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Keywords:

  • renovascular hypertension;
  • traumatic renal artery thrombosis

Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Case report
  5. Discussion
  6. References

Abstract  A 15-year-old boy, who tumbled from a fourth-floor window, was transported to our hospital. Enhanced computed tomography (CT) 1.5 h after the injury showed a non-contrasted right kidney, and a repeat CT 6 h after the injury showed a growing retroperitoneal hematoma. The angiography showed complete obstruction of the right renal artery and bleeding from the subcapsular artery, which was successfully embolized. Renovascular hypertension developed on the second day after the injury; therefore, simple nephrectomy was performed.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Case report
  5. Discussion
  6. References

Traumatic renal artery thrombosis, which was first described by Von Recklinghausen in 1862, is an uncommon complication of blunt abdominal trauma, with an incidence of 1% to 4%. In the present study, we report a case of traumatic renal artery thrombosis. In this case, renovascular hypertension occurred immediately after the injury and was treated using simple nephrectomy.

Case report

  1. Top of page
  2. Abstract
  3. Introduction
  4. Case report
  5. Discussion
  6. References

A 15-year-old boy, who tried to kill himself by leaping from a fourth-floor window, was admitted to our Emergency Center. He had clear consciousness and complained of pain in his right flank, right upper arm and left lower limb. On physical examination, there were open wounds in the right humerus and left ankle joint. He exhibited hypotension at the scene (80 mmHg systolic), and pulse 100/min. Laboratory data indicated: hemolobin, 13.7 g/dL; hematocrit (Hct), 41.9%; blood urea nitrogen, 15 mg/dL; creatinine, 1.1 mg/dL; glutamic-oxaloacetic transaminase, 315 IU; glutamic-pyruvic transaminase, 268 IU; lactate dehydrogenase, 3133 IU; creatinine phosphokinase, 866 IU; bilirubin, 0.9 mg/dL; blood sugar, 235 mg/dL; and C-reactive protein, 0.0 mg/dL. A urine sample showed evidence of gross hematuria. Radiographs showed a mild pneumothorax in the left lung, an oppression fracture on L1, a right sacroiliac joint dislocation, a right acetabular fracture, right humerus fracture and left ankle fracture. The enhanced computed tomography (CT), taken immediately after admission, showed a non-contrasted right kidney (Fig. 1) and hematoma in the pelvis. Six units of blood were transfused 4 h after the injury because of anemia (Hct 22.2%) and uncontrollable hypotension. A CT scan taken 6 h after the injury showed new bleeding around the non-contrasted right kidney. The arteriogram identified occlusion of the right renal artery (Fig. 2), at 3 cm from its origin. Only a branch of the inferior adrenal artery fed the upper pole of the kidney. There was also bleeding from the subcapsular artery, which was embolized with gelatin. There was no marked bleeding from the internal iliac and lumbar arteries. The patient underwent a pinning operation for his humerus and left ankle fractures under general anesthesia 10 h after the injury.

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Figure 1. Enhanced computed tomography of the abdomen showed no contrast in the right kidney, but did show the right renal vein.

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Figure 2. Aortography showed complete occlusion of the right renal artery.

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Two days after the injury, the patient's blood pressure increased to over 160 mmHg systolic. The serum levels of renin, angiotensin I, angiotensin II and aldosterone were 12.2 ng/mL/h (normal range, <1.2), 2040 pg/mL (normal range, <500), 67 pg/mL (normal range, <47) and 47.4 ng/dL (normal range, <13), respectively, on the twelfth  day  after  the  injury.  The  serum  levels  of  renin  in the right renal vein, left renal vein and inferior vena cava (IVC) under the renal veins were 51.4 ng/mL/h, 4.1 ng/mL/h and 3.9 ng/mL/h, respectively. Although the patient's blood pressure was controlled with an angiotension-converting enzyme inhibitor, orthopedists planned anterior spinal fusion 2 months after the injury. Therefore, a right simple nephrectomy was performed with a single flank incision. The patient became normotensive, and the serum levels of renin and aldosterone decreased to 0.5 ng/mL/h and 3.2 ng/dL, respectively.

Pathological examination showed coagulation necrosis in almost all of the right kidney with a small number of glomerular apparatuses remaining around some patent arteries. The tunica intima and tunica media of the renal artery were disconnected and white thrombus filled the lumen of the renal artery with some reperfusion area (Fig. 3). The renal vein was filled with red thrombus.

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Figure 3. Pathological examination showed that the tunica intima (arrow head) and tunica media (arrow) of the renal artery were disconnected, and white thrombus filled the lumen of the renal artery with some reperfusion area.

