Medical, diet, family hx

By rray, 28 November, 2014
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<sup>1</sup> Malabsorptive GI states associated w/ stone dz: bowel resection, bariatric surgery, bowel/pancreatic dz.<br><br><sup>2</sup> Stone-provoking meds: probenecid, some protease inhibitors, lipase inhibitors, triamterene, chemo, vit C, vit D, Ca++, CAIs (topiramate, acetazolamide, zonisamide).<br><br>
<sup>3</sup> If urine pH >7 or urea-splitting organisms (e.g., <i>Proteus</i>): struvite stones possible.<br><br>
<sup>4</sup> Suspicion may also arise w/ predominantly Ca++ phosphate stones w/ ↑ urinary Ca++, or mid-range PTH in face of higher serum Ca++. Measuring vit D levels may help, as low D may mask 1° HPT, or contribute to 2° HPT.<br><br>
<sup>5</sup> High risk = (+)FHx, malabsorptive dz, recurrent UTI, obesity, medical dz (RTA type 1, 1° HPT, gout, DM type 2), solitary kidney.<br><br>
<sup>6</sup> Do not perform “fast and calcium load” testing to distinguish hypercalciuria type [R/C].<br><br>
<sup>7</sup> Suspect 1° hyperoxaluria if urinary oxalate excretion >75 mg/day in adults w/o bowel dysfxn (refer for genetic test/specialized urine tests).<br><br>
<sup>8</sup> Multiple/BL renal calculi @ initial presentation may signal ↑ recurrence risk. Nephrocalcinosis implies metabolic dz (RTA type 1, 1° HPT, 1° hyperoxaluria) or anatomic dz (medullary sponge kidney).
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