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Abstract: TH-PO377

Severe, Symptomatic, and Resistant Hypokalemia in Peritoneal Dialysis

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical


  • Agraharkar, Mahendra L., The University of Texas Medical Branch at Galveston School of Medicine, Galveston, Texas, United States
  • Vanteru, Abinay Siva kumar Reddy, Max Healthcare Institute Limited, New Delhi, Delhi, India
  • Nemalidinne, Krishna Vani, Max Hospital Gurgaon, Gurgaon, Haryana, India

Hypokalemia is common in peritoneal dialysis (PD) patients and it affects a third of all PD patients. According to the Peritoneal Dialysis Outcomes and Practice Patterns Study (PDOPPS), the prevalence of hypokalemia in PD patients ranges from 3% to 47%. The reason can be poor intake, increased losses from sweat, urine, stool or dialysis and intracellular shift. Hypokalemia is associated with an increased risk of arrythmia and cardiovascular mortality.

Case Description

A 53-year-old female ESRD patient with a history of diabetes, hypertension and dyslipidemia on peritoneal dialysis presented with bilateral leg weakness. She had hypokalemia that was resistent to potassium chloride, ACE inhibitors and spironolactone. Magnessium level was low and was replaced. Her medication list included potassium chloride 80 mg BID, lantus insulin, lisinopril and spironolactone. Her aldosterone level was 5 ng/dl (4 - 31). Dialysate effluent potassium was only 1.7 mmol/L. The patient was discharged home hypokalemic but symptom free. A month later, she was readmitted with persistent bilateral leg weakness and pain. She had severe hypokalemia despite high dose oral potassium, ACE inhibitors and spironolactone. She was switched to hemodialysis and insulin dose decreased. Her potassium levels normalized on a standard bath of 2K (2 mEq/L). She is off potassium and spironolactone. Her symptoms improved dramatically.


Hypokalemia is very common in peritoneal dialysis patients and can leed to fatal cardiac arrhythmia. In most cases it is amenable to treatment with potassium supplements or addition of ACE inhibitors or spironolactone. In our patient, we failed to treat her hypokalemia while on PD.
The normal distribution of potassium between cells and the extracellular fluid is maintained by the Na-K-ATPase pump in the cell membrane. In our case, we believe that it was disrupted due to presence of insulin resulting in hypokalemia from increased potassium entry into cells. We are not aware of any other means to maintain normokalemia and have not encountered any case that needed a change in modality due to hypokalemia.

Persistent Hypokalemia in Peritoneal Dialysis