ORIGINAL ARTICLE

Prevalence and severity of atherosclerosis in renal arteryin Northwest Indian population: an autopsy study

Anjali Aggarwal Æ Kanchan Kapoor ÆBalbir Singh

Received: 21 July 2008 / Accepted: 3 December 2008 / Published online: 19 December 2008

� Springer-Verlag 2008

Abstract

Background Atherosclerosis has been described as the

most common cause of renal artery stenosis. The purpose

of this autopsy study was to assess the preponderance and

severity of atherosclerotic changes in renal artery in dif-

ferent age groups in normal population.

Methods Ninety renal arteries from 45 cadavers above

30 years of age were obtained at autopsy. Fifty-four renal

arteries were studied grossly after Sudan IV staining for

extent and severity of fatty deposits in terms of Athero-

sclerotic index (AI). Another 36 renal arteries were studied

microscopically for changes in different layers and at dif-

ferent sites of artery and luminal narrowing, if any with

advancing age.

Results In grossly stained specimens, incidence and AI

which is the marker of extent and severity of lesions were

found to increase gradually with advancement of age.

Increased incidence of atherosclerotic changes with better

nutritional status was recorded. In microscopically studied

specimens, intimal thickness which is a marker of disease

also showed upward rise with advancing age. Renal artery

stenosis was prevalent in 13.8% cases. Lesions were most

commonly detected at renal ostium and proximal segment.

Conclusions Fatty changes appear with advancing age.

Advanced types of changes including fibrous plaques,

calcification and ulceration were noticed first in fifth dec-

ade. The changes were usually bilateral. Proximal segment

was the most affected part. Four cases had less than 50%

and one case had 70% luminal narrowing. The changes

were only moderately severe in most of the cases.

Keywords Renal artery stenosis � Renovascular disease �Renal ostium � Atherosclerotic index

Introduction

Atherosclerosis has been described as the most common

cause of renal artery stenosis [15]. Over the past two dec-

ades, renal artery stenosis has become the predominant

indication for renovascular surgery, responsible for 60–97%

cases of renovascular disease [17]. Its prevalence is con-

tinually increasing and it represents a potentially reversible

cause of hypertension and renal failure [5]. Majority of

patients with renal artery stenosis are those with clinically

silent process [2]. Most lesions that decrease renal blood

flow originate within the renal artery. However, a large

aortic atherosclerotic plaque can overhang the renal ostium

producing functional renal artery stenosis. Stenosis within

renal artery responds very well to angioplasty. Conversely,

when aortic plaques are responsible for obstruction at renal

ostium, there is a poor response to balloon dilatation [7].

This disparity of response reflects the anatomic differences

in the orientation of elastic and collagen fibers of muscular

and adventitial layers of renal artery and aorta.

Until recently, the distinction between these two ana-

tomic configurations was not considered to be of critical

importance since surgical bypass efficiently restored renal

A. Aggarwal

Department of Anatomy, M.M. Institute of Medical Science

and Research, Mullana, India

K. Kapoor � B. Singh

Department of Anatomy, Government Medical College,

Chandigarh 160 036, India

A. Aggarwal (&)

123-C Old Type V, Sector 24-A, Chandigarh, India

e-mail: anjli_doc@yahoo.com; agg_adityadoc@yahoo.co.in

123

Surg Radiol Anat (2009) 31:349–356

DOI 10.1007/s00276-008-0452-0

blood flow regardless of location of obstructive lesion [7].

The outcome of balloon angioplasty may depend not only

on an obstructive lesion consistency but also vary with

lesion location. Besides this, it is also essential to know the

changes in renal artery with advancing age. However, little

is known about severity of these age bound changes and

their association with morbidity and mortality rate. Ath-

erosclerosis affecting coronary, carotid and peripheral

arteries has been exhaustively studied in terms of inci-

dence, sequelae, treatment and outcome. This is not true of

atherosclerosis of renal arteries, which has been difficult to

detect and even more difficult to monitor over time [4].

