Acid-base homeostasis during chronic PTH excess in humans.

Abstract

The chronic renal and systemic acid-base effects of hyperparathyroidism in humans remain controversial and unresolved. The present studies evaluated the acid-base response of normal human subjects to a 13-day intravenous infusion of synthetic b(1-34) PTH sufficient to result in sustained hypercalcemia and hypophosphatemia. The acid-base response was biphasic: an initial transient renal acidosis developed on the first day of PTH infusion, followed by a prompt increase in net acid excretion and plasma [HCO3-] of sufficient magnitude to result in a steady state of mild metabolic alkalosis. The results indicate that: 1) sustained, continuous, experimentally produced hyperparathyroidism results in a steady state of mild metabolic alkalosis; 2) the alkalosis is both generated and maintained, at least in part, by renal mechanisms; and 3) reported renal acidosis in sustained clinical conditions of primary hyperparathyroidism is not attributable to either direct or indirect effects of PTH excess when present for a 2-week period, an interval sufficient to re-establish a new steady state of renal and systemic acid-base equilibrium.

• Authors: H N Hulter, J C Peterson
• Journal: Kidney international (Kidney Int) Vol. 28 Issue 2 Pg. 187-92 (Aug 1985) ISSN: 0085-2538 [Print] United States
• PMID: 3834229 (Publication Type: Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Parathyroid Hormone
• Peptide Fragments
• Teriparatide

Topics

• Acid-Base Equilibrium
• Acidosis, Renal Tubular (chemically induced)
• Adult
• Alkalosis (chemically induced)
• Diet
• Humans
• Hypercalcemia (chemically induced)
• Hyperparathyroidism (chemically induced, metabolism)
• Infusions, Parenteral
• Kidney (metabolism)
• Male
• Parathyroid Hormone (administration & dosage)
• Peptide Fragments (administration & dosage)
• Teriparatide