) in urine and WBC casts – where is the infection?

ACUTE PYELONEPHRITIS Ascending infection

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During urethral instrumentation catheterization and cystoscopy

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Urinary tract obstruction – stasis – infection

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vesicouretral reflux in children

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prostatic hypertrophy

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uterine prolapse Hematogenous - septicemia, emboli from bacterial endocarditis

ACUTE PN

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One or both kidneys involved.

Gross - discrete yellow raised abscesses on the surface.

Micro - suppurative necrosis with abscess formation, pus cell casts in the urine.

Necrotizing papillitis or papillary necrosis in diabetes Neutrophils in tubules & interstitium

ACUTE PN CLINICAL/LAB FEATURES

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Fever, chills, costovertebral angle pain Urinalysis – pyuria, pus cells (may be present in upper & lower UTI), pus cell casts (WBC casts, only in upper UTI), bacteriuria Self-limiting infection, if recurrent - progress to chronic PN PUS CELL CAST PUS CELLS

ACUTE RENAL FAILURE CAUSES

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ATN – commonest cause of ARF – due to renal ischemia – eg: due to hypotension, shock

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Patient presents with oliguria, azotemia, hyperkalemia

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RPGN Acute papillary necrosis Drug induced interstitial nephritis – penicillin derivatives, NSAIDs

CHRONIC PN MICROSCOPY

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Interstitium – chronic inflammation Tubules - atrophy, dilatation and “thyroidization” Blood vessels – arteriosclerosis Glomeruli – periglomerular fibrosis Thyroidization

DISEASES OF THE BLOOD VESSELS

Benign nephrosclerosis

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Renal changes in benign hypertension.

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Kidneys are atrophic with fine granularity and microscopically shows hyaline arteriosclerosis Malignant Nephrosclerosis

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Malignant hypertension-

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Fibrinoid necrosis of arterioles

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hyperplastic arteriosclerosis.

Grossly “flea bitten kidney”

Chronic glomerulonephritis Chronic pyelonephritis GRANULAR CONTRACTED KIDNEYS Benign nephrosclerosis Gross small symmetrically atrophic with fine granularity Micro – Hyalinized glomeruli, secondary tubulointerstitial and vascular changes Gross asymmetric contraction with coarse scarring Mic.- i nterstitial chronic inflammation fibrosis, secondary vascular and glomerular involvement Gross - small symmetrically atrophic with fine granularity Mic.

- hyaline arteriolosclerosis, secondary ischemic atrophy of other structures

CYSTIC DISEASES OF THE KIDNEY INHERITANCE PATHOLOGICAL FEATURE CLINICAL FEATURE AND OUTCOME Adult polycystic kidney disease hypertension Autosomal Large multicystic kidneys hematuria, pain, CRF at 40-60 dominant liver cysts, berry aneurysms Childhood polycystic kidney disease

Autosomal Enlarged cystic kidneys renal failure and death in infancy recessive at birth hepatic fibrosis if child survives

Simple cysts

none single or multiple cysts

usually asymptomatic

in normal sized kidneys

Autosomal dominant adult polycystic kidney Autosomal recessive childhood polycystic kidney Liver cysts in ADPKD

RENAL STONES

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Calcium oxalate stones Struvite stones – triple phosphate stones (Mg, NH 3 Ca PO 4 ) staghorn calculi - UTI

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Uric acid stones - gout, radiolucent Cystine stones

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Urine obstruction, colicky pain, hematuria, infection, Stag horn calculus squamous metaplasia in renal pelvis – squamous cell ca.

OBSTUCTIVE UROPATHY

HYDRONEPHOSIS – atrophy of kidneys

RENAL CELL CARCINOMA

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Adenocarcinoma of the Kidney, Clear cell carcinoma, hypernephroma Tobacco most significant risk factor – cigarettes, pipes and cigars 70-80% of RCC – clear cell carcinoma Grows into renal vein – IVC – right atrium Mass, hematuria, weight loss, polycythemia, Cushing syndrome, hypercalcemia

RENAL CELL CARCINOMA Yellow C/S, hemorrhage, necrosis Cells with clear or granular cytoplasm with glycogen or lipid

RENAL CELL CARCINOMA CLINICAL

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Paraneoplastic syndromes - polycythemia, hypercalcemia, hypertension, Cushing syndrome, leukemoid reaction METHODS OF SPREAD:

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Local, hematogenous, lymphatic

CYSTITIS

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ETIOLOGY – patient’s fecal flora, Proteus, Klebsiella, candida (prolonged antibiotics),TB (secondary to renal TB), Schistosomiasis (Egypt)

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PREDISPOSING FACTORS instrumentation bladder calculi diabetes mellitus, immune deficiency radiation (radiation cystitis) cyclophosphamide (hemorrhagic cystitis)

TUMORS OF URINARY BLADDER

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Benign papillomas – 1-2 cm frond like structures with fibrovascular cores covered by transitional epithelium – usually solitary lesions which rarely recur

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Transitional cell carcinoma Squamous cell ca – 5% of bladder carcinomas –

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calculi, Schistosomiasis Adenocarcinoma – rare - urachul remnants

URINARY BLADDER CA

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Cigarette smoking, radiation naphthylamines (industry), analgesics, cyclophosphamide S. hematobium – inflammation, squamous metaplasia, dysplasia, carcinoma (SCC) Benign papillomas, TCC Squamous cell ca – 5% Adenocarcinomas – rare TCC - M>F, 50-80 years Painless hematuria, dysplastic cells in urine