Only a few studies [10, 21, 23] have been reported on

atherosclerosis in renal artery. Most of these are based on

clinico-radiological aspects of the disease. Fujii et al. [9], in

autopsy subjects with stroke, reported the relationship

between extent of renal parenchyma damage, renal artery

stenosis and clinical characteristics. Coexisting renal

parenchymal damage was more severe in renal artery ste-

nosis, hypertension, diabetes mellitus, proteinuria and renal

insufficiency than those without such complications. Age

related changes in renal artery have not been studied hist-

opathologically and described in the literature. Mathur et al.

in 1961, [16] studied atherosclerotic changes in renal artery

on gross examination only. However, the authors have

neither reported about the exact location of atherosclerotic

lesions nor about the degree of renal artery stenosis.

It is true that in the present scenario, the presence of the

atherosclerosis and the vascular stenosis may be well

appreciated by angiography and ultrasound, more effi-

ciently in clinic on the living patient. However, all kinds of

atherosclerotic lesions can not be detected in living per-

sons. Only calcified and severe areas of stenosis in arteries

can be detected in the living persons [22]. Because of these

limitations, the autopsy provides the only means for thor-

ough and direct examination of the arterial system in order

to evaluate atherosclerotic lesions precisely [22]. There has

been much debate about the role of autopsy in present-day

medical practice, teaching and research. ‘‘The Pathobio-

logical Determinants of Atherosclerosis in Youth’’ (PDAY)

research group also stressed upon the value of the autopsy

as a powerful research tool [25].

The purpose of this study was to determine the preva-

lence and severity of age related atherosclerotic changes in

renal artery as a whole in random population, with special

reference to specific sites and nature of lesions.

Materials and methods

The subjects were non-catastrophic persons, above 30 years

of age who died of non-renal causes and were autopsied

within 48 h after death. The subjects were divided into 4

age groups viz. 30–39, 40–49, 50–59 and 60 years or above.

Brief history of cause of death, smoking, alcoholism,

hypertension and diabetes mellitus was obtained from

medical records as well as from relatives. Body mass index

(BMI) was calculated using formula weight (kg)/height

(m)2. The Cases were categorized as thinly, moderately and

well built with BMI \ 20, 20–25 and[25, respectively.

After ventral midline incision on the cadaver, aorta was

cut 1 cm proximal and 1 cm distal to the origin of renal

artery. This segment of aorta was removed along with both

renal arteries. Renal arteries were cut just distal to the

origin of segmental branches. The renal artery atheroscle-

rosis was studied in 90 renal arteries; 54 renal arteries from

27 cadavers were obtained for macroscopic evaluation and

36 renal arteries from 18 cadavers were subjected to

microscopic examination.

Gross examination

Aorta and renal arteries were opened by a longitudinal

incision on the ventral surface. The specimen was covered

with freshly made Sudan IV solution for 10–20 min. The

intimal surface was stained red initially. The specimen was

then washed with water and differentiated with 70%

alcohol. After washing, fatty streaks retained the red stain

while normal endothelium lost its deep red stain and

became pinkish. Fibrous plaques remained unstained. The

specimens were fixed in 10% formal-saline.

For measuring atherosclerotic lesions, the outlines of

specimen and various lesions were marked on cellophane

paper. Percentage of atherosclerotic area out of the total

area of renal artery was calculated with the help of a

transparent graph paper (Fig. 1).

Atherosclerotic index (AI) was calculated from the

above measurements according to the formula recom-

mended by the Special Committee on Lesions of American

Society for the Study of Atherosclerosis [13].

Atherosclerotic index AIð Þ ¼ 1=2pTþ 1=4pFþ 1=2pC

where

pT % of total atherosclerotic area

pF % of total fibrous plaque

pC % of total complicated lesions

Student’s ‘t’ test was performed to correlate the extent

of atherosclerosis with increasing age. The site and location

of atherosclerotic lesions on the two sides were also

compared.

