Albumin turnover in renal disease.

Hypoalbuminemia is found in patients both with the nephrotic syndrome and with end-stage renal disease (ESRD) treated either with continuous ambulatory peritoneal dialysis (CAPD) or hemodialysis. In nephrotic patients the primary causes of hypoalbuminemia are urinary albumin losses, an inappropriate increase in the fractional catabolic rate (FCR) of albumin and an insufficient increase in the rate of albumin synthesis to replace these losses. Nevertheless, the albumin synthetic rate is increased significantly. In patients on CAPD, albumin losses into the urine and across the peritoneal membrane contribute significantly to hypoalbuminemia. In contrast to nephrotic patients, albumin FCR decreases as serum albumin falls and serum albumin levels are significantly greater than in nephrotic patients with the same external losses of albumin. CAPD patients, like nephrotic patients with normal renal function, can increase albumin synthesis to replace losses. Thus ESRD does not directly suppress albumin synthesis. In contrast, hypoalbuminemia in hemodialysis patients results from reduced albumin synthesis. The cause of decreased albumin synthesis is a combination of response to inflammation (acute-phase response) and, to a lesser extent, inadequate nutrition. There is no evidence that shifts of albumin to the extravascular space or that dilution of the plasma by volume expansion play any role in causing hypoalbuminemia in ESRD or nephrotic patients.