Figure 114

Nephrocalcinosis in type I (distal) renal tubular acidosis. Nephrocalcinosis and nephrolithiasis are common complications in distal renal tubular acidosis (RTA-1). Several factors contribute to the pathogenesis. The most important of these factors are a reduction in urinary excretion of citrate and a persistently alkaline urine. Citrate inhibits the growth of calcium stones; its excretion is reduced in RTA-1 as a result of both systemic acidosis and hypokalemia. The high urine pH favors precipitation of calcium phosphate (CaPO4). Thus, RTA-1 should be suspected in any patient with pure calcium phosphate stones [4]. Systemic acidosis also promotes hypercal-ciuria, although not all patients with RTA-1 have excessive urinary calcium excretion [5]. Hypercalciuria results from resorption of bone mineral and the consequent increased filtered load of calcium as acidosis leads to consumption of bone buffers. Acidosis also has a direct effect of inhibiting renal tubular calcium reabsorption. Conversely, nephrocalcinosis from other causes can impair urinary acidification and lead to RTA in some patients. The mainstay of therapy for RTA-1 is potassium citrate, which corrects acidosis, replaces potassium, restores urinary citrate excretion, and reduces urinary loss of calcium [5]. (From Buckalew [5]; with permission.)

51 Tips for Dealing with Kidney Stones

51 Tips for Dealing with Kidney Stones

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