Acute Anuria Secondary to Renal Artery Stenosis JAMES M. THOMAS, M.D., WILLIAM W. PFAFF, M.D.*
From the Department of Surgery, College of Medicine, University of Florida, Gainesville, Florida
Three patients with acute onset of anuria secondary to renal malperfusion were successfully treated by revascularization. Twelve such patients have previously been reported. The role of surgery for prophylaxis in stenosing renal artery disease is advocated.
DIMINUTION in renal perfusion is associated with the appearance of systemic hypertension which can be reversed by re-establishing flow to the affected organ. Severe malperfusion or total arterial occlusion leads to irreversible ischemic injury, renal atrophy or infarction. Intermediate levels of malperfusion have been demonstrated experimentally wherein viability may be maintained even though function may cease.7 In clinical confirmation, several reviews5'9'11 have described the return of function in the acutely anuric patient following renal revascularization. Smith et al. 12 reported the twelfth and most recent case in 1974. Three such patients have been encountered and are the basis of the present report.
Case Reports A 51-year-old man was referred to the Shands Teaching Hospital, University of Florida, with a three-year history of hypertension. Peripheral renin activity was 5.3 ng/ml (normal 1.0-2.8 ng/ml), serum creatinine was 2.5 mg%o and endogenous creatinine clearance was 37 ml/min. Arteriography showed complete occlusion of the left renal artery with an atrophic left kidney perfused by collaterals. The right renal artery was partially occluded (Fig. 1) and the left common iliac artery was completely occluded. A left nephrectomy was performed. Five weeks after surgery he was seen in the Emergency Room; he had a 24-hour history of anuria. Blood urea nitrogen was 81 mg%o and serum creatinine was 6.5 mg%o. Emergency aortogram demonstrated further narrowing of the right renal artery (Fig. 2). A small amount of contrast was seen to traverse the stenotic segment, but opacification of the distal artery was slight. No collateral vessels were identified. Aortorenal bypass with reversed saphenous vein graft was performed (Fig. 3), with prompt resumption of urine production. He was discharged on the eighth postoperative day with a serum creatinine of 1.5 mg%o and a creatinine clearance of 76 ml/min. After 4 years, his creatinine was 1.3 mg%o and the clearance 76 ml/min.
Submitted for publication September 26, 1975. Reprint requests: William W. Pfaff, M.D., Department of Surgery, College of Medicine, University of Florida, Gainesville, Florida 32610
A 63-year-old female, when seen by her local physician, had a twoweek history of headache and was found to have a blood pressure of 210/110. Her creatinine clearance was 80 ml/min. Arteriography showed extensive atherosclerotic changes of the infra-renal aorta with near complete occlusion of the left renal artery, and mild stenosis of the right. She was transferred to the Shands Teaching Hospital, University of Florida, where differential function study showed no urine production by the left kidney. Renal vein renin activity was 10.3 ,ug/ml on the right and 15.3 ,ug/ml on the left. A left nephrectomy was performed with immediate fall in pressure to 140/80. On the fourth postoperative day, it was discovered that she had been anuric for over 12 hours. An emergency aortogram demonstrated total occlusion of the right renal artery with no discernible perfusion of the kidney. Reversed saphenous vein aortorenal bypass graft was completed after approximately 18 hours of total arterial occlusion. After a period of oliguria immediately after surgery, urine output improved and 3 weeks later she was discharged with a serum creatinine of 5 mg% and a creatinine clearance of 12 ml/min.3 Five months after revascularization, her serum creatinine was 3.7 mg%o with a clearance of 17 ml/min. In the interim she had developed rapidly enlarging subcutaneous masses on both thighs. Biopsy diagnosis was malignant mesenchymoma. An 84-year-old man was admitted to the Gainesville Veterans Administration Hospital with a one-month history of gross hematuria. After the right kidney failed to visualize on IVP, an aortogram was performed. Severe aortic atherosclerosis was seen, with marked stenosis at the origin of the left renal artery (Fig. 4). The right kidney and right renal artery were not identified. Blood urea nitrogen was 17 mgo. No further urinary tract anomalies could be found other than outlet obstruction secondary to prostatic hypertrophy, and a transurethral resection was performed. Four months later he returned with a 36-hour history of anuria. Aortography shoed progression of the renal artery stenosis (Fig. 5) with diminished flow in the distal artery. Emergency aortorenal bypass with reversed saphenous vein was performed. The right kidney was not palpable. A carcinoma of the sigmoid colon was found and was resected at a later operation. Two days after revascularization the serum creatinine was 8.7 mgo and the creatinine clearance 0.8 ml/min. After one month, creatinine was 2.6 mg%o and clearance 17 ml/min. He was discharged after two months with a serum creatinine of 2.3 mg%o and was doing well when last seen in the clinic 12 months after surgery.
