Hyperkalemia in a Dialysis Patient After Colon Diversion
Abstract and Introduction
Introduction: Potassium (K) homeostasis in healthy subjects is maintained mainly by urinary excretion of K. In patients with end-stage renal disease, the intestinal tract might assume an accessory K excretory role in the face of declining renal excretory function. Here, we report the case of a patient with end-stage renal disease who developed severe hyperkalemia following colon diversion surgery.
Case Presentation: A 56-year-old Caucasian woman undergoing hemodialysis experienced ischemic colitis, leading to ileocecal resection and a temporary ileostomy. She made a good recovery and her dietary intake improved. However, her pre-dialysis serum K level three weeks later was 7.2mmol/L, which was much higher than her previous level (range 4.9 to 6.1mmol/L). Despite dietary restriction of K and use of oral cation-exchange resin and low K dialysate, her serum K level remained high (6.1 to 8.3mmol/L). Six months later, her bowel continuity was restored and her serum K decreased to the previous level. Her fecal K concentration before and after stoma reversal showed a marked difference: 23mmol/L before and 60mmol/L after.
Conclusions: We assume that the severe hyperkalemia seen in our patient was caused by reduced colonic K secretion due to the colon diversion. Our patient's case demonstrates the importance of colonic K secretion for the maintenance of K homeostasis in patients with end-stage renal disease.
Potassium (K) is an essential dietary mineral and major intra-cellular cation. It constitutes the main intra-cellular electrolyte and osmolyte necessary for fundamental processes such as membrane excitability, ion and solute transport or cell volume regulation. Homeostatic maintenance of plasma K is therefore a critical physiological function. Total body exchangeable K, measured with the use of radioactive K, averages 46mEq/kg in men and 39mEq/kg in women. Only 1.5 to 2.5 percent of total body K (about 65mEq) is found in the extracellular fluid. Under conditions of a normal dietary K intake (80 to 100mmol per day), about 90 percent of dietary K is absorbed in the small intestine and an equivalent amount of the absorbed K is excreted mainly by the distal tubules of the kidney (about 90mmol per day). The contribution of the colon to net K absorption and secretion is trivial, and fecal K averages about 10mmol per day in healthy subjects.
During the development of end-stage renal disease (ESRD), many patients remain normokalemic for long periods, although renal excretory function deteriorates progressively. This can be explained by an increase in the K secretory capacity of remaining functional renal tubules, an adaptive response dependent on enhanced K uptake across the basolateral membrane, which is mediated by increased cortical and outer medullary Na/K-adenylpyrophosphatase (ATPase) activity. However, this response cannot entirely explain the maintenance of K homeostasis in such patients, because urinary K excretion is generally substantially lower than in healthy individuals. Metabolic studies indicated increased fecal K losses in patients with ESRD, raising the possibility that the intestinal tract might assume an accessory K excretory role in the face of declining renal excretory function.
Here, we report on an unusual case of severe hyperkalemia following ileocecal resection and a temporary ileostomy in a patient undergoing chronic hemodialysis (HD), and discuss the possible pathophysiological mechanisms to account for the clinical picture.