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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2013  |  Volume : 24  |  Issue : 5  |  Page : 1062-1067
Characteristics of atheromatous renovascular disease in Dubai: A single-center experience

1 NMC Specialty Hospital, Dubai, United Arab Emirates
2 Al-Nahrain College of Medicine, Baghdad, Iraq

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Date of Web Publication12-Sep-2013


To determine the characteristics of atherosclerotic renal artery stenosis (ARAS) in a cohort of patients who attended the Nephrology Department of NMC Specialty Hospital in Dubai from 2006 through 2010, including their clinical and investigational features and their response to various remedial modalities, we studied 20 patients with a diagnosis of ARAS based on magnetic resonance angiography. Three (15%) patients developed acute renal failure (ARF) after the initiation of angiotensin converting enzyme inhibitors or angiotensin II receptor blockers and 13 (65%) patients presented with chronic kidney disease (CKD) of either ischemic nephropathy or nephroangiosclerosis etiology. Four (20%) patients presented with resistant arterial hypertension (RAH). Plasma renin activity was elevated in all the patients. Fifteen (75%) patients were diabetics. We conclude that CKD was the main presentation of ARAS followed by RAH and ARF in our study. Diabetes Mellitus was the main risk factor for ARAS found in our study.

How to cite this article:
Jebur WL, Abdulla K, Tomaraei S. Characteristics of atheromatous renovascular disease in Dubai: A single-center experience. Saudi J Kidney Dis Transpl 2013;24:1062-7

How to cite this URL:
Jebur WL, Abdulla K, Tomaraei S. Characteristics of atheromatous renovascular disease in Dubai: A single-center experience. Saudi J Kidney Dis Transpl [serial online] 2013 [cited 2020 Jul 7];24:1062-7. Available from: http://www.sjkdt.org/text.asp?2013/24/5/1062/118102

   Introduction Top

Two diagnoses are closely related in patients with atherosclerotic renal artery stenosis (ARAS): Ischemic nephropathy (IN) and nephroangiosclerosis (NAS). They probably involve two different mechanisms. While IN is ischemialed glomerulosclerosis, NAS is hypertensionled glomerulosclerosis. The histopathological features are similar in both, including glomerulosclerosis and interstitial fibrosis; secondary to ischemia in IN and to hypertension in NAS.

IN secondary to longstanding ARAS is a frequently reported culprit for idiopathic renal failure in the elderly and for resistant hypertension in general. While ARAS-associated IN is secondary to bilateral RAS, or to stenosis in a solitary functioning kidney, ARAS is associated with NAS in the case of unilateral renal artery stenosis (URAS) and often normal-sized contralateral kidney.

Renal artery angiography is the gold standard for the diagnosis of renal artery stenosis (RAS), although non-invasive magnetic resonance angiography (MRA) is more feasible and widely used in daily practice. The renal artery should be at least 70% stenosed in order to be categorized as a hemodynamically significant RAS.

The aim of our study was to characterize the clinical and the investigational features of ARAS patients in our area (Dubai, United Arab Emirates), with a special insight into the interplaying mechanisms and the response to treatment.

   Patients and Methods Top

We enrolled 25 patients into the study (15 males and five females). Their age ranged between 50 and 70 years. The study was conducted in the period 2006 through 2010 in the NMC Specialty Hospital in Dubai. All patients were followed-up with regular monitoring of blood pressure, serum creatinine, electrolytes and glomerular filtration rate (eGFR) estimated by the Modified Diet in Renal Disease (MDRD) equation along with regular reviewing of the medical records for any cardiovascular complications throughout the study period. Chronic kidney disease (CKD) was diagnosed and classified according to the Kidney Disease Outcome Quality Initiative (KDOQI) guidelines.

ARAS was associated with three clinical scenarios:

  1. Acute renal failure (ARF) after the initiation of angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor blocking (ARB) drugs.
  2. CKD in elderly patients with small or borderline kidney size (8-8.5 cm in long axis) in whom no other cause could be detected.
  3. Resistant hypertension with or without normal renal function.
The diagnosis of ARAS was established in all patients by MRA with Gadolenium contrast (done either in our hospital or in other centers), which revealed the presence of more than 70% reduction in the main renal artery lumen diameter in three categories: (a) bilateral ARAS, (b)ARAS in a solitary functioning kidney and (c) URAS with a small-sized kidney and a normal-sized contralateral kidney, with or without a discrepancy of more than 1.5 cm in the long axis between the two.

