POSTGRAD. MED. J. (1966), 42, 183

ARTERIOGRAPY AND RENAL ARTERY STENOSISDAVID SUTTON, M.D., F.R.C.P., F.F.R.

Director, Radiological Department, St. Mary'sHospital, London, W.2.

IT is now well recognised that renal ischaemia isan important cause of hypertension. There areseveral renal vascular lesions -which may cause,or may be associated with, renal ischaemia.These include:

1. Renal artery stenosis and thrombosis.2. Renal artery aneurysm.3. Angiomatous malformation of the renal

artery.4. Arterio-venous fistula involving the renal

arteries.5. Embolus of the renal artery or its branches.Of the lesions listed, renal artery stenosis is

much the most frequent and important.This condition is now generally accepted as a

significant and important cause for hypertensionof renal origin. Various pathological lesionshave been cited as causes of renal artery steno-sis. These and the number of cases encounteredin our material are:

1. Atheroma, of which we have seen 135examples.

2. Fibromuscullar hyperplasia, and the possi-bly allied condition of fibrous hyperplasia,of which we have seen 43 cases.

3. External pressure, of which we have seen2 examples.

4. Congenital hypoplasia of the renal arteryorigin-3 examples.

Numerically atheroma is clearly the most im-portant cause of renal artery stenosis.The clinical aspect of atheromatous renal

artery stenosis have been discussed in detail ina previous paper from St. Mary's Hospital(Brown, Owen, Pealt, Robertson and Sutton,1960), and we have also reviewed the radio-logical aspects. (Sutton, Starer and Brunton,1961; 'Sutton, 'Brunton, Foot and Guthrie, 1963.)I propose here to bring up to date the radio-logical analysis of our material, and the opin-ions previously expressed.We have now examined over 700 known

hypertensives with the deliberate object of con-firming or excluding renal artery stenosis, or ofdemonstrating other vascular lesions causing, or

associated with, the hypertension. We have alsoexamined about 2,500 patients with aorto-iliacdisease by aortography. Amongst these we haveseen 69 cases of renal artery stenosis mostlyassociated with hypertension. However, the trueincidence amongst patients with aorto-iliacatheroma is not reflected in this figure since themajority of the patients investigated werenormo-tensive and had low aortic punctures,i.e. below the level of the renal arteries.

TABLE 1RENAL ARTERY STENOSIS Total1. Arteriography for aorto-iliac disease

Cases investigated-2,500 Stenosis 692. Arteriography for Hypertension 135

Case investigated- 700(a) Stenoses 66

(b) FibromuscularHyperplasia 43

(c)Other lesions 10

Our hypertensive cases were largely un-selected and the procedure was carried out onmost of the hypertensive patients admitted tothe Medical Unit under Professor Peart at St.Mary's Hospital, and on some hypertensivesadmitted to other units. Among these 700 caseswe have discovered 65 cases of simple renalartery stenosis, i.e. ren-al artery stenosis of thestraightforward atheromatous stricture type.(Fig. 1).

We have previously described the changesobserved at IVP in cases of renal arterystenosis, and *which we regard as diagnosticor suggestive of renal artery stenosis (Suttonand others, 1961). We have now extended ourexperience in this field and have examined thepyelograms in about 100 cases of proven renalartery stenosis. The following changes are re-garded by us as virtually pathognomonic offunctional renal artery stenosis. (Fig. 2).

1. The affected kidney is smaller than thenon-affected kidney.

2. The kidnev contour is smooth, in contrastto the irregular contour of the smallkidney in chronic pyelonephritis.

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FIG. 1.-Severe atheromatous stenosis at the originof the left renal ar.tery.

3. Contrast values are denser on the affectedside.

4. The calyces appear "spastic" though, aswe have previously pointed out, this isnot due to true spasm but to underfillingof the calyces associated with a reduced

urine flow. This of course is secondary tothe reduced blood pressure distal to thestenosis, and to relatively increased waterresorption.

These changes are to be expected on physio-logical grounds. This is because there is a re-duced volume of glomerular filltrate, but thetubular resorption of water remains excellent.The final urine therefore is of low volume buthas a high concentration of contrast medium,on the side of the stenosis. This may be wellbrought out in a water-diuresis pyelogram.While we now regard the pyelogram syn-

drome I have described as diagnostic of renalartery stenosis there are several qualificationsthat must be made.

First, the full pyelogram syndrome of renalartery stenosis will only be seen in a proportionof cases where arteriography demonstrates astenosis. In our material it has been present inover one-third of 100 cases where adequatepyelograms were available for examination, andin these cases it provides strong evidence, ifnot absolute proof, of the presence of a func-tional renal artery stenosis. In some casesonly part of the syndrome has been present.Here also the diagnosis can be correctly sug-gested in particular if there is increased con-

FIG. 2.-IVP in a case of right renal artery stenosis.The affected kidney is smaller, with "spastic"calyces but there is denser contrast in the smallpelvis.

