Systemic vascular hemodynamics and transplanted kidney survival.

INTRODUCTION

High blood pressure and arterial stiffness contribute independently to cardiovascular mortality in uremic patients. High blood pressure is an established risk factor for chronic allograft nephropathy, recently named interstitial fibrosis/tubular atrophy (IF/TA). We sought to assess whether heart afterload determinants: arterial stiffness and vascular resistance or impedance accelerate kidney graft failure upon long-term observation.

METHODS

Using a noninvasive method of blood pressure waveform analysis, (HDI/PulseWave/CR-2000), we studied 160 consecutive kidney transplant recipients, who were at least 3 months after transplantation, for systolic (SBP), diastolic, and mean blood pressure; pulse rate; systemic vascular resistance and impedance as well as large and small artery compliance. The associations of the hemodynamic parameters with relative increases in serum creatinine for every year of graft survival (ΔCreat) were assessed using multiple linear regression analysis. Relationships between systemic hemodynamics and kidney graft loss due to IF/TA were evaluated by Cox regression analysis, including serum creatinine, time after transplantation, delayed graft function, human leukocyte antigen mismatch, panel-reactive antibodies, cold ischemia time, donor age glomerular filtration rate as well as prescribed cardiovascular and immunosuppressive drugs.

RESULTS

Over 6.6±0.4 years of follow-up, excluding four noncompliant patients, 11 patients died and 32 lost their kidney grafts, including 25 due to IF/TA. ΔCreat (10.3%±22.0%/y) was independently and positively associated with the initial SBP (β=0.26; P=.001) and serum creatinine values (β=0.16; P=.04). The risk of graft loss due to IF/TA was greater among patients with an increased serum creatinine (relative risk [RR]=59.5 per nlog-unit increase; P<.001) or higher SBP (RR=51.1 per nlog-unit increase; P=.04). Besides SBP, no other hemodynamic parameter was associated with graft failure.

CONCLUSIONS

The rate of kidney graft function deterioration and risk of transplant loss due to IF/TA are not independently influenced by systemic arterial compliance, resistance, or impedance. SBP appears to be the key circulatory parameter independently affecting the progression of IF/TA, and should be a therapeutic target.