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Valsartan-induced hematocrit changes in renal transplant patients
C A Flores1, L G Ardiles, C A Aros
1Unidad de Nefrología, Hospital Regional de Valdivia, Valdivia, Chile. eflores@uach.cl
Insights
Valsartan significantly reduced hematocrit in stable renal transplant patients with elevated levels. This angiotensin II receptor blocker was well-tolerated, offering potential benefits for managing post-transplant erythrocytosis.
Area of Science:
- Nephrology
- Pharmacology
- Transplantation
Background:
- Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor type 1 blockers (ARBs) are common in renal transplant patients.
- These drugs may prevent chronic renal allograft dysfunction and improve transplant survival.
- ACE inhibitors and ARBs are also used to manage post-transplant erythrocytosis.
Purpose of the Study:
- To evaluate the effect of the ARB valsartan on hematocrit levels in stable renal transplant patients.
- To assess valsartan's impact on patients treated with cyclosporine, azathioprine, and prednisone.
Main Methods:
- A study involving 26 stable renal transplant patients treated with valsartan 80 mg/day orally.
- Patients were monitored for 6 months, with evaluations at baseline, 3 months, and 6 months.
Main Results:
- A significant decrease in hematocrit was observed at 3 months in patients with baseline levels over 38% (P < .0001).
- No further reduction in hematocrit was noted at 6 months.
- No significant hematocrit reduction occurred in recipients with baseline levels below 38%.
- Valsartan was well-tolerated with no significant side effects.
Conclusions:
- Valsartan may reduce and stabilize hematocrit in stable renal transplant patients.
- Potential mechanisms include inhibition of angiotensin II's proerythropoietic effects, reduced renal tubulointerstitial hypoxia, and efferent arteriole vasodilation.
Background:
Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor type 1 blockers (ARB) are frequently prescribed for renal transplant patients. The main reasons for their use are that their antihypertensive and antifibrogenic effects may prevent chronic renal allograft dysfunction, potentially improving transplant survival. Furthermore, ACE and ARB have been used to reduce the hematocrit in patients with posttransplant erythrocytosis. We evaluated the effects of the ARB valsartan on the evolution of hematocrit in stable renal transplant patients treated with cyclosporine (CsA), azathioprine (Aza), and prednisone.
Patients And Methods:
Twenty-six stable renal transplant patients treated with valsartan 80 mg/d orally were followed for 6 months. Evaluations were performed prior to as well as at 3 and 6 months following the initiation of valsartan.
Results:
The hematocrit levels decreased significantly at 3 months (46.1 +/- 7.3 vs 39.9 +/- 5.8 ; P < .0001) in patients with a normal hematocrit, namely a level over 38%, with no further reduction at 6 months. In recipients with an hematocrit less than 38%, there was no significant reduction, either at 3 or 6 months follow-up. Valsartan was well tolerated without significant side effects.
Conclusion:
We postulate that inhibition of the proerythropoietic effects of angiotensin II and/or the reduction in hypoxia within the renal tubulointerstitium as well as the vasodilator effects on the efferent arterioles, represent possible mechanisms for the reduction and stabilization of the hematocrit in stable renal transplant patients.
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