A 3-mo perdialytic parenteral nutrition (PDPN) regimen was tested in 26 malnourished adults receiving hemodialysis (HD). Subjects were randomly assigned to receive PDPN (n = 12) or not to receive it (n = 14). PDPN was intravenously infused three times a week during HD; each infusion was made up of 1.6 g fat/kg body wt, 0.08 g N/kg body wt, essential and nonessential amino acids, and glycyl-tyrosine. PDPN, together with a PDPN-induced increase in spontaneous eating, increased intakes from 30 +/- 8.4 kcal.kg body wt-1.d-1 (mean +/- SD) and 1 +/- 0.27 g protein.kg body wt-1.d-1 to 39 +/- 8.5 kcal.kg body wt-1.d-1 and 1.25 +/- 0.30 g protein.kg body wt-1.d-1. Compared with control subjects, PDPN patients were characterized by increases in body weight (P less than 0.01), arm-muscle circumference (P less than 0.02), serum transthyretin and albumin concentrations (P less than 0.05), interdialytic creatinine appearance (P less than 0.01), skin-test reactivity (P less than 0.02), plasma leucine (P less than 0.05) without modifications of other amino acids, and plasma apolipoprotein A-I (P less than 0.01) without significant changes in apolipoprotein B, cholesterol, triglyceride, and phospholipid concentrations. Thus, PDPN appeared to be effective and safe with respect to plasma lipids.

In hemodialysis (HD) patients, serum prealbumin (TBPA) is correlated to nutritional status and outcome despite usually elevated serum levels. The purpose of this work was to study the role of TBPA-retinol-binding-protein (RBP)-retinol complex changes in the elevation of serum TBPA in HD patients. Serum TBPA, RBP, and retinol were measured in 30 otherwise healthy HD patients (15 men, 15 women) and in 30 healthy volunteers (15 men, 15 women). The dependence of TBPA on RBP was studied by covariance and regression methods. TBPA (p less than 0.05), RBP (p less than 0.01), and retinol (p less than 0.05) were elevated in HD patients. Elevated TBPA was associated with a decrease of TBPA free from RBP (p less than 0.01). The decrease of free TBPA may explain the reduction of TBPA breakdown and its elevation in HD patients.

Metabolic changes due to chronic renal failure (CRF) were studied in isolated liver cells. In 14 CRF and 14 sham-operated rats, liver cells were isolated by the Berry and Friend method and incubated with various substrates in order to study gluconeogenesis, ureagenesis, ketogenesis, oxygen consumption as well as cytosolic and mitochondrial adenine nucleotide content. CRF rat hepatocytes exhibited a 25% to 45% decrease in gluconeogenesis and ureagenesis (P < 0.05) from all the tested substrates (lactate plus pyruvate, fructose, glycerol, dihydroxyacetone, alanine and glutamine for gluconeogenesis and alanine, glutamine, ammonia and ammonia plus ornithine for ureagenesis), while endogenous rates were unaffected. CRF did not alter ketone body production (acetoacetate and beta-hydroxybutyrate) from oleate or octanoate. In the presence of either oleate, lactate plus pyruvate or ammonia, oxygen uptake as well as cytosolic and mitochondrial total adenine nucleotides were unaffected by CRF, while the mitochondrial ATP/ADP ratio decreased (P < 0.001). Thus, this study of hepatocyte intermediary metabolism during CRF showed an alteration of only gluconeogenesis and ureagenesis pathways. Moreover, the association of normal oxygen uptake together with decreased mitochondrial ATP/ADP ratio suggest a possible increase in hepatocyte ATP demand during uremia.

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