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SUTTON: Arteriography and Renal Stenosis

trast concentration on one side.More difficult to assess are the cases where

there was no IVP function on the side of thestenosis and this happened in some cases; orthe cases where function on the two sides atIVP appear equal-this was so in 40 of ourcases. In some cases there may be severeischaemic damage to the kidney or there maybe a co-incidental lesion such as hydrone-phrosis or pyelonephritis. Again, where a branchartery or an accessory artery only is involvedthen only a part of the kidney is affected bythe stenosis and the remainder will functionexactly as does the non-affected kidney.

Finally, stenosis does not necessarily meansignificant ischaemia of the kidney or significantinterference with function. Before accepting astenosis as functional we require confirmationby divided function studies and other investiga-tions.We have attempted to correlate the degree of

stenosis as measured at arteriography with thepyelogram changes. We did this by arbitrarilygrading the degree of encroachment on therenal artery lumen. Whilst aware of the theoret-ical objections to arbitrary gradings of thlis typethe exercise was useful in demonstrating asignificant relationship between the degree ofstenosis and the pyelogram changes. Thus, al-though less than half our cases showed increasedconcentration of the medium, most of thesecases were among the severer grades of stenosis.We have strong evidence therefore that there

is a close relationship between the degree ofstenosis and the pyelographic change in thek;idney, unless the picture is complicated byother features. We have in conjunction with theMedical Unit used various refinements of theIVP as tests of differential function of the twokid'neys. These have included the water loadtest; IVP after administration of Pitressin;studies with and without abdominal com-pression, and serial films at rapid and differentintervals after IVP.

Early films taken within 60 seconds of in-jection may be useful in showing differencesin contrast at IVP as pointed out by Siggers(1961) but our own impression is that differ-.nces of contrast density in the pyelogram arebest appreciated in the later stages of an IViPand are best seen in the films at 15 to 20minutes.

Clearly, functional studies by modiificationof the normal pyelogram investigation can becarried out in many different ways. On thebasis of our present experience however anIVP carried out with standard technique

seems ithe most practical mode of routine in-vestigations, because of the many complexfactors involved.As regards kidney size, measurements of

both kidney ilengths were possible in about 100cases. In 80(% of these the kidney on thestenotic side was smaller, and in about two-third's of these the difference in size was morethan 1 cm. In ten cases the kidneys were equalin size and in eight cases the kidney on theside of the stenosis was larger. In all itheseeight cases the difference in size was minimaland it was the left kidney which was affected.It should be remembered that the left kidneycan normally be a little larger than the right.Fibromuscular Hyperplasia and Fibrous

HyperplasiaWe have now encountered 43 cases where

there was a diffuse lesion involving a largesegment of a renal artery, or one of its majorbranches. It has been claimed that this typeof abnormality represents a specific entity whichWylie and Wellington (1960) have 'termed"fibromuscular hyperplasia" of the renalarteries. Hunt, 'Harrison, Kincaid, Bernatz andDavies (1962) also include the condition offibrous hyperplasia in this group of cases.The evidence for regarding fibromuscular

hyperplasia of the renal artery as a specificentity is both pathological and radiological. It isclaimed that the histology in these cases is quitedifferent from that observed in cases of athe-roma. The picture is said to be one of irregularmuscular hypertrophy and quite unlike thehistological picture seen in atheroma. Furtheratheroma tends 'to involve the origin of therenal artery but fibromuscular hyperplasia in-volves'the middle third of the artery, and mayextend over its whole course and into brancharteries. Fibromuscular hyperplasia is bilateraland diffuse in the majority of cases, though itcan be unilateral. It may be associated wi'thsaccular aneurysm formation. Atheromatousstenosis on the other hand affects only the originof the renal artery, and in most examples en-countered is unilateral or primarily so.The radiological appearances of fibromuscu-

lar hyperplasia are also quite different fromthose of atheroma and reflect the differences inpathology. In atheroma the lesion is only afew mm. in length and nearly always affectsthe origin of the main renal artery.

In fibromuscular hyperplasia, the lesion usu-ally affects a long segment of the artery and ismaximal in the middle one third of the renalartery. (Fig. 3.) It may also involve brancharteries.

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FIG. 3.-Fibromuscular hyperplasia affecting thedistal half of the main right renal artery. Thereis also a cyst in the lower pole of the kidney.

There are also clinical features in whichfibromuscular'hyperplasia differs from atheromaof the renal arteries. Atheroma of the renalartery, like atheroma elsewhere in the body hasa predominantly male sex incidence. In ourmaterial the number of male cases has outnum-bered the female cases by over two to one.Fibromuscular hyperplasia on the other handhas a predominantly female sex incidence. Theseries of 11 cases reported by Falubinska andWylile were all female cases. Our own figuresconfirm this female sex incidence, but it isimportant that we have encountered a few malecases. Our 43 patients consisted of 37 femalesand 6 males.