Histological examination

A 2–3 mm tissue from proximal and distal segment was

cut. Middle segment was not subjected to examination as it

350 Surg Radiol Anat (2009) 31:349–356

123

was found to be the least affected part after gross exami-

nation. Serial sections of 5 lm thickness were selected for

H&E staining.

The stained slides were viewed under microscope and

various histological features were noted and the extent of

luminal narrowing was evaluated with a micrometer. The

subjects with stenotic lesions were divided into three

grades of luminal narrowing –mild, moderate and severe

stenosis [27]. The cases were tabulated and correlated with

all the above-mentioned parameters.

Results

Gross examination

Type of lesions

Lesions were classified into three types as per WHO [27]

classification:

1. Fatty streaks

2. Fibrous plaques

3. Complicated lesions

All the arteries showed mainly fatty streaks except for

two arteries in fifth and seventh decades which showed

fibrous plaque at ostium (Fig. 2). At all other sites, lesions

appeared as small, scattered patches or dots.

Incidence During the fourth decade, atherosclerotic

lesions were found in 75% of renal arteries. In the fifth

decade, the incidence increased to 85% with a small

decline in sixth decade to 70%. Out of ten renal arteries

falling in sixth decade, six were from male subjects and

four from female cases. All six arteries from males (n = 6)

showed atherosclerotic lesions (100% involvement).

However, Out of four arteries from females, only one

showed evidence of atherosclerotic lesions (25%

involvement); other three were free from atherosclerotic

lesions. A steep rise in the incidence of arteries was seen in

seventh decade with 100% involvement (Table 1).

Sex Out of 27 subjects (54 renal arteries), only 3 subjects

(6 renal arteries) were females. Two (2) subjects (4 renal

arteries) belonged to 50–59 years age group, whereas one

subject (2 renal arteries) was from above 60 years age group.

Extent The extent of lesions was calculated in terms of

atherosclerotic area and atherosclerotic index (Table 1).

These followed the same trend as incidence. AI was the

highest in fifth decade. The difference in the extent was not

statistically significant.

Site Lesions were studied at four sites: at ostium, proxi-

mal one-third, middle one-third and distal one-third of

renal artery. Most lesions were found near ostium

(85%).The next common site was proximal segment with

Fig. 1 Measurement of

atherosclerotic area (dark area)

on a graph paper

Fig. 2 Renal arteries in 60 years old well built male. A big fibrous

plaque (as indicated by arrows) is seen in the aorta on the left side,

overhanging the renal ostia. Right renal artery shows fatty streaks at

ostium. The middle and distal segments are free of lesions

Surg Radiol Anat (2009) 31:349–356 351

123

27% incidence (Table 2). The middle segment was the

least involved site. Lesions near the ostium were relatively

larger than at other sites. The same renal artery demon-

strated atherosclerotic lesions at more than one site, i.e.,

ostium as well as distal segment. There were patchy

involvements of renal arteries. In some of the cases, there

was involvement of more than one segment (Fig. 3).

Side of involvement Distribution of lesions was essen-

tially similar on both the sides. The right renal artery was

involved in 77% whereas left renal artery had lesions in

88% cases. Lesions were bilateral in 77% cases and uni-

lateral in 11.11% cases. Incidentally, all the arteries with

unilateral involvement were on the left side. Two cases

with accessory renal artery on left side were seen. In both

cases, lesions were found close to ostium.

Mean atherosclerotic index was also found to be higher

on left than right side. The incidence as well as extent of

atherosclerosis was more on left side but the difference was

not statistically significant (Table 3).

Social distribution

Nutritional factor Incidence of atherosclerotic lesions

was found to increase with better nutritional status but no

statistically significant correlation was found between

severity of atherosclerosis and nutritional status (Fig. 4).

Smoking Incidence of atherosclerosis in smokers was

almost equal that of nonsmokers but as far as percentage of

intimal surface involvement is concerned, smokers had

higher atherosclerotic area. No statistically significant

correlation was observed between the relationship of renal

artery atherosclerosis with smoking (P value 0.74) in our

study.

