Clinical Renal

Question 1

Nephritic syndrome

Answer 1

• commonly results from inflammation of glomeruli
• hematuria
• red cell casts in urine: agrregates of RBC held together by kidney protein
• mild proteinuria
• Acute Glomerulonephritis

Question 2

Nephrotic syndrome?

Answer 2

• commonly occurs as a result of increased permeability of the basement membrane to proteins
• massive proteinuria
• hypoalbuminemia
• generalised edema
• Minimal Change Disease
• Membranous Glomerulopathy

Question 3

Acute Renal Failure

Answer 3

• Oliguria/anuria
• Azotemia: only biochemal; increased BUN & Cr without Sx
• Commonly seen in Hypovolemic Shock

Question 4

Chronic Renal Failure

Answer 4

• Prolonged Sx
• Uremia
• End result of all chronic renal disease

Question 5

Adult Polycystic Kidney Disease

Answer 5

• Berry aneurysm in circle of Willis
• Multiple expanding cysts of both kidneys
• Cysts generally also seen in other organs like liver
• Fibrocystin protein affected in Infantile disorder
• Detected late in adulthood - renal failure
• Polycystin protein affected
• ARPKD - the cysts are dilated elongations of the collecting tubules and radially arranged
• Rx: transplant

Question 6

Acute/Post-Streptococcal Glomerulonephritis

Answer 6

• immunologically mediated disease: IgG to strep
  
  • sore throat & upper resp tract
  • massively increased cellularity in glomerulus due to influx of cell
  • leucocytes, mainly neutrophils therefore acute
• No proliferation of epithelial cells so urinary space remains clear
• Antigen-Ab complexes circulating in blood & get trapped w/in glomerulus
• Complexes cause injury to glomerulus, leading to activation and binding of complement system
• Electron dense deposits on epithelial side of membrane-humps representing deposition of immune complexes
• Granular deposits of IgG & complement on glomerular BM

Question 7

Minimal Change Disease

Answer 7

• commonest cause of nephrotic syndrome in children; less commonly seen in adults
• clinically, seen in association with resp infections & immunization
• best response to cort out of the renal diseases
• injury to visceral epithelial cells -> increased capillary permeability to proteins -> massive proteinuria
• nl appearance of glomeruli on light microscopy - minimal change
• EM: loss of pedical (effacement); sometimes referred to as fusion
• Lipoid Nephrosis: Cells of Prox. Tubules often laden with protein & lipid
• Immunofluorescence shows no deposition of immune complexes

Question 8

Membranous Nephropathy

Answer 8

• common cause of nephrotic syndrome in adults
• diffuse thickening of glomerular capillary wall due to accumulation of immune deposits
• basement membrane problem; diffusely thickened and appear eosinophilic
• causes include:
  
  • drugs like penicillamine, NSAIDs
  • carcinoma of lung & colon
  • SLE
  • infections - hepatitis
• no epithelial proliferation
• no change in Bowman’s Capsule
• Pathogenesis: circulating antigen complexes get deposited -> recruit MAC -> complement mediated basement membrane injury -> proteinuria
• EM: dense deposits of immune complexes b/w BM & overlying epithelial cells which lose their foot processes
• extra BM material laid down b/w deposits as spikes -> Uniform BM thickening due to IgG
• spikes grow over deposits & eventually cover them -> Dome & Spike
• Immunofluorescence: immune complexes containing both IgG & complement

Question 9

Mesangial proliferative GN / IgA nephropathy

Answer 9

• Nephritic syndrome
• diffuse and global glomerular damage
• deposition of IgA in mesangial regions
• commonly seen in association with Henoch - Schonlein purpura (HSP)
• Light microscopy:
  
  • increased mesangial matrix & cellularity
  • No BM abnormality
• Immunofluorescence: Mesangial deposition of IgA

Question 10

Acute Tubular Necrosis

Answer 10

• Clinicopath entity
• Acute diminution of renal fx
• most common cause of acute renal failure
• common cause: ischaemia
  
  • but reversible
  • should be called Acute Tubular Injury
• Light microscopy:
  
  • most clearly seen in PCT
  • dilated tubules
  • flattened epithelium
  • loss of brush border

Question 11

Acute Pyelonephritis

Answer 11

• Acute suppurative (puss forming) inflammation of kidney
• Predisposing conditions:
  
  • UTI, ascending
  • Cath
  • Pregnancy
  • Diabetes mellitus
• Clinical features
  
  • sudden onset
  • +ve Goldflam sign
  • fever & malaise
  • urinary sx including pyuria
  • finding of leucocyte casts in urine is highly suggestive of pyelonephritis
  • Dx of urine culture
  • White cell cast
• Light microscopy:
  
  • extensive infiltration by neutrophils
  • dilated tubules also filled with neutrophils
  • glomeruli appear nl, especially in early stages
  • abscess formation very common

Question 12

Hypertensive Nephrosclerosis

Answer 12

• renal failure very commonly results from untreated hypertension, as a result of changes in renal vessels
• Light microscopy:
  
  • thickening of vessel walls of large renal vessels
  • Hyaline thickening of walls of arterioles
  • Sclerosis/hyalisation of glomerulus
• Disuse atrophy of tubuluar part of nephron
• End stage Renal Disease

Question 13

Diabetic nephropathy

Answer 13

• increased susceptibility to infections - repeated pyelonephritis
• metabolic effects of hyperglycemia & glycosylation of proteins - BM changes
• Massive thickening of BM - may be 4-5 times its usual thickness
• atherosclerosis - renal ischemia & vascular changes
• Light microscopy:
  
  • nodular glomerulosclerosis
  • increase in mesangial matrix - localised gives Kimmelstiel Wilson nodules
  • Hyalinisation of both afferent & efferent arterioles
  • diffuse & global increase in mesangial matrix - diffuse diabetic glomerulosclerosis
  • Fibrin caps (FC) - outer surface of glomerular tuft; plasma protein that has leaked out

Question 14

Renal Cell Carcinoma

Answer 14

• most common primary malignancy of the kidney
• derived from renal tubular epithelial cells
• Clinical Sx:
  
  • Classic Triad: Hematuria, Flank Pain, Palpable Mass
  • Path subtypes:
  • Clear cell: most common
  • Papillary
  • Chromophobe
• Light microscopy
  
  • Large & polygonal tumour cells
  • Clear cytoplasm due to accumulation of glycogen & lipids