Abnormal Renal Sodium Excretion in the Nephrotic Syndrome after Furosemide: Relation to Glomerular Filtration Rate

Danielsen H, Pedersen EB, Madsen M, Jensen T. (Department of Internal Medicine C, Aarhus Kommunehospital, and University of Aarhus, Aarhus, Denmark.) Abnormal renal sodium excretion in the nephrotic syndrome after furosemide: relation to glomerular filtratoni rate. The effect of 40 mg furosemide intravenously on sodium excretion, the renin‐aldosterone system and arginine vasopressin (AVP) was studied in 14 patients with the nephrotic syndrome and in 13 control subjects. Creatinine clearance (Ccr) was reduced in all patients but four. Before furosemide, AVP, but not angiotensin II (AII) or aldosterone (Aldo), was increased in the nephrotic patients. After fursoemide, sodium excretion (NaE) increased less and changes in AVP, AII and Aldo were blunted in the patients. Ccr and NaE were positively correlated in the nephrotic syndrome. The reduced sodium response after furosemide in the nephrotic syndrome seems to be closely correlated to a reduced glomerular filtration rate but not to an increased activity of the renin‐angiotensin‐aldosterone system. The reduced response of AVP, AII and Aldo after furosemide is consistent with a lower degree of volume depletion in nephrotic patients.