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HYPERTENSION AND RENAL ARTERY DISEASE By KENNETH OWEN, M.S., F.R.C.S. Consultant Surgeon, St Mnry’s Hospital, St Pnul’s Hospital and Royul Nortlirrn Hospital, Londoii THIS paper is a preliminary communication based upon work proceeding at St Mary’s Hospital. the medical investigations being performed by Professor W. S. Peart and the radiography by Dr David Sutton. FIG. I FIG. 2 Renal arteriograms of a patient with clinically malignant hypertension showing a normal right renal artery and a stenosed left renal artery with. post-stenotic dilatation. The lower part of the left kidney was supplied by an aberrant artery. This patient was treated successfully by nephrectomy. Following the discovery in experimental animals by Goldblatt ef a/. (1934) that partiat obstruction of the renal artery could produce hypertension, many efforts were made to link the known relationship between renal disease and hypertension in man with hypothetical vascular lesions. It is only, however, within the last few years that developments in vascular surgery and in renal arteriography have led to the demonstration of specific arterial lesions responsible for reversible malignant hypertension (Thompson and Smithwick, 1952 ; Freeman et a/., 1954 ; Poutasse, 1956). The first cases to be described were patients in whom partial renal artery obstruction associated with hypertension was found coincidentally in the investigation of other vascular disease. In 1956, Professor Rob and the writer operated upon such a patient, aged 39. who presented with symptoms of aortic thrombosis, severe buttock claudication, and inability to maintain an erection. He had a blood-pressure of 205/110 mm. and an aortogram (Fig. 1) revealed an aortic thrombosis from the level of the renal arteries downwards, with narrowing of the left renal artery. The origin of the right artery was not clearly seen. At operation, both renal arteries were found to be involved in atheromatous narrowing. A thrombendarterectomy Read at the Fifteenth Annual Meeting of the British Association of Urological Surgeons (combined meeting with the Canadian Urological Association) at Glasgow, July 1959. 414

HYPERTENSION AND RENAL ARTERY DISEASE

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Page 1: HYPERTENSION AND RENAL ARTERY DISEASE

HYPERTENSION AND RENAL ARTERY DISEASE

By KENNETH OWEN, M.S., F.R.C.S. Consultant Surgeon, St Mnry’s Hospital, St Pnul’s Hospital and

Royul Nortlirrn Hospital, Londoii

THIS paper is a preliminary communication based upon work proceeding at St Mary’s Hospital. the medical investigations being performed by Professor W. S. Peart and the radiography by Dr David Sutton.

FIG. I FIG. 2 Renal arteriograms of a patient with clinically malignant hypertension showing a normal right renal artery and a stenosed left renal artery with. post-stenotic dilatation. The lower part of the left kidney was supplied by an aberrant artery. This patient was treated successfully by nephrectomy.

Following the discovery in experimental animals by Goldblatt ef a/. (1934) that partiat obstruction of the renal artery could produce hypertension, many efforts were made to link the known relationship between renal disease and hypertension in man with hypothetical vascular lesions. I t is only, however, within the last few years that developments in vascular surgery and in renal arteriography have led to the demonstration of specific arterial lesions responsible for reversible malignant hypertension (Thompson and Smithwick, 1952 ; Freeman et a/., 1954 ; Poutasse, 1956). The first cases to be described were patients in whom partial renal artery obstruction associated with hypertension was found coincidentally in the investigation of other vascular disease. I n 1956, Professor Rob and the writer operated upon such a patient, aged 39. who presented with symptoms of aortic thrombosis, severe buttock claudication, and inability to maintain an erection. He had a blood-pressure of 205/110 mm. and an aortogram (Fig. 1) revealed an aortic thrombosis from the level of the renal arteries downwards, with narrowing of the left renal artery. The origin of the right artery was not clearly seen. At operation, both renal arteries were found to be involved in atheromatous narrowing. A thrombendarterectomy

Read a t the Fifteenth Annual Meeting of the British Association of Urological Surgeons (combined meeting with the Canadian Urological Association) a t Glasgow, July 1959.

414

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H Y P E R T E N S I O N A N D R E N A L A R T E R Y D I S E A S E 415

was performed on the right from within the aorta, but this was not possible on the left side and the left kidney was removed. The aorta was reconstructed. The patient made a straightforward recovery and is now, three years after operation, normotensive. A similar case has been described by Gellman (1958) in which nephrectomy was performed by Sir Eric Riches.

Such cases led to a search in patients with hypertension for an isolated renal vascular lesion which might be responsible for the disease, and a number of such cases have been described, the biggest series being those of Poutasse from the Cleveland Urological Clinic, and De Camp from New Orleans.

In most of the cases described, the cause of the arterial obstruction has been an atheromatous plaque, but other lesions have been described such as aneurysm, embolus, thromboangiitis obliterans, tumours and cysts, and congenital stenosis.

