British Journal of Urology ( I 976), 48, 41 9-425
0
Embolism in a Single Functioning Kidney: Report of Two Cases c. SELLI, D.
TURINI and G . BERNI
Institute of Urology, University of Florence and Santa Maria Nicova Hospital, Florence, Italy
Embolism in a single functioning kidney is a rare cause of acute renal failure due to vascular occlusion; reviewing the world literature in English we found only 1 1 cases. In the future its detection will probably become more frequent. Increasing reports of renal functional recovery after disobstructive surgery (Brest, Bower and Heider, 1964; Smithwick et a/., 1964; Baird, Yendt and Firor, 1965; Erskine and Blaisdell, 1965; Perkins et a/., 1967; Peterson and McDonald, 1968; Smith, Shapiro and Messner, 1968; Fergus, Jones and Thomas, 1969; Mundth, Shine and Austen, 1969; Thomas, Faulconer and Lansing, 1969; Birkenstock, Rabkin and Stables, 1972; Morton and Crawford, 1972; Quantock and Thatcher, 1972; Sheil et a/., 1973; Morgan el a/., 1974; Smith ct a/., 1974) and after medical anticoagulant therapy (Moyer r?a / . , 1973) have changed the attitude towards acute renal artery occlusion, which is no longer considered such a catastrophic event. This is valid even in the extreme case of a solitary kidney. Case Reports Case 1 A 72-year-old woman was admitted to the Urologic Clinic because of anuria which had developed 3 days earlier following left flank pain. 3 years previously she had undergone right nephrectomy for a large cyst. The patient had dso a rheumatic rnitral valve stenosis, with chronic atrial fibrillation. On admission her BUN was 1.8 nig %, WBC 24,000 and serum potassium 5.7 mEq/l. A retrograde pyelography did not show any obstruction. The patient \+;is treated by haemodialysis. A radioperthecnetate renal scan was later performed, demonstrating no uptake from the left kidney (Fig. 1). Finally, retrograde transfemoral aortography showed multiple translucent emboli in the left renal artery (Fig. 2). The patient was explored through a transverse transperitoneal approach. The aorta and the left renal artery were isolated and 2 longitudinal arteriotomies were performed, 1 on the left renal artery and the other on a major branch; 5 emboli were removed. After disobstruction good back bleeding was observed from the distal artery branches, which were irrigated with Ringer lactate solution, to which heparin was added, at a temperature o f 4°C. The longitudinal arteriotomies were closed transversely with 5-0 synthetic sutures to widen the vessel lumen. At the end of the procedure the kidney had resumed normal colour and good pulse could be palpated in the renal artery. Urinary output began on the 3rd day after operation, reaching a peak of 500 ml the 12th day. An average of 3 dialyses a week were necessary during the postoperative course (Fig. 3). A technetium scan performed 15 days after surgery demonstrated a good uptake from the left kidney (Fig. 1). Unfortunately the patient died 22 days after surgery with symptoms of cerebral embolism. Permission for autopsy was not granted. Case 2 A 72-year-old woman was admitted with left hemiparesis, hypotension and severe oliguria. She was known to have
rheumatic mitral valve stenosis and 1 year earlier had a femoral artery embolectomy. An aortography performed before that intervention had also shown complete left renal artery occlusion. At hospital admittance BUN was 0.54 mg %,, WBC 15,000and serum potassium 4.4 mEq/l. Anticoagulant therapy with sodium warfarine (Couniadine) WBS immediately begun, and a regimen of limited salt intake was started. Retrograde transfemoral aortography demonstrated an embolus inside a major branch of the right renal artery (Fig. 4). After a week the urinary output decreased to 50 ml/day, BUN raised to 1.19 mg/lO nil serum potassium to 6.5 mEq/l and serum creatinine was 6 mg/100 ml (Fig. 5 ) . I t seemed likely that more branches of the renal artery were obstructed by emboli arising from 419 ;I
4’0
BRITISH JOURNAL O F UROLOCiY
Fig. 2 Case I; retrograde translbmoral aortography: arrows indicate translucent emboli inside the Icft renal
artery.
Fig. I Case 1 ; perfusion radionuckie study with technetiuni-9Y M . Posterior view. 7on: Dreoperatively; poor perfusion ofthe left kidney. Boti;m: 1 5 days after surgery; improved perfusion of the left kidney. (Previous right
ncphrectomy.)
V ‘lJJ
5
1 (I
20
\
V 1
I
,,
.’
