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Acute hemodialysis in a young man with severe symptomatic hyponatremia and kidney injury
Author(s) -
Courteau Catherine,
Al Khoury Alex,
Michel Rene P.,
Weber Catherine L.
Publication year - 2018
Publication title -
hemodialysis international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.658
H-Index - 47
eISSN - 1542-4758
pISSN - 1492-7535
DOI - 10.1111/hdi.12636
Subject(s) - medicine , hyponatremia , hemodialysis , acute kidney injury , low sodium , urology , renal replacement therapy , surgery , gastroenterology , sodium , chemistry , organic chemistry
A 35‐year‐old man presented with severe hypo‐osmolar hyponatremia (serum sodium 99 mmol/L), profound nonoliguric renal failure (serum creatinine 1240 μmol/L), and nephrotic range proteinuria. Computed tomography of the abdomen revealed nephromegaly and no obstruction. The patient was admitted to the intensive care unit (ICU) and conventional hemodialysis was initiated. To avoid rapid sodium correction, we prescribed concurrent dialysate flow, a low dialysate sodium concentration, a small surface area dialyzer, and a low blood flow rate. We infused dextrose 5% water into the venous return line and adjusted the infusion rate according to hourly sodium concentration. The rate of sodium correction was 7.7 mmol/day over the first 3 days of admission. A subsequent renal biopsy revealed focal segmental glomerulosclerosis and interstitial infiltration with extranodal NK/T‐cell lymphoma nasal type. The patient died of massive lower gastrointestinal bleeding secondary to lymphomatous involvement day 19 in the ICU. In the setting of acute kidney injury requiring renal replacement therapy and concomitant severe hyponatremia, it is challenging to avoid overcorrection of serum sodium. We describe several key prescription modifications to conventional hemodialysis, factors that affect sodium diffusion at the level of the dialyzer membrane, and the importance of frequent laboratory monitoring.