Aims Although multiple recent studies have confirmed an association between chronic proton-pump inhibitor (PPI) use and hypomagnesemia, the physiologic explanation for this association remains uncertain. To address this, we investigated the association of PPI use with urinary magnesium excretion. Methods We measured 24-hour urine magnesium excretion in collections performed for nephrolithiasis evaluation in 278 consecutive ambulatory patients and determined PPI use from contemporaneous medical records. Results The mean daily urinary magnesium was 84.6±42.8 mg in PPI users, compared to 101.2±41.1 mg in non-PPI users (p=0.01). In adjusted analyses, PPI use was associated with 10.54±5.30 mg/day lower daily urinary magnesium excretion (p=0.05). Diuretic use was associated with increased magnesuria, but did not significantly modify the effect of PPI on urinary magnesium. As a control, PPI use was not associated with other urinary indicators of nutritional intake. Conclusions Our findings suggest that PPI use is associated with lower 24-hour urinary magnesium excretion. Whether this reflects decreased intestinal uptake due to PPI exposure, or residual confounding due to decreased magnesium intake, requires further study.
Background Although vitamin D deficiency has been associated with increased insulin resistance, a causal link has not been established. Interpreting the relationship has been confounded by a close correlation between vitamin D deficiency and obesity. The current clinical approach of assessing endogenous 25-hydroxyvitamin D (25(OH)D) concentrations in patients with Chronic Kidney Disease(CKD), and independently administering activated vitamin D(AD), allows a unique opportunity to clarify cause and effect in the relationship of vitamin D, obesity, and insulin resistance. Methods We assessed how 25(OH)D and body mass index(BMI) related to fasting insulin concentrations in 120 nondiabetic CKD patients. In addition, we described how treatment with AD modified these relationships. Results In the full cohort, fasting insulin concentrations varied inversely with both 25(OH)D (r=−0.22, P=0.02) and BMI (r=−0.36, P<.0001). The administration of AD altered these relationships. In individuals treated with AD, there was no association between 25(OH)D and fasting insulin, and the mean fasting insulin concentrations were significantly lower than in those not receiving AD (40.5 ± 22.0 vs 54.1 ± 30.9 pmol/L, P=0.01). In a multivariate analysis, both AD treatment and BMI were independent predictors of fasting insulin. Furthermore, obese patients treated with AD had insulin concentrations similar to nonobese patients (46.1 ± 24.9 vs 40.2 ± 21.5 pmol/L), whereas untreated obese patients had markedly higher fasting insulin concentrations (74.4 ± 33.4 pmol/L, P=0.003). Conclusion 25(OH)D deficiency is associated with insulin resistance in CKD. Replacement with pharmacologic doses of AD is associated with lower fasting insulin concentrations, especially in obese patients.
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