ELSEVIER
Benefit of Angiotensin II Receptor Blockade in the Treatment Posttransplant Polycythemia in Renal Transplant Recipients W. Kupin, K.K. Venkat, M. Goggins,
M. Abouljoud,
F. Escobar, and M. Mozes
P
OSTTRANSPLANT polycythemia (PTP), defined as a persistent hematocrit (HCT) greater than 51%, develops in approximately 10% to 15% of both cadaveric and living-related renal transplant recipients.’ Although individual risk factors have been identified including cyclosporine-based immunosuppression, acute rejection, transplant renal artery stenosis, retained native kidneys, and urinary obstruction, the majority of patients have no clearly defined etiology for PTP.’ An increased incidence of thrombotic events (stroke, venous thrombosis, pulmonary embolism) may occur in up to 20% of PTP patients? Spontaneous resolution occurs in less than 25% of patients necessitating early therapeutic intervention with either repeated phlebotomies or adenosine A2 receptor inhibitors (theophylline). Recently, the beneficial effects of angiotensin-converting enzyme inhibitors (ACEI) have been reported in PTP but the potential adverse side effects of cough or angioedema may preclude their widespread use.” The recent introduction of a specific angiotensin II type I receptor blocker (Losartan) may offer an alternative to ACEI therapy but its use in PTP has not been reported.‘,”
METHODS The patient (8 cadaveric
population consisted of 10 renal transplant recipients and 2 living-related) with persistent HCT greater than
51% for three consecutive weeks in the presence of normovolemia and absence of intrinsic pulmonary disease. All patients were initially treated with ACEI therapy (enalapril or prinivil) at 5 to 10 mgid. When the HCT normalized to less than 45%. ACEI was discontinued. When the HCT increased back to greater than 51%, were performed Losartan (50 mgid) was initiated. No phlebotomies during drug therapy.
of
60
.
55 50 Ha(%)
45
._
40
Mean 35
44fi I
5-w I
L p <0.05-I
54+3 I
L p <0.05
30 1 Pre ACEI
-
Fig 1. Effect of sequential tients with PTP.
ACEI
Losartan P&-
ACEI and Losartan therapy
in pa-
in both groups. No episodes of acute renal failure were encountered. No patient developed cough requiring discontinuation of either drug and no cases of angioedema were noted.
DISCUSSION
Angiotensin II type I receptor blockade appears to be an effective alternative management option for patients with PTP. This finding substantiates the dependence of PTP on endogeneous erythropoietin production but could not discern between increased erythropoietin levels versus enhanced tissue sensitivity since levels were not measured in this study. This new class of drugs may carry a reduced risk of cough and/or angioedema compared to ACEI due to their lack of effect on bradykinin metabolism.’ Angiotensin II type I receptor blockers may be added to the list of phlebotomy, theophylline, and ACEI therapy for the management of PTP.
RESULTS
Patient demographics consisted of a baseline creatinine of 1.8 5 0.3 mg/dl, male sex (SO%), hypertension (lOO%), prior rejection (40%), and no prior thromboembolic complications. The HCT response to ACEI and Losartan therapy is shown in Figure 1. A significant decrease in HCT of approximately 22% was noted for both agents. A significant but clinically benign increase in serum potassium (4.3 meq/L
baseline;
4.6 meq/L
posttherapy,
P < .OS) occurred
0 1997 by Elsevier Science Inc. 655 Avenue of the Americas, New York, NY 10010
From the Division of Nephrology and Hypertension and Department of Transplantation Surgery, Henry Ford Hospital, Detroit, Michigan. Address reprint requests to Warren Kupin, MD, Division of Nephrology and Hypertension, Henry Ford Hospital, 2799 West Grand Blvd, Detroit, MI 48202.
0041-1345/97/$17.00 PII SO041 -1345(96)00065-6
207
Transplantation
Proceedings,
29, 207-208
(1997)
208
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