Alcoholism Incidence of atherosclerosis in alcoholics was

found to be higher than nonalcoholic but AI was less in

alcoholics. No statistically significant correlation was

observed between the relationship of renal artery athero-

sclerosis and alcoholism (P value 0.38).

Histopathological examination

Proximal segment

Intimal thickening was the most common finding and was

present in 72% of total cases. Incidence of thickening was

found to increase with age except for the age group of 50–

59 years. Seventh decade onwards, intimal thickening was

a universal phenomenon. It was localized in most of the

cases and crescentic in some cases with little or no luminal

narrowing. In two cases, intimal thickening was substantial

enough to result in uniform narrowing of lumen (Fig. 5).

First evidence of fibrous plaque was seen in the fifth

decade. The prevalence of fibrous plaque was found to

increase with increasing age except in 50–59 years age

Table 1 Incidence and extent

of atherosclerosis in different

age groups

Ath. atherosclerosis, AIatherosclerotic index

Age(yrs.) No. Incidence of Ath. (%). Mean Ath. area (%) Mean AI P value

30–39 16 12 (75%) 7.24 3.69 ± 2.17 0.36

40–49 14 12 (85%) 13.28 6.64 ± 5.18

50–59 10 7 (70%) 9.74 4.87 ± 2.03

[60 14 14 (100%) 11.86 5.93 ± 5.26

Table 2 Location of

atherosclerois in the renal artery

(More than one segment was

involved in one artery so total

was more than 100%)

Side Number

of arteries

Location

Ostium Proximal segment Middle segment Distal segment

Right 27 21 (77%) 8 (29%) 1 (3.7%) 0

Left 27 25 (92%) 7 (25%) 1 (3.7%) 3

Total 54 46 (85%) 15 (27%) 2 (3.7%) 3 (5.5%)

Fig. 3 Renal arteries showing patchy atherosclerotic lesions in

different segments (as indicated by arrows); Fatty streaks are seen

at ostium and middle segment in right renal artery and distal segment

in left artery

352 Surg Radiol Anat (2009) 31:349–356

123

group. The fibrous plaques followed the same trend as

intimal thickening. In advanced fibrous plaques, the deep

core was full of cholesterol clefts and foam cells. These

changes were predominantly seen in the sixth and the

seventh decades. The fibrous plaque showed good amount

of thrombus formation. In these cases, internal elastic

lamina was found to be attenuated. Fibrous plaques

encroached on the media, resulting in thinning of media

(Fig. 6). Complicated lesions made their appearance in the

fifth decade in the form of calcification (Table 4; Fig. 7).

Ulceration was also seen in one case (Fig. 8) in the age

group of 40–50 years.

Arterial stenosis was assessed on transverse section of

arterial segments. Three grades of luminal narrowing were

recognized as recommended by World Health Organiza-

tion, 1958 [27]. Out of 36 renal arteries studied, luminal

narrowing was seen only in 5 arteries. One case showed

stenosis in arteries on both the sides. The overall preva-

lence of renal artery stenosis was found to be 13.8%.

However, as the age advanced, the incidence of stenosis

increased from 14% in fourth decade to 50% of the total

cases in seventh decade. Severe stenosis was seen only in

one case belonging to seventh decade (Table 5).

Distal segment

As observed in gross examination, the distal segment

showed minimal involvement. The atheromatous changes

were observed in 16% specimens in the form of focal

intimal thickness. The distal segment showed evidence of

Table 3 Incidence and extent of atherosclerosis

Age Right renal artery Left renal artery P value

No. Incidence Mean AI ± SD No Incidence Mean AI ± SD

30–39 8 6 2.99 ± 1.59 8 6 4.39 ± 2.57 0.28

40–49 7 5 6.02 ± 6.16 7 7 7.07 ± 4.83 0.74

50–59 5 3 4.97 ± 2.89 5 4 4.8 ± 1.65 0.93

[60 7 7 6.17 ± 6.88 7 7 5.68 ± 3.53 0.87

Total 27 21 (77%) 5.05 ± 5.02 27 24 (88%) 5.62 ± 3.52 0.66

64%

87.5%93%

0

20

40

60

80

100

120

Inci

den

ce %

WellModeratelyThinly

Built

Relation Between Nutrition Status & Incidence of Atherosclerosis

Fig. 4 Bar diagram showing positive correlation between nutritional

status and incidence of Atherosclerosis

Fig. 5 TS of proximal segment of left renal artery in a 45 years old

male. Marked thickening of intima with intact internal elastic lamina

is seen (9280, H&E)

