1 Department of Medical Imaging 2 Department of Nephrology 3 Department of Diabetology Grenoble, France
Sir,
Renal artery stenosis (RAS) is a recognized factor during ischaemic nephropathy and chronic renal failure in type 2 diabetic patients and involves 13 out of ten patients with chronic renal insufficiency (CRI) [1]. Although little is known about the mechanisms of RAS, they may be related to atherosclerosis, or to specific processes linked to diabetes.
Imaging patterns and pathologic signs of artery stenosis in other vascular regions are different in type 2 diabetic compared with non-diabetic patients, suggesting differing underlying mechanisms [2]. Magnetic renal angiography (MRA) is a non-invasive means of diagnosis that allows detection of RAS in patients with CRI without using nephrotoxic iodinated contrast media. It has been validated in CRI patients by using comparisons with conventional arteriography [3].
We retrospectively studied charts and X rays of 125 patients with CRI, of whom 39 were diabetic (36 were type 2). Mean serum creatinine levels were 210 µmol/l (96570) and creatinine clearance was 35 ml/min/1.73 m2 (865). Ninety per cent of the population were treated or non-treated hypertensives. No differences were found between diabetic (creatininaemia: 185±89 µmol/l, clearance: 40±13 ml/min) and non-diabetic patients (creatininaemia: 196±114 µmol/l, clearance: 32±15 ml/min) in terms of renal function parameters measured at the time of MRI.
Patients were studied using MRA combined with iv. injection of Gadolinium (0.2 µmol/kg). We evaluated the presence or absence of stenosis, the degree of narrowing, localization within the artery, and the length of RAS, defined as either long (>5 mm) or short (<5 mm).
Thirteen RAS were found in 10 (type 2 only) out of 39 diabetic patients (26%), and 39 RAS were found in 32 out of 86 non-diabetic patients (37%, NS). Truncular RAS was significantly more frequent in diabetic (7/13) than in non-diabetic patients (9/39, p<0.05), and long stenosis occurred more frequently in diabetic (5/12) than in non-diabetic patients (3/32, p<0.01). There were no differences in terms of the presence of post-stenotic dilatation. The presence of parietal calcifications could not be evaluated using MRA. Seven thromboses were found in non diabetic patients and one in diabetic patients (NS). The prevalence of hypertension was not different between patients with or without RAS.
In conclusion, RAS MRA patterns in diabetic patients were different from those in non-diabetic patients with CRI in the present series. We found that RAS in diabetics was longer and more frequently located in the arterial trunk. If these results are confirmed in larger populations, they should allow easier endovascular angioplasties in diabetic patients. If confirmed in prospective studies, they may be of pathophysiological significance (arteriosclerosis being not the only, and in addition not the same process as in non-diabetic patients). These findings may also be of therapeutic relevance and are similar to the coronary stenosis pattern differences observed in diabetic and non-diabetic patients after angioplasty [2].
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