Urinary magnesium and pH are known to modulate urinary calcium excretion, but the mechanisms underlying these relationships are unknown. In this study, the data from 17 clinical trials in which urinary magnesium and pH were pharmacologically manipulated were analyzed, and it was found that the change in urinary calcium excretion is directly proportional to the change in magnesium excretion and inversely proportional to the change in urine pH; a regression equation was generated to relate these variables (R 2 ϭ 0.58). For further exploration of these relationships, intravenous calcium chloride, magnesium chloride, or vehicle was administered to rats. Magnesium infusion significantly increased urinary calcium excretion (normalized to urinary creatinine), but calcium infusion did not affect magnesium excretion. Parathyroidectomy did not prevent this magnesium-induced hypercalciuria. The effect of magnesium loading on calciuria was still observed after treatment with furosemide, which disrupts calcium and magnesium absorption in the thick ascending limb, suggesting that the effect may be mediated by the distal nephron. The calcium channel TRPV5, normally present in the distal tubule, was expressed in Xenopus oocytes. Calcium uptake by TRPV5 was directly inhibited by magnesium and low pH. In summary, these data are compatible with the hypothesis that urinary magnesium directly inhibits renal calcium absorption, which can be negated by high luminal pH, and that this regulation likely takes place in the distal tubule. 19: 153019: -153719: , 200819: . doi: 10.1681 The amount of calcium excreted in the urine (calciuria) is tightly regulated by a complex interaction between numerous calcitropic hormones, extracellular volume, acid-base status, and plasma and urinary concentration of various ions. 1 Calciuria is a continuous trait in the general population, and hypercalciuria is a major risk factor for nephrolithiasis found in high incidence in the stone former and/or in the osteoporotic populations. 2 The first description of an effect of magnesium on calciuria was made in a seminal article by Mendel and Benedict in 1909. 3 They observed increased calcium excretion and decreased fecal calcium content when magnesium salts were injected to various animal species. Similar observations were later reported in humans in preeclamptic pregnant women who were treated with magnesium sulfate and in normal individuals. 4,5 This effect was attributable to magnesium and not sulfate. 6 Attempts have been made to localize the segment where urinary magnesium could mediate its effect on calcium reabsorption in different animal models. Metabolic experi- J Am Soc Nephrol

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We report a case of an African American woman who presented with fatigue, generalized weakness, and hypophosphatemia in the setting of a recent hospitalization for severe, symptomatic iron deficiency anemia requiring ferric carboxymaltose infusions. Parental iron is indicated in numerous clinical settings including chronic kidney disease, inflammatory bowel disease, and iron deficiency anemia. Ferric carboxymaltose is one of the most common forms of parental iron infusions used due to administration procedure and minimal reported side effects. The most common side effect reported is a transient decrease in serum phosphate. This case highlights the necessity of monitoring serum phosphate in the setting of parental iron infusions, especially ferric carboxymaltose, and when severe hypophosphatemia occurs management includes intravenous phosphorous and calcitriol.

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