Proteinuria, hyperlipidemia, and the kidney.

Hyperlipidemia in the nephrotic syndrome is the result of abnormalities in both synthesis and catabolism of lipids and lipoproteins. The etiology of nephrotic hyperlipidemia has not been established, but both abnormal glomerular permeability to plasma proteins and reduced serum oncotic pressure may contribute. Although standard hypolipemic drugs are effective in nephrotic patients, therapies such as dietary protein restriction and angiotensin-converting enzyme inhibitors which reduce proteinuria and increase serum oncotic pressure ameliorate hyperlipidemia as well. Hyperlipidemia may also induce proteinuric renal disease in normal animals and worsen renal injury in a variety of animal models of kidney disease. Conversely, treatment of hyperlipidemia prevents renal injury and lessens proteinuria. Potential mechanisms by which hyperlipidemia may cause renal injury include inflammatory and immunologically mediated injury and alteration of glomerular paracrine function.