Renal Pathology Flashcards
Describe the basic anatomy and histology of the kidney
What are the types of glomerular disease?
- Glomerulonephritis
- Pyelonephritis
- Acute Tubular Necrosis
- Kidney stones
- Renal cell carcinoma
- Transitional cell carcinoma
- Polycystic kidney disease
What is glomerulonephritis and the different types?
- Inflammation of the glomerulus
- Glomeruli diseases are by and large immune-related
- Antibody-antigen complexes build and become trapped -> block filtration -> cause tissue injury -> long term complement or phagocyte activation
- Proliferation of mesangial cells
- Entrapment of leukocytes
- Blockage of glomeruli
- Hematuria, proteinuria, edema
Types:
- Nephrotic Syndrome
- Nephritic Syndrome
- Crescentic Glomerulonephritis
What is nephrOtic syndrome?
- Derangement of capillary walls or thinning of foot processes
- Proteinuria -> decreased serum albumin -> decreased oncotic pressure –> increased interstitial
volume = edema - Swelling in the legs and ankles, fatigue, poor appetite, high lipids in urine, hypoalbuminemia and edema
Causes:
- Minimal-change disease
- Membranous Nephropathy
Describe minimal-change disease and membranous nephropathy as causes of nephrOtic syndrome
Minimal-change disease:
- Diffuse thinning of foot processes of epithelial cells in glomeruli
- Pathogenesis: Absence of immune deposits but may involve some immune dysfunction
- Damage to glomerulus -> Proteinuria - mainly albumin
- Loss of oncotic pressure results in edema
- Benign, resolves with corticosteroid therapy
Membranous Nephropathy:
- Very common cause of the nephrotic syndrome in adults
- Basement membrane markedly thickened by immune complex deposits
What is nephritic syndrome?
Acute post-infection glomerulonephritis:
- Type III hypersensitivity reaction followingstreptococcal infection in children
- 1-2 weeks after sore throat
- 6 weeks after skin infection
- Injury through immune complexes deposition in the kidney
- Dominated by acute onset of usually grossly visible hematuria, oliguria; possibly some proteinuria and edema, azotemia
Histology:
- Inflammatory cells in the glomeruli
What is Cresentic glomerulonephritis (Rapidly progressiveglomerulonephritis)?
- Extensive crescents (usually >50%)
- Cause of crescent formation: rupture of glomerular capillaries -> cellular and humoral inflammatory mediators spill into Bowman’s space - Rapid loss of renal function
Describe acute pyelonephritis (kidney infection)
- Suppurative inflammation of kidney and pelvi
- Most commonly caused by Escherichia col
Risk factors:
1. Female
2. Recent catheterization
3. Vesico-ureteral reflux
4. Urinary tract obstruction
- A complication of UTI e.g. cystitis, prostatitis, urethritis
Routes by which bacteria can reach the kidney:
- Haematogenous infection (less common) e.g. septicaemia, endocarditis
- Ascending Infection UTI, urinary tract obstruction e.g. renal calculi
Describe chronic pyelonephritis
- Pathogenesis: bacterial infection + vesicoureteral reflux and obstruction
- Cause: almost always includes chronic urinary tract obstruction and repeated bouts of acute inflammation
- Intrarenal reflux causes scarring and chronic inflammation
What are Urinary Tract Infections (UTI) and the main causes and symptoms ?
- Bacterial infection
- 40% of women get urinary tract infections
- Short urethra of females can allow fecal bacteria to easily enter urethra
- Most occur in sexually active women
a) Urethritis: inflammation of urethra
b) Cystitis: inflammation of bladder
c) Pyelitis or pyelonephritis: inflammation of kidneys
Symptoms: dysuria, urinary urgency and frequency, fever, and sometimes cloudy or blood-tinged urine
- Back pain when kidneys are involved
Treatment: antibiotics can cure most urinary tract infections
What are kidney stones (renal calculi)?
- Crystallized salts in renal pelvis -> stones block ureter, causing pressure and pain
Types:
- Calcium stones
- 15% Struvite stones
- 10% Uric acid stones
- 1-2% Cysteine stones
Causes:
- Chronic bacterial infection
- Urine retention
- Increased Ca2+ in blood
- Increased pH of urine (Diet rich in purines)
What is polycystic kidney disease and the different types?
Hereditary disorder of multiple expanding cysts, which ultimately destroy the renal parenchyma
Types:
- Autosomal-dominant
- Autosomal-recessive
What is autosomal-dominant (adult) polycystic kidney disease?
- Partial replacement of renal parenchyma by cysts
- Bilateral; kidneys enlarged
- 1:500 – 1:1000 persons affected - Manifests between 15 and 30 years of age
- Up to 90% defective PKD1 gene on chromosome 16
-> encodes for polycystein-1
-> involved in cell-cell, cell-matrix adhesion
Palpable renal masses and progression to chronic renal failure
- Hypertension, hematuria, often urinary infection, pressure of cysts leads to ischemic atrophy of the intervening renal substance
- Histology: Serous filled cysts with normal nephrons between cysts
What is autosomal-recessive (infantile) polycystic kidney disease?
- Bilateral renal cysts without dysplasia
- 1:20,000 - 1:40,000 and a heterozygote carrier rate of 1:70
- Mutations in polycystic kidney and hepatic disease 1 (PKHD1) - Multiple cysts (smaller) evident at birth or early childhood
Cystic dilatation of renal collecting ducts
- marked renal enlargement, leading to hypertension and progressive renal failure
- alsobiliary dysgenesis, leading to abnormal bile duct formation with progressive periportal congenital hepatic fibrosis
Name and describe the phases of renal failure
- Acute Renal Failure:
- Failure of complete filtration of waste products from the blood
- Symptom: Oliguria or anuria & recent onset of azotemia
2. Chronic Renal Failure/Disease
- Progressive loss in kidney function over a period of months or years
- Characterized by prolonged symptoms and signs of uremia, is the end result of all chronic renal parenchymal diseases (example, glomerular or tubulointerstitial lesions)
- 1:10 Australians affected
- End stage Renal Failure:
- Defined as Glomerular Filtration Rate < 15 ml/min
- Causes uremia: ionic and hormonal imbalances, metabolic abnormalities, toxic molecule accumulation
- Symptoms: fatigue, anorexia, nausea, mental changes, cramps, pain
- Treatment: hemodialysis or transplant