The pathology in the first two categories was considered to be IN due to the significant reduction of the arterial lumen. In the third cate gory, it was considered to be NAS at least in the contralateral kidney as it has a normal blood supply and is subjected to high arterial pressure. Blood pressure of 140/90 mmHg or more was considered hypertension. Resistant arterial hypertension (RAH) was diagnosed when hypertension was not controlled despite the use of more than three antihypertensive drugs, including a diuretic. Plasma renin activity (PRA) was measured in all patients after abandoning the use of ARB or ACEI and β-blockers for two weeks. Peripheral venous sampling was used with the patient in a recumbent position.

Renal angiography and percutaneous transluminal angioplasty (PTRA) was done for four patients in other centers. Full screening for connective tissue diseases and vasculitis was performed for four patients with nephrotic range protienuria, and the results were negative.

Kidney biopsy was considered unjustifiable due to the risk involved, kidney size discrepancy and the high probability of diabetic nephropathy being the cause of the heavy proteinuria. Kidney biopsy was done for one patient.

   Statistical Analysis Top

Correlation between the degree of narrowing of the renal artery as shown in the MRA and the degree of impairment of kidney function as shown by the eGFR was estimated in patients presenting with CKD using PPSP statistical software. Patients presenting with ARF were not included in the analysis because it was thought that the main factor responsible for ischemia in these patients was hemodynamic rather than organic narrowing of the artery.

   Results Top

The degree of narrowing of the renal artery as shown by the MRA ranged from 70% to 75% [Table 1]. Thirteen patients were diagnosed as CKD (serum creatinine ranged between 1.5 and 3 mg/dL and eGFR between 20 and 50 mL/ min), six as NAS and seven as IN. The rise of serum creatinine after the initiation of ACEI or ARB was trivial (0.5-1 mg/dL) in these patients.
Table 1: Patients' clinical, radiological and laboratory characteristics.

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ARF was diagnosed in three patients, with a serum creatinine rise to twice to thrice the baseline (1-3 mg/dL) value after initiation of ACEI or ARB, returning to baseline after discontinuation of the medications. They then maintained normal renal function throughout the follow-up period of two to three years. All the patients were hypertensive and RAH was diagnosed in four patients with CKD.

There was no significant correlation between the degree of narrowing of the renal artery and the degree of impairment of kidney function in the patients who presented as CKD (Pearson correlation coefficient 0.16, P-value = 0.58).

Fifteen patients were diabetic. Evidence of diabetic microangiopathy (retinopathy and peripheral neuropathy) and macrovascular complications was present in five and 10 patients, respectively [Table 2].
Table 2: Clinical and ultrasonographic features in patients with different diagnostic categories.

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Variable range and generally mild proteinuria was identified in all patients except for four who had idiopathic nephrotic range proteinuria [Table 2].

Abdominal arterial bruit was detected in eight patients. Diffuse clinical atherosclerotic vascular disease in terms of cerebral, coronary and peripheral arterial disease were identified in 14 patients. And, finally, resting PRA was remarkably elevated in all patients (30-44 ng/L).

While renal function did not improve in three out of four patients who underwent percutaneous transmural renal angioplasty (PTRA), the fourth patient's renal function improved promptly after the procedure (creatinine dropped to 1.3 mg from 3.2 mg prior to the procedure) and he maintained the improvement throughout the follow-up period of one year.

The only kidney biopsy performed on our patients showed focal segmental glomerulosclerosis.

