title: Valsartan-induced hematocrit changes in renal transplant patients.
abstract: 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.
  
  
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Unidad de Nefrología, Hospital Regional de Valdivia, Valdivia, Chile. eflores@uach.cl
authors.forename: C A
authors.initials: CA
authors.lastname: Flores
authors.forename: L G
authors.initials: LG
authors.lastname: Ardiles
authors.forename: C A
authors.initials: CA
authors.lastname: Aros
authors.forename: C C
authors.initials: CC
authors.lastname: Muñoz
authors.forename: H O
authors.initials: HO
authors.lastname: Schneider
authors.forename: J A
authors.initials: JA
authors.lastname: Ramírez
authors.forename: V
authors.initials: V
authors.lastname: Jerez
authors.forename: M G
authors.initials: MG
authors.lastname: Valderrama
authors.forename: S A
authors.initials: SA
authors.lastname: Mezzano
mesh_terms: D000328:Adult; D000368:Aged; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D003404:Creatinine / Q000097:blood; D004359:Drug Therapy, Combination; D005260:Female; D006400:Hematocrit; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D016030:Kidney Transplantation / Q000276:immunology / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D011188:Potassium / Q000097:blood; D013777:Tetrazoles / Q000627:therapeutic use*; D014633:Valine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000068756:Valsartan
chemical_list: D000959:Antihypertensive Agents; D007166:Immunosuppressive Agents; D013777:Tetrazoles; D000068756:Valsartan; D003404:Creatinine; D014633:Valine; D011188:Potassium