1,
Fig. 3 Case I,; changes i n B U N and urinc output d u r i n g
the preoperative and postopcrativc period.
the left atrium. Exchange-ion resins were given orally with the purpose of reducing serum potassium concentration. Because of the critical general condition the patient was considered a poor risk for surgery. She was therefore immediately haeniodialysed, and this treatment was repeated twice a week. Anticoagulant therapy was o f course continued, maintaining the prothrombin time in therapeutic range. In order to improve the urinary output and the renal blood How a single dose of I ,OOO mg of fruseinide was given intravenously. An IVP with tornography performed 3 months after her admission (Fig. 6) demonstrated a small right kidney (length 10 cm, width 4 cni) with an irregular outline, late opacification of the cavities and grouping of the calyces o n the upper pole. The right kidney surface. measured on the X-ray film, was calculated to be 30 sq cni while 3 months before it had been 63 sq cm. On her discharge from hospital the urinary output was ROO cc/day, B U N 0.80, serum creatinine 3.8 mg1100 ml, serum potassium 4.7 niEq/l.
Discussion
It is not rare to find renal infarction at autopsy (Hoxie and Coggin, 1940; Schoenbaum, Goldman and Siegelman, 1971) and some authors have pointed out that there is a discrepancy between
42 1
EMBOLISM IN A SINGLE FUNCTIONING KIDNEY
Fig. 4 (left). Case 2 ; retrograde transfemoral aortography : embolic occlusion of a major branch of the right renal artery. Fig. 5 (right). Case 2; changes in serum creatinine, B U N and urine output during hospitalisation.
1
1
b,(left). Case 2 ; IVP performed 3 months after renal artery embolisation: small.kidney with irregular outlines and grouping of the calyces on the upper pole. I;ig. 7 (right). Graphic showing the absence of correlation between the duration of preoperative anuria and the length 01' the recovery period in 16 cases of surgically treated renal artery occlusion.
422
BRITISH JOURNAL OF UR(II.OCY
these findings and the relatively scarce number of clinically recognised cases (Sullivan ul., 1972; Schramek et al., 1973). The presence of a single functioning kidney doubles the risk of damage, but makes easier the recognition of arterial obstruction, since the symptom of anuria or severe oliguria is constant. This finding, often associated with flank pain, stimulated towards a prompt angiographic investigation. Sometimes the symptoms of occlusion of other arteries are present at the same time ( c J . , ~ . neurologic disturbances, myocardial or mesenteric infarction). The patient’s history is of paramount importance, for it often reveals that there is functional absence of a kidney and the presence of a potential source of emboli, generally heart disease with fibrillation. Arteriography is by far the most accurate diagnostic tool in case of renal artery obstruction. Not only does it reveal the exact site of obstruction, but it has also a prognostic value, showing the development of a collateral circulation, or a certain amount of flow around the emboli. Both factors result in a nephrographic effect, which demonstrates the presence of viable renal parenchyma. In this case a functional recovery can reasonably be expected after embolectomy. However (Sproul, 1969; Lacombe, 1971) even angiographically silent kidneys can still be viable, and surgery may be effective. Until a few years ago it was believed, according to experimental studies, that acute renal artery occlusion caused irreversible lesions after a period of 90 min., in normothermic conditions (Kerr ct a/ . , 1960). If this were so, the problem would be of little clinical interest, since it would be very difficult to treat the patients in the short time interval. On the contrary a considerable amount of clinical reports and more recent experiments have increased our knowledge of the collateral circulation which is established even in the case of acute obstruction. Therefore acute vascular renal failure in man is an entity quite different from some experimental situations; as a matter of fact, reviewing the literature, we can observe that: 1. There is no correlation between the duration of preoperative anuria and the length of the recovery period, ranging from revascularisation to the return of the renal function (Fig. 7). 2 . In most cases a correlation can be demonstrated between the development of collateral circulation and the precocity of renal functional recovery. The collateral flow ensures to a part of the renal parenchyma a perfusion pressure of al least 15 mm/Hg. This pressure is sufficient for tissue survival, even if inadequate for thc filtration (Morris, Heider and Moyer, 1955). The collateral circulation development and extension depend mainly on the level of the obstruction and a more favourable result can be expected when the obstruction is situated near to the origin of the renal artery. Collateral flow in man originates mainly from the lumbar arteries and, to a lesser extent. f r o m the aorta directly, the gonadal, intercostal, adrenal and sometimes external iliac arteries (Abrams and Cornell, 1965). These collateral vessels communicate with 3 niajor systems: the capsular, peripelvic periureteric, through which a flow to the intrarenal arteries is established (Abrams and Cornell, 1965). In the case of renal artery embolism, reflex vasoconstriction produces a loss of the renal function (Lacombe, 1971; Schoenbaum, Goldman and Siegelman, 1971) but after a few days the spasm ceases and an opacification of the distal branches can be angiographically demonstrated. From our review of the I 1 cases of embolism to a single functioning kidney all except I were treated surgically and the functional recovery was observed in 7 cases out of 10 (Table). According to these figures we believe that surgical disobstruction is advisable whenever the general conditions allow it, though a severe cardiac disease, which is also the source of emholi, may sometimes contraindicate surgery.
