Gastrointestinal Protein Loss and Intestinal Function in the Nephrotic Syndrome

Abstract

In the nephrotic syndrome the renal loss of albumin is often insufficient to explain the hypoalbuminaemia. Studies with labelled albumin have in many cases revealed an increased ‘endogenous’ catabolism of albumin. In the present investigations the significance of abnormal gastrointestinal protein loss as a source of endogenous hypercatabolism was assessed by means of the ⁵¹Cr-albumin test. Thirteen patients were examined. In 4 a slight increase of faecal ⁵¹Cr-output was observed, in the remaining 9 faecal ⁵¹Cr-excretion was normal. It is concluded that gastrointestinal protein loss at most plays a contributory role for the endogenous hypercatabolism. Other intestinal function tests, histological and radiological examination of the small intestine were performed. The results of these investigations were normal in the majority of the patients.

Role of the kidney in the metabolism of apolipoprotein A-IV: influence of the type of proteinuria

“…ApoA-IV could also be lost into the intestinum by an intestinal hyperpermeability, resulting in a leakage of enterocyte-derived apoA-IV into the intestinal lumen (38). Similar intestinal losses in patients with nephrotic syndrome have been described for albumin (39,40).…”

The Role of the Kidney in the Metabolism of Plasma Proteins

“…It is not the major factor as Jensen el «/. [52] have shown that protein-losing gastroenteropathy is not present in most patients with nephrotic syndrome accompanied by protein hypercatabolism: even when hypercatabolism can be demonstrated, protein-losing enteropathy only partially explains the increased fractional catabolic rate. A much more likely explanation of the increased fractional catabolic rate for proteins of inter mediate MW is increased exposure of these proteins to renal tubular catabolic sites.…”

Gastrointestinal Protein Loss in the Nephrotic Syndrome Studied with ⁵¹Cr-Albumin

“…Given by mouth, chromium is completely recovered in the feces indicating no enteral reabsorption. Using this substance, Jensen et al [6] found only moderate enteral protein loss in 4 out of 13 nephroticadults. Regarding the incidence of urinary contamination of the stool as an important source of error, especially in children, 5flFe-dextran has been applied by Yssing et al [17].…”

“…Increased fractional catabolic rate [7,8,14] and gastrointestinal protein loss are of more significance. The latter factor has been established in several papers since 1960 by Barandun et al [ 1 ], Klutlie et a!., [9], Nussle et al [10] and Nussle and Royer [ 11], However, in recent years there have only been few investigations on this matter with the result that there was no or only small enteral protein loss in nephrotic patients [6,8,17], This important question seems to be still controversial and that is why the present study has been initiated.…”