In order to evaluate the renal contribution to the metabolism of arginine, we have evaluated its biosynthesis and catabolism in the isolated perfused rat kidney. The kidneys of eight male Sprague-Dawley rats were perfused with Krebs-Ringer-bicarbonate buffer containing albumin and amino acids. Twenty-five muCi of L-[guanidino-14C]arginine or 25 muCi L-[guanidino-14C]citrulline were added to the system and radiochromatograms of the perfusate were obtained at 0, 30, 60, and 90 min. Perfusate levels of urea, creatine, and guanidine derivatives were measured with high-pressure liquid chromatography. During perfusion there was net utilization of arginine and net production of creatine, guanidinoacetic acid (GAA) and guanidinosuccinic acid (GSA). The guanidino carbon of arginine was incorporated by the kidney into urea, creatine GSA, GAA, and guanidinobutyric acid. The production of 14C-labeled urea from L-[guanidino-14C]citrulline was substantially lower than that previously demonstrated in the liver, while that of arginine was approximately 20 times greater. These studies demonstrate the important contribution of the kidney to the synthesis and metabolism of arginine.

The diagnosis of ketoacidosis with an inordinately high plasma and urinary concentration ratio of beta-hydroxybutyrate (beta-OHB) to acetoacetate (AcAc) is difficult, because only AcAc and acetone react with the diagnostic reagents used clinically to detect ketones. The purpose of this study was to assess the validity of the claim that beta-OHB can be identified with a simple modification of the usual bedside test for ketones, using hydrogen peroxide (H2O2) and Ketostix (Ames Division, Miles Laboratories, Inc., Elkhart, Indiana). Unfortunately, the lowest detectable concentration of urinary beta-OHB was 50 mmol/L, and serum beta-OHB could not be detected at levels less than 100 mmol/L, a clinically irrelevant level. The relative insensitivity, the inapplicability to serum, and the potential hazard of the routine use of 30% H2O2 by practicing physicians or houseofficers render the method of limited value.

The effect of hyperkalemia on insulin secretion remains undefined. We evaluated portal and peripheral insulin levels in anesthetized dogs after infusions of KCl. The mean maximal increase in peripheral plasma potassium at infusion rates of 0.2 mEq/kg/h was 0.68 +/- 0.20 mEq/l. There were no significant increases in either portal or peripheral insulin levels. In contrast, in six dogs whose plasma potassium concentration increased in each case by more than 2.0 mEq/l (infusion rate of 0.5 mEq/kg/h), portal insulin levels increased fivefold (p less than 0.05). We concluded that only marked increases in plasma potassium concentration stimulate pancreatic insulin secretion.

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