423
EMBOLISM IN A SINGLE FUNCTIONING KIDNEY
Table Cases of Embolism in a Single Functioning Kidney Reference
Age
Sex
Side
73
R R
75 66 66 66
M F M F M F
Peterson (1968) 57 Smithwick (1964) 63
F F
R R
Schramek (1973) Sullivan (1972) Thomas (1969)
F F M
L L
Hrest (1964)
Goldsmith (1968) 62 Lacombe (1971) Kaiser (1951)
55 70
45
L
R R R
R
Treatment Embolectomy Embolectomy Embolectomy Embolectomy Embolectomy Supportive Medical Embolectomy Embolectomy Partial nephrectomy Embolectomy Embolectomy Embolectomy
Time interval between symptoms onset and treatment
Outcome
5 days 12 hours 4 days 5 days 9 days 5 days
Functional recovery Death Death Death Functional recovery Death
43 days 2 days
Functional recovery Functional recovery
18 hours 9 days 2 days
Functional recovery Functional recovery Functional recovery
In the case of embolism in a solitary kidney embolectomy is recommended when the main trunk of the renal artery is occluded; in this case all the kidney is in danger, and obviously every efTort must be made to save it. Modern dialysis techniques can help in equilibrating the patient’s condition before operating, especially when diagnosis is made after some days of anuria. Haemodialysis is of course vital in the postoperative period, supporting the patient until tubular ischaemic damage is repaired. When angiography demonstrates the occlusion of a distal branch and the general condition is poor, medical anticoagulant therapy is advisable (Lacombe, 197 I ). The efficiencyof local fibrinolytic treatment ceases a few hours after vascular occlusion and is therefore of little clinical advantage. Some diuretics (frusemide, ethacrynic acid) improve the cortical blood flow and can be useful i n reducing the ischaemic damage to the renal parenchyma (Birtch et al., 1967). “Blind” anticoagulant therapy before angiography is unacceptable, since it may complicate subsequent surgical treatment. Back bleeding after arterial disobstruction has a great prognostic value, since it proves an adequate collateral circulation. Another favourable sign is the presence of normal kidney colour afler embolectomy (Lacombe, 1971; Tse and Leberman, 1972; Schramek e l nl., 1973). Conclusions
We agree with some authors (Moyer et al., 1973) about adopting non-operative treatment initially but only as a means of improving the patient’s condition, thus reducing the risks of surgery. Even if it is demonstrated that the renal parenchyma remains viable after acute vascular occlusion, the ischaemic damage often progresses after some weeks and tends to become irreversible. Moreover repeated embolic extensions can cause rapid deterioration in the renal haemodynamic \ituation, as probably occurred in the second case that we reported. In the case of embolism in a single functioning kidney the whole renal function is very often at stake and an aggressive approach is more justified than when the presence of a normal contralateral organ prevents renal failure.
424
EMBOLISM IN A SINGLE FUNCTIONING KIDNEY
Summary
2 cases of embolism in single functioning kidneys are reported. In the first case there was an occlusion of the main trunk of the renal artery; the patient was treated by embolectomy. In the second case the occlusion of a major arterial branch was demonstrated; because of the bad general conditions the patient was treated with medical therapy. The authors review the literature and the indications for embolectomy in embolism in a solitary kidney. References ABRAMS, H. L. and CORNELL, S. H. (1965). Patterns of collateral flow in renal ischemia. Radiology, 84, 1001-1012. BAIRD,R. J., YENDT,E. R. and FIROR, W. B. (1965). Anuria due to acute occlusion of the artery to a solitary kidney. New England Journal of Medicine, 272, 1012-1014. BIRKENSTOCK, W. E., RABKIN, R. and STABLES, D. P. (1972). Bilateral traumatic renal artery occlusion with survival after late reconstitution of arterial flow. British Journal of Surgery, 59, 915-917. BIRTCH, A. G., ZAKHEIM, R. M., JONES, L. G. and BARGER, A. C. (1967). Redistribution of renal blood flow produced by furosemide and ethacrynic acid. Circulation Research, 21, 869-878. BREST,A. N., BOWER, R. and