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Discussion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Case report
  5. Discussion
  6. References

Traumatic renal artery thrombosis is an uncommon disorder, whose actual incidence is unknown. The left kidney of young men is usually affected. Two mechanisms of renal artery thrombus have been presented. One involves a sudden deceleration of the artery wall, where the intima, being less elastic than the media or adventitia, is damaged. The injured endothelium activates the collagen cascade and the development of a thrombus occludes the arterial lumen. The other mechanism involves a contusion of the right renal artery between the anterior abdominal wall and the vertebral bodies. In the present case, the right renal artery was occluded by the first mechanism because the pathology did not show detritions of the arterial wall, but showed tunica intima and media laceration. The impact was so high that both the intima and the media were torn.

In order to rescue the ischemic kidney, it is important to revascularize the injured renal artery as soon as possible. The procedures for revascularization include thrombectomy with vein patch angioplasty, excision of the thrombosed segment with end-to-end anastomosis, aortorenal bypass using a venous graft from the saphena or cava, autotransplantation, or intervention therapy such as stenting. The limit of warm ischemic time for the kidney is known to be 30 min. In fact, it is impossible to revascularize within this time. However, the kidney can survive longer than this because of the collateral arteries. Spirnak stated that the ratio of recovery of renal function was 5 : 35 in patients who had undergone revascularization within 12 h.1 Bilateral renal artery thrombosis is a more severe disorder and the indication of revascularization does not depend on the ischemic time. Immediately after the diagnosis is confirmed, the revascularization should be performed to prevent the need for permanent hemodialysis. Brunetti et al. reported the avoidance of permanent hemodialysis in six of 12 patients whom he had revascularized.2 In the present case, the angiography was performed 7 h after the injury; therefore, the kidney might have been repaired if rapid revascularization, such as stenting, had been performed. Hirota reported the success of stenting in bilateral renal artery thrombosis, thus avoiding permanent hemodialysis (unpublished data, 2001). Revascularization of unilateral renal artery thrombosis is indicated within 12 h of the injury. In the case of a solitary kidney or bilateral renal artery thrombosis, the indication should be expanded.

Principal complications of an infracted kidney include delayed hypertension and infection. The hypertension in the present case was induced by renin generated by the ischemic kidney. This was confirmed with the selective renin sampling in the bilateral renal veins. The renin ratio of the right to left renal vein was 12.5, and the renin levels in the left renal vein and the IVC under the renal veins were at almost the same level. This result shows the excess production of renin in the responsible kidney, and renin suppression in the contralateral kidney; this result was also obtained in an experiment carried out by Goldblatt et al. involving a two-kidney, one-clip model.3 The incident rate of delayed hypertension ranges from 15 to 57%, and can take several months, or even years. Considering the low incidence of hypertension, an early nephrectomy should not be performed in the absence of complications. If hypertension develops, a nephrectomy is inevitable.4 Similarly, a nephrectomy should be performed if medical treatment is ineffective.5 In the present case, the renovascular hypertension occurred immediately after the injury. The adequate collateral arteries, including the inferior adrenal artery and the subcapsular artery, made the ischemic kidney produce excess renin. Because of his age, long-term antihypertensive medical control would be necessary for the patient in the present study. Therefore, a nephrectomy was performed at the same time as the orthopedic operation, using a single skin incision.

We conclude that it is possible to incur renal artery thrombosis in trauma, and its complications can include early renovascular hypertension.

References

  1. Top of page
  2. Abstract
  3. Introduction
  4. Case report
  5. Discussion
  6. References
  • 1
    Spirnak JP, Resnick MI. Revascularization of traumatic thrombosis of the renal artery. Surg. Gynecol. Obstet. 1987; 164: 226.
  • 2
    Brunetti DR, Sasaki TM, Friedlander G et al. Successful renal autotransplantation in a patient with bilateral renal artery thrombosis. Urology 1994; 43: 2357.
  • 3
    Goldblatt H, Lynch J, Hanzal RF. Studies on experimental hypertension. The production of persistent elevation of systolic blood pressure by means of renal ischemia. J. Exp. Med. 1934; 59: 347.
  • 4
    Von Knorring J, Fyhrquist F, Ahonen J et al. Renin/angiotensin system in hypertension after traumatic renal-artery thrombosis. Lancet 1976; 1: 9346.
  • 5
    Munoz D, Gutierrez C, Hidalgo F. Traumatic renal artery thrombosis. Scand. J. Urol. Nephrol. 1998; 32: 2968.