A Case of Unresolving Hypokalemia

Introduction: Renal Tubular acidosis are a group of disorders that occur in the tubules of nephrons. They have multiple causes and all result in acidosis and electrolyte defects. Type 1 RTA is caused by a defect of H+ secretion in distal tubules, due to multiple drugs, autoimmune or genetic disorders causing: acidosis, Urine pH>5.5 and hypokalemia. Case Description: Our case is a 35 years old female with Hx of SCD s/p splenectomy and allo SCT complicated by steroid refractory GVHD, for which she is currently on belumosudil. She also has acyclovir resistant HSV rectal lesions for which she was on cidofovir-stopped 08/13, restarted on 1/2024 then stopped again on 2/17/2024.Pt has long Hx of hypokalemia since 2014. On her last admission for sickle cell crisis, she was found to have a serum potassium of 2.1. She was placed on maximum oral and IV potassium of total around 160 Meq with amiloride which only raised potassium to 3.4. On follow up after discharge, she was found to have serum potassium of around 3. She states that her chronic hypokalemia has become more severe and persistent over the last year, since her BMT. She has been getting regular IV potassium infusions in addition to taking PO supplementation. Although Pt had always denied any emesis/diarrhea or Poor PO intake some of her labs are suggestive of malnutrition including her urine potassium which was 18.6 and 25.4 on 2 consecutive days, with urine pH of 6-7 during inpatient stay. She was discharged with following admissions for IV potassium needed to maintain serum potassium above 3. Discussion: We conclude that Pt has a mixed etiology of potassium malabsorption, cidofovir use and RTA 1, as she has low urine potassium which goes against RTA 1 but at the same time still doesn’t achieve full compensation even with IV replacement and observed oral compliance and high potassium diet. A final solution would be bilateral Nephrectomy with at least 3 times/week HD with IV potassium supplementation if needed to improve potassium control and decrease risk of sudden death. Literature previously reported hypokalemia post BMT, SCT but by themselves they are amenable to oral and may need temporary IV management. Antiretroviral induced Fanconi has been rarely noted previously. This case shows that: 1-Hypokalemia can be refractory when multifactorial and certain pathologies have additive effects. 2-Full treatment is sometimes difficult as therapy ends up being too radical for Pt.