HEIDER, C. (1964). Renal functional recovery following anuria secondary to renal artery embolism. Journal of the American Medical Association, 187, 540-542. ERSKINE, J. M. and BLAISDELL, F. W. (1965). Acute bilateral renal artery occlusion in man. Archives of Surgery, 90, 247-252. FERGUS, J. N., JONES, N. F. and THOMAS, M. L. (1969). Kidney function after renal arterial embolism. Bririih Medical Journal, 4, 587-590. GOLDSMITH, E. I., FULLER, F. W., LABREW, C. T. and MARSHALL, V. F. (1968). Embolectomy of the renal artery. Journal of Urology, 99, 366-370. HOXIE,H. J. and COGGIN, C. B. (1940). Renal infarction: statistical study of 205 cases and detailed report of an unusual case. Archives of Internal Medicine, 65, 587-594. KAISER, T. F. and ROSS, R. R. (1951). Total infarction of the kidneys from bilateral arterial emboli. J ~ J ~ W N oJ’U I Urology, 66, 500-505. KERR,W. K., KYLE,V. N., KERESTECI, A. G . and SMYTHE, C. A. (1960). Renal hypothermia. Journal of Urolox)’, 84, 236-242. LACOMBE, M. (1971). The surgical treatment of renal artery embolism with anuria. Surgerjs, Gj’/7C’C.O/O~g.I’ urrtl Obstetrics, 133, 419-424. MORGAN, T., JOHNSTON, W., WILSON, M., CLUNIE, G. J. and GORDON, R. (1974). Restoration of rcnal function by arterial surgery. Lancer, 1, 653-656. MORRIS, G. C., HEIDER, C. F. and MOYER, J. G. (1955). Protective effect of subfiltration arterial pressure in kidney. Surgical Forum, 6, 623. MORTON, J. R. and CRAWFORD, E. S. (1972). Bilateral traumatic renal artery thrombosis. Anierican Surgwn. 176, 62. MOYER, J. O., RAO,C. N . , WIDRICH, W. C. and OLSSON,C. A. (1973). Conservative management of renal artery embolus. Journal of Urology. 109, 138-143. MUNDTH,E. D., SHINE, K. and AUSTEN, W. G . (1969). Correction of malignant hypertension and return of renal function following late renal arterial embolectomy. American Journal of Medicine, 46, 985-988. PERKINS, R. P., JACOBSEN, D. S., FEUER, F. P., LIPCHIK, E. 0. and FINE,P. H. (1967). Return of renal function after late embolectomy. New England Journal of’ Medicine, 276, 1194-1 195. PETERSON, N . E. and MCDONALD, D. F. (1968). Renal embolization. Journal o/ Urologj,, 100, 140-135. QUANTOCK, 0.P. and THATCHER, G . N. (1972). Reversible renal failure with renal artery occlusion. BtYliJh Mc,r/ic,~7/ Journal, 2, 27-28. SCHOENBAUM, S., GOLDMAN, M. A. and SIEGELMAN, S. (I 971). Renal arterial embolization. Angiology, 22, 331-343. SCHRAMEK, A., HASHMONAI, M., CHAIMOVITZ, C. and BETTER, 0. S. (1973). Survival following late renal cmbolectomy in a patient with a single functioning kidney. Journal ~f Urology, 109, 342-344. SHEIL,A. G. R., STOKES, G. S., TILLER, D. J., MAY,J., JOHNSON, J. R. and STEWART, J. H. (1973). Revcrsal of renal failure by revascularisation of kidneys with thrombosed renal arteries. Lancet, 2, 865-866. SMITH, H. T., SHAPIRO, F. L. and MESSNER, R. D. (1968). Anuria secondary to renovascular disease. Jorrrnol o / / l i e American Medical Association, 204, 176. SMITH, S. P., HAMBURGER, R. J., DONOHUE, J. P. and GRIM, C. E. (1974). Occlusion of the artery to a solitary kidney. Journal of’ the American Medical Association, 230, 1306-1307. SMITHWICK, R. H., NEWTON, R. C., CROCKER, D. H. and HARRISON, J. H. (1964). Surgical management of renal hypertension. American Journal of Surgery, 107, 104-120.
42 5
EMBOLISM IN A SINGLE FUNCTIONING KIDNEY
SPROUL,G . (1969). Total aortic occlusion with anuria: late embolectorny with survival. Journal of Urology, 102, 383-385. SULLIVAN, M. J., CRONIN, R., LACKNER, L. H. and EDWARDS,W. S. (1972). Embolization of a solitary kidney. Joirrnal of’ the American Medical Association, 222, 82-83. PtioMAs, T. V., FAULCONEII, H. T . and LANSING,A. M. (1969). Management of embolic occlusion of renal arteries. Siirgery, 65, 576-583. PSI., R. and LEBERMAN, P. R. (1972). Acute renal artery occlusion: etiology, diagnosis and treatment: report of a case with subsequent revascularization. Jortrrial of’ Urology, 108, 32-34.
The Authors C . Selli, Assistant, Institute of Urology. I).Turini, Assistant Professor, Institute of Urology. G . Berni, Assistant Professor, Santa Maria Nuova Hospital.