293
294
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THOMAS AND PFAFF
Ann. Surg.
9
March 1976
tion of the kidney can improve function in selected patients.3'6'8 There is also evidence that renal revascularization for hypertension can be associated with functional improvement, although Simon and del Greco10 have shown that the revascularized kidney may improve at the expense of the contralateral kidney. The projected success for renovascular surgery depends not only on the accessiblity of the lesion, but also on the arhount of functional tissue distal to the lesion. Kaufman4 expressed doubt that a serum creatinine chronically greater than 4 mgo would be caused only by a central and thereby surgically-accessible lesion. Schiel et al.8 and others have pointed out that the compromised kidney might be protected by the obstructing lesion from the damaging effects of the resultant and associated hypertension, but peripheral emboli from a central atheromatous lesion have been shown to produce renal failure as well,2 indicating that the ipsilateral kidney is also at risk. The problem at present is that of selecting patients for operative management of existing or potential renal failure secondary to vascular compromise. Clearly the acute onset of anuria attributable to renal malperfusion is an opportunity for timely surgery. In almost all such instances however, anuria will occur only after FIG. 1. Patient 1. Initial aortogram demonstrating near total occlusion of left renal artery, marked stenosis of right renal artery at its origin. Hepatic and splenic arteries are opacified superior to renals.
Discussion Of the three patients described, only the second experienced total renal arterial occlusion, possibly the consequence of reduced pressure and flow through an abnormal right renal artery during a postoperative period of hypercoagulability. The first and third patients demonstrate a phenomenon of critical arterial stenosis, the vessel narrowed to a degree that pressure distal to the stenosis was insufficient for glomerular filtration, but viability was maintained. All three patients resumed renal function, the first patient at near normal levels. Renal arterial stenosis is thought to have little effect on organ perfusion unless the luminal diameter is reduced by approximately 70%.1 Beyond that point, a narrow spectrum of anatomic progression may be associated with a wide spectrum of functional distortion. Moderate diminution in renal perfusion may produce hypertension with minimal change in fuction, while more marked narrowing of the vessel may result in severe malperfusion resulting in initially reversible, then irreversible loss of function. Over this narrow anatomic range, it would appear that graded alterations in perfusion might produce corresponding alterations in function. Several authors have in fact shown that revasculariza-
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present. Progressive stenosis of right renal artery without total clusion.
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ANURIA SECONDARY TO RENAL ARTERY STENOSIS
Vol. 183 . No. 3
295 ..ir
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FIG. 5. Patient 3. Progressive stenosis of left renal artery, nephrogram longer evident.
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FIG. 3. Patient I after aortorenal bypass. Graft is patent and well filled, good nephrogram and pyelogram are demonstrated.
sive nature of occlusive vascular disease, granting variability, the presence of significant vascular lesions of the renal artery is in and of itself an indication for revascularization to preserve renal function. Certainly the lesion must be considered in the context of other elements noted in the individual patient, but to delay revascularization until renal dysfunction appears is to needlessly sacrifice significant renal mass.
