Renal Pathology

high blood flow = susceptible to circulatory problems

Four Cell Compartments

1. glomerulus
2. tubules
3. interstitium
4. vessels

Glomerulus

electron microscopy used in renal pathology - can show immune complex deposits, minimal change pathology  (foot process effacement)


normal = open capillary loops, normal mesangium (3 cells per cluster)


Glomerular diseases

• primary - kidney only/predominate organ affected
• secondary - to systemic conditions; e.g., SLE, diabetes, hypertension
• clinical manifestations
• nephrotic syndrome - proteinuria    
• 3.5 g protein/24 h
• hypoalbuminemia
• hypercholesterolemia
• edema
• low oncotic pressure
• increased Na and H2O retention
• inactive urinary sediment
• mechanisms of injury
• damage to epithelial cells
• immune processes
• deposition diseases
• complications
• hyperlipidemia
• susceptible to infections (loss of immunoglobins)
• hypercoagulability
• primary causes
• children - minimal change disease
• peak age 2-6 years
• dramatic response to steroids
• etiology hypothesis - immune dysfunction - elaboration of cytokine that damages foot processes
• Primary FSGS - damage to podocytes - affect podocyte slit diaphragm nephrin molecules - sclerosis - occlusion of capillaries by acellular matrix (healing process from damage).  Hyalinosis- accumulation of plasma proteins.  Foot process effacement (similar to minimal change disease),
• Secondary FSGS - reduced nephron mass (loss of kidney), drug damage, pre-existing renal disease.  secondary to adaptive change (POSITIVE feedback loop = bad goes to worse.
• 

• nephritic syndrome - hematuria

• rapidly progressing glomerulonephritis (acute renal failure)
• asymptomatic hematuria or proteinuria
• chronic renal failure

 Pathogenesis of Glomerular Diseases

• immune mechanisms
• injury by antibodies
• injury from deposition of antigen-antibody complexes