4816-C
0
Embolism in a Single Functioning Kidney: Report of Two Cases c. SELLI, D.
TURINI and G . BERNI
Institute of Urology, University of Florence and Santa Maria Nicova Hospital, Florence, Italy
Embolism in a single functioning kidney is a rare cause of acute renal failure due to vascular occlusion; reviewing the world literature in English we found only 1 1 cases. In the future its detection will probably become more frequent. Increasing reports of renal functional recovery after disobstructive surgery (Brest, Bower and Heider, 1964; Smithwick et a/., 1964; Baird, Yendt and Firor, 1965; Erskine and Blaisdell, 1965; Perkins et a/., 1967; Peterson and McDonald, 1968; Smith, Shapiro and Messner, 1968; Fergus, Jones and Thomas, 1969; Mundth, Shine and Austen, 1969; Thomas, Faulconer and Lansing, 1969; Birkenstock, Rabkin and Stables, 1972; Morton and Crawford, 1972; Quantock and Thatcher, 1972; Sheil et a/., 1973; Morgan el a/., 1974; Smith ct a/., 1974) and after medical anticoagulant therapy (Moyer r?a / . , 1973) have changed the attitude towards acute renal artery occlusion, which is no longer considered such a catastrophic event. This is valid even in the extreme case of a solitary kidney. Case Reports Case 1 A 72-year-old woman was admitted to the Urologic Clinic because of anuria which had developed 3 days earlier following left flank pain. 3 years previously she had undergone right nephrectomy for a large cyst. The patient had dso a rheumatic rnitral valve stenosis, with chronic atrial fibrillation. On admission her BUN was 1.8 nig %, WBC 24,000 and serum potassium 5.7 mEq/l. A retrograde pyelography did not show any obstruction. The patient \+;is treated by haemodialysis. A radioperthecnetate renal scan was later performed, demonstrating no uptake from the left kidney (Fig. 1). Finally, retrograde transfemoral aortography showed multiple translucent emboli in the left renal artery (Fig. 2). The patient was explored through a transverse transperitoneal approach. The aorta and the left renal artery were isolated and 2 longitudinal arteriotomies were performed, 1 on the left renal artery and the other on a major branch; 5 emboli were removed. After disobstruction good back bleeding was observed from the distal artery branches, which were irrigated with Ringer lactate solution, to which heparin was added, at a temperature o f 4°C. The longitudinal arteriotomies were closed transversely with 5-0 synthetic sutures to widen the vessel lumen. At the end of the procedure the kidney had resumed normal colour and good pulse could be palpated in the renal artery. Urinary output began on the 3rd day after operation, reaching a peak of 500 ml the 12th day. An average of 3 dialyses a week were necessary during the postoperative course (Fig. 3). A technetium scan performed 15 days after surgery demonstrated a good uptake from the left kidney (Fig. 1). Unfortunately the patient died 22 days after surgery with symptoms of cerebral embolism. Permission for autopsy was not granted. Case 2 A 72-year-old woman was admitted with left hemiparesis, hypotension and severe oliguria. She was known to have
rheumatic mitral valve stenosis and 1 year earlier had a femoral artery embolectomy. An aortography performed before that intervention had also shown complete left renal artery occlusion. At hospital admittance BUN was 0.54 mg %,, WBC 15,000and serum potassium 4.4 mEq/l. Anticoagulant therapy with sodium warfarine (Couniadine) WBS immediately begun, and a regimen of limited salt intake was started. Retrograde transfemoral aortography demonstrated an embolus inside a major branch of the right renal artery (Fig. 4). After a week the urinary output decreased to 50 ml/day, BUN raised to 1.19 mg/lO nil serum potassium to 6.5 mEq/l and serum creatinine was 6 mg/100 ml (Fig. 5 ) . I t seemed likely that more branches of the renal artery were obstructed by emboli arising from 419 ;I
4’0
BRITISH JOURNAL O F UROLOCiY
Fig. 2 Case I; retrograde translbmoral aortography: arrows indicate translucent emboli inside the Icft renal
artery.
Fig. I Case 1 ; perfusion radionuckie study with technetiuni-9Y M . Posterior view. 7on: Dreoperatively; poor perfusion ofthe left kidney. Boti;m: 1 5 days after surgery; improved perfusion of the left kidney. (Previous right
ncphrectomy.)
V ‘lJJ
5
1 (I
20
\
V 1
I
,,
.’
