Abstract
A 48 yr old man suffering from acute myeloid leukemia presented a hypokalemia that persisted almost constantly during 18 mo. despite total hematological remission. The renal investigation demonstrated a hypokalemic nephropathy with an impairment of urinary concentrating function. Light and electron microscopy showed renal lesions related to K depletion. Specific lesions explaining the renal K wasting were not observed. Metabolic studies showed persistent hyperkaluresis, which appeared to be the main kaliopenic factor. Hypomagnesemia and changes of the renin-aldosterone system were also found. A hyperreninism, probably due to hypokalemia and a slight hyperaldosteronism, which could have been 1 of the kaluretic agents were observed.