References earlier infarction or resection of one kidney, and the former is generally an insidious event, perhaps associated with hypertension but unheralded by local or systemic symptoms. Similar progression of vascular occlusive disease in the remaining kidney may occur acutely, as herein reported, or gradually, but in either instance is an overwhelming threat to life. In view of the progres-
1. Berguer. R. and Hwang, N. H. P.: Critical Arterial Stenosis: A Theoretical and Experimental Solution. Ann. Surg., 180:39, 1974. 2. Dalakos, T. G., Streeten, D. H. P.. Jones, D. and Obeid, A.: Malignant Hypertension Resulting from Atheromatous Embolization Predominantly of One Kidney. Am. J. Med., 57: 135, 1974. 3. Kaufman. J. J.: Renal Artery Stenosis and Azotemia. Surg. Gynecol. Obstet., 137:949, 1973. 4. Kaufman, J. J.: Renal Artery Stenosis and Azotemia: Does Correction of Renovascular Hypertension Improve Renal Function? Trans. Am. Assoc. Genitourin. Surg.. 65:12. 1973. 5. Loomis, R. C., Ocher, J. N., Jr. and Hodges, C. V.: Dynamic Treatment of Renal Artery Embolism: A Case Report and Review of the Literature. J. Urol., 96:131, 1966. 6. Morgan, T., Wilson, M., Johnston, W., et al.: Restoration of Renal Function by Arterial Surgery. Lancet, 1:653, 1974. 7. Morris, G. C., Jr., Heider, C. and Moyer, J. H.: The Protective Effect of Subfiltration Arterial Pressure on the Kidney. Surg. Forum, 5:623, 1956. 8. Schiel, A. G. R., May, J., Stokes. G. S.. et al.: Reversal of Renal Failure by Revascularisation of Kidneys with Thrombosed Renal Arteries. Lancet, 2:865, 1973. 9. Schranck, A., Hashmonai, M., Chaimovitz, C. and Bette. 0. S.: Survival Following Late Renal Embolectomy in Patient With a Single Functioning Kidney. J. Urol., 109:342. 1973. 10. Simon, N. M. and delGreco, F.: Kidney Function after Renal Devascularization for Hypertension. Circulation, 29:376. 1964. 11. Smith, H. T., Shapiro, F. L. and Messner, R. P.: Anuria Secondary to Renal Vascular Disease. JAMA. 204:928, 1968. 12. Smith, S. P.. Jr., Hamburger, R. J., Donahue, J. P. and Grim. C. E.: Occlusion of the Artery to a Solitary Kidney. JAMA. 230:1306, 1974. a
FIG. 4. Patient 3. Initial aortogram. The right renal artery is not demonstrated. There is marked stenosis of the proximal left renal artery but
nephrogram is present.
From the Department of Surgery, College of Medicine, University of Florida, Gainesville, Florida
Three patients with acute onset of anuria secondary to renal malperfusion were successfully treated by revascularization. Twelve such patients have previously been reported. The role of surgery for prophylaxis in stenosing renal artery disease is advocated.
DIMINUTION in renal perfusion is associated with the appearance of systemic hypertension which can be reversed by re-establishing flow to the affected organ. Severe malperfusion or total arterial occlusion leads to irreversible ischemic injury, renal atrophy or infarction. Intermediate levels of malperfusion have been demonstrated experimentally wherein viability may be maintained even though function may cease.7 In clinical confirmation, several reviews5'9'11 have described the return of function in the acutely anuric patient following renal revascularization. Smith et al. 12 reported the twelfth and most recent case in 1974. Three such patients have been encountered and are the basis of the present report.
Case Reports A 51-year-old man was referred to the Shands Teaching Hospital, University of Florida, with a three-year history of hypertension. Peripheral renin activity was 5.3 ng/ml (normal 1.0-2.8 ng/ml), serum creatinine was 2.5 mg%o and endogenous creatinine clearance was 37 ml/min. Arteriography showed complete occlusion of the left renal artery with an atrophic left kidney perfused by collaterals. The right renal artery was partially occluded (Fig. 1) and the left common iliac artery was completely occluded. A left nephrectomy was performed. Five weeks after surgery he was seen in the Emergency Room; he had a 24-hour history of anuria. Blood urea nitrogen was 81 mg%o and serum creatinine was 6.5 mg%o. Emergency aortogram demonstrated further narrowing of the right renal artery (Fig. 2). A small amount of contrast was seen to traverse the stenotic segment, but opacification of the distal artery was slight. No collateral vessels were identified. Aortorenal bypass with reversed saphenous vein graft was performed (Fig. 3), with prompt resumption of urine production. He was discharged on the eighth postoperative day with a serum creatinine of 1.5 mg%o and a creatinine clearance of 76 ml/min. After 4 years, his creatinine was 1.3 mg%o and the clearance 76 ml/min.