Fig. 6 TS of proximal segment of left renal artery in a 50 years old

male showing well formed atheroma (as shown by arrows) with

thinning of media. Intima is markedly thickened (955, H&E)

Surg Radiol Anat (2009) 31:349–356 353

123

atheromatous changes in only six cases. Five cases showed

focal intimal thickness. Diffuse intimal thickening involv-

ing half or more of the circumference of intima was seen in

only one case.

Discussion

The aim of the present study was to find out the incidence,

extent and severity of atherosclerosis in renal arteries in

persons who were apparently normal before death.

Incidence and severity of renal artery atherosclerosis

was found to increase with age. There was a slight dip in

the sixth decade. This was possibly because the number of

cases in this age group was relatively small (10) and out of

these, 4 (40%) were females. Thus the results were

severely influenced by less involvement of arteries from

female subjects in this age group.

Extent and severity of atherosclerotic lesions in terms of

AI was found to increase from 3.69 ± 2.17 in fourth

decade to the 6.64 ± 5.18 in fifth decade with decline to

4.87 ± 2.03 in sixth decade and again increase to

5.93 ± 5.26 in the seventh decade. In the seventh decade,

AI was higher than the sixth but relatively low for this age.

This was possibly due to absorption of fatty streaks and/or

their transformation into complicated lesions. Maximum

AI was seen in the fifth decade. Since AI is predominantly

dependent upon the atherosclerotic area, it is quite possible

that AI may not increase proportionately with age. The

same can not be stated for the degree of lesions and

appearance of complicated lesions in the arteries. In the

fourth and fifth decades, fatty streaks occupied most of the

atherosclerotic area whereas from sixth decade onwards,

fibrous plaques and complicated lesions were more

prominent. No complicated lesions were seen in renal

arteries in the grossly stained specimens. Thus in our

study, renal artery atherosclerosis was of mild to moderate

severity in terms of AI. This is consistent with the

observation of Roberts et al. [18] that atherosclerosis in

renal artery is only moderately severe. However, this study

[18] graded the severity of lesions, based on the percent-

age of intimal surface involvement only. Moreover, no

lipid staining was performed and hence probably might

have missed out certain lesions. In our study, lipid staining

was done for facilitating better delineation of the athero-

sclerotic lesions.

Table 4 Type of lesions in proximal and distal segment of renal artery

Age No. Proximal segment Distal segment

IT Internal elastic

lamina attenuation

Any other

lesion

Lumen

narrowing

IT Internal elastic

lamina attenuation

Any other

lesion

Lumen

narrowing

30–39 10 6 (60%) – – – 1 (10%) – – –

40–49 14 11 (78%) 6 (42%) 2 (14%) 2 (14%) 4 (28%) – – –

50–59 8 5 (62%) 2 (25%) 1 (12.5%) 1 (12.5%) – – – –

[60 4 4 (100%) 2 (50%) 2 (50%) 2 (50%) 1 (25%) – – –

Total 36 26 (72%) 10 (27%) 5 (13.8%) 5 (13.8%) 6 (16%) – – –

IT intimal thickness

Fig. 7 TS of proximal segment of left renal artery in a 60 years old

male, showing calcification (arrow) within an atheromatous plaque

(9280, H&E)

Fig. 8 TS of proximal segment of left renal artery in a 45 years old

male, showing well formed atheromatous plaque with superficial

ulceration (arrow) (9140, H&E)

