A comparison of the effects of glucose ingestion and NH4Cl acidosis on urinary calcium and magnesium excretion in man.
Both glucose ingestion and NH(4)Cl acidosis have been reported to augment urinary calcium (U(Ca) V) and magnesium (U(Mg) V) excretion. Both also cause acidification of the urine and an increase in renal acid excretion. To examine whether a common mechanism of action was involved, the effects of glucose ingestion and NH(4)Cl acidosis on U(Ca) V and U(Mg) V were tested in the same subjects. Glucose ingestion caused significant increases in both U(Ca) V and U(Mg) V. During stable NH(4)Cl acidosis, U(Ca) V increased significantly, while U(Mg) V was unaffected. When a glucose load was given during acidosis, the separate effects of acidosis and glucose on U(Ca) V were additive, whereas U(Mg) V increased less than observed during normal acid-base balance. Although renal acid excretion increased and the urine was acidified after glucose in the normal steady state, when glucose was administered during NH(4)Cl acidosis urine pH rose and there was no change in renal acid excretion. We concluded that NH(4)Cl acidosis and glucose ingestion reduce the renal tubular reabsorption of magnesium and (or) calcium, but they act through separate mechanisms.
D000138:Acidosis / Q000139:chemically induced*; D000643:Ammonium Chloride; D002118:Calcium / Q000652:urine*; D004231:Diuresis; D005919:Glomerular Filtration Rate; D005947:Glucose / Q000378:metabolism / Q000494:pharmacology*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007444:Inulin; D007668:Kidney / Q000502:physiology*; D007684:Kidney Tubules / Q000502:physiology; D008274:Magnesium / Q000652:urine*; D008297:Male; D009994:Osmolar Concentration; D012964:Sodium / Q000652:urine
D000643:Ammonium Chloride; D007444:Inulin; D012964:Sodium; D008274:Magnesium; D005947:Glucose; D002118:Calcium