Submitted for publication September 26, 1975. Reprint requests: William W. Pfaff, M.D., Department of Surgery, College of Medicine, University of Florida, Gainesville, Florida 32610
A 63-year-old female, when seen by her local physician, had a twoweek history of headache and was found to have a blood pressure of 210/110. Her creatinine clearance was 80 ml/min. Arteriography showed extensive atherosclerotic changes of the infra-renal aorta with near complete occlusion of the left renal artery, and mild stenosis of the right. She was transferred to the Shands Teaching Hospital, University of Florida, where differential function study showed no urine production by the left kidney. Renal vein renin activity was 10.3 ,ug/ml on the right and 15.3 ,ug/ml on the left. A left nephrectomy was performed with immediate fall in pressure to 140/80. On the fourth postoperative day, it was discovered that she had been anuric for over 12 hours. An emergency aortogram demonstrated total occlusion of the right renal artery with no discernible perfusion of the kidney. Reversed saphenous vein aortorenal bypass graft was completed after approximately 18 hours of total arterial occlusion. After a period of oliguria immediately after surgery, urine output improved and 3 weeks later she was discharged with a serum creatinine of 5 mg% and a creatinine clearance of 12 ml/min.3 Five months after revascularization, her serum creatinine was 3.7 mg%o with a clearance of 17 ml/min. In the interim she had developed rapidly enlarging subcutaneous masses on both thighs. Biopsy diagnosis was malignant mesenchymoma. An 84-year-old man was admitted to the Gainesville Veterans Administration Hospital with a one-month history of gross hematuria. After the right kidney failed to visualize on IVP, an aortogram was performed. Severe aortic atherosclerosis was seen, with marked stenosis at the origin of the left renal artery (Fig. 4). The right kidney and right renal artery were not identified. Blood urea nitrogen was 17 mgo. No further urinary tract anomalies could be found other than outlet obstruction secondary to prostatic hypertrophy, and a transurethral resection was performed. Four months later he returned with a 36-hour history of anuria. Aortography shoed progression of the renal artery stenosis (Fig. 5) with diminished flow in the distal artery. Emergency aortorenal bypass with reversed saphenous vein was performed. The right kidney was not palpable. A carcinoma of the sigmoid colon was found and was resected at a later operation. Two days after revascularization the serum creatinine was 8.7 mgo and the creatinine clearance 0.8 ml/min. After one month, creatinine was 2.6 mg%o and clearance 17 ml/min. He was discharged after two months with a serum creatinine of 2.3 mg%o and was doing well when last seen in the clinic 12 months after surgery.
293
294
-':~ .}e1
THOMAS AND PFAFF
Ann. Surg.
9
March 1976
tion of the kidney can improve function in selected patients.3'6'8 There is also evidence that renal revascularization for hypertension can be associated with functional improvement, although Simon and del Greco10 have shown that the revascularized kidney may improve at the expense of the contralateral kidney. The projected success for renovascular surgery depends not only on the accessiblity of the lesion, but also on the arhount of functional tissue distal to the lesion. Kaufman4 expressed doubt that a serum creatinine chronically greater than 4 mgo would be caused only by a central and thereby surgically-accessible lesion. Schiel et al.8 and others have pointed out that the compromised kidney might be protected by the obstructing lesion from the damaging effects of the resultant and associated hypertension, but peripheral emboli from a central atheromatous lesion have been shown to produce renal failure as well,2 indicating that the ipsilateral kidney is also at risk. The problem at present is that of selecting patients for operative management of existing or potential renal failure secondary to vascular compromise. Clearly the acute onset of anuria attributable to renal malperfusion is an opportunity for timely surgery. In almost all such instances however, anuria will occur only after FIG. 1. Patient 1. Initial aortogram demonstrating near total occlusion of left renal artery, marked stenosis of right renal artery at its origin. Hepatic and splenic arteries are opacified superior to renals.
