In chronic azotemic renal failure, the kidneys may lose their ability to conserve sodium efficiently. The resultant urinary sodium loss seldom exceeds the average sodium intake, and therefore is usually of minor clinical significance unless dietary salt is restricted. Rarely, however, urinary sodium loss may be great enough to result in the rapid onset of sodium depletion unless the diet is adequately supplemented (10-20 gm NaCl or equivalent daily). Hyponatremia, dehydration, increasing azotemia, and generalized weakness occur, often associated with nausea and vomiting. Death may ensue.
In 1944 Thorn and associates reported upon two young azotemic patients who appeared to have adrenal insufficiency. It was subsequently found that there was no response to adrenal cortical hormone and that salt and fluids alone controlled the clinical manifestations.1 Since this first description of salt-losing nephritis, 28 additional cases have been reported, designated variously as salt-losing nephritis, renal disease with saltlosing syndrome,
HUGHES JM. Salt-Losing Nephritis: A Case Report and a Review. Arch Intern Med. 1964;114(2):190–195. doi:10.1001/archinte.1964.03860080040002
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