Renal resistance index-think of more than just the kidney.

Sir,

In a recent Nephroquiz, Mitsides et al. describe Doppler ultrasound of the segmental renal arteries of a renal allograft obtained from a patient with bigeminus [1]. They and others point out that extrarenal factors can affect the intrarenal resistance index (RI) [2]. To extend the list of these factors, we want to report the case of a 60-year-old woman, who had preemptively received a living donor kidney allograft from her husband.

The cause of her renal disease was vascular nephropathy. Immunosuppressive therapy consisted of tacrolimus, mycophenolate and prednisolone, and she also received several antihypertensive drugs (metoprolol, indapamide, doxazosin, felodipine). The post-operative course was uneventful, and serum creatinine at discharge was 90 µmol/L. Despite normal renal function, a Doppler ultrasound of the allograft showed a complete absence of diastolic flow in the interlobar and segmental arteries, giving an RI of 1 (Figure 1). A transplant biopsy taken 6 months later showed a mild polyoma virus nephropathy. Acute rejection was excluded, and arteries and arterioles appeared 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.

Fig. 1

Doppler signal of the distal segmental artery

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.