1,
Fig. 3 Case I,; changes i n B U N and urinc output d u r i n g
the preoperative and postopcrativc period.
the left atrium. Exchange-ion resins were given orally with the purpose of reducing serum potassium concentration. Because of the critical general condition the patient was considered a poor risk for surgery. She was therefore immediately haeniodialysed, and this treatment was repeated twice a week. Anticoagulant therapy was o f course continued, maintaining the prothrombin time in therapeutic range. In order to improve the urinary output and the renal blood How a single dose of I ,OOO mg of fruseinide was given intravenously. An IVP with tornography performed 3 months after her admission (Fig. 6) demonstrated a small right kidney (length 10 cm, width 4 cni) with an irregular outline, late opacification of the cavities and grouping of the calyces o n the upper pole. The right kidney surface. measured on the X-ray film, was calculated to be 30 sq cni while 3 months before it had been 63 sq cm. On her discharge from hospital the urinary output was ROO cc/day, B U N 0.80, serum creatinine 3.8 mg1100 ml, serum potassium 4.7 niEq/l.
Discussion
It is not rare to find renal infarction at autopsy (Hoxie and Coggin, 1940; Schoenbaum, Goldman and Siegelman, 1971) and some authors have pointed out that there is a discrepancy between
42 1
EMBOLISM IN A SINGLE FUNCTIONING KIDNEY
Fig. 4 (left). Case 2 ; retrograde transfemoral aortography : embolic occlusion of a major branch of the right renal artery. Fig. 5 (right). Case 2; changes in serum creatinine, B U N and urine output during hospitalisation.
1
1
b,(left). Case 2 ; IVP performed 3 months after renal artery embolisation: small.kidney with irregular outlines and grouping of the calyces on the upper pole. I;ig. 7 (right). Graphic showing the absence of correlation between the duration of preoperative anuria and the length 01' the recovery period in 16 cases of surgically treated renal artery occlusion.
422
BRITISH JOURNAL OF UR(II.OCY
these findings and the relatively scarce number of clinically recognised cases (Sullivan ul., 1972; Schramek et al., 1973). The presence of a single functioning kidney doubles the risk of damage, but makes easier the recognition of arterial obstruction, since the symptom of anuria or severe oliguria is constant. This finding, often associated with flank pain, stimulated towards a prompt angiographic investigation. Sometimes the symptoms of occlusion of other arteries are present at the same time ( c J . , ~ . neurologic disturbances, myocardial or mesenteric infarction). The patient’s history is of paramount importance, for it often reveals that there is functional absence of a kidney and the presence of a potential source of emboli, generally heart disease with fibrillation. Arteriography is by far the most accurate diagnostic tool in case of renal artery obstruction. Not only does it reveal the exact site of obstruction, but it has also a prognostic value, showing the development of a collateral circulation, or a certain amount of flow around the emboli. Both factors result in a nephrographic effect, which demonstrates the presence of viable renal parenchyma. In this case a functional recovery can reasonably be expected after embolectomy. However (Sproul, 1969; Lacombe, 1971) even angiographically silent kidneys can still be viable, and surgery may be effective. Until a few years ago it was believed, according to experimental studies, that acute renal artery occlusion caused irreversible lesions after a period of 90 min., in normothermic conditions (Kerr ct a/ . , 1960). If this were so, the problem would be of little clinical interest, since it would be very difficult to treat the patients in the short time interval. On the contrary a considerable amount of clinical reports and more recent experiments have increased our knowledge of the collateral circulation which is established even in the case of acute obstruction. Therefore acute vascular renal failure in man is an entity quite different from some experimental situations; as a matter of fact, reviewing the literature, we can observe that: 1. There is no correlation between the duration of preoperative anuria and the length of the recovery period, ranging from revascularisation to the return of the renal function (Fig. 7). 2 . In most cases a correlation can be demonstrated between the development of collateral circulation and the precocity of renal functional recovery. The collateral flow ensures to a part of the renal parenchyma a perfusion pressure of al least 15 mm/Hg. This pressure is sufficient for tissue survival, even if inadequate for thc filtration (Morris, Heider and Moyer, 1955). The collateral circulation development and extension depend mainly on the level of the obstruction and a more favourable result can be expected when the obstruction is situated near to the origin of the renal artery. Collateral flow in man originates mainly from the lumbar arteries and, to a lesser extent. f r o m the aorta directly, the gonadal, intercostal, adrenal and sometimes external iliac arteries (Abrams and Cornell, 1965). These collateral vessels communicate with 3 niajor systems: the capsular, peripelvic periureteric, through which a flow to the intrarenal arteries is established (Abrams and Cornell, 1965). In the case of renal artery embolism, reflex vasoconstriction produces a loss of the renal function (Lacombe, 1971; Schoenbaum, Goldman and Siegelman, 1971) but after a few days the spasm ceases and an opacification of the distal branches can be angiographically demonstrated. From our review of the I 1 cases of embolism to a single functioning kidney all except I were treated surgically and the functional recovery was observed in 7 cases out of 10 (Table). According to these figures we believe that surgical disobstruction is advisable whenever the general conditions allow it, though a severe cardiac disease, which is also the source of emholi, may sometimes contraindicate surgery.
