Kidney International (1985) 28, 187–192; doi:10.1038/ki.1985.139
Acid-base homeostasis during chronic PTH excess in humans
Henry N Hulter1 and John C Peterson1
1Renal Laboratory, Veterans Administration Medical Center and Department of Medicine, University of Florida, Gainesville, Florida, USA
Correspondence: Dr H N Hulter, Division of Nephrology, 1065 HSE, University of California, San Francisco, California 94143 USA
Received 9 October 1984; Revised 28 January 1985.
Top of pageAbstract
Acid-base homeostasis during chronic PTH excess in humans. 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.
Homéostasie acido-basique pendant un excès chronique de PTH chez l'homme. Les effets acido-basiques rénaux et systémiques de l'hyperparathyroïdisme chez l'homme sont sujets à controverse et restent non résolus. Ces études ont évalué la réponse acido-basique de sujets humains normaux à une perfusion intraveineuse de 13 jours de b(1–34) PTH synthétique suffisante pour induire une hypercalcémie et une hypophosphatémie prolongées. La réponse acido-basique était biphasique: une acidose rénale transitoire initiale se développait le premier jour de la perfusion de PTH, suivie par une élévation rapide de l'excrétion nette d'acides et du [HCO3-] plasmatique d'importance suffisante pour entraîner à l'équilibre une alcalose métabolique modérée. Ces résultats indiquent que: 1) une hyperparathyroïdie soutenue, continue, produite expérimentalement, entraîne une alcalose métabolique modérée; 2) l'alcalose est générée et maintenue, au moins en partie, par des mécanismes rénaux; 3) l'acidose rénale rapportée dans des conditions cliniques d'hyperparathyroïdie primitive prolongée n'est pas attribuable à des effets directs ou indirects de l'excès de PTH lorsqu'il est présent sur une période de deux semaines, un intervalle suffisant pour ré-établir un nouvel état d'équilibre acido-basique rénal et systémique.
Top of pageReferences
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