The incidence of such disease in unselected cases of malignant hypertension is probably not very high, but the method of screening adopted has been so variable in different clinics that no reliable figure is at present available. Whatever the incidence, the possibility of a cure in an otherwise incurable disease would seem to justify a large number of negative investigations, as in the search for other primary causes of hypertension, such as phzochromocytoma. Clinically, suspicion of such a cause may be aroused by the occurrence of malignant hypertension in young or old patients outside the usual age group for the disease, In these patients, as well as in others in the usual age group, a history of loin pain (suggesting renal infarction) and the detection of a systolic murmur over the renal artery on abdominal auscultation, may suggest this possible diagnosis. On intravenous pyelography a slight disparity may be seen in the size or function of the two kidneys, and such a disparity may be so slight as to need a much more critical evaluation of the pyelogram than is usual in searching for a renal cause of hypertension.

Na. l Flow.

I , - .

w. F. .

A . T . .

E. J. .

in I. /ni I n . Right, 4.0 Left, 2.0

Right, 0.2 Left, 4.5

Right, 3.9 Left. 1.1

mEq./li t re 60 50

67 I35

64 91

TABLE I .-

PA H PA H I Clearmce 1 Concentra- Extraction. ' PA H

1 :Ion. I

mEq.jlitre. 52 45

32 123

~~~

nil iniin. lmg. per cent.1 Per cent. 236 I ...

95 181 96

40 152 ... 234 168 ...

242

I

70 48 1 236 232 59 56 187

Divided renal function studies on two patients (W. F. and A. T.) with renal artery stenosis and one patient (E. J.) with hydronephrosis. Tn W. F. the left renal artery was stenosed and in A. T. the right renal artery was stenosed. In both cases there is a marked reduction in the water and electrolyte secretion on the involved side. By contrast the patient E. J. with a severe left hydronephrosis shows a reduced water excretion on the left diseased side, but there is an

increased excretion of sodium and chloride.

Selective renal function studies are of great help. It was shown experimentally by Mueller et a/. (1951) that the urinary sodium concentration is the first function to be depressed in renal ischxmia, and this is the basis of the Howard test (Howard et a/., 1956). It has been found that the sodium concentration and water excretion have been significantly depressed on the obstructed side in cases in the present series (Table I ) .

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416 B R I T I S H J O U R N A L O F U R O L O G Y

Arteriography.-This is the most important investigation, and the diagnosis in most of the present cases has been made possible by the excellent visualisation of the renal arteries obtained by Dr David Sutton. The lesion may be shown on percutaneous aortography, but better results are obtained by selective renal artery catheterisation, the catheter being introduced through the femoral artery. The most common lesion is a narrowing of the renal artery close to the aorta. Post-stenotic dilatation may be seen (Figs. 2 and 3). The nephrogram may confirm reduction in size of the kidney and reveal areas of infarction.

Despite the importance of arteriography, it is felt that reliance should not be placed upon this procedure alone, as an apparent anatomical abnormality may not be associated with functional abnormality. At operation, pressure recordings are taken simultaneously from the aorta and renal artery distal to the lesion. Only when a pressure drop can be demon- strated, together with functional impairment on selective renal catheterisation, is the radiological lesion regarded as a functional stenosis. Pre- operative percutaneous renal biopsy has not been used, as the ischmiia may be limited to part of the kidney which may be missed by a blind procedure. At operation, however. biopsies are taken from each kidney.

TREATMENT

FIG. 3 Right rena! arteriogram of a patient with hypertensive retinopathy. The tight steiiosis of the renal artery was treated by thrombendarterectoniy. The patient's blood- pressure returned to normal and his eye,changes regressed after a period of several months following the operation.

The simplest treatment is nephrectomy. and this may be indicated when the patient is unfit for a more major operation or is not prepared to take the added risk, or when a previous arterial reconstructive operation has failed.

When the patient's general condition allows, a reconstructive arterial operation would seem preferable as the kidney itself is usually healthy,

and may indeed be the better kidney, as it is protected from secondary hypertensive changes by the arterial lesion. The possible reconstructive operations are the following :-

I . Thr0mbendarterectomy.-This is the simplest reconstructive operation, and by analogy with similar operations in vessels of comparable size, such as the iliac and carotid arteries. the long-term results can be expected to be good (Table 11). It would seem important to open the aorta in performing the operation, in order to remove irregular intima from around the renal artery orifice.

2. Excision of the Narrowed Segment and End-to-end Anastomosis.-This method is suitable when the stenosis is in the middle of the renal artery.

3. Excision and Grafting.

4. By-pass Grafting.

5. Anastomosis of Splenic Artery to Renal Artery.-This operation is applicable only to disease of the left renal artery.

In most cases there seems little to be gained by using a graft, although this may occasionally be necessary as, for example, in congenital lesions.

