1 Departments of Renal Medicine and 2 Radiology, Hope Hospital, Salford, UK
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Abstract |
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Methods. A cohort of 71 patients had creatinine clearance measured at the time of digital subtraction angiography; eight patients were diabetics and were excluded from further analysis. The severity of proximal renovascular lesions was estimated by standard methodology, and patients were sub-grouped according to residual patency of the proximal renal arteries (e.g. normal=2.0; unilateral occlusion )RAO(=1.0). Renal bipolar lengths at ultrasound were also assessed.
Results. Sixty-three non-diabetic patients (mean±SD age 67.7±5.8 years; 34 males) were suitable for study. No differences in renal function (mean±SD creatinine clearance (ml/min)) were seen between patients with unilateral (32.1±18.9, n=36) or bilateral (31.7±20.9, n=27) disease, or between sub-groups with RAS <60% (28.3±13.9, n=15), unilateral RAS >60% (38.9±24.6, n=12), bilateral RAS >60% (36.3±20.4, n=6) or unilateral RAO (30.3±17.7, n=28), and mean average renal size similarly did not differ between the sub-groups. No correlation existed between residual patency and creatinine clearance (r=0.015); mean±SD renal function was almost identical in the four patency sub-groups, and average renal size mirrored this pattern. Mean 24-h urinary protein excretion was similar for the four groups, but patients with minimal ARVD had significantly less comorbid vascular disease.
Conclusions. These findings suggest that the severity of proximal renal artery lesions is often unrelated to the severity of renal dysfunction in patients with ARVD. Associated renal parenchymal damage is the more probable arbiter of renal dysfunction, and this should be considered when revascularization procedures are contemplated.
Keywords: atherosclerotic renovascular disease; bipolar renal length; creatinine clearance; proximal lumen patency; renal function; renal parenchymal damage; ultrasound
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Introduction |
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The natural history of proximal arterial lesions in ARVD has previously been defined by non-invasive [3] and invasive [4] studies that have demonstrated a rapid rate of progression of high-grade renal artery stenoses (RAS) to renal arterial occlusion (RAO) with consequent loss of functioning renal mass. This has underpinned the rationale of maintaining renal arterial patency by angioplasty, with or without endovascular stent placement, in order to preserve renal function in patients with severe RAS. However, more recent studies, performed in an era when aspirin and lipid-lowering therapy are widely used in patients with ARVD, show a lower rate of RAS progression [5] and that other factors, such as hypertension, may be more important than RAO in determining progression to renal atrophy.
Further, outcomes in ARVD seem to vary; some patients with severe proximal artery lesions maintain well-preserved renal function, yet others with lesser lesions can still progress to ESRF. This has been highlighted by isotopic techniques that estimate single kidney glomerular filtration rate (SK-GFR) [6]. The effects of revascularization with renal angioplasty [7,8], stenting [9], or renovascular surgery [10,11] upon renal functional outcome are similarly unpredictable. Thus, although individual patients with ARVD have been rescued from dialysis treatment by surgery [12] or angioplasty, the majority of patients manifest no improvement in renal function, or indeed, some show progressive renal functional decline, after revascularization. There is now an increasing recognition that, in many patients with ARVD, the extent of renal parenchymal injury rather than the severity of proximal vascular lesions is the chief determinant of renal functional outcome. This study sought to investigate the relationship of renal dysfunction to the extent of proximal arterial lesions in a cohort of patients with ARVD.
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Subjects and methods |
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The renal angiographic findings were categorized as unilateral or bilateral disease, taking account of whether the renal arterial anatomy demonstrated insignificant disease (normal vessel up to <25% narrowing), mild-moderate RAS (>25 to <60% stenosis), severe RAS (>60% RAS) or occlusion (RAO) in either or both arteries. As the purpose of the study was to examine the relationship between renal arterial anatomy and renal function at the time of angiography, a simple scoring system for proximal renovascular disease severity was developed which also denoted the residual lumen patency of the proximal renal arteries (patency index).
Examples of patency index calculation:
Bilateral normal arteries=2.0
Unilateral RAO (contralateral normal) or bilateral 50% RAS=1.0
Unilateral RAO with contralateral 60% RAS, or bilateral 80% RAS=0.4
Bilateral RAO=0.
Where a kidney was supplied by more than one renal artery, the residual patency was estimated from the proportionate narrowing of the total arterial supply of that kidney (e.g. if a kidney was supplied by two arteries, one having 80% RAS and the other being normal, the patency score for that kidney would be 0.6). Renal function was assessed by creatinine clearance just prior to the angiographic procedure. Bipolar renal length of all kidneys was determined by renal ultrasound and 24-h urinary protein excretion was also measured. Other demographic data including age at presentation, sex, blood pressure, and presence of other vascular disease (angina, myocardial infarction, or cerebrovascular or peripheral vascular disease) were also recorded. The renal function of patients with RAO was also further classified with respect to accompanying contralateral disease, as this provided an important insight into pathogenetic mechanisms.
