Hepatitis C virus core antigen test in virological monitoring of patients on long-term dialysis

normal. Therefore, the high RI could not be explained by intrarenal abnormalities, pointing to an extrarenal cause. One such cause could be stiffness of the pre-renal arterial vessels. Our patient had suffered from coronary heart disease, insufficiency of the aortic valve and an aneurysm of the ascending aorta. Therefore, 7 years before transplantation, she had undergone to aerotocoronary bypass grafting and implantation of a prosthetic aortic valve, and a vascular graft (Hemashield Vantage) of the ascending aorta. Dacron grafts are extremely stiff compared to the healthy aorta [3]. Therefore, they cannot expand during systole, and contraction during diastole, the main determinant of diastolic aortic flow, is absent. We suggest that this phenomenon explains the missing diastolic perfusion in the patient's renal allograft. In addition, Doppler ultrasound of the abdominal aorta and the superior mesenteric artery also showed a complete absence of diastolic perfusion. In conclusion, this case demonstrates that an increased RI in a renal allograft may not always be a consequence of intrarenal pathology, but may also be caused by impairment of the function of pre-renal arterial vessels. Whether the absence of diastolic blood flow in the transplanted kidney will have a negative impact on long-term graft function is, at present, unknown. Eighteen months after transplantation, the patient's allograft function is excellent with an actual serum creatinine of 120 μmol/L.