A long course of juvenile DM and the presence of pathologic calcifications were associated with the TNFalpha-308A allele and with the increased production of TNFalpha, which may perpetuate the inflammatory response.

SF consumed less calcium, presumably to prevent more stones, and displayed a bone mineral responsiveness to calcium loss and ammonium excretion not present among NSF, who ate more calcium. Lowered calcium consumption in IH, perhaps in response to stone formation, alters bone responses in a direction that can predispose to mineral loss and eventual fracture.

Although idiopathic hypercalciuria (IH) is associated with reduced bone mineral density (BMD), no studies to date have identified predictors of BMD change over an extended period of observation. We have studied change in femoral neck and spine BMD z-scores in men and women with IH and stone disease (IHSF) and their first-degree relatives in order to determine the predictive value of commonly made clinical measurements. Urine calcium excretion was inversely correlated with change in femoral neck z-score over 3 years, and marginally correlated with fall in spine z-score. Markers of bone turnover, serum calcitriol, and urine measurements of acid-base balance such as ammonium and sulfate had no predictive value, nor did calcium intake assessed using a well-established questionnaire. It would appear that IHSF with the highest 24-h urine calcium excretion rates are at highest risk for loss of femoral neck bone mineral over a 3-year period.