354 Surg Radiol Anat (2009) 31:349–356

123

In Mathur et al.’s [16] study, mean AI was lower (Mean

AI: 0.013 in the second decade to 1.880 in the eighth

decade) than our study. Despite lower values of AI, this

study also reported calcified lesions in sixth decade

onwards which were not seen in our grossly stained spec-

imens. Our study showed almost similar trends and fibrous

plaques made their first appearance in the fifth decade. This

discrepancy might be probably due to the fact that north-

west Indian population has a better nutritional and eco-

nomic status as compared to the population involved in the

other study. In addition, no microscopic examination was

performed in this study. In our study, there was a definite

correlation between nutritional status or built of person and

atherosclerosis. Incidence was found to increase with

improvement of nutritional status (Fig. 3).

Increase in intimal thickness is considered to be an

integral part of atherosclerosis. Increase in intima to media

ratio serves as an indicator of atherosclerosis [8]. Abdel-

ghaffar et al. 2003 [1] studied the role of ultrasound for

determining the presence of subclinical atherosclerosis

(measured as carotid intima-media thickness [cIMT] in

adolescents with type 1 diabetes. The mean aggregate

cIMT was higher in diabetics than controls. Non-invasive

methods such as ultrasound for monitoring vascular chan-

ges as cIMT might be useful in clinical practice for early

diagnosis of sub clinical atherosclerosis [1].

In our study, the incidence of intimal thickness was

found to increase with increasing age. It was present in all

cases after the seventh decade. In 5% of cases, circum-

ferential thickening was enough to cause uniform luminal

narrowing.

Microscopically, fibrous plaques appeared first in the

fifth decade with an incidence of 14% which increased to

50% in the seventh decade. Calcification and ulceration

were noticed first in fifth decade. Overall incidence of

calcification was 5%. The severity of renal artery athero-

sclerosis in terms of type of lesions was found to increase

with age.

On extensive review of literature, no recent autopsy

studies on renal artery atherosclerosis have been found. As

old studies (1959, 1961) [18, 16] have been the major

autopsy studies extensively done in renal arteries, hence we

have compared with these studies.

Different authors have used different scales to express

stenosis [12, 27]. WHO 1958 [27] classification was used

in our study. The overall prevalence reported in our study

was 13.8% which was close to the observations of Harding

et al. [11] but less than that reported by Choudhri et al. [6]

and Valentine et al. [24]. Stenosis was noticed first in the

fifth decade with 14% incidence. It increased with age with

almost 50% arteries in the seventh decade, showing evi-

dence of atherosclerotic renal artery stenosis. Less than

25% luminal narrowing and 25–50% narrowing were

reported in 5.5% of cases each. Severe stenosis ([50%

luminal narrowing) was seen in only one case (2.7%).

Holley et al. [12] in his autopsy study reported preva-

lence of severe renal artery stenosis as 27%. In another

autopsy study, Schwartz et al. [20] found a prevalence rate

of 5% in patient less than 64 years. These investigators

defined significant stenosis as[50% of luminal narrowing.

Angiographic studies done by various authors showed a

wide variation in the evaluation of luminal narrowing.

Angiography does provide anatomic information on loca-

tion and extent of disease but is not suitable for long term

studies to document the natural history of disease [4]. In a

study by Androes et al. in 2007 [3], 200 consecutive

patients undergoing angiographic evaluation of symptom-

atic peripheral vascular disease were studied retrospectively

for renal artery stenosis. Over all incidence of any degree of

renal artery stenosis was 26%. A 12% had incidental finding

of[50% stenosis in either renal artery. Choudhri et al. [6]

reported narrowing in 33–39%, Harding et al. [11] in 11%

and Valentine et al. [24] in 23% of cases. Thus prevalence

of atherosclerotic renal artery stenosis as reported by these

authors was found in the range of 11–39%.

In current study, the most common site of atheroscle-

rotic stenotic plaques was the proximal third of renal artery

where the prevalence of stenosis was 13.8% followed by

distal segment. The middle third of renal arterial trunk was

the least affected site.

