Gastrointestinal Protein Loss and Intestinal Function in the Nephrotic Syndrome

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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.

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