Lvad-a cause of cola-colored urine.
Agarwal S, Farooq M, Vini S, Reddy, S. Lvad-a cause of cola-colored urine. Am J Kidney Dis 2017; 69(4):A18-A18.
Am J Kidney Dis
LVAD thrombosis is rarely reported causeof heme-induced kidney injury. Two such cases have been reported so far in the literature.
A 53 year old African American woman presented with complaints of generalized abdominal pain, diarrhea and cola colored urine. She had a history of non-ischemic cardiomyopathy, ejection fraction of 25% and underwent placement of an LVAD two years prior with a complicated LVAD line infection post-operatively needing long-term parenteral antibiotic therapy. Additionally, she remained on warfarin for protein C deficiency. On clinical examination, she was hemodynamically stable, LVAD hum, generalized abdominal tenderness and no pedal edema were appreciated. Her initial diagnostics revealed a serum creatine of 2.7 mg/dL, hemoglobin of 8.7 g/dl and an INR of 3.19. A diptstick analysis of a grossly bloody urine sample showed glycosuria, 9-10 RBCs/hpf 20-25 WBCs/hpf, and 100mg/dl protein. A sediment analysis was suggestive of severe tubular injury with the presence of 9-10 muddy granular casts/lpf. Imaging with computed tomography was unremarkable for abnormal findings in the abdomen and pelvis. Creatine phosphokinase was minimally elevated 171U/L. A reticulocyte count of 3.2%, haptoglobin of <30mg/dl, lactate dehydrogenase (LDH) of 2100 U/L was suggestive of hemolytic anemia. However, a peripheral blood smear with 1-2 schistocytes was inconcusive for a microangiopathic process. Transthoracic echcardiogram and LVAD interrogation failed to identify any definitive malfunction. Right heart catheterization findings were suggestive of LVAD pump thrombus which was treated with intravenous thrombolytic therapy. There was rapid improvement in the urine discoloration with no urgent requirements for initiation of renal replacement therapy. Definitive management with LVAD exchange was deferred given her overall comorbidities.
Heme pigment may cause direct proximal tubular cell injury secondary to free radical release or by vasoconstriction leading to reduced blood flow in the outer medulla. With the increasing incidence of LVAD implants as definitive therapy for advanced heart failure, hemoglobin induced injury should remain high in the differential for AKI in these patients. Definitive treatment is LVAD replacement if therapy fails. In such cases, expected renal survival with recovery and progression to end stage renal disease is unknown and needs to be further investigated.