It is also suggested in the literature thatfibromuscular hyperplasia is predominantly adisease of young patients and is unusual in theelderly. Our own material however does notsupport this contention. The age distributionin our cases did not differ appreciably from thatof the atheromatous stenosis cases at the time ofdiagnosis. There were 8 cases aged over 60, 13cases aged 50-60, 11 aged 40-50 and 11 under40. It should be remembered however that wehave no evidence as to the length of time forwhich the disease was present before hyperten-sion was diagnosed. This is a facinating condi-tion and considerable further work needs to bedone for its elucidation. Unfortunaltely, relativelyfew cases have been operated on because ofthe bilateral or extensive nature of the arterialdisease.

In some of the cases 'operated on an im-provement in the hypertension has been ob-tained where the disease was predominantly

unilateral. In the original communication ofWylie and Wellington it was thought possiblethat there might be a relationship between thiscondition and toxaemia of pregnancy, becausethe hypertension in their first three patientswas first noted during pregnancies. This interest-ing speculation was not supported by their fur-ther experience and it could hardly be relevantto our own male cases, or to the reported casesin children. However, it is a point which re-quires further investigation.

It is of interest that a few of our femalecases suffered from hypertension which was firstnoticed during pregnancy. It is also interestingthat many of our cases of fibromuscular hyper-plasia showed clinically features suggestive ofrenal artery stenosis. Thus in some cases therewas a loud 'bruit over the abdomen, and someof {the predominantly unilateral cases showedtypical IVP changes.

It is thus clear that fibromuscular hyperplasiacan simulate simple atheromatous stenosis inits presentation both clinically and at pyelo-graphy if one artery is dominantly affected. Thisis not surprising as the condition does in factproduce a stenosis of the renal artery. However,differences between the kidneys on plain x-rayand pyelography will only be apparent if the'lesion is more marked on one iside. As thedisease is commonly bilateral, this is the excep-tion rather than the rule.

Fibrous HyperplasiaCases have been described where stenosis

of the renal artery has been due to a fibrousstenosis which was (a) perimuscular, or (b) inti-mal. Hunt and others '(1962) classified this con-dition as a variant of fibromuscular hyperplasia,despite the very different histology.We have seen two verified cases bu't, radio-

logically we were unable to differentiate themfrom fibromuscular hyperplasia. The diagnosiswould thus appear to be largely pathological.Some of the cases of fibromuscular stenosis

reported in the literature occurred in children.We have seen three such cases of renal arterystenosis in children and we think they do notreally fall into the same category though theymight be classified as "fibrous hyperplasia".

In one verified case our pathologist consi-dered the ilesions to represent areas of mal-development, i.e. to be congenital hypoplasiawith some secondary intimal fibrosis rather thanbelonging to the fibromuscular or fibrous hyper-plasias.

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March, 1966 SUTTON: Arteriography and Renal Stenosis 187

Extrinsic Pressure BandsWe have seen two examples of this very rare

condition where the renal artery is compressedby a fibrous or fibromuscular band (D'Abreuand Strickland, 1962). In both our cases theband was found to contain lumber sympatheticfibres and ganglion cells (Sutton and others,1963), suggesting that it was part of the lumbersympathetic chain.

SummaryRenal artery stenosis is an important cause of

hypertension. One hundred and eighty eightcases have been diagnosed by angiography atSt. Marys' Hospital in the past ten years. Onehundred and nineteen of 'the cases were foundamong 700 hypertensive patients. The majorcause was atheroma, but fibromuscular hyper-plasia (43 cases) was also an important cause,particularly among the female patients. Othercauses are fibrous hyperplasia, extrinsic pressurebands, and congenital arterial hypoplasia, butthese are rare.

REFERENCES

BROWN, J., OWEN, K., PEART, W., ROBERTSON, J., andSUTTON, D. 1(1960): The Diagnosis and Treatmentof Renal Artery Stenosis, Brit. med. J., ii, 327.

D'ABREU, F., and STRICKLAND, B., ((1962): Develop-mental Renal Artery Stenosis, Lancet, ii, 517.

HUNT, J. C., HARRISON, E. C., OWINGS, W., KINCAID.O. W., IBERNATZ, P. E., and DAVIES, G. D. (1962):Idiopathic Fibrous and Fibromuscular Stenosis ofthe Renal Arteries Associated with Hypertension.Proc. Mayo. Clin., 37, 187.

PALUBINSKAS, A. J., and WYLIE, E. J. (1961): Fi,bro-musoular Hyperpl'asia of the Renal Arteries,Radiology, 76, 634.

SIGGERS, R. L. (1961): Differential Renal Function inGoldblatt Type of Hypertension, Acta radiol.(Stockh), 56, 94.

SUTTON, D., BRUNTON, F., FOOT, E. C., GUTHRIE, J.(1963): Fibromuscular, Fibrous and Non-Athero-matous Renal Artery Stenosis and Hypertension,Clin. Radiol., 14, 381.

SUTTON, D., STARER, F., and BRUNTON, F. (1961):Renal Artery Stenosis, Clin. Radiol., 12, 80.

WYLIE, E. J., and WELLINGTON, J. S. (1960): Hyper-tension Caused by Fibromsucular Hyperplasia ofthe Renal Arteries, Amer. J. Surg., 100, 183.

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