BackgroundConcerns about hyperkalemia limit the use of angiotensin‐converting enzyme inhibitors (ACE‐I) and angiotensin receptor blockers (ARBs), but guidelines conflict regarding potassium‐monitoring protocols. We quantified hyperkalemia monitoring and risks after ACE‐I/ARB initiation and developed and validated a hyperkalemia susceptibility score.Methods and ResultsWe evaluated 69 426 new users of ACE‐I/ARB therapy in the Stockholm Creatinine Measurements (SCREAM) project with medication initiation from January 1, 2007 to December 31, 2010, and follow‐up for 1 year thereafter. Three fourths (76%) of SCREAM patients had potassium checked within the first year. Potassium >5 and >5.5 mmol/L occurred in 5.6% and 1.7%, respectively. As a comparison, we propensity‐matched new ACE‐I/ARB users to 20 186 new β‐blocker users in SCREAM: 64% had potassium checked. The occurrence of elevated potassium levels was similar between new β‐blocker and ACE‐I/ARB users without kidney disease; only at estimated glomerular filtration rate <60 mL/min per 1.73 m2 were risks higher among ACE‐I/ARB users. We developed a hyperkalemia susceptibility score that incorporated estimated glomerular filtration rate, baseline potassium level, sex, diabetes mellitus, heart failure, and the concomitant use of potassium‐sparing diuretics in new ACE‐I/ARB users; this score accurately predicted 1‐year hyperkalemia risk in the SCREAM cohort (area under the curve, 0.845, 95% CI: 0.840–0.869) and in a validation cohort from the US‐based Geisinger Health System (N=19 524; area under the curve, 0.818, 95% CI: 0.794–0.841), with good calibration.ConclusionsHyperkalemia within the first year of ACE‐I/ARB therapy was relatively uncommon among people with estimated glomerular filtration rate >60 mL/min per 1.73 m2, but rates were much higher with lower estimated glomerular filtration rate. Use of the hyperkalemia susceptibility score may help guide laboratory monitoring and prescribing strategies.
Over the past few years, chloride has joined the league of essential electrolytes for critically ill patients. Dyschloremia can occur secondary to various etiologic factors before and during patient admission in the intensive care unit. Some cases are disease-related; others, treatment-related. Chloride abnormalities were shown in animal models to have adverse effects on arterial blood pressure, renal blood flow, and inflammatory markers, which have led to several clinical investigations. Hyperchloremia was studied in several settings and correlated to different outcomes, including death and acute kidney injury. Baseline hypochloremia, to a much lesser extent, has been studied and associated with similar outcomes. The chloride content of resuscitation fluids was also a subject of clinical research. In this review, we describe the effect of dyschloremia on outcomes in critically ill patients. We review the major studies assessing the chloride content of resuscitation fluids in the critically ill patient.
Antibody-mediated anti-glomerular basement membrane (anti-GBM) disease occurs rarely in the presence of another B-cell disorder, membranous nephropathy. The coexistence of these two autoimmune disorders would be anticipated to require differing, specific therapies targeted to each disease process. We describe a case of concomitant membranous nephropathy and anti-GBM disease in which conventional therapy, including steroids, plasmapheresis and cyclophosphamide, failed to attenuate the anti-GBM disease, yet responded to an alternative treatment of rituximab. This B-cell directed, monoclonal, chimeric antibody treatment substantially reduced anti-GBM antibody titers and led to discontinuation of plasmapheresis, while maintaining the remission of membranous nephropathy and anti-GBM disease.
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