111 bilateral cases, conservative surgery is, of course, essential.

Failure to do this may result in further thrombosis.

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H Y P E R T E N S I O N A N D R E N A L A R T E R Y D I S E A S E 417

Operative Technique.-The operative approach is through a transverse upper abdominal incision. On the left side the spleen is reflected to the right, and the splenic flexure is displaced downwards, while on the right the pancreatic head and duodenum are mobilised and displaced to the left. The aorta and vena cava are exposed, and during the operation the aorta is clamped obliquely between the renal arteries so as not to interfere with the renal blood flow on the unaffected side. Pressures are measured in the renal artery and aorta using a capacitance manometer, and biopsies are taken from both kidneys. Heparin is injected into the renal artery distal to the clamp, but anticoagulants are not otherwise used except later in convalescence as a long-term measure, in an attempt to reduce the chances of recurrence of the lesion.

Case. Sex

1 E., aged 39 M.

I

I F., aged 50 1 M I

TABLE I1

Post-operative Blood-pressure.1 Blood-pressure.

Lesion. Pre-operative Operation. I

Aortic thrombosis a n d b i l a t e r a l r e n a l a r t e r y stenosis

Left renal artery stenosis

F., aged 50 M. Left renal artery stenosis

~ T., aged 48 M. I

I

Right renal artery stenosis ,

W , aged 48 1 F Right renal artery I

stenosis 1

I ~~ .~ ~~ ~-

2051 I I0

2301

2301

50

50

2401 I50

2201 I20

~

Aortic reconstruction. Left nephrectomy. Right renal throni- bendarterectoniy

First operation. Left renal thrombendar-

i terectomy

Second opera t ion . Left nephrectoniy.

Three months after thrombendarterec- toniy

Right a o r t o - r e n a l t h r o ni be n d a r t e r - ectoniy

Right nephrectomy

I20/90

Initial droo.

Follow-up ' Period.

Three years I

-

... then rose to pre-operative I level

130/90 Nine months

I30/90 Twelve months

I50/90 Six months

RESULTS

A number of cases have been investigated and have either refused operation or have been thought unfit o r unsuitable for operation. Table I1 shows the results of four cases treated surgically, one of these patients requiring two operations. There has been no operative mortality or morbidity apart from one superficial wound infection. Although the follow-up periods are short in the last few cases the blood-pressure has fallen progressively during the weeks following operation, unlike the change sometimes seen i n hypertensive patients after non-specific surgery.

The lesion in the last patient was anatomically suitable for thrombendarterectomy, but frozen section biopsy of the kidney revealed such considerable atrophy that it was doubted whether it would regenerate. Nevertheless, this operation would have been done, with the possibility in mind of later nephrectomy should it have been unsuccessful, but the patient lived abroad and it was therefore felt that she should have the operation offering the highest chance of permanent success.

Thrombendarterectomy in the second patient was performed through the renal artery alone, and it is felt that the reason for subsequent thrombosis was the failure to open the aorta and remove a circle of intima around the renal arterial orifice. During the course of the operation on the third patient (T.) it was found that after removal of the renal atheroma there was an

Page 5: HYPERTENSION AND RENAL ARTERY DISEASE

418 B R I T I S H J O U R N A L O F U R O L O G Y

irregular fringe of aortic intima around the renal arterial orifice, and it is believed that the removal of this fringe is essential to the success of the operation.

Patients F. and T. are of interest in that they both presented with incapacitating eye changes of malignant hypertension, and they have both now returned to work with normal eyesight. Patient T. had considerable exudates and hamorrhages before operation, and these had almost completely resolved three months after operation.

SUMMARY

The diagnosis of renal artery stenosis as a cause of hypertension is discussed together with the results of operative treatment of four patients. Whatever the incidence of this lesion may be, it is of considerable importance in that its treatment offers the chance of survival from an otherwise incurable disease.

Indiscriminate surgery on the renal artery in patients with hypertension is likely to produce a crop of disappointing results, and it is felt that surgery should follow only a careful correlation of split renal function studies, renal arteriography, renal biopsy, and arterial pressure measurements. The use of these, and possibly additional methods of investigation, may not only reduce the chances of misdirected surgery, but may possibly give some clue as to the mechanism of renal hypertension.

It is thought that aorto-renal thrombendarterectomy is the most suitable operation available at present for the atheromatous juxta-aortic stenosis.

REFERENCES

DE CAMP, P. T. (1958). Sw.pnly, 43, 134. FREEMAN, N . E., LEEDS, F. H . , ELLIOTT, W. G., and ROLAND, S. 1. (1954). J. Auier. /ired. A s . , 156, 1077. GELLMAN, D. D. (1958). Qunvf. J . Med., 51, 103. GOLDBLATT, H., LYNCH, J . , HANZEL, R. F., and SUMMERVILL~, W. W. (1934). J. exp. Med., 59, 347. HOWARD, J . E., CONNOR. T. B., and THOMAS, W. C. (1956). Trans. Ass. Atner. Pbyriis., 69, 291.

POUTASSE, E. F. (1956). THOMPSON, J . E., and SMITHWICK, P. J . (1952). Aitgioloy-v, 3, 493.

MUELLER, c. B. , SURTSHIN, A,, CARLIN, M. R., and WHITE, H. L. (1951). Anlev. J. Physio/., 165, 41 1. Civculntioit, 13, 37.