Clinical Investigation

Kidney International (1979) 16, 736–742; doi:10.1038/ki.1979.190

Differing effects of acid versus neutral phosphate therapy of hypercalciuria

Kai Lau1, Charles Wolf1, Paul Nussbaum1, Bernard Weiner1, Peter DeOreo1, Eduardo Slatopolsky1, Zalman Agus1 and Stanley Goldfarb1

1Renal-Electrolyte Section, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania

Correspondence: Dr Kai Lau, Renal Section, 860 Gates Building, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, Pennsylvania 19104, USA

Received 12 March 1979; Revised 11 June 1979.

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Abstract

Differing effects of acid versus neutral phosphate therapy in idiopathic hypercalciuria. Studies were performed on 12 patients with idiopathic hypercalciuria to evaluate the hypothesis that the acid load accompanying potassium acid phosphate would adversely affect renal calcium reabsorption and citrate excretion compared to the neutral form of the phosphate salt. During acute clearance studies, neutral phosphate (NP) led to a fall in FECa (2.2 plusminus 0.6% to 0.8 plusminus 0.1%, P < 0.02) and no change in titratable acidity (TA) or net acid excretion (NAE). Acid phosphate (AP) did not reduce FECa acutely, and led to a rise in TA (22 plusminus 4 to 62 plusminus 6 microEq/min, P < 0.02) and NAE (46 plusminus 6 to 89 plusminus 7 microEq/min, P < 0.02). During chronic administration, AP resulted in higher urinary calcium excretion in both absorptive (187 plusminus 29 vs. 141 plusminus 18 mg/day, P < 0.02) and renal hypercalciuric patients (233 plusminus 24 vs. 173 plusminus 190.02 mg/day, P < 0.02). Also, TA and NAE were higher following AP, whereas citrate excretion was lower (375.4 plusminus 64.6 vs. 633.4 plusminus 28.8 mg/day, P < 0.01). These data suggest that the reported ineffectiveness of AP in the therapy of nephrolithiasis may be related to the deleterious effects of the acid load on calcium and citrate metabolism.

Effets différents du traitement de l'hypercalciurie par les formes acide ou neutre du phosphate. Douze malades atteints d'hypercalciurie idiopathique ont été étudiés pour évaluer l'hypothèse selon laquelle la charge acide incluse dans le phosphate acide de potassium pourrait défavorablement influencer la réabsorption rénale de calcium et l'excrétion urinaire de citrate par comparaison avec la forme neutre du phosphate. Au cours d'études aiguës, le phosphate neutre (NP) a déterminé une chute de FECa (2,2 plusminus 0,6% à 0,8 plusminus 0,1%; P < 0,02) et pas de modification de l'acidité titrable (TA) ou de l'excrétion nette d'acide (NAE). Le phosphate acide ne diminue pas FECa et détermine une augmentation de TA (22 plusminus 4 à 62 plusminus 6 microEq/min; P < 0,02) et de NAE (46 plusminus 6 à 89 plusminus 7 microEq/min; P < 0,02). Au cours de l'administration chronique, le phosphate acide détermine une excrétion urinaire de Ca plus importante aussi bien chez les malades atteints d'hypercalciurie par hyperabsorption (187 plusminus 29 vs. 141 plusminus 18 mg/jour; P < 0,02) que chez ceux ayant des hypercalciuries rénales (233 plusminus 24 vs. 173 plusminus 190,02 mg/jour; P < 0,02). De même TA et NAE étaient plus élevées après l'administration de phosphate acide alors que l'excrétion de citrate était diminuée (375,4 plusminus 64,6 vs. 633,4 plusminus 28,8 mg/jour P < 0,01). Ces observations suggèrent que l'inefficacité du phosphate acide dans le traitement de la lithiase rénale peut être liée aux effets nuisibles de la charge acide sur les métabolismes du citrate et du calcium.

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