Some of the earlier autopsy studies [12, 20] showed the

same trend with stenotic plaques, most frequently found in

the proximal third of renal arterial trunk near aortic ostia.

Elsewhere, the lesions were relatively uncommon. The site

of stenosis was essentially same on both sides. Propensity

of stenosis to occur at ostium and proximal segment, as

explained by these authors, was due to either some struc-

tural preponderance or the rules of fluid haemodynamics

causing turbulence at these particular sites [19]. Non-ostial

lesions comprised only 15–20% of renal artery stenoses

with middle third as the least common site. Schwartz and

Mitchell [19] in their study on renal arteries in 336 patients

reported the most frequent occurrence of the atheroscle-

rotic lesions at the ostia of the artery. Libby [14] found

Table 5 Degree of stenosisNumber

of arteries

No stenosis Moderate stenosis \50% Severe

stenosis [50%\25% [25%

36 31 2 2 1

Surg Radiol Anat (2009) 31:349–356 355

123

proximal segment of renal artery as the common site for

development of atherosclerotic plaque.

Like stenosis in carotid and vertebral arteries [20], renal

stenosis has a marked propensity to occur bilaterally [12].

Schwartz and White [20] stressed upon the bilateral nature

of the disease. Our study also recorded similar finding.

In Our study, atherosclerotic changes were seen more

commonly on left side. In all the age groups, left renal

artery was more commonly involved. Mean AI was higher

on the left side in all age groups, though the difference was

not statistically significant. The incidence of atherosclero-

sis was much higher on the left side. This has never been

explained. However, it is postulated that it could be prob-

ably due to the fact that left renal artery is given off slightly

proximal to the right and turbulence might be compara-

tively greater here.

Schwartz and White [20] noticed a slight but inconsis-

tent difference in right and left renal arteries. In general,

the left renal artery showed a slightly greater prevalence of

stenosis and atherosclerosis than right. Wollenweber [26]

on the other hand, claimed that in cases with unilateral

atherosclerosis, the right renal arteries were involved more

frequently. Both the authors could not explain this pre-

dominance of one side or the other.

Conclusion

Incidence and severity of renal artery atherosclerosis was

found to increase with age. There was a slight dip in the

sixth decade. Proximal segment was the most commonly

and severely affected site. Most of the case showed bilat-

eral involvement; in unilaterally affected cases, left artery

was more affected.

References

1. Abdelghaffar S, El Amir M, El Hadidi A, El Mougi F (2006) Carotid

intima-media thickness: an index for subclinical atherosclerosis in

type I diabetes. J Trop Pediatr 52(1):39–45 Epub 2005 July 6

2. Albers FJ (1994) Clinical characteristics of atherosclerosis

renovascular disease. Am J Kid Dis 24(4):636–641

3. Androes MP, Langan EMIII, Kalbaugh CA, Blackhurst DW,

Taylor SM, Youkey JR (2007) Is incidental renal arteriography

justified in a population of patients with symptomatic peripheral

arterial disease? Vasc Endovascular Surg 41(2):106–110

4. Caps MT, Perissinotto C, Zierler RE et al (1998) Prospective

study of atherosclerotic disease progression in the renal artery.

Circulation 98:2866–2872

5. Carmichael P, Carmichael AR (1999) Atherosclerotic renal artery

stenosis from diagnosis to treatment. Curr Concepts Med 75:527–

535

6. Choudhri AH, Cleland JG, Rowlands PC, Tran TL, McCarty M,

Al Kutoub MA (1990) Unsuspected renal artery stenosis in

peripheral vascular disease. BMJ 301:1197–1198

7. Cicuto KP, McLean GK, Oleaga JA, Freiman DB, Grossman RA,

Ring EJ (1981) Renal artery stenosis: anatomic classification for

percutaneous transluminal angioplasty. Am J Radio 137:599–601

8. Ferro M, Novero D, Botto Micca F, Palestro G (1991) Compar-

ative morphological study of the structure of the normal and

arteriosclerotic internal mammary, coronary and renal artery.

