American Journal of Medicine, internal medicine, medicine, health, healthy lifestyles, cancer, heart disease, drugs

Hypokalemia in an End-Stage Renal Disease Patient

Computer tomography without contrast of abdomen showing colonic distension with air fluid levels without mechanical obstruction.

Kidneys play an essential role in K+ homeostasis, but the role of the colon in K+ homeostasis is not well recognized. Increased colonic K+ excretion plays a vital role in regulating plasma K+ level in patients with end-stage renal disease.1 We present a case of hypokalemia in a patient with end-stage renal disease with colonic pseudo-obstruction.

Case Report

A 66-year-old man with a history of end-stage renal disease on hemodialysis every Monday, Wednesday, and Friday presented with acute onset of abdominal distension and diarrhea for the past 1 week. The patient had a known history of colonic pseudo-obstruction and had colonic decompression 1 month ago. The patient had persistent hypokalemia refractory to oral potassium replacement with potassium chloride (KCl) 20 mEq 3 times a day and use of 4 mmol/L dialysates during hemodialysis. Initial vital signs were normal. On physical examination, the abdomen was distended, soft and nontender on palpation, tympanic on percussion, and hypoactive bowel sounds were present. Laboratory investigation showed serum Na+ 141 mmol/L, K+ 2.5 mmol/L, Cl– 109 mmol/L, bicarbonate 18 mmol/L, blood urea nitrogen 43 mg/dL, and creatinine 5.2 mg/dL. Stool studies showed no Clostridium difficile or other bacterial infections. Computed tomography of the abdomen showed colonic distension with air-fluid levels without mechanical obstruction (Figure). Fecal electrolytes showed Na+ <10 mmol/L, K+ 162 mmol/L, and chloride 65 mmol/L. Esophagogastroduodenoscopy showed a gastric antrum ulcer and esophagitis with biopsy negative for Helicobacter pylori; colonoscopy was normal. The rectal tube was inserted for decompression. Potassium replacement was started with KCl 40 mEq intravenously 3 times daily and K+ (4 mmol/L)-rich fluid for hemodialysis. In addition to all of these interventions, K+ was still <3 mmol/L. Profound hypokalemia complicating colonic pseudo-obstruction led to colonic perforation. Laparoscopic colectomy was performed, revealing colonic dilation with edematous appearance. Colectomy histology showed findings favoring acute colonic ischemia and chronic patchy active colitis. Following colectomy, the patient’s potassium level returned to normal without supplementation.

Discussion

The colon plays an important role in maintaining K+ in patients undergoing chronic dialysis by adapting to be an important accessory organ of K+ secretion.2 Rectal K+ secretion was found to be 3 times more in patients with end-stage renal disease compared with control with normal renal function.3 BK channels play an important role in potassium secretion in the colon. These channels are highly expressed in both the colonic surface and crypt cell in a patient with end-stage renal disease compared with those only on surface cells in patients with normal renal function evidenced by immunostaining.3 Severe K+ secretory diarrhea secondary to an active K+ secretory process has been explained in colonic pseudo-obstruction associated with profound hypokalemia.4 Increased K+ in stool illustrated increased colonic secretion in this patient, who had multiple episodes of colonic pseudo-obstruction with secretory diarrhea leading to profound hypokalemia. Because of the recurrent colonic pseudo-obstruction, our patient developed acute chronic ischemia causing perforation. Ischemia causing increased BK channel expression has been explained before with immunostaining using a specific antibody to the high conductance BK channels.4 Potassium levels returned to normal without any KCl supplementation following colectomy. This case elucidates the critical mechanism of hypokalemia in end-stage renal disease through increased potassium secretion in the colon secondary to colonic pseudo-obstruction and chronic ischemia.

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– Ashish Verma, MBBS, Muhammad Hassaan Shahid, MBBS, Laura Youngblood, MD

This article originally appeared in the September issue of The American Journal of Medicine.

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