Abstract: FR-PO156
Spurious Hyperphosphatemia in Patients with ESRD on Hemodialysis
Session Information
- Bone and Mineral Metabolism: Phosphorus, FGF23, Vascular Calcification
November 08, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Dialysis
- 704 Dialysis: Vascular Access
Authors
- Tamvada, Dheera, Saint Vincent Hospital, Worcester, Massachusetts, United States
- Black, Robert Mark, Saint Vincent Hospital, Worcester, Massachusetts, United States
Background
Hyperphosphatemia is common in patients with CKD. In most instances, the high phosphorus is due to a combination of increased intake and reduced urinary excretion. Despite the frequency of this finding, some patients with high phosphorus levels have normal kidney function. This can be associated with hypoparathyroidism, a monoclonal gammopathy or extracellular shifts as can be seen with lactic acidosis or rhabdomyolysis. Here we present three patients on hemodialysis with sudden, transient very high phosphorus levels.
Methods
Three patients with ESRD on hemodialysis were noted to have high phosphorus levels of 29.6 mg/dL, 31.5 mg/dL and 25.0 mg/dL during routine monthly laboratory evaluation. All were compliant with phosphate binders and a low phosphate diet. Blood samples were drawn from the hemodialysis catheter ports which had been locked with tissue plasminogen activator (tPA). In these patients, tPA was used to limit blood clot formation and poor blood flow through the hemodialysis catheters. tPA contains phosphoric acid to balance the pH.
Results
Below are the phosphorus levels in patients before tPA (first column) and with tPA (second column) administration. In these three patients, 5 ml of blood or less was discarded from the dialysis catheters at the time the highest phosphorus levels were resulted (second column). The third column shows improvement in phosphorus levels after we removed at least 10 ml of blood from the dialysis catheters containing tPA before sending for laboratory evaluation for phosphorus levels.
Conclusion
The severe hyperphosphatemia in our three patients appears to be secondary to the blood draw technique employed. If tPA contaminates the blood sample, high phosphorus levels are likely to result. Hence we recommend always discarding the first 10 ml of blood drawn from the hemodialysis catheter with tPA dwelling before sending the required sample for analysis. While these findings are unusual, even small quantities of tPA could lead to inappropriate conclusions of patients’ non-compliance with oral phosphate binders. When possible, phosphorus levels should not be drawn if tPA has been administered and is still dwelling in the dialysis catheter.