Effects of pentoxifylline on renal function and blood pressure in cardiac transplant recipients: a randomized trial.
BACKGROUND
The current success of cardiac transplantation is in part attributable to the development of effective immunosuppressive agents such as cyclosporine. However, concern remains regarding the potential for cyclosporine-induced nephrotoxicity. Animal studies and early reports of renal protective effects of pentoxifylline in bone marrow transplant recipients prompted a randomized trial in cardiac transplant recipients.


METHODS
Twenty-nine patients were randomized to receive pentoxifylline 400 mg p.o. t.i.d. or matching placebo for 1 year after cardiac transplantation. Renal function was assessed preoperatively and at 1, 6, and 12 months postoperatively. Glomerular filtration rate and renal plasma flow were measured with iothalamate and para-aminohippurate, respectively. Serum creatinine was also measured. Ambulatory blood pressure monitoring after withdrawal of antihypertensives for 3 days was performed 12 months postoperatively.


RESULTS
Twenty-seven patients completed the study. Glomerular filtration rate rose between 1 and 6 months after transplantation, presumably due to the reduction in goal cyclosporine level in that period, and then fell modestly between 6 and 12 months, presumably due to ongoing nephrotoxic effects of cyclosporine. No difference in glomerular filtration rate or creatinine was seen between pentoxifylline and placebo groups at any interval. Renal plasma flow increased modestly between baseline and 6 months in the pentoxifylline group, but not in the placebo group, and then fell between 6 and 12 months. Serum creatinine increased between baseline and 6 months in both groups, apparently due to increased body weight. Results of 18-hr ambulatory blood pressure monitoring obtained 1 year after transplantation was not different between groups.


CONCLUSIONS
Renal function declines only modestly in the first year after cardiac transplantation. Pentoxifylline did not attenuate this process and had no effect on blood pressure. The modest decline in renal function may be related to current immunosuppressive strategies.
Frantz
R P
RP
Division of Cardiovascular Diseases, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905, USA.
Edwards
B S
BS
Olson
L J
LJ
Schwab
M K
MK
Adams
T F
TF
Textor
S C
SC
Daly
R C
RC
McGregor
C G
CG
Rodeheffer
R J
RJ
D000328:Adult; D000368:Aged; D001794:Blood Pressure; D018660:Blood Pressure Monitoring, Ambulatory; D001835:Body Weight / Q000502:physiology; D016572:Cyclosporine / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology; D004311:Double-Blind Method; D004357:Drug Synergism; D016027:Heart Transplantation / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000139:chemically induced; D007166:Immunosuppressive Agents / Q000009:adverse effects / Q000494:pharmacology; D007668:Kidney / Q000502:physiology*; D007674:Kidney Diseases / Q000139:chemically induced; D008875:Middle Aged; D010431:Pentoxifylline / Q000494:pharmacology*; D014665:Vasodilator Agents / Q000494:pharmacology*; D015430:Weight Gain / Q000502:physiology
D007166:Immunosuppressive Agents; D014665:Vasodilator Agents; D016572:Cyclosporine; D010431:Pentoxifylline