by Felix C.

Describe the pathophysiology of underlying conditions.

  • Diabetic nephropathy [6]

    • Hyperglycemia → nonenzymatic glycation of proteins → varying degrees of damage to all types of kidney cell.

    • Pathological changes include:

      • Hypertrophy and proliferation of mesangial cells, GBM thickening, and ECM protein accumulation → eosinophilic nodular glomerulosclerosis

      • Thickening and diffuse hyalinization of afferent and efferent arterioles/interlobular arteries

      • Interstitial fibrosis, TBM thickening, and tubular hypertrophy

  • Hypertensive nephropathy: Due to protective autoregulatory vasoconstriction of preglomerular vessels, increases in systemic blood pressure do not normally affect renal microvessels. [7]

    • Increased systemic blood pressure (e.g., due to chronic hypertension) below the protective autoregulatory threshold → benign nephrosclerosis (sclerosis of afferent arterioles and small arteries) → ↓ perfusion → ischemic damage

    • In case BP exceeds threshold → acute injury → malignant nephrosclerosis (petechial subcapsular hemorrhages, visible infarction with necrosis of mesangial and endothelial cells, thrombosis of glomeruli capillaries, luminal thrombosis of arterioles, and red blood cell extravasation and fragmentation) → failure of autoregulatory mechanisms → ↑ damage

  • Glomerulonephritis (GN)

    • Noninflammatory GN (e.g., minimal change GN, membranous nephropathy, focal segmental glomerulosclerosis)

    • Inflammatory GN (e.g., lupus nephritis, poststreptococcal GN, rapid progressive GN, hemolytic uremic syndrome)


Felix C.


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