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The classic definition of hypercalciuria, an upper normal limit of 200  mg/day, is based on a constant diet restricted in calcium, sodium, and animal protein; however, random diet data challenge this. Here our retrospective study determined the validity of the classic definition of hypercalciuria by comparing data from 39 publications analyzing urinary calcium excretion on a constant restricted diet and testing whether hypercalciuria could be defined when extraneous dietary influences were controlled. These papers encompassed 300 non-stone-forming patients, 208 patients with absorptive hypercalciuria type I (presumed due to high intestinal calcium absorption), and 234 stone formers without absorptive hypercalciuria; all evaluated on a constant restricted diet. In non-stone formers, the mean urinary calcium was well below 200  mg/day, and the mean for all patients was 127±46  mg/day with an upper limit of 219  mg/day. In absorptive hypercalciuria type I, the mean urinary calcium significantly exceeded 200  mg/day in all studies with a combined mean of 259±55  mg/day. Receiver operating characteristic curve analysis showed the optimal cutoff point for urinary calcium excretion was 172  mg/day on a restricted diet, a value that approximates the traditional limit of 200  mg/day. Thus, on a restricted diet, a clear demarcation was seen between urinary calcium excretion of kidney stone formers with absorptive hypercalciuria type I and normal individuals. When dietary variables are controlled, the classic definition of hypercalciuria of nephrolithiasis appears valid.

Background: This study was undertaken to ascertain the effect of dietary modification on urinary stone risks, and to determine whether the response depends on the prevailing urinary calcium., Methods: A retrospective data analysis was conducted from our stone registry involving 951 patients with calcareous stones undergoing ambulatory evaluation, whereby 24-hour urine samples were collected during random diet and after dietary modification composed of restriction of calcium, oxalate, sodium, and meat products. Samples were analyzed for stone risk factors. Urinary calcium was also obtained after overnight fast and following a 1 g-calcium load. Changes produced by dietary modification from the random diet were evaluated in 356 patients with moderate-severe hypercalciuria (>6.88 mmol/day, group I), 243 patients with mild hypercalciuria (5.00-6.88 mmol/day, group II), and 352 with normocalciuria (<5.00 mmol/day, group III)., Results: Urinary calcium postcalcium load and the percentage of patients with absorptive hypercalciuria type I were highest in group I, intermediate in group II, and lowest in group III. During dietary modification, urinary calcium declined by 29% in group I, 19% in group II, and 10% in group III. Urinary oxalate did not change. Urinary saturation of calcium oxalate declined by only 12% in group I, 6% in group II, and nonsignificantly in group III, owing to various physicochemical changes in urinary biochemistry, which attenuated the effect of the decline in urinary calcium. Urinary saturation of brushite declined in all 3 groups due to the fall in urinary calcium, phosphorus, and pH. This reduction was more marked in the hypercalciuric groups than in the normocalciuric group. Urinary saturation of monosodium urate also decreased from a decline in urinary sodium and uric acid., Conclusion: Secondary rise in urinary oxalate occurring from calcium restriction can be avoided by concurrent dietary oxalate restriction. Dietary modification (restriction of dietary calcium, oxalate, sodium, and meat products) is more useful in reducing urinary saturation of calcium oxalate among patients with hypercalciuria than among those with normocalciuria.

Background: Potassium citrate is commonly used in combination with a thiazide diuretic in the medical management of recurrent hypercalciuric nephrolithiasis. However, concerns have been raised that administration of this nonchloride potassium alkali with a kaliuretic and natriuretic agent such as thiazide may not be efficacious in correcting or preventing hypokalemia, and may produce hypochloremic metabolic alkalosis. This retrospective analysis was conducted to determine if these two potential complications are encountered in patients on long-term potassium citrate and thiazide therapy., Methods: Data were collected on 95 patients who had been on combination therapy for at least 4 months from the stone clinics of the University of Texas Southwestern Medical Center, Duke University Medical Center, and Ochsner Clinic., Results: Mean serum potassium concentration remained within normal limits without a significant decrease during combined therapy. Serum chloride was significantly lower from pretreatment but by only 1 mEq/L and remained within normal limits throughout treatment. There was a small increase in serum bicarbonate concentration compared to the baseline level of less than 1 mEq/L at 8 to 12 and 18 to 24 months, but not at other treatment periods., Conclusion: Co-administration of potassium citrate did not induce hypokalemia or hypochloremic metabolic alkalosis in our thiazide-treated patient population.