423
EMBOLISM IN A SINGLE FUNCTIONING KIDNEY
Table Cases of Embolism in a Single Functioning Kidney Reference
Age
Sex
Side
73
R R
75 66 66 66
M F M F M F
Peterson (1968) 57 Smithwick (1964) 63
F F
R R
Schramek (1973) Sullivan (1972) Thomas (1969)
F F M
L L
Hrest (1964)
Goldsmith (1968) 62 Lacombe (1971) Kaiser (1951)
55 70
45
L
R R R
R
Treatment Embolectomy Embolectomy Embolectomy Embolectomy Embolectomy Supportive Medical Embolectomy Embolectomy Partial nephrectomy Embolectomy Embolectomy Embolectomy
Time interval between symptoms onset and treatment
Outcome
5 days 12 hours 4 days 5 days 9 days 5 days
Functional recovery Death Death Death Functional recovery Death
43 days 2 days
Functional recovery Functional recovery
18 hours 9 days 2 days
Functional recovery Functional recovery Functional recovery
In the case of embolism in a solitary kidney embolectomy is recommended when the main trunk of the renal artery is occluded; in this case all the kidney is in danger, and obviously every efTort must be made to save it. Modern dialysis techniques can help in equilibrating the patient’s condition before operating, especially when diagnosis is made after some days of anuria. Haemodialysis is of course vital in the postoperative period, supporting the patient until tubular ischaemic damage is repaired. When angiography demonstrates the occlusion of a distal branch and the general condition is poor, medical anticoagulant therapy is advisable (Lacombe, 197 I ). The efficiencyof local fibrinolytic treatment ceases a few hours after vascular occlusion and is therefore of little clinical advantage. Some diuretics (frusemide, ethacrynic acid) improve the cortical blood flow and can be useful i n reducing the ischaemic damage to the renal parenchyma (Birtch et al., 1967). “Blind” anticoagulant therapy before angiography is unacceptable, since it may complicate subsequent surgical treatment. Back bleeding after arterial disobstruction has a great prognostic value, since it proves an adequate collateral circulation. Another favourable sign is the presence of normal kidney colour afler embolectomy (Lacombe, 1971; Tse and Leberman, 1972; Schramek e l nl., 1973). Conclusions
We agree with some authors (Moyer et al., 1973) about adopting non-operative treatment initially but only as a means of improving the patient’s condition, thus reducing the risks of surgery. Even if it is demonstrated that the renal parenchyma remains viable after acute vascular occlusion, the ischaemic damage often progresses after some weeks and tends to become irreversible. Moreover repeated embolic extensions can cause rapid deterioration in the renal haemodynamic \ituation, as probably occurred in the second case that we reported. In the case of embolism in a single functioning kidney the whole renal function is very often at stake and an aggressive approach is more justified than when the presence of a normal contralateral organ prevents renal failure.
424
EMBOLISM IN A SINGLE FUNCTIONING KIDNEY
Summary
2 cases of embolism in single functioning kidneys are reported. In the first case there was an occlusion of the main trunk of the renal artery; the patient was treated by embolectomy. In the second case the occlusion of a major arterial branch was demonstrated; because of the bad general conditions the patient was treated with medical therapy. The authors review the literature and the indications for embolectomy in embolism in a solitary kidney. References ABRAMS, H. L. and CORNELL, S. H. (1965). Patterns of collateral flow in renal ischemia. Radiology, 84, 1001-1012. BAIRD,R. J., YENDT,E. R. and FIROR, W. B. (1965). Anuria due to acute occlusion of the artery to a solitary kidney. New England Journal of Medicine, 272, 1012-1014. BIRKENSTOCK, W. E., RABKIN, R. and STABLES, D. P. (1972). Bilateral traumatic renal artery occlusion with survival after late reconstitution of arterial flow. British Journal of Surgery, 59, 915-917. BIRTCH, A. G., ZAKHEIM, R. M., JONES, L. G. and BARGER, A. C. (1967). Redistribution of renal blood flow produced by furosemide and ethacrynic acid. Circulation Research, 21, 869-878. BREST,A. N., BOWER, R. and HEIDER, C. (1964). Renal functional recovery