REVERSIBLE HYPONATREMIC ENCEPHALOPATHY TRIGGERED BY DIURETIC-INDUCED DYSELECTROLYTEMIA IN STAGE IIIB CKD: A CAUTIONARY CASE REPORT

Abstract

Electrolyte imbalances are a major concern for chronic kidney disease (CKD) patients, particularly with diuretic use. Unmonitored loop and thiazide diuretics can cause severe fluid and electrolyte disturbances, leading to acute neurological and metabolic problems. Timely identification and correction of these imbalances are essential to prevent morbidity and mortality in patients with impaired kidney function.
We present a 65-year-old male with stage 3b chronic kidney disease, type 2 diabetes, hypertension, and a stroke history. After 7 days of severe diarrhea, reduced food intake, and increasing weakness, he experienced an acute change in mental status. Upon admission, he exhibited encephalopathy, rapid breathing, and dehydration. Lab results indicated severe hyponatremia (Na+127 mmol/L), hypokalemia (K+3.1 mmol/L), hypochloremia, and elevated serum creatinine (6.6 mg/dL), along with high-anion-gap metabolic acidosis. His medication review revealed unsupervised use of furosemide and hydrochlorothiazide for leg edema, contributing to his electrolyte imbalances and metabolic instability.
This case emphasizes the nephrotoxic risks associated with excessive diuretic use in individuals with impaired kidney function and demonstrates the critical need for careful monitoring of electrolytes and tailored medication strategies in the management of chronic kidney disease (CKD). It underscores the importance of collaborative efforts across disciplines to avert drug-induced metabolic disturbances and to maintain both renal and neurological stability. This case underscores the nephrotoxic risks of excessive diuretic use in patients with impaired kidney function, highlighting the need for careful electrolyte monitoring and tailored medication strategies in CKD management.