Elisa Del Valle

Hypomagnesaemia/hypokalemia associated with the use of esomeprazole.

Magnesium homeostasis is essential for many intracellular processes and depends on dynamic interplay of intestinal absorption, exchange with the bone reservoir, and renal excretion. Hypomagnesaemia may arise from various disorders. We review the case of a 59 year-old man whose only complaint was irritability with a routine analysis showing hypomagnesaemia and hypokalemia while using esomeprazole, a proton pump inhibitor (PPI). Fractional magnesium excretion was low, excluding excessive renal loss. Potassium excretion was 80 mEq/24 Hr in the presence of hypokalemia suggesting hypomagnesaemia-induced kaliuresis as its cause. Hypomagnesaemia partially resolved after oral magnesium supplementation. Esomeprazol suppression corrected hypomagnesaemia. A causal relationship with esomeprazol use was supported by the recurrence of hypomagnesaemia after rechallenge. We review the literature on hypomagnesaemia due to the use of proton pump inhibitors. In the past decade our understanding of transcellular magnesium transport was enhanced by the discovery of the magnesium channel, transient receptor potential (TR PM) 6 and 7 and other proteins that play an important role in its transport. In this light we discuss the possible etiology of proton pump inhibitor related hypomagnesaemia/hypokalemia.

Weekly high-dose ergocalciferol to correct vitamin D deficiency/insufficiency in hemodialysis patients: A pilot trial

Controversy exists on which vitamin D (D2 or D3) and which dosage scheme is the best to obtain and maintain adequate 25 OH D levels in dialysis patients safely. We tried to determine whether high‐dose vitamin D2 supplementation could obtain optimal vitamin D status without inducing hypercalcemia. We studied 82 patients on dialysis not taking active vitamin D therapy and supplemented them with oral vitamin D2 72,000 IU/week for 12 weeks followed by 24,000 IU/week as maintenance therapy during 36 weeks. By week 12, serum 25(OH)D increased from 15.2 ± 5.4 to 42.5 ± 13.2 ng/mL (P < 0.01) at week 12 and remained optimal (34.7 ± 12.0); 84.8% of the patients reached values ≥30 ng/mL. iPTH and alkaline phosphatase did not change at 48 weeks compared with baseline, but bone alkaline phosphatase decreased significantly (54.3 ± 46.0 to 44.3 ± 25.0; P = 0.02). Uncorrected serum Ca increased significantly at the end of follow‐up (9.03 ± 0.42 to 9.14 ± 0.62; P = 0.04); hypercalcemia was presented in two patients in the first control visit (week 12), in one patient in the second control (week 30), and in one patient in the third control (week 48). In 222 serum calcium determinations during follow‐up, hypercalcemia was observed in only 1.8% of cases. This vitamin D2 oral regimen with initial high doses was safe and sufficient to obtain and maintain optimal serum 25(OH)D concentrations and prevent vitamin D insufficiency in chronic kidney disease patients on dialysis.

Which Vitamin D in Chronic Kidney Disease: Nutritional or Active Vitamin D? Or Both?

As vitamin D insufficiency is very common world-wide, vitamin D supplementation has generated much debate and subsequent research not only in the general population but also in patients with chronic kidney disease (CKD). Several observational and mechanistic studies have suggested that vitamin D’s actions may be more broad and significant than originally appreciated, far exceeding bone and mineral metabolism. This is probably due to the fact that most tissues in the body express vitamin D receptors. As patients with kidney disease cannot convert 25-hydroxyvitamin D [25(OH)D] to its more active form, 1,25-dihydroxy vitamin D [1,25(OH)2D] because of reduced activity of the enzyme 1α-hydroxylase in the kidneys to produce classic bone and mineral effects, nephrologists have traditionally replaced patients with kidney disease with active vitamin D, 1,25-dihydroxvitamin D, or related analogs. Multiple observational studies in patients with CKD have shown that they not only have low levels of 1,25(OH)2D, but also low 25(OH)D levels. The fact that there is also extrarenal conversion of 25(OH) vitamin D to 1,25(OH)2 vitamin D in CKD in multiple tissues leading to autocrine effects, has led to the speculation that CKD patients should also need to be supplemented with nutritional vitamin D. This chapter outlines the available evidence on the controversy about which vitamin D is better for patients with kidney disease: Active vitamin D, nutritional or both.