HEPARIN-INDUCED RENAL TUBULAR ACIDOSIS MASQUERADING AS HYPERKALEMIA IN A PATIENT WITH SARS-COV-2

Abstract

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Renal tubular acidosis (RTA) is defined as inadequate excretion of acids via the kidneys to maintain the acid-base balance. In RTA type 4, there is either deficiency or resistance to aldosterone leading to impaired regulation of electrolytes and hydrogen ions. This leads to hyponatremia, hyperkalemia, and acidemia. We present an unsuspecting etiology to RTA type 4 in a critically ill. SARS-CoV-2 patient as noted by heparin use for VTE prophylaxis. [1,2] CASE PRESENTATION: A 72-year-old male with history of chronic kidney disease, leukemia in remission presents with 6-day history of flu-like symptoms including intermittent diarrhea, fevers, decreased appetite, shortness of breath and generalized malaise with exposure to several known sick contacts with SARS-CoV-2. The patient was admitted to the ICU for acute hypoxic respiratory failure and started on Decadron, Remdesivir, Azithromycin, Ceftriaxone, Lovenox, Zinc, and vitamin C and subsequently intubated on day 10. Creatinine up trended and peaked at 3.51 mg/dL on hospital day 14. He developed hyperkalemia initially presumed to be secondary to acute kidney injury. His platelet counts declined by >50%, >10 days after hospitalization. Due to concern for HIT, argatroban was started but stopped due to bleeding. As fondaparinux is contraindicated in renal failure, he was restarted on heparin when HIT ab (-) result was obtained. Serum potassium peaked at 6.7 mmol/L on day 21. He was treated with calcium gluconate, insulin D50, Patiromer 8.4 g with no significant improvement in potassium levels. Due to concerns that use of heparin may be causing hyperkalemia by suppressing aldosterone, heparin was discontinued. Subsequently, serum potassium levels improved to normal range. DISCUSSION: In RTA type 4, either low levels of aldosterone or from kidneys not responding to aldosterone, impaired sodium reabsorption and potassium secretion occurs.[2]. Persistent hyperkalemia in whom there is no apparent cause such as potassium supplements or a potassium-sparing diuretic or renal failure, hypoaldosteronism must be considered [3-5].In COVID-19, there exists a higher propensity for thromboembolic disease and often prevention with heparin can serve as the best treatment. Heparin has a direct toxic impact on the adrenal zona glomerulosa cells, which may be facilitated by a drop in the number and affinity of adrenal angiotensin II receptors [4,6]. This reduction in aldosterone can lead to severe hyperkalemia [6]. CONCLUSIONS: This case is unique because hyperkalemia was noted to be refractory to the typical standard treatment given the etiology was hypoaldosteronism likely secondary to heparin use. Most patients with RTA if treated adequately in the early stages do not develop permanent kidney failure, have better mortality and morbidity outcomes and necessitate a broad etiologic differential. REFERENCE #1: Rodriguez Soriano J. Renal tubular acidosis: the clinical entity. J Am Soc Nephrol 2002;13:2160. REFERENCE #2: Renal Tubular Acidosis. www.kidney.niddk.nih.gov.U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. National Institutes of Health, NIH Publication No. 09–4696, October 2008. REFERENCE #3: DeFronzo RA. Hyperkalemia and hyporeninemic hypoaldosteronism. Kidney Int 1980;17:118. DISCLOSURES: No relevant relationships by Vidya Baleguli, source=Web Response No relevant relationships by Martin Herrera, source=Web Response No relevant relationships by Riaz Mahmood, source=Web Response No relevant relationships by Erine Raybon-Rojas, source=Web Response