Although maintenance hemodialysis (MHD) patients are often wasted, little is known about their dietary energy needs. We studied four men and two women in a clinical research center while they received diets providing 45, 35 and 25 kcal/kg desirable body weight/day; diets were fed, in random order, for 21 to 23 days each. Protein intake, 1.13 +/- 0.02 (SEM) g protein/kg/day, was similar with all three diets. Body weight rose with 45 and 35 kcal/kg/day (P less than 0.05) and fell with 25 kcal/kg/day (P less than 0.05). Nitrogen balance, adjusted for estimated unmeasured losses, was neutral with 45 and 35 kcal/kg/day and negative with 25 kcal/kg/day. Balance was neutral or positive in 6 of 6, 4 of 6, and 0 of 6 patients fed 45, 35, 25 kcal/kg/day, respectively. Nitrogen balance, many plasma amino acids and changes in body weight, mid-arm circumference, mid-arm muscle area and body fat each correlated with energy intake. Resting energy expenditure was normal. The energy intake estimated from regression equations to maintain neutral nitrogen balance was 38.5 kcal/kg desirable weight/day; for body fat and weight, it was 32 kcal/kg/day. These data suggest that MHD patients have normal energy expenditure and approximately normal requirements for maintenance of protein balance, body weight and body fat. An average energy intake of about 38 kcal/kg desirable weight/day may be necessary to maintain nitrogen balance in these patients.

An oral protein load or infusion of amino acids induces a rise in renal hemodynamics in normal subjects, but the mechanisms mediating this phenomenon are unknown. We investigated whether glucagon may mediate the increase in RPF and GFR induced by an arginine infusion and whether prostaglandins are required for this effect. In four different studies, normal subjects underwent 13 inulin and PAH clearances of 30 minutes each. During the fourth and tenth clearance periods arginine HCl, 250 mg/kg, was infused over 30 minutes. At the beginning of the fifth clearance period several subjects ingested indomethacin, 150 mg, (N = 8) or ibuprofen, 800 mg (N = 6). Control subjects (N = 4) did not receive cyclooxygenase inhibitors. Six subjects underwent a similar protocol except that they were infused with glucagon, 6 ng/kg/min, instead of arginine, for 30 minutes during the fourth and tenth periods. They also ingested indomethacin, 150 mg, in the fifth period. In all four studies, a transient and significant rise in RPF and GRF and fall in RVR occurred during the first arginine or glucagon infusion. These changes in renal hemodynamics were blocked when the arginine or glucagon infusion was repeated after administration of indomethacin or ibuprofen. Urinary excretion of 6-keto-PGF1 alpha did not rise with either arginine infusion in the control subjects or in the individuals who received indomethacin. As predicted, urinary 6-keto-PGF1 alpha fell significantly after ingestion of indomethacin before the second infusion of arginine. Plasma norepinephrine and epinephrine concentrations were unaffected by the arginine infusions or by indomethacin.(ABSTRACT TRUNCATED AT 250 WORDS)

This study examined whether patients with insulin-dependent diabetes mellitus and normal renal function have an altered response to an amino acid infusion when they are pretreated with a converting-enzyme inhibitor. Three groups of adults received amino acid infusions for 20 min on two occasions separated by a 240-min interval. Groups 1 (6 normals) and 2 (6 diabetics) ingested captopril (12.5 mg) 120 min before starting the second infusion. Group 3 (4 diabetics) did not receive captopril. Diabetics had normal base-line renal plasma flow, as indicated by para-aminohippuric acid clearance (CPAH), and glomerular filtration rate (GFR). In group 1, the maximum increase in CPAH was significant and similar with both infusions, 23 +/- 5 vs. 15 +/- 3% (SE); maximal changes in GFR were also significant and similar, 20 +/- 5 vs. 20 +/- 6%. In Group 2, the maximal increase in CPAH and GFR with the first infusion was 28 +/- 7 and 23 +/- 6%, respectively. After captopril, the increases in CPAH and GFR were significantly greater than with the first infusion (64 +/- 8%, P less than 0.002, and 67 +/- 9%, P less than 0.002, respectively). In Group 3 diabetics, there was no difference in either CPAH or GFR with the first vs. the second infusion. Thus captopril enhances the renal hemodynamic response to an amino acid load in diabetic patients but not in normal adults.