   Discussion Top

Our results showed that the most common presentation was CKD, followed by RAH and ARF, contrary to the findings of some other studies, [1] which showed that RAH was the main presentation of ARAS. This difference might be attributed to the higher incidence of diabetes mellitus in our patients. In the CKD group in our patients, the chronic organic nature of ARAS-related parenchymal kidney disease was highlighted by the trivial deterioration of renal function after the initiation of ACEI or ARB, which is in line with the failure of PTRA to improve renal function in three out of four patients who underwent the procedure in this group. This is consistent with long-term ischemia and/or hypertension-related glomerulosclerosis and interstitial fibrosis shown in one of the patients biopsied for nephrotic syndrome. It is the most common histological pattern in relation to ARAS, and is consistent with the conclusions of other studies. [2]

The absence of a significant correlation between the degree of narrowing of the renal artery as shown in the MRA and the degree of impairment of renal function as shown by the eGFR is the result of the variable development of renal arterial collaterals in different patients and the variable degree of intrarenal activation of RAAS, and this is consistent with the conclusion of other studies. [3] Furthermore, this indicates the insensitivity of kidney size as an indicator of reversibility of ARAS-related nephropathy in those with mildly reduced kidney size, contrary to what is recommended by other larger studies that PTRA is advisable for patients with a kidney size of more than 8 cm in the long axis. [4] On the other hand, it explicitly highlights the importance of acuteness, reversibility and rate of deterioration of renal function as the potential predictive factors in determining the outcome, which is in agreement with other studies. [5]

Being the most common presentation, CKD indicates the long-term and progressive effect of ischemia imposed by the stenotic lesions as well as the effect of other factors adversely impacting renal function in long-standing ARAS, such as hypertension, hyperreninisim (both were elevated in all patients in this study) and, importantly, the showering of cholesterol emboli by the atheromatous stenotic lesions. [6] This would bolster the significance of ARAS-related nephropathy as a missed and probably preventable cause of CKD.

The fact that PRA is a non-specific feature, having had a universal and comparable elevation in all our patients, would highlight its significance as a predictor of ARAS-related nephropathy and an enhancing factor for glomerulosclerosis and interstitial fibrosis. However, it is neither a distinctive measurement of the reversibility of the ARAS-related nephropathy nor a discriminative sign of parenchymal versus vascular nephropathy. This is in agreement with the results from the Masayuki et al study. [7]

In most of our patients, ARAS was part of a diffuse atherosclerotic cardiovascular disease, clinically manifested as ischemic heart disease, cerebrovascular and peripheral vascular disease, which is in common with other studies. [8] We have considered the diagnosis of NAS in six out of 13 patients presenting with CKD and URAS, adopting the criteria cited by other investigators. [9] In patients with CKD, there were no distinctive clinical features between IN and NAS patients [Table 2], in consistence with the Jornet et al [9] study.

Our patients were mostly diabetic, with macrovascular and microvascular disease, in contrast with other studies showing a lower incidence of diabetes-related ARAS. [8],[9] This may be explained by the higher incidence of diabetes mellitus in this country, with its cosmopolitan population of Arabic, Persian, Indian and Asian descents, implying an apparently important genetic background for the predisposition to ARAS in diabetic patients, a finding that is still debatable and is discussed in other studies. [10],[11]

The higher ARAS-related nephropathy in diabetic patients might be thought of as a possible etiologic factor for CKD in diabetics presenting solely with an impaired renal function and minimal protienuria. IN-related proteinuria is usually mild (less than 1 g/day), as it was in the majority of our patients and in other studies. [9],[12]

The high proportion of diabetic patients would also explain the higher incidence in our study of nephrotic range proteinuria for which investigations failed to find another primary or secondary renal disease. In these patients, both diabetic nephropathy and atheromatous renal disease contributed to the impairment of kidney function.

Because of the apparent chronicity of the renal disease in most of our patients, and the significant morbidity associated with the procedure, PTRA was performed in only four out of 20 patients. Only one of four patients had improved renal function after the procedure, in consistence with the ASTRAL study outcome [13] and many other studies. However, we feel that our results might be attributed to selection criteria, given the fact that all four patients were diagnosed initially with CKD secondary to IN, and all of them were diabetics. We are inclined to the conclusion drawn by other investigators considering diabetic nephropathy-related IN as a bad prognostic factor for recovery after PTRA. [14]

Regular follow-up of the three patients who had ARF revealed no deterioration of kidney function after 2-4 years with medical therapy excluding ACEI and ARB. Conversely, the prognosis in the patients with RAH secondary to ARAS was invariably worse. While all the patients with RAH were treated medically with multiple antihypertensives, including ACEI or ARB, universal deterioration of kidney function was the rule, as shown elsewhere. [15]

Hyponatremic hypertensive syndrome and flash pulmonary edema, noticeable findings in other studies, [16] were conspicuously absent in this study. Despite the fact that Gadolinium-enhanced magnetic resonance imaging studies have been noted to be associated with systemic nephrosclerosis in some patients with advanced renal failure, there has been no similar complication in any of our patients throughout the study period.

