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Background: Patiromer and sodium polystyrene sulfonate (SPS) are cation-exchangers approved for the treatment of chronic hyperkalemia. Data regarding their efficacy acutely is lacking. Despite this, both drugs are frequently used in the emergent setting. Objective: The purpose of this study was to compare the potassium reduction of patiromer to SPS within 6 to 24 hours following a single dose. Methods: This retrospective quality improvement project included hyperkalemic patients receiving 1 dose of patiromer or SPS and had a second potassium level drawn in 6 to 24 hours. Doses of 8.4 g of patiromer and 15 g of SPS were considered "low dose" while 16.8 g of patiromer and 30 g of SPS were considered "high dose." The presence of a dose-response relationship was assessed through a linear regression analysis. Results: Mean (SD) potassium reduction was higher in SPS than patiromer [0.76 (0.63) mEq/L vs 0.32 (0.65) mEq/L, (P = .001)]. A dose response relationship was not demonstrated in low versus high dose groups [-0.21 (0.14), P = .13] and CKD, ESRD, and renal transplant patients when compared to patients with normal renal function [0.11 (0.17), P = .51, -0.07 (0.19), P = -0.07 (0.19), P = .73, and -0.10 (0.22), P = .65]. Conclusions: This study suggests a clinically significant reduction in potassium with SPS compared to patiromer. Although SPS was successful in demonstrating this outcome, due to well-documented adverse reactions in the literature and a time to onset of 6 hours, it cannot be recommended for use in acute hyperkalemia either.
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Patiromer is a novel potassium-binding compound which has recently received FDA approval. This ion exchange resin releases calcium when it binds potassium. We describe the development of hypercalcemia after initiation of patiromer. The calcium levels fell when the drug was stopped but recurred when it was later resumed. Patiromer was again discontinued, and the serum calcium level fell back into the normal range. We believe this patient manifested patiromer-induced hypercalcemia.
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We present a patient with steroid-resistant nephrotic syndrome due to focal segmental glomerulosclerosis along with smoldering multiple myeloma. While investigating the cause of proteinuria, a monoclonal gammopathy with a negative kidney biopsy for myeloma-related pathology was discovered.
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We describe the case of a 24-year-old woman who intentionally ingested between 400 and 600 mg of amlodipine along with a large number of simvastatin and trazodone tablets.
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Renal artery stenosis and renovascular hypertension are important considerations in patients with hypertension that is difficult to control. The diagnosis may also have prognostic significance for progressive renal disease. The most common causes of renal artery stenosis are atherosclerotic disease and fibromuscular dysplasia. The pathophysiology of renal artery stenosis is reviewed, and the pros and cons of various imaging studies in the appropriate clinical setting are discussed. Treatment includes aggressive control of hypertension, dealing with associated cardiac risk factors, and angioplasty or surgery in specific circumstances.
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Amiodarone is a class III antiarrhythmic drug widely used for both ventricular and supraventricular tachyarrhythmias. Due to its high iodine content and structural similarity to thyroxine, abnormalities in thyroid function are common in patients taking amiodarone, especially with long-term use. Both hypo- and hyperthyroidism have been associated with amiodarone, with the former far more common in the United States. We present a patient with medically refractory amiodarone-induced thyrotoxicosis after a 2-year history of amiodarone use, resulting in cardiac arrest and encephalopathy. The patient ultimately required total thyroidectomy for symptomatic control.