Jeffrey H. William

Proton-pump inhibitor use is associated with low serum magnesium concentrations.

Although case reports link proton-pump inhibitor (PPI) use and hypomagnesemia, no large-scale studies have been conducted. Here we examined the serum magnesium concentration and the likelihood of hypomagnesemia (<1.6 mg/dl) with a history of PPI or histamine-2 receptor antagonist used to reduce gastric acid, or use of neither among 11,490 consecutive adult admissions to an intensive care unit of a tertiary medical center. Of these, 2632 patients reported PPI use prior to admission, while 657 patients were using a histamine-2 receptor antagonist. PPI use was associated with 0.012 mg/dl lower adjusted serum magnesium concentration compared to users of no acid-suppressive medications, but this effect was restricted to those patients taking diuretics. Among the 3286 patients concurrently on diuretics, PPI use was associated with a significant increase of hypomagnesemia (odds ratio 1.54) and 0.028 mg/dl lower serum magnesium concentration. Among those not using diuretics, PPI use was not associated with serum magnesium levels. Histamine-2 receptor antagonist use was not significantly associated with magnesium concentration without or with diuretic use. The use of PPI was not associated with serum phosphate concentration regardless of diuretic use. Thus, we verify case reports of the association between PPI use and hypomagnesemia in those concurrently taking diuretics. Hence, serum magnesium concentrations should be followed in susceptible individuals on chronic PPI therapy.

Proton-pump inhibitor-induced hypomagnesemia: Current research and proposed mechanisms

Since the early reports nearly a decade ago, proton-pump inhibitor-induced hypomagnesemia (PPIH) has become a well-recognized phenomenon. While many observational studies in the inpatient and outpatient populations have confirmed the association of PPI exposure and serum magnesium concentrations, there are no prospective, controlled studies to support causation. Molecular mechanisms of magnesium transporters, including the pH-dependent regulation of transient receptor potential melastatin-6 transporters in the colonic enterocyte, have been proposed to explain the effect of PPIs on magnesium reabsorption, but may be a small part of a more complicated interplay of molecular biology, pharmacology, and genetic predisposition. This review explores the current state of research in the field of PPIH and the proposed mechanisms of this effect.

Magnesium Deficiency and Proton‐Pump Inhibitor Use: A Clinical Review

The association of proton‐pump inhibitor (PPI) use and hypomagnesemia has garnered much attention over the last 5 years. A large body of observational data has linked chronic PPI use with hypomagnesemia, presumably due to decreased intestinal absorption and consequent magnesium deficiency. However, despite the increasing prevalence of this highly popular class of medicine, and despite potential significant risks associated with magnesium depletion, including cardiac arrhythmias and seizures, there are no well‐designed studies to delineate the nature of this observed association. Consequently, providers must use best judgment to inform clinical decision making. This review summarizes the current body of evidence linking PPI use with hypomagnesemia, acknowledges the possibility of significant residual confounding in the observational data, explains potential physiologic mechanisms, and offers clinical recommendations.

Proton-pump inhibitor use is associated with lower urinary magnesium excretion.

Although multiple recent studies have confirmed an association between chronic proton‐pump inhibitor (PPI) use and hypomagnesaemia, the physiologic explanation for this association remains uncertain. To address this, we investigated the association of PPI use with urinary magnesium excretion.

How we make nephrology easier to learn: Computer-based modules at the point-of-care

Background: Novel educational tools, such as case-based learning in a web-based module format, are an effective approach to teaching clinical concepts to medical trainees, especially if the situations are clinically relevant and the intervention is delivered at the point-of-care. Though studies have evaluated the effectiveness of point-of-care reference materials, limited literature addresses active web-based interventions designed for completion at the point-of-care. Aims: By taking advantage of existing technological resources and integrating an effective learning modality into the clinical environment, we can increase trainee understanding of high-yield topics in clinical nephrology. Methods: We designed interactive, case-based computer-based modules in Principles of Dialysis, Hyponatremia, and Acid–Base abnormalities, with interwoven multiple-choice and free text questions with immediate feedback, supplemental practice questions, and enrichment material to be completed in the clinical environment. All medicine trainees at an urban, academic institution were invited to participate in a needs assessment, pre and post knowledge tests, and module completion. Results: Most trainees believed the modules were “very” or “extremely helpful” in understanding the selected topic and that they would likely change their clinical practice. Those who completed the modules performed better on a post-intervention knowledge assessment. Free-text feedback was overwhelmingly supportive of the modules. Conclusion: Our findings confirmed that a novel, simplified approach to renal content by making it readily applicable to a clinical context and available at the point-of-care improves trainee understanding of high-yield topics in nephrology.

Keeping an eye on dialysis: the association of hemodialysis with intraocular hypertension.

Intraocular hypertension is common during hemodialysis. Dialysis disequilibrium syndrome and intraocular hypertension occur via similar pathophysiologic mechanisms. These mechanisms may contribute to the development of glaucoma and cataracts in a patient population already at high risk for ocular abnormalities, given the common risk factors for chronic kidney disease and impaired aqueous humor outflow. We describe a patient with complicated diabetes mellitus, end-stage renal disease, and recent cataract surgery who developed severe intraocular hypertension during hemodialysis. We recommend increased awareness of the symptoms of intraocular hypertension and subsequent ophthalmologic surveillance in order to prevent long-term visual complications.

Magnesium and Drugs Commonly Used in Chronic Kidney Disease

As with other electrolytes, magnesium homeostasis depends on the balance between gastrointestinal absorption and kidney excretion. Certain drugs used commonly in patients with CKD can decrease gastrointestinal ingestion and kidney reclamation, and potentially cause hypomagnesemia. Other magnesium-containing drugs such as laxatives and cathartics can induce hypermagnesemia, particularly in those with impaired glomerular filtration and magnesium excretion. In this review, we will discuss the potential magnesium complications associated with a range of commonly encountered drugs in the care of CKD patients, discuss the potential mechanisms, and provide basic clinical recommendations.