Michael Emmett M.D.

Emmett, M. and A. Mehta (2016). “Gastrointestinal potassium binding-more than just lowering serum [k(+)]: Patiromer, potassium balance, and the renin angiotensin aldosterone axis.” Kidney Int 90(3): 484-486.

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Hyperkalemia limits the use of renin-angiotensin-aldosterone axis (RAAS) blockers in patients with renal insufficiency. This can be managed by efforts to increase kaliuresis and by gastrointestinal potassium binding with sodium polystyrene sulfonate, a relatively ineffective agent. Now with the availability of patiromer, RAAS blockers can be used more liberally. In addition, potassium reduction decreases aldosterone, which may be beneficial. Adverse nonepithelial aldosterone effects such as endothelial dysfunction and cardiac fibrosis may be ameliorated.

Hundemer, G. L., A. Z. Fenves, K. M. Phillips and M. Emmett (2016). “Sodium Thiosulfate and the Anion Gap in Patients Treated by Hemodialysis.” Am J Kidney Dis. Mar 15. [Epub ahead of print]

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Calciphylaxis is a syndrome of microvascular calcification and thrombosis leading to painful purpuric skin lesions that progress to necrotic ulcers. Calciphylaxis occurs primarily in patients with ESRD, for which its prevalence has been estimated at 1% annually, and carries a high mortality rate. Increasingly, sodium thiosulfate (STS) is used off-label for treating calciphylaxis. The STS mechanism of action in this condition is unknown. One postulated mechanism is by binding to calcium phosphate salts to form soluble calcium thiosulfate, though additional antioxidant, vasodilatory, and direct inhibitory actions on vascular calcification have been proposed. Dosing of STS, which contains 12.7 mEq/g of sodium and thiosulfate, is empirical and typically 12.5 or 25 g is given during the final 30 to 60 minutes of a hemodialysis (HD) session. A retrospective study showed that 73% of patients treated for calciphylaxis with STS had clinical improvement, with 26% having complete resolution of skin lesions . . . Using an electronic database, we identified all patients with a diagnosis of calciphylaxis who were treated with STS at Massachusetts General Hospital and Brigham and Women’s Hospital between January 2005 and December 2014. . . We found that HD patients treated with STS for calciphylaxis develop an elevated anion gap that is variable and often severe. In addition, we found a dose-response effect of STS on anion gap elevation. Future studies should address the exact mechanism of how STS improves calciphylaxis, which anion accumulates with STS treatment, why such high variability in anion gap effect exists, and clinical effects of the anion gap elevation. (Excerpts from text; no abstract.)

Emmett, M. (2016). “Approach to the Patient With a Negative Anion Gap.” American Journal of Kidney Diseases 67(1): 143-150.

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When anion gap calculation generates a very small or negative number, an explanation must be sought. Sporadic (nonreproducible) measurement errors and systematic (reproducible) laboratory errors must be considered. If an error is ruled out, 2 general possibilities exist. A true anion gap reduction can be generated by either reduced concentrations of unmeasured anions such as albumin or increased concentrations of unmeasured cations such as magnesium, calcium, or lithium. This teaching case describes a patient with aspirin (salicylate) poisoning whose anion gap was markedly reduced (−47 mEq/L). The discussion systematically reviews the possibilities and provides the explanation for this unusual laboratory result.