The effects of acute and chronic metabolic acidosis on serum immunoreactive parathyroid hormone (iPTH) were studied. Acute metabolic acidosis induced by administration of ammonium chloride (NH4Cl) produced a barely detectable increase in serum iPTH. Chronic NH4Cl administration produced a marked elevation of serum iPTH that was well correlated with the magnitude of acid-induced hypercalciuria but not with the degree of acidosis. Acetazolamide administration produced an equivalent degree of acidosis, but hypercalciuria was minimal and iPTH increased only marginally. Methionine administration caused moderate hypercalciuria and a significant but moderate increase in iPTH. Chronic NH4Cl-induced acidosis produced no hypercalciuria when dietary sodium intake was rigidly restricted, and under these conditions serum iPTH remained normal. When sodium intake was suddenly increased while maintaining the acid load, hypercalciuria appeared and was followed by progressive rise in serum iPTH equivalent to that observed during chronic NH4Cl-induced acidosis in subjects consuming salt ad lib. These results indicate that chronic acidosis elevates iPTH mainly by producing hypercalciuria and that acidosis itself is not a primary stimulus to PTH secretion.
Plasma concentrations of 25 essential (EAA) and nonessential (NEAA) amino acids were measured pre- and postdialysis in 46 chronic hemodialysis therapy (CDT) patients. Sixteen of these patients with prior weight loss of 14.5 +/- 2.37 pounds in 24 months were administered a GAA solution (EAA + NEAA + glucose) for 20 weeks during each dialysis. Eight of these patients (group 1) responded with improved appetite and weight gain; the remaining eight patients (group 2) with clinically advanced metabolic bone disease continued to lose weight. Five other patients (group 14), biochemically similar to group 1 but with shorter prior dialysis experience, who received EAA (plus glucose) hyperalimentation (including oral I-histidine), experienced weight gain similar to group 1 but displayed significantly different plasma aminograms indicating a deficit of NEAA. When EAA and glucose hyperalimentation was administered without histidine (1 patient) no weight gain occurred and aminograms differed significantly from other groups. Plasma aminograms of 25 weight-stable, nonhyperalimented CDT patients were obtained for comparison. Results indicate GAA hyperalimentation can promote weight gain in catabolic CDT patients with inadequate prior nutritional intake (as in groups 1 and 14) but cannot reverse weight loss when the primary clinical setting is advanced metabolic bone disease and myopathy due to hyperparathyroidism (group 2). Hyperalimentation with glucose and an amino acid solution specifically tailored to the needs of CDT patients may improve results. Plasma phosphoethanolamine levels, normal for weight-stable and elevated in catabolic CDT patients, suggest a possible role for phosphoethanolamine as a marker for catabolism.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.