Statistical analyses
Patients were stratified into sub-groups based upon their residual patency index; their clinical and investigational characteristics were compared in the context of these sub-groups. The angiographic findings were also represented in standard groupings (unilateral/bilateral, RAS <60%, RAS >60% or RAO), and renal function as well as renal size were also analysed between these groups. Means, standard deviations (SD), and median values are displayed where appropriate. Mean renal size for each sub-group was derived from the average ultrasound bipolar renal length (i.e. (right+left)/2) for each patient. Variables were analysed by two-way analysis of variance (ANOVA). When the ANOVA indicated significant differences among patient groups, differences in categorical data were analysed with 2 tests. For continuous data, means were compared by t tests. A P value of less than 0.05 was considered a significant difference. A correlation study was used to test the relationship between renal function and residual lumen patency.
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Results |
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The relationship between standard angiographic findings, renal function and ultrasonographic renal size is depicted in Table 1. The 36 patients with unilateral disease (i.e. insignificant RAS, significant RAS or RAO affecting one kidney, the contralateral vessel being normal) had similar renal function (creatinine clearance 32.1±18.9, range 366 ml/min) to the 27 patients who had bilateral disease (clearance 31.7±20.9, range 671 ml/min). Renal function was also remarkably similar when sub-group analysis compared patients with mild-moderate or severe RAS (in both unilateral or bilateral categories), and also those patients with unilateral RAO. There were no significant differences in renal length between patients with unilateral or bilateral RAS, but kidneys with RAO were significantly smaller (e.g. in the 28 patients with unilateral RAO, the RAO kidney was 7.68±1.3 cm compared to 10.02±1.15 cm for the contralateral kidney; P<0.001). These findings suggest that, with the exception of kidneys shrunken by RAO, chronic renal parenchymal damage is the chief determinant of renal dysfunction in patients with ARVD.
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Discussion |
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It is likely that the pathogenesis of renal dysfunction in patients with ARVD is multi-factorial. This has been inferred by Caps et al. [5] who used serial duplex ultrasound to examine factors that determine progression to renal atrophy in a cohort of patients with ARVD. The cumulative risk of renal atrophy was greatest in patients with poorly controlled hypertension; although kidneys with RAS >60% had a high rate of atrophy, the vast majority had not progressed to RAO. These data suggest that hypertension and ischaemia are likely to provoke renal parenchymal damage by different mechanisms. A limitation of the study was that although renal atrophy appeared to correlate with renal dysfunction, the possible contribution of injury (e.g. hypertensive damage) in the contralateral (non-atrophied) kidney was not excluded. Indeed, isotopic studies have shown that the SK-GFR may be similar in the paired kidneys from patients with high-grade unilateral RAS and normal contralateral vessel [6]. Further, SK-GFR may not correlate with bipolar renal length as determined by ultrasound [16].
In the current study, the severity of ARVD was described by both standard renal angiographic anatomy and by residual luminal patency. Although the study was only cross-sectional and the division of patients into sub-groups of differing patency was arbitrary, there was absolutely no relationship between proximal renovascular narrowing and overall renal dysfunction. Renal impairment was equally marked in patients with mild proximal ARVD as in those with severe bilateral disease, or in those patients who had unilateral RAO. Kidneys affected by RAO were significantly smaller than those with RAS, but just as for renal function, average renal size was not predictive of the sub-grouping of ARVD severity. Renal histology was only obtained in a minority of patients, but it was representative of the spectrum of changes described as ischaemic nephropathy [17]. Perhaps the renal parenchymal damage might be more appropriately termed atherosclerotic nephropathy [18] in some patients, as intra-renal atheroma, hypertensive damage, and cholesterol emboli may develop independently of the ischaemia that would be consequent upon a high-grade stenosis. Such a hypothesis would explain the findings of this and other [5,8,9,15] studies, as well as the previously described inconsistencies in renal functional outcome seen after revascularization in ARVD. Proteinuria has recently been shown to be a non-specific marker of this parenchymal damage in patients with ARVD [19].
Our findings suggest that underlying renal parenchymal damage is a major determinant of renal dysfunction in ARVD, and, with the exception of kidneys affected by RAO, it should be considered independently of the proximal renal arterial disease in these patients. Studies that help distinguish the varying contributions of renal ischaemia, hypertensive damage, and intra-renal atherosclerosis to the pathogenesis of renal dysfunction in these patients are now required. Only such clinicopathological clarity will enable appropriate selection of patients, and indeed, those particular kidneys, most likely to benefit from revascularization, thereby facilitating the chances of optimal long-term renal functional outcome after surgery, angioplasty, or endovascular stenting in the future.
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Notes |
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References |
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