Discussion Of the three patients described, only the second experienced total renal arterial occlusion, possibly the consequence of reduced pressure and flow through an abnormal right renal artery during a postoperative period of hypercoagulability. The first and third patients demonstrate a phenomenon of critical arterial stenosis, the vessel narrowed to a degree that pressure distal to the stenosis was insufficient for glomerular filtration, but viability was maintained. All three patients resumed renal function, the first patient at near normal levels. Renal arterial stenosis is thought to have little effect on organ perfusion unless the luminal diameter is reduced by approximately 70%.1 Beyond that point, a narrow spectrum of anatomic progression may be associated with a wide spectrum of functional distortion. Moderate diminution in renal perfusion may produce hypertension with minimal change in fuction, while more marked narrowing of the vessel may result in severe malperfusion resulting in initially reversible, then irreversible loss of function. Over this narrow anatomic range, it would appear that graded alterations in perfusion might produce corresponding alterations in function. Several authors have in fact shown that revasculariza-
renalarr..............
_mee sk
a, ..............X~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~... .....
.....~~~~~~~~~~~~~~~~~~~~.
.........
present. Progressive stenosis of right renal artery without total clusion.
oc-
.. :,*ei,: .: :
ANURIA SECONDARY TO RENAL ARTERY STENOSIS
Vol. 183 . No. 3
295 ..ir
.: :.: .::
., ;*'.' 4.U': .: ,£
L .:
:0,'fl' .: ::^.
FIG. 5. Patient 3. Progressive stenosis of left renal artery, nephrogram longer evident.
no
FIG. 3. Patient I after aortorenal bypass. Graft is patent and well filled, good nephrogram and pyelogram are demonstrated.
sive nature of occlusive vascular disease, granting variability, the presence of significant vascular lesions of the renal artery is in and of itself an indication for revascularization to preserve renal function. Certainly the lesion must be considered in the context of other elements noted in the individual patient, but to delay revascularization until renal dysfunction appears is to needlessly sacrifice significant renal mass.
References earlier infarction or resection of one kidney, and the former is generally an insidious event, perhaps associated with hypertension but unheralded by local or systemic symptoms. Similar progression of vascular occlusive disease in the remaining kidney may occur acutely, as herein reported, or gradually, but in either instance is an overwhelming threat to life. In view of the progres-
1. Berguer. R. and Hwang, N. H. P.: Critical Arterial Stenosis: A Theoretical and Experimental Solution. Ann. Surg., 180:39, 1974. 2. Dalakos, T. G., Streeten, D. H. P.. Jones, D. and Obeid, A.: Malignant Hypertension Resulting from Atheromatous Embolization Predominantly of One Kidney. Am. J. Med., 57: 135, 1974. 3. Kaufman. J. J.: Renal Artery Stenosis and Azotemia. Surg. Gynecol. Obstet., 137:949, 1973. 4. Kaufman, J. J.: Renal Artery Stenosis and Azotemia: Does Correction of Renovascular Hypertension Improve Renal Function? Trans. Am. Assoc. Genitourin. Surg.. 65:12. 1973. 5. Loomis, R. C., Ocher, J. N., Jr. and Hodges, C. V.: Dynamic Treatment of Renal Artery Embolism: A Case Report and Review of the Literature. J. Urol., 96:131, 1966. 6. Morgan, T., Wilson, M., Johnston, W., et al.: Restoration of Renal Function by Arterial Surgery. Lancet, 1:653, 1974. 7. Morris, G. C., Jr., Heider, C. and Moyer, J. H.: The Protective Effect of Subfiltration Arterial Pressure on the Kidney. Surg. Forum, 5:623, 1956. 8. Schiel, A. G. R., May, J., Stokes. G. S.. et al.: Reversal of Renal Failure by Revascularisation of Kidneys with Thrombosed Renal Arteries. Lancet, 2:865, 1973. 9. Schranck, A., Hashmonai, M., Chaimovitz, C. and Bette. 0. S.: Survival Following Late Renal Embolectomy in Patient With a Single Functioning Kidney. J. Urol., 109:342. 1973. 10. Simon, N. M. and delGreco, F.: Kidney Function after Renal Devascularization for Hypertension. Circulation, 29:376. 1964. 11. Smith, H. T., Shapiro, F. L. and Messner, R. P.: Anuria Secondary to Renal Vascular Disease. JAMA. 204:928, 1968. 12. Smith, S. P.. Jr., Hamburger, R. J., Donahue, J. P. and Grim. C. E.: Occlusion of the Artery to a Solitary Kidney. JAMA. 230:1306, 1974. a
FIG. 4. Patient 3. Initial aortogram. The right renal artery is not demonstrated. There is marked stenosis of the proximal left renal artery but
nephrogram is present.
