Renal Pathology. Introduction: 150gm: each kidney 1700 liters of blood filtered  180 L of G. filtrate  1.5 L of urine / day. Kidney is a retro-peritoneal.

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Presentation transcript:

Renal Pathology

Introduction: 150gm: each kidney 1700 liters of blood filtered  180 L of G. filtrate  1.5 L of urine / day. Kidney is a retro-peritoneal organ Blood supply: Renal Artery & Vein One half of kidney is sufficient – reserve kidney function: Filtration, Excretion, Secretion, Hormone synthesis.

Kidney Location:

Kidney Anatomy:

Renal Pathology Outline Glomerular diseases: Glomerulonephritis Tubular diseases: Acute tubular necrosis interstitial diseases: Pyelonephritis Diseases involving blood vessels: Nephrosclerosis Cystic diseases Tumors

Clinical Syndromes: Nephritic syndrome. –Oliguria, Haematuria, Proteinuria, Oedema. Nephrotic syndrome. –Gross proteinuria, hyperlipidemia, Acute renal failure –Oliguria, loss of Kidney function - within weeks Chronic renal failure. –Over months and years - Uremia

Introduction Functions of the kidney: –excretion of waste products –regulation of water/salt –maintenance of acid/base balance –secretion of hormones Diseases of the kidney –glomeruli –tubules –interstitium –vessels

Azotemia:  BUN, creatinine Uremia: azotemia + more problems Acute renal failure: oliguria Chronic renal failure: prolonged uremia Abnormal findings

Hematuria Oliguria Azotemia Hypertension Nephritic syndrome Massive proteinuria Hypoalbuminemia Edema Hyperlipidemia/-uria Nephrotic syndrome

Glomerular diseases –Nephrotic syndrome Minimal change disease Focal segmental glomerulosclerosis Membranous nephropathy –Nephritic syndrome Post-infectious GN IgA (immune) nephropathy

Nephrotic Syndrome Massive proteinuria Hypoalbuminemia Edema Hyperlipidemia

Adults: systemic disease (diabetes) Children: minimal change disease Characterized by loss of foot processes Good prognosis Causes

Minimal change disease

Normal glumerular structure

Normal glomerulusMinimal change disease

Focal Segmental Glomerulosclerosis Primary or secondary Some (focal) glomeruli show partial (segmental) hyalinization Unknown pathogenesis Poor prognosis

Focal segmental glomerulosclerosis

Membranous Glomerulonephritis Autoimmune reaction against unknown renal antigen Immune complexes Thickened GBM Subepithelial deposits

Membranous glomerulonephritis

Nephritic Syndrome Hematuria Oliguria, azotemia Hypertension

Post-infectious GN, IgA nephropathy Immunologically-mediated Characterized by proliferative changes and inflammation Causes

Post-Infectious Glomerulonephritis Child after streptococcal throat infection Immune complexes Hypercellular glomeruli Subepithelial humps

Post-infectious glomerulonephritis

IgA Nephropathy Common! Child with hematuria after (URI) Upper Respiratory Infection IgA in mesangium Variable prognosis

IgA nephropathy

Tubular and interstitial diseases –Inflammatory lesions pyelonephritis

Pyelonephritis Invasive kidney infection Usually ascends from UTI Fever, flank pain Organisms: E. coli, Proteus

Women, elderly Patients with catheters or mal-formations Dysuria, frequency Organisms: E. coli, Proteus Urinary Tract Infection

Acute pyelonephritis with abscesses

Pyelonephritis

Cellular cast

Chronic pyelonephritis

Drug-Induced Interstitial Nephritis Antibiotics, NSAIDS IgE and T-cell-mediated immune reaction Fever, eosinophilia, hematuria Patient usually recovers Analgesic nephritis is different (bad)

Drug-induced interstitial nephritis

Acute Tubular Necrosis The most common cause of ARF! Reversible tubular injury Many causes: ischemic (shock), toxic (drugs) Most patients recover

Acute tubular necrosis

Benign Nephrosclerosis Found in patients with benign hypertension Hyaline thickening of arterial walls Leads to mild functional impairment Rarely fatal

Benign nephrosclerosis

Malignant nephrosclerosis Arises in malignant hypertension Hyperplastic vessels Ischemia of kidney Medical emergency

5% of cases of hypertension Super-high blood pressure, encephalopathy, heart abnormalities First sign often headache, scotomas Decreased blood flow to kidney leads to increased renin, which leads to increased BP! 5y survival: 50% Malignant Hypertension

Malignant hypertension

Adult Polycystic Kidney Disease Autosomal dominant Huge kidneys full of cysts Usually no symptoms until 30 years Associated with brain aneurysms.

Adult polycystic kidney disease

Childhood Polycystic Kidney Disease Autosomal recessive Numerous small cortical cysts Associated with liver cysts Patients often die in infancy

Childhood polycystic kidney disease

Medullary Cystic Kidney Disease Chronic renal failure in children Complex inheritance Kidneys contracted, with many cysts Progresses to end-stage renal disease

Tumors –Renal cell carcinoma –Bladder carcinoma

Renal Cell Carcinoma Derived from tubular epithelium Smoking, hypertension, cadmium exposure Hematuria, abdominal mass, flank pain If metastatic, 5y survival = 5%

Renal cell carcinoma

Bladder Carcinoma Derived from transitional epithelium Present with painless hematuria Prognosis depends on grade and depth of invasion Overall 5y survival = 50%

Bladder carcinoma