Pentoxifylline Improves Hemoglobin Levels in Patients with... : Journal of the American Society of Nephrology (original) (raw)

Clinical Nephrology

Pentoxifylline Improves Hemoglobin Levels in Patients with Erythropoietin-resistant Anemia in Renal Failure

Cooper, Angela*,†; Mikhail, Ashraf*; Lethbridge, Mark W.†; Kemeny, D. Michael†; Macdougall, Iain C.*

Departments of *Renal Medicine and †Immunology, GKT School of Medicine, King’s College Hospital, London, United Kingdom.

Correspondence to Dr. Iain Macdougall, Department of Renal Medicine, King’s College Hospital, Bessemer Road, London, SE5 9PJ, United Kingdom. Phone: 44-207-346-6234; Fax: 44-207-346-6472; E-mail: [email protected]

Accepted April 08, 2004

Received January 16, 2004

Journal of the American Society of Nephrology 15(7):p 1877-1882, July 2004. | DOI: 10.1097/01.ASN.0000131523.17045.56

Abstract

ABSTRACT. It was hypothesized that pentoxifylline might improve the response to recombinant human erythropoietin (rh-Epo) in anemic renal failure patients. Sixteen patients with ESRD and rh-Epo-resistant anemia, defined by a hemoglobin of <10.7 g/dl for 6 mo before treatment and a rh-Epo dose of ≥12,000 IU/wk, were recruited. They were treated with oral pentoxifylline 400 mg o.d. for 4 mo. Ex vivo T cell generation of tumor necrosis factor alpha (TNF-α) and interferon gamma (IFN-γ) from the patients was assessed before treatment and 6 to 8 wk after therapy. A total of 12 of 16 patients completed the study. Before therapy, the 12 patients’ mean hemoglobin concentration was 9.5 ± 0.9 g/dl. After 4 mo of pentoxifylline treatment, the mean hemoglobin concentration increased to 11.7 ± 1.0 g/dl (P = 0.0001). Baseline ex vivo T cell expression of TNF-α decreased from 58% ± 11% to 31% ± 23% (P = 0.0007) after therapy. Likewise, IFN-γ expression decreased from 31% ± 10% to 13% ± 10% (P = 0.0002). Pentoxifylline therapy may significantly improve the hemoglobin response in patients with previously rh-Epo-resistant anemia in renal failure. This may occur due to inhibition of proinflammatory cytokine production, which could interfere with the effectiveness of rh-Epo.