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Citrate Excretion in Renal Tubular Acidosis
- JAMES F. MORRISSEY, M.D.;
- MANUEL OCHOA, JR., M.D.;
- WILLIAM D. LOTSPEICH, M.D.; and
- CHRISTINE WATERHOUSE, M.D., F.A.C.P.
Excerpt
Metabolic and respiratory acidosis has been shown to decrease the urinary citrate excretion in man (1). Conversely, metabolic or respiratory alkalosis will increase this parameter, without associated increase in the plasma citrate level (2). In these situations, usually the urine pH varies directly with the pH of the blood which does not allow one to differentiate the significance of either factor in the renal excretion of citrate. Recently, Evans, Maclntyre, Macpherson, and Milne (2) have shown that potassium repletion in a patient with primary aldosteronism was associated with an increased urinary citrate excretion. In their case, this occurred in the
This 100-word excerpt has been provided in the absence of an abstract.
Summario in Interlingua
In recente tempores il ha essite postulate que in acidosis reno-tubular le restringite excretion renal de ion de hydrogeno contra un gradiente de concentration es possibilemente le consequentia de un defecto quantitative in le production de energia ab le cyclo de Kreb intra le cellulas reno-tubular. Plure observationes, incluse nostres, ha confirmate le constatation de basse concentrationes de citrato urinari in acidosis reno-tubular. Viste que citrato es un importante componente del cyclo de Kreb, il pareva pertinente mesurar le excretion de illo in le mentionate morbo sub varie conditiones. In un patiente adulte, con ben-documentate acidosis reno-tubular, qui esseva studiate in un departimento pro problemas de metabolismo, le valores de base pro le citrato urinari esseva inter 10 e 15 mg per die in despecto de un normal pH del sanguine. (Le correspondente valores normal es inter 200 e 1000 mg.) Le induction de depletion de kalium per Diuril e de sever acidosis per NH4Cl causava nulle alteration. Repletion con KCl, durante que le acidosis esseva mantenite, produceva nulle augmento. Post un secunde periodo de inducite depletion de kalium, le repletion de iste ion—associate in iste occasion con un augmento del pH del sero a valores normal—de novo habeva nulle influentia super le excretion de citrato. Le subsequente administration de NaHCO3 (in un dosage de 45 mEq per die) produceva de facto un augmento del citrato usque a nivellos normal basse (attingente un maximo de 220 mg per die). Quando plus grande quantitates de NaHCO3 (360 mEq per die) esseva administrate, le excretion de citrato montava additionalmente a plus que 500 mg per die. In le curso de quatro horas de infusion intravenose de NaHCO3 o tampon tris, le excretion de citrato attingeva nivellos de 300 mg intra quatro horas, lo que es comparabile al valores inducite per alcalosis metabolic experimental in subjectos normal. A base de iste observationes il es postulate que le defective excretion de citrato in acidosis reno-tubular es relationate con un alterate ambiente intracellular in le tubulos, possibilemente acidosis, plus tosto que con un defecto enzymatic in le cyclo de Kreb. Assi il pare que le basse excretion de citrato in iste disordine es un phenomeno secundari plus tosto que un evento primari.
Article and Author Information
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From the Departments of Medicine and Physiology, University of Rochester School of Medicine and Dentistry, Rochester, New York.
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This study was supported by grant OG-22 from the United States Public Health Service.
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- Received June 4, 1962.
- Accepted June 25, 1962.
