Renal Pathology Flashcards

1
Q

Describe basic kidney anatomy and histology

A
  • Renal corpuscule (glomerulus / bowmans capsule)

- PCT, loop of henle, DCT, collecting tubules

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2
Q

List the different glomerular diseases

A
  • Glomerulonephritis
  • Pyelonephritis
  • Acute Tubular Necrosis
  • Kidney Stones
  • Renal Cell Carcinoma
  • Transitional Cell Carcinoma
  • Polycystic Kidney Disease
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3
Q

What is glomerulonephritis and list the types

A
  • Inflammation of the glomerulus
  • Immune related
  • Antibody-antigen complexes build and become trapped (block filtration, tissue injury, long term complete / phagocyte activation), proteinuria
  • Proliferation of messengial cells, entrapment of leukocytes, blockage of glomeruli, hematuria, edema
  • Enlarged hyper-cellular glomeruli and humps of antigen-antibody complexes
  • Types: Nephritic, nephrotic and cresentic
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4
Q

What is nephrotic glomerulonephritis

A
  • Minimal change disease
  • Focal segmental glomerulosclerosis
  • Membranous nephropathy and membranoproliferative glomerulonephritis
  • Derangement of capillary walls / thin of foot processes
  • Proteinuria, decreased serum albumin / oncotic pressure
  • Increased edema, swelling in legs / ankles, fatigue, poor appetite, high lipids in urine, hypoalbuminemia
  • Absence of immune deposits, immune dysfunction, damage to glomerulus, benign
  • Resolves with corticosteroid therapy
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5
Q

What is nephritic glomerulonephritis

A
  • Acute post infectious (post-streptococcal)
  • IgA nephropathy (Berger disease) and hereditary nephritis
  • Inflammatory cells in glomeruli
  • Type III HS reaction (1-2 w after sore throat or 6 w after skin infection)
  • Acute onset of hematuria, oliguria, proteinuria, azotemia
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6
Q

What is crescent glomerulonephritis

A
  • Extensive glomerular crescents
  • Proliferating cells in Bowmans capsule (histologic marker)
  • Rapidly progressive
  • Rupture of glomerular capillaries causes cellular and humoral inflammatory mediators to fill BC
  • Rapid loss of renal function, glomerular injury
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7
Q

What is acute pyelonephritis

A
  • Kidney infection
  • suppurative inflammation of kidney and pelvis
  • Caused by E. coli
  • Risk factors (female, UTO, catheterisation, vesicoureteral reflux)
  • Complication of UTI (cystitis, prostatitis, urethritis)
  • Bacteria reach kidney by haematogenous infection (septicaemia / endocarditis) or ascending UTI / UTO (renal calculi)
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8
Q

What is chronic pyelonephritis

A
  • Bacterial infection
  • Vesicoureteral reflux / obstruction
  • Caused by chronic UTO / repeated bouts of acute inflammation
  • Intrarenal reflux (scarring / chronic inflammation)
  • Border of cortex / medulla focal infiltrations of lymphocytes / plasma cells
  • Renal tubes are dilated and filled with pink protein casts
  • Connective tissue in interstitium, thickening of arteriole walls, lumen narrows (secondary hypertension)
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9
Q

What is a UTI

A
  • Short urethra of females allows faecal bacteria to easily enter urethra
  • More common in sexually active women
  • Urethritis, cystitis or pyelitis / pyelonephritis (complications)
  • Dysuria, urinary urgency / frequency, fever, cloudy / blood tinged urine, back pain (kidneys)
  • Treated with antibiotics
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10
Q

What is acute tubular necrosis

A
  • Destruction of tubular epithelial cells
  • Caused by ischaemia, toxic injury, hypersensitivity to drugs, UTO (tumour)
  • Loss of renal function, common cause of acute renal failure
  • Tubule cell injury and disturbances in BF
  • Loss of brush border, flattening cells, intratubular cast formation, sloughing
  • Intratubular obstruction
  • Pre-renal, initiation, extension, maintenance and repair
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11
Q

What is renal cell carcinoma

A
  • Primary carcinoma of the kidney parenchyma arising from the tubular epithelium
  • Risk Factors: Smoking, obesity, hypertension, occupational exposure (asbestos, petroleum, heavy metals) and genetics
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12
Q

What is transitional cell carcinoma

A
  • Bladder can expand significantly (transitional epithelium)
  • Most common cancer of bladder, ureter, urethra and rarely the renal pelvis
  • Risk Factors: Smoking, industrial exposure, schistosoma haematobium infection, drugs and radiation
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13
Q

What are cystic kidney diseases

A
- Heterogenous group of kidney diseases 
Cysts: 
- Single / multiple cystic spaces
- Variable size (1-5 cm)
- Clear fluid
- Confined to cortex
- Membrane singe layer of cuboidal or flattened cuboidal epithelium
- No clinical significance
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14
Q

What is polycystic disease

A
  • Hereditary disorder
  • Multiple expanding cysts which ultimately destroy renal parenchyma
  • Autosomal dominant or recessive
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15
Q

What is autosomal dominant polycystic disease

A
  • Partial replacement of renal parenchyma by cysts, bilateral, kidneys enlarged
  • 15-30 years
  • Defective PKD1 gene on chromosome 16
  • Palpable renal masses and progression to choleric renal failure
  • Hypertension, hematuria, UTI, ischemic atrophy of intervening renal substance
  • Serous filled cysts with normal nephrons between cysts
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16
Q

What is autosomal recessive polycystic disease

A
  • Bilateral renal cysts without dysplasia
  • Mutation in PKHD1
  • Multiple cysts (smaller) evident at birth or early childhood
  • Cystic dilation of renal collecting ducts
  • Marked renal enlargement, leading to hypertension and progressive renal failure
  • Biliary dysgenesis, abnormal bile duct formation with progressive periportal congenital hepatic fibrosis
17
Q

What is acute renal failure

A
  • Failure of complete filtration of waste products from the blood
  • Oliguria or anuria
  • Recent onset of azotemia
  • Sudden loss of kidney function
  • Illness / injury / toxins that increase stress of kidney
18
Q

What is chronic renal failure

A
  • Progressive loss in kidney function over months / years
  • Prolonged uraemia
  • Chronic renal parenchymal diseases (glomerular / tubulointerstitial lesions)
19
Q

What is end stage renal failure

A
  • Kidneys permanently shut down, glomerular filtration rate < 15 mL / min
  • Uraemia, ionic and hormonal imbalances, metabolic abnormalities, toxic molecule accumulation
  • Fatigue, anorexia, nausea, cramps and pain
  • Treated by hemodialysis or transplantation
  • Stage 1 (damage, proteinuria, GFR < 90), 2 (damage, GFR 60-88), 3 (GFR 30-59), 4 (GFR 15-29) and 5 (failure, end stage, GFR >15)
20
Q

What are kidney stones

A
  • Renal calculi, crystallised salts in renal pelvis
  • Stones block ureter causing pressure / pain
  • Causes: Chronic bacterial infection, urine retention, increase Ca in blood and increased pH of urine
21
Q

What are the types of kidney stones

A
  • 70% Calcium stones
  • 15% Struvite stones (UTI)
  • 10% Uric acid stones (acidic urine)
  • 1-2% Cysteine stones (genetic disorder)