Abstract
Alterations in renal tubular and cellular function have been reported in clinical and experimental nephrolithiasis1-3, and it has been suggested that the presence of calcium oxalate stones within the kidney elicits these changes as a result of mechanical injury to the tubular cells. Evidence in support of this possibility was provided by studies in experimental animals where the induction of calcium oxalate crystal formation led to renal tubular damage (enzymuria, proteinuria, etc,4, 5). The present studies assessed the possibility that oxalate produces alterations in cell function in the absence of overt crystal formation. Specifically we determined whether or not exposure to physiological levels of oxalate would elicit changes in intracellular calcium levels in isolated papillary cells from normal rat kidneys.
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