Abstract: FR-PO575
Hemodialysis Access Failure Caused by Hyperviscosity due to Secondary Polycythemia in Polycystic Kidney Disease
Session Information
- Dialysis and Vascular Trainee Case Reports
November 08, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 704 Dialysis: Vascular Access
Authors
- Jamal, Yusra, Northwell Health, Forest Hills, New York, United States
- Lopez-Padilla, Christian J., Northwell Health, Forest Hills, New York, United States
- Schrier, Peter B., Park Avenue Nephrology, Fresh Meadows, New York, United States
Introduction
Hemodialysis (HD) access failure is one the gravest complications that can lead to morbidity and mortality in End Stage Renal Disease (ESRD) patients. We present a rare case of an Autosomal Dominant Polycystic Kidney disease (ADPKD) patient with ESRD on HD who developed overt secondary polycythemia that led to hyperviscosity, recurrent hemodialysis access clotting and hemodialysis failure.
Case Description
A 44-year-old male with ADPKD on HD presented with dyspnea following several missed HD sessions. He was found to have respiratory failure secondary to pulmonary edema and required intubation. His laboratory studies revealed potassium of 6.9 mmol/L (non-hemolyzed), hemoglobin level of 18.1mg /dl and hematocrit of 58%. EKG showed widened QRS complex with peaked T waves. Emergent HD was planned but multiple attempts at hemodialysis were unsuccessful due to clotted arteriovenous fistula followed by recurrent clotting of three temporary dialysis catheters. Repeated phlebotomy was attempted with no significant drop in hemoglobin. He received multiple doses of intravenous calcium gluconate, insulin and kayexalate. Eventually, the patient developed refractory hyperkalemia of 8.7 mmol/L leading to arrythmia and cardiac arrest. Further laboratory evaluation revealed erythropoietin level (EPO) was 139.0 mlU/ml (normal range 2.6-34 mIU/ml). JAK 2 mutation was negative. There was no history of obstructive sleep apnea, smoking or use of performance enhancing agents. Autopsy confirmed ADPKD and did not reveal any evidence of malignancy. There was no evidence of abnormal cardiopulmonary physiology or chronic lung disease.
Discussion
Patients with ADPKD tend to have excess EPO production by renal cysts. Secondary polycythemia can occur in these patients as a result. In this case, patient’s hyperviscosity from secondary polycythemia caused clotting of hemodialysis access sites despite treatment with repeat phlebotomy. Hemodialysis was therefore unsuccessful. In literature, there are few cases of hemodialysis access failure caused by secondary polycythemia due to ADPKD which led to such serious intractable hyperviscosity leading to the ultimate death of the patient. This case illustrates that early recognition of this complication in patients with ADPKD is essential for appropriate management and avoid subsequent complications in this population.