PLASMA NATRIURETIC FACTOR(S) IN PATIENTS WITH INTRACRANIAL DISEASE, RENAL SALT WASTING AND HYPERURICOSURIA

To test our hypothesis that a circulating factor(s) may be causing the renal salt and urate wasting in patients (pts) with intracranial dise ases, we exposed rats to the plasma of these patients and studied sodi um and lithium transport. We selected 21 neurosurgical pts, 13 of whom had increased fractional excretion (FE) of urate, and 14 age and sex- matched controls. Plasma from pts and controls were injected IP (0.5 m L) and infused, 0.2 ml prime and 1.8 mL at 0.01 mL/min, to Sprague Daw ley rats anesthetized with Inactin. Renal transport of sodium (Na), li thium (Li) and potassium (K) was determined. There were higher mean +/ - SEM for FENa, 0.59 +/- 0.07% vs 0.29 +/- 0.05%, P < 0.01, FELi, 36.6 +/- 1.9% vs 24.0 +/- 1.6%, P < 0.001 and K excretion rates, 1.69 +/- 0.13 vs 1.31 +/- 0.09 mumol/min, p < 0.02, in rats infused with plasma of pts as compared to controls, respectively. FENa decreased with inc reasing dilution of plasma of 2 pts with ICD. There was no difference in mean weight of rats, blood pressure, urine flow rate or inulin clea rance between pts and controls. These data suggest that pts with ICD h ave a plasma factor(s) which decreases net Na, Li and K reabsorption.