Albumin metabolism in the nephrotic syndrome

Nephrotic syndrome is characterized by increased urinary excretion of albumin and other serum proteins, accompanied by hypoproteinemia and edema formation. Nephrotic patients have lower serum albumin concentrations than do patients undergoing continuous ambulatory peritoneal dialysis when albumin and protein losses are the same in both groups, suggesting that nephrotic patients may not maximally adapt to loss of protein. The fractional rate of albumin catabolism is increased in nephrotic patients, possibly as a result of increased albumin catabolism by the kidney, but the absolute albumin catabolic rate is decreased in nephrotic patients. The rate of albumin synthesis may be increased, but not sufficiently to maintain normal serum albumin concentration or albumin pools. Augmentation of dietary protein in nephrotic rats directly stimulates albumin synthesis by increasing albumin mRNA content in the liver, but also causes an increase in glomerular permeability to macromolecules so that much if not all of the excess albumin synthesized is lost in the urine. When dietary protein is restricted, the rate of albumin synthesis is not increased either in nephrotic patients or in rats, despite severe hypoalbuminemia. Although dietary protein supplementation may lead to positive nitrogen balance, dietary protein supplementation alone does not cause an increase in serum albumin concentration or body albumin pools, and may instead cause further albumin pool depletion because of changes induced in glomerular permselectivity. The use of angiotensin-converting enzyme inhibitors may blunt the increased albuminuria caused by dietary protein supplementation and allow albumin stores to be increased.