Renal artery stenosis following transplantation: Etiology, diagnosis, and prevention

Arterial stenosis following renal transplantation may produce serious hypertension and accelerated graft failure. To determine etiologic factors associated with the development of renal artery stenosis (RAS), records of 319 renal transplants were reviewed. Arterial stenosis (<70% diameter narrowing) occurred in 16 patients. Review of their arteriograms demonstrated that kinking and/or torsion of the renal artery was the cause of stenosis in seven instances. The kinking was caused by excessive length of the donor renal artery or restricted rotation of the recipient hypogastric artery. Postanastamotic stenoses were present in four cases and clearly were caused by trauma to the renal artery during graft harvest and flushing or preservation in two. Thus failure to excise an adequate portion of renal artery prior to implantation accounted for two thirds of our cases of RAS. A bruit was heard in all of the patients with RAS when this sign was sought. In the group of post-transplant hypertensive patients, the RAS group had (1) more severe hypertension (diastolic blood pressure, 119 ± 6 vs. 96 ± 6 mm Hg, (2) higher transplant vein renin activity (7.03 ± 1.74 vs. 1.6 ± .6 mg/ml/hr), and (3) significantly higher systemic plasma renin activity 4.74 ± 1.41 vs. 0.9 ± 0.26 mg/ml/hr. Our experience with transplant RAS suggests that this complication is largely technical and is not a consequence of, the rejection process. The diagnosis should be suspected in any patient with a bruit and severe, difficult-to-control hypertension. Peripheral plasma renin activity was elevated impressively in transplant patients with significant RAS, indicating both a pathophysiological and diagnostic role for the renin-angiotensin system in this group of patients.