Inulin and mannitol clearances, BUN concentrations and renal morphologic alterations were studied in rats 24 h after the injection of low doses of mercuric chloride. Water drinking rats given 4.7 mg/kg body weight of HgCl₂ developed renal failure and severe tubular necrosis. Their clearance of inulin was decreased to the same degree as their simultaneously determined mannitol clearance. Any significant change in tubular permeability should have resulted in a greater loss of mannitol than inulin, and it is suggested that tubular permeability to neither molecule was greatly increased. This is supported by the fact that rats drinking one percent saline in place of tap water for a month prior to receiving the same dose of HgCl₂ showed insignificant changes in inulin clearance and minimal elevations in BUN concentration. Nevertheless, histologic sections of their kidneys showed frank tubular necrosis that was equally severe as, but slightly less extensive than that observed in the water drinking rats whose inulin clearance was 6 % of normal. In view of these findings, it seems unlikely that alterationin tubular permeability per se are responsible for the development of acute renal failure in low dose mercury poisoning. The protective effect of salt loading does not depend on the prevention of tubular injury, and may well reflect inhibition of pre-glomerular vasoconstriction by suppression of the renin-angiotensin axis.

Diminished taste acuity may account for the persistence of protein and caloric malnutrition observed in a majority of hemodialysis patients inspite of liberalization of the prescribed amount of dietary protein. Twenty-two patients undergoing thrice weekly hemodialysis for more than 6 months were tested for taste acuity and plasma zinc concentration, after which a double-blind study was instituted using a zinc supplement (50 mg of elemental zinc as zinc acetate per day) or a placebo. The threshold of taste detection and recognition for salt (NaCl), sweet (sucrose), and bitter (urea) but not for sour (HCl) improved significantly in all patients on zinc supplementation. None of these parameters improved in those taking placebo. During the study period, the mean plasma zinc level increased from 75 +/- 8 to 97 +/- 10 microgram/dl (P less than 0.001) in patients receiving zinc acetate. There was not significant change in plasma zinc level in the placebo group (75 +/- 15 to 80 +/- 15). The results of this study show that uremic hypogeusia improved in association with zinc supplementation and elevation of plasma zinc concentration.

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Rats depleted of renin by chronic saline loading are largely protected from glycerol induced acute renal failure. For some 4 h after glycerol injection, these animals showed the same apparent renal ischemia, cessation of filtration and tubule collapse seen in rats that are not renin depleted. Despite this ischemia, renal function returned rapidly, individual nephron GFR reaching 75 % of normal within the succeeding 12 h. Significant outflow obstruction was evident transiently early in recovery, but was found not to be the prime cause of the low GFR. Recovery of glomerular filtration occurred quickly despite the presence of grossly elevated hydrostatic pressure in some nephrons. It is suggested that renin depletion produced by long term saline ingestion may prevent the protracted afferent arteriolar constriction which is chiefly responsible for the pathophysiologic events in this model of acute renal failure in the rat.

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One day after rats were injected with 4.7 mg/kg HgCl₂ subcutaneously, their surface nephrons usually were fluid filled, had a normal intratubular pressure, but formed minimal volumes of filtrate. Proximal tubule fluid flow rate was greatly diminished, material resembling cell debris obstructing the outflow of fluid. The finding of normal, rather than elevated, intratubular pressure in obstructed tubules indicates that effective filtration pressure probably was grossly reduced. Fluid absorption in the proximal tubule appeared to be greatly impaired. Despite slow flow in the undisturbed nephron, fluid could be collected from the proximal tubule at a normal rate, single nephron GFR being some 80% of control. The return of filtration on ‘venting’ the nephron during collections, and sustained normal single nephron GFR values after obstruction was relieved by washout of debris suggest a feed-back mechanism between impairment of tubular flow and intraglomerular filtration pressure. Intravenously injected lissamine green appeared promptly in distal tubule segments after release of obstruction, confirming the return of a normal proximal tubule fluid flow rate. Evidence for pathologically increased absorption of filtrate was not found. It is concluded that effective filtration pressure is significantly reduced in acute renal failure produced in the rat with low doses of HgCl₂ that tubular obstruction plays a role in the maintenance of the low filtration pressure, and that the discrepancy between whole kidney and single nephron inulin clearance values is artifactual. The latter features appear to be unique to low dose mercury poisoning and differ significantly from findings in other models of experimental acute renal failure in the rat.

A B S T R A C T Micropuncture studies of the recovery phase of glycerol-induced myohemoglobinuric acute renal failure were performed in rats whose blood urea nitrogen (BUN) had fallen at least 20% below its peak value. The