Pathophysiology - Hypoalbuminemia via low plasma oncotic pressure causes increased hepatic synthesis of lipoproteins, esp apoprotein B, and cholesterol. Protective HDL are lost in urine. Decreased clearance of VLDL due in part to decreased lipoprotein lipase activity. Decrease in clearance correlates better with renal albumin clearance than with plasma oncotic pressure suggesting loss of a factor involved in VLDL metabolism. In addition, increased levels of fibrinogen and evidence of activation of both fibrin formation and degradation are found.
All abnormalities resolve with remission of underlying disease.
Clinically manifests as renal vein thrombosis and pulmonary embolism. Kidneys are small, with glomerular scarring and tubular atrophy and underlying pathologic process may be obscurred by advanced scarring of kidney. Ab reacts with GBM, specifically the noncollagenous domain of a 3 chain of Type IV collagen. Recent evidence suggests that anti-GBM Ab alone can cause loss GBM charge barrier and proteinuria. PMN, macrophages and complement are required for development of proliferative and destructive lesions.