following anuria secondary to renal artery embolism. Journal of the American Medical Association, 187, 540-542. ERSKINE, J. M. and BLAISDELL, F. W. (1965). Acute bilateral renal artery occlusion in man. Archives of Surgery, 90, 247-252. FERGUS, J. N., JONES, N. F. and THOMAS, M. L. (1969). Kidney function after renal arterial embolism. Bririih Medical Journal, 4, 587-590. GOLDSMITH, E. I., FULLER, F. W., LABREW, C. T. and MARSHALL, V. F. (1968). Embolectomy of the renal artery. Journal of Urology, 99, 366-370. HOXIE,H. J. and COGGIN, C. B. (1940). Renal infarction: statistical study of 205 cases and detailed report of an unusual case. Archives of Internal Medicine, 65, 587-594. KAISER, T. F. and ROSS, R. R. (1951). Total infarction of the kidneys from bilateral arterial emboli. J ~ J ~ W N oJ’U I Urology, 66, 500-505. KERR,W. K., KYLE,V. N., KERESTECI, A. G . and SMYTHE, C. A. (1960). Renal hypothermia. Journal of Urolox)’, 84, 236-242. LACOMBE, M. (1971). The surgical treatment of renal artery embolism with anuria. Surgerjs, Gj’/7C’C.O/O~g.I’ urrtl Obstetrics, 133, 419-424. MORGAN, T., JOHNSTON, W., WILSON, M., CLUNIE, G. J. and GORDON, R. (1974). Restoration of rcnal function by arterial surgery. Lancer, 1, 653-656. MORRIS, G. C., HEIDER, C. F. and MOYER, J. G. (1955). Protective effect of subfiltration arterial pressure in kidney. Surgical Forum, 6, 623. MORTON, J. R. and CRAWFORD, E. S. (1972). Bilateral traumatic renal artery thrombosis. Anierican Surgwn. 176, 62. MOYER, J. O., RAO,C. N . , WIDRICH, W. C. and OLSSON,C. A. (1973). Conservative management of renal artery embolus. Journal of Urology. 109, 138-143. MUNDTH,E. D., SHINE, K. and AUSTEN, W. G . (1969). Correction of malignant hypertension and return of renal function following late renal arterial embolectomy. American Journal of Medicine, 46, 985-988. PERKINS, R. P., JACOBSEN, D. S., FEUER, F. P., LIPCHIK, E. 0. and FINE,P. H. (1967). Return of renal function after late embolectomy. New England Journal of’ Medicine, 276, 1194-1 195. PETERSON, N . E. and MCDONALD, D. F. (1968). Renal embolization. Journal o/ Urologj,, 100, 140-135. QUANTOCK, 0.P. and THATCHER, G . N. (1972). Reversible renal failure with renal artery occlusion. BtYliJh Mc,r/ic,~7/ Journal, 2, 27-28. SCHOENBAUM, S., GOLDMAN, M. A. and SIEGELMAN, S. (I 971). Renal arterial embolization. Angiology, 22, 331-343. SCHRAMEK, A., HASHMONAI, M., CHAIMOVITZ, C. and BETTER, 0. S. (1973). Survival following late renal cmbolectomy in a patient with a single functioning kidney. Journal ~f Urology, 109, 342-344. SHEIL,A. G. R., STOKES, G. S., TILLER, D. J., MAY,J., JOHNSON, J. R. and STEWART, J. H. (1973). Revcrsal of renal failure by revascularisation of kidneys with thrombosed renal arteries. Lancet, 2, 865-866. SMITH, H. T., SHAPIRO, F. L. and MESSNER, R. D. (1968). Anuria secondary to renovascular disease. Jorrrnol o / / l i e American Medical Association, 204, 176. SMITH, S. P., HAMBURGER, R. J., DONOHUE, J. P. and GRIM, C. E. (1974). Occlusion of the artery to a solitary kidney. Journal of’ the American Medical Association, 230, 1306-1307. SMITHWICK, R. H., NEWTON, R. C., CROCKER, D. H. and HARRISON, J. H. (1964). Surgical management of renal hypertension. American Journal of Surgery, 107, 104-120.
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EMBOLISM IN A SINGLE FUNCTIONING KIDNEY
SPROUL,G . (1969). Total aortic occlusion with anuria: late embolectorny with survival. Journal of Urology, 102, 383-385. SULLIVAN, M. J., CRONIN, R., LACKNER, L. H. and EDWARDS,W. S. (1972). Embolization of a solitary kidney. Joirrnal of’ the American Medical Association, 222, 82-83. PtioMAs, T. V., FAULCONEII, H. T . and LANSING,A. M. (1969). Management of embolic occlusion of renal arteries. Siirgery, 65, 576-583. PSI., R. and LEBERMAN, P. R. (1972). Acute renal artery occlusion: etiology, diagnosis and treatment: report of a case with subsequent revascularization. Jortrrial of’ Urology, 108, 32-34.
The Authors C . Selli, Assistant, Institute of Urology. I).Turini, Assistant Professor, Institute of Urology. G . Berni, Assistant Professor, Santa Maria Nuova Hospital.
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