**4.4 Role of proteinuria**

20 Chronic Kidney Disease

Fig. 5. Capillary tufts almost replaced by the fibous tissue forming glomerular scarring.

Fig. 6. Immunofluorescent stain shows deposition of coarsely granular deposits of

With progression of kidney disease the afferent arteriole tone decreases to a much larger extent than the efferent tone. As a result intra-glomerular pressure rises leading to hyperfiltration. Angiotensin II aides in hyperfiltration through its vasoconstrictor effect predominantly on the efferent arteriole. Apart from its hemodynamic effects, Angiotensin II acts directly on the glomerular membrane. It acts on the angiotensin II receptors on the surface of the podocytes, altering their permselective property, by contracting the foot

Angiotensin II also induces proliferation ofglomerular cells and fibroblasts. It acts on AT1 receptors on tubular cells causing hypertrophy, which results in increased synthesis of collagen type IV. It increases macrophage activation and phagocytosis responsible for the

**4.3 Role of angiotensin II, hypertension and hyperfiltration** 

processes. This allows proteins to escape in the urinary space.

inflammatory component associated with CKD.

complement C3.

Proteinuria is not only a marker of kidney damage, but also contributes to nephron damage. Filtered proteins are reabsorbed from the proximal tubule. Damaged tubular basement membrane causes leakage of tubular content into the interstitium, thereby causing macrophage infiltration. Macrophages produce inflammatory mediators thus mounting an immense inflammatory reaction inside the renal interstitium.

Fig. 7. Focal segmental and global Glomerulosclerosis and nephron loss is a vicious circle ultimately leading to proteinuria.
