A Case of Decreased Urine Output with Loop Diuretics

Introduction: Loop diuretics are used in escalating doses to treat volume overload and to overcome diuretics resistance. We present a case of a patient who had a decreased urine output despite receiving high doses of intravenous loop diuretics. Case Description: A 65-year-old obese male presented with acute hypoxic/hypercapnic respiratory failure requiring intubation. He had non pitting edema, without other clinical or radiological evidence of pulmonary edema. His Right atrial pressure was elevated 13 mmHg, right ventricular pressure of 85/15 mmHg, and pulmonary artery pressure of 87/27 mmHg with normal ejection fraction. Due to inability to wean the patient off ventilator, he received a trial of high dose furosemide infusion for 4 days. Over the course of diuretic therapy, his blood urea nitrogen (BUN) and Serum Creatinine (Scr) increased from 13 to 38 mg/dl, and from 0.97 to 2.43 mg/dl respectively. He was given furosemide 200-300 mg/day with less than 1 L urine output and urine sodium (UNa) of 10 during diuretic therapy. Following nephrology recommendation, diuretic administration ceased, resulting in a subsequent increase in urine output to 100-150 ml/hr within 4 hours. Discussion: This case presents a fascinating unusual antidiuretic response to furosemide with the swift and complete reversal upon diuretic withdrawal is particularly noteworthy. The underlying mechanism is likely rooted in an extreme hemodynamic event within the kidney, precipitated by severe pulmonary hypertension, heightened right heart pressure, and cor pulmonale, possibly from obesity related Pickwickian syndrome. Increased right heart pressure with omental fat deposits in a recumbent position elevates systemic and renal venous pressures, exacerbated by positive pressure ventilation. In the above situation, loop diuretics exacerbates tubular fluid accumulation, increasing renal pressures, reducing net filtration pressure, resulting in a decrease in estimated glomerular filtration rate (eGFR) and urine output. Increased interstitial pressure contributes further compresses capillaries, hindering renal blood flow. Discontinuation of diuretics rapidly alleviates tubular pressure, facilitating the renal function recovery. This underscores the importance of tailored interventions in managing patients with such intricate pathophysiological profiles.