ABSTRACT We studied prospectively 18 patients with sodium-losing nephropathy. In 12 patients (66.7 per cent) the sodium-losing nephropathy was owing to obstructions, challenging the hitherto existing concept that the most common cause of the condition is pyelonephritis. The diagnosis of sodium-losing nephropathy is important in urological practice since sodium repletion in these cases shortens significantly the hospitalization and preoperative waiting time.
- [show abstract] [hide abstract]
ABSTRACT: Studies were made on the biochemical and pathological conditions of kidneys of 20 brain-dead patients who were maintained for 0 to 48 days after brain death by administration of vasopressin and epinephrine. Twenty specimens were obtained by percutaneous biopsy or at autopsy. The biochemical and pathological degrees were compared with those on the day of brain death (day 0). Biochemical tests on day 0 indicated that they showed the diuretic phase of prerenal failure, and then glomerular hyperemia was extensive. Renal function recovered on day 1 and remained almost normal during the 14 day period. Their urine retained high levels of sodium and osmolarity for days 0 to 14, with mild hyponatremia and hypo-osmolarity of the plasma. Tubulointerstitial nephritis gradually became extensive. There was no significant change in the degrees of mesangial widening, mesangial cell proliferation or hyalinosis. Arterial intimal proliferation was gradually extensive after day 3 and glomerular endothelial proliferation was gradually extensive after a week. Brain-dead patients have been mostly reported to develop diabetes insipidus, but our brain-dead patients did not show any manifestation of this disease. We suggest that constant natriuresis and continuing high level of urine osmolarity might have been caused by prerenal renal failure, brain death followed by neurogenic impairment, high level of serum vasopressin, or interstitial nephritis.Kidney International 07/1993; 43(6):1363-70. · 7.92 Impact Factor