Conflict of Interest: None to declare

   References Top

1.Rognanate RA, Obell JW, Gordon P. Renal artery stenosis: Clinical and therapeutic implications. Med Health Rhode I 2008;91:315-9.  Back to cited text no. 1
2.Kendrick J, Chonchol M. Renal Artery Stenosis and chronic Ischemic Nephropathy: Epidemiology and Diagnosis. Adv Chronic Kidney Dis 2008;15:355-62.  Back to cited text no. 2
3.Suresh M, Laboi P, Mamtora H, Kalra PA. Relationship of renal dysfunction to proximal arterial disease severity in atherosclerotic renovascular disease. Nephrol Dial Transplant 2000;35:573-87.  Back to cited text no. 3
4.Chrysochou C, Karla PA. Current management of atherosclerotic renovascular disease - What have we learned from ASTRAL? Nephron Clin Pract 2010;115:c73-81.  Back to cited text no. 4
5.Textor SC. Stable patients with atherosclerosis renal artery stenosis should be treated first with medical management. J Kidney Dis 2003;42: 573-87.  Back to cited text no. 5
6.Textor SC, Lerman L. Renovascular hypertension and Ischemic Nephropathy. Am J Hypertens 2010;23:1159-69.  Back to cited text no. 6
7.Tanemoto M, Suzuki T, Abe M, Abe T, Ito S. Hemodynamic Index of Atheromatous renal artery stenosis for Angioplasty. Clin J Am Soc Nephrol 2009;4:651-5.  Back to cited text no. 7
8.Balk E, Raman G, Chung M, et al. Effectiveness of management strategies for renal artery stenosis: A systemic review. Ann Intern Med 2006;14:901-12.  Back to cited text no. 8
9.Rodríguez Jornet A, Ibeas J, Ribera L, et al. Ischemic nephropathy: Revascularization or conservative medical therapy. Nefrologia 2005;25:258-68.  Back to cited text no. 9
10.Jazrawi A, Darda S, Burke P, et al. Is Race a risk factor for the development of renal artery stenosis? Cardiol Res Pract 2009;2009:817987.  Back to cited text no. 10
11.Meyrier A, Hill GS, Simon P. Ischemic renal disease: New insights into old entities. Kidney Int 1998;54:2-13.  Back to cited text no. 11
12.Makanjuola AD, Scoble JE. Ischemic nephropathy is the diagnosis excluded by heavy proteinuria. Nephrol Dial Transplant 1999;14: 2795-7.  Back to cited text no. 12
13.ASTRAL investigators, Wheatley K, Ives N, Gray R, et al. Revascularization versus medical therapy for renal-artery stenosis. N Engl J Med 2009;361:1953-62.  Back to cited text no. 13
14.Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): Executive summary. J Am Coll Cardiol 2006;47:573-87.  Back to cited text no. 14
15.Krijnen P, Van Jaarsveld BC, Deinum J, Steyeberg EW, Habbema JD. Which patients with hypertension and atherosclerotic renal artery stenosis benefit from immediate intervention? J Hum Hypertens 2004;18:91-6.  Back to cited text no. 15
16.Tomson C, Anderson K. Hypertension in Chronic Kidney Diseases; In: Barrat J, Harris K, Topham P, editors. Oxfortd Desk Reference Nephrology, Chapter 1.4., 2009. p. 18-22.  Back to cited text no. 16

Correspondence Address:
Wael Lateef Jebur
NMC Specialty Hospital, P. O. Box 7832, Dubai
United Arab Emirates
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DOI: 10.4103/1319-2442.118102

PMID: 24029285

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