Pathologica 83(1084):159–166

9. Fujii H, Nakamura S, Kuroda S et al (2006) Relationship between

renal artery stenosis and intrarenal damage in autopsy subjects

with stroke. Nephrol Dial Transplant 21(1):113–119 Epub 2005

September 2

10. Hansen KJ (1994) Prevalence of ischemic nephropathy in the

atherosclerotic population. Am J Kid Dis 24:615–621

11. Harding MB, Smith LR, Himmelsteen SI (1992) Renal artery

stenosis: prevalence and associated risk factors in patients

undergoing routine cardiac catheterization. J Am Soc Nephrol

2:1608–1614

12. Holley KE, Hunt JC, Brown AL, Kincaid OW, Sheps SG (1964)

Renal artery stenosis: a clinico-pathologic study in normotensive

and hypertensive patients. Am J Med 37:14–22

13. Holman RL, Brown BW, Gore I, McMillan GC, Paterson JC,

Pollack OJ, Roberts JC, Wissler RW (1960) An Index for the

evaluation of arteriosclerotic lesions in the abdominal aorta. A

report by the ‘‘Committee on lesion of the American society for

the study of arteriosclerosis’’. Circulation 22:1137–1143

14. Libby P (1998) Atherosclerosis. In: Fauci AS, Braunwald E, Is-

selbacher KJ, Wilson JD, Martin JB, Kasper DL, Hauser SL,

Longo DL (eds) Harrisons’ principles of internal medicine, 14th

edn. McGraw-Hill, New York, p 1345

15. Mann J, Allenberg JR, Reisch C, Dietz R, Weber M, Luft FC

(1992) Renovascular hypertension. In: Cameron S, Davison AM,

Grunfeld JP, Kerr D, Ritz E (eds) Oxford text book of clinical

nephrology, vol 3. Oxford University Press, Oxford, p 2096

16. Mathur KS, Patney NL, Kumar V (1961) Atherosclerosis in

India: an autopsy study of the aorta and coronary cerebral, renal

and pulmonary arteries. Circulation 24:68–74

17. Novick AC, Stewart BH (1979) Surgical treatment of renovas-

cular hypertension. Curr Probl Surg 16:1–74

18. Roberts JC, Moses C, Wilkins RH (1959) Autopsy studies in

atherosclerosis I. Distribution and severity of atherosclerosis in

patients dying without morphologic evidence of atherosclerotic

catastrophe. Circulation 20:511–519

19. Schwartz CJ, Mitchell JR (1962) Observation of localization of

arterial plaques. Circ Res 11:63–73

20. Schwartz CJ, White TA (1964) Stenosis of renal artery: an

unselected necropsy study. BMJ 2:1415–1421

21. Strandness DE (1994) Duplex imaging for detection of renal

artery stenosis. Am J Kid Dis 24:674–678

22. Strong JP, Richards ML (1976) Cigarette smoking and athero-

sclerosis in autopsied men. Atherosclerosis 23:451–476

23. Thomas MG (1994) Magnetic resonance angiography of renal

artery stenosis. Am J Kid Dis 24(4):700–712

24. Valentine RJ, Myer SI, Miller GL, Lopez MA, Clagett GP (1993)

Detection of unsuspected renal artery stenosis in patients with

abdominal aortic aneurysm: refined indication for preop aortog-

raphy. Ann Vasc Surg 7:220–224

25. Wissler RW, Strong JP, PDAY Research Group (1998) Risk

factors and progression of atherosclerosis in youth. Am J Pathol

153(4):1023–1033

26. Woollenweber J, Sheps SG, Davis GD (1968) Clinical course of

athero-sclerotic renovascular disease. Am J Cardiol 21:60–171

27. World Health Organization (1958) Classification of Atheroscle-

rotic lesions. World Health Organization Technical Report Series

143, Geneva

356 Surg Radiol Anat (2009) 31:349–356

123