EXPERIMENTAL AND CLINICAL TRANSPLANTATION

Subcapsular hematoma after kidney transplant may result in kidney ischemia and graft loss. In this report, we present a patient who had a subcapsular hematoma that had no intraoperative enlargement but ruptured after surgery. A man who had chronic kidney disease secondary to hypertension had a preemptive living-donor kidney transplant from his wife. After declamping, appropriate renal perfusion and urinary output were observed. At perfusion, a subcapsular hematoma (diameter, 3 cm) was observed at the upper pole of the kidney. The hematoma did not enlarge during the surgery. Capsulotomy was not performed due to possible risks, and transplant surgery was completed with the plan for close postoperative ultrasonography and hemodynamic follow-up. Decreased urinary output was observed early after surgery. Renal Doppler ultrasonography showed decreased diastolic flow and a hematoma (width, 9 mm) that completely surrounded the transplanted kidney. The patient had emergency reoperation due to active hemorrhage from his surgical drain at 40 hours after surgery. Rupture of the capsule and hemorrhage from the surface of the kidney were observed. Extended capsulotomy and hemostasis of the kidney were performed. After surgery, urinary flow increased and renal Doppler ultrasonography findings improved. In summary, intervention for a subcapsular hematoma after kidney transplant is controversial. Capsulotomy should be considered for treatment of increased pressure to the graft, risk of permanent damage, and risk of graft loss.

Key words : Complications, End-stage renal disease, Hemorrhage, Treatment

Page kidney phenomenon is the occurrence of kidney hypoperfusion and ischemia due to pressure on the kidney by a subcapsular hematoma. Hypoperfusion and microvascular ischemia in the kidney may stimulate the renin-angiotensin-aldosterone system and cause hypertension. Tumors, lymphoceles, and urinomas are other causes of Page kidney phenomenon.^1-3 There is controversy about the treatment of subcapsular hematoma. There are papers that report spontaneous resolution of subcapsular hematomas.^4,5 Antihypertensive treatment, percu-taneous drainage, surgical decortication, laparoscopic intervention, and nephrectomy are the other treatment options.^6,7 In this case report, we describe a subcapsular hematoma that occurred and had no intraoperative enlargement but ruptured after surgery.

A 50-year-old man who had chronic kidney disease secondary to hypertension had preemptive living-donor kidney transplant from his wife (wife’s age, 48 y). The recipient had no history of antiplatelet drug use and had platelet count > 150 ×10⁹/L. Basiliximab 20 mg was given as an inducing agent, and other immunosuppressive drugs were tacrolimus, mycophenolic acid, and methylprednisolone. After declamping, appropriate renal perfusion and urinary output were observed, and a subcapsular hematoma (diameter, 3 cm) was observed at the upper pole of the kidney. The hematoma did not enlarge during surgery. Capsulotomy was not performed due to possible risks, and transplant surgery was completed with the plan for close postoperative ultrasonography and hemodynamic follow-up.

Early postoperative urinary output was > 500 mL/h. At 10 hours after the operation, urinary flow decreased to 100 to 150 mL/h, despite normal central venous pressure. Renal Doppler ultraso-nography showed decreased diastolic flow and a hematoma (width, 9 mm) that completely surrounded the transplanted kidney. Resistant hypertension was not observed. Control renal Doppler ultraso-nography showed a resistive index of 0.85, and the hematoma width was 11 mm.

Preoperative serum creatinine level was 4.52 mg/dL. Postoperative day 1 creatinine level was 4.25 mg/dL, and this level was higher than expected. Urinary output increased at 36 hours after surgery. After active hemorrhage was observed from the surgical drain at 40 hours, the patient had emergency exploratory surgery. Rupture of the capsule and hemorrhage from the surface of the kidney were observed. Extended capsulotomy, wedge biopsy, and hemostasis of the kidney were performed (Figure 1 and 2). After reoperation, urinary flow increased and renal Doppler ultrasonography findings improved (Figure 3). Creatinine levels decreased after reoperation, and the last serum creatinine level was 1.87 mg/dL. Pathologic evaluation of the kidney biopsy showed acute tubular necrosis.

Page kidney phenomenon was first described in an experimental model in the 1930s.⁸ Cromie and associates described this event as renal allograft pseudorejection; after living-donor renal transplant, the patient had refractory hypertension, perinephric hematoma was observed by renal ultrasonography, and blood pressure was normalized after intervention to treat the hematoma.⁹ Hypertension is the characteristic finding in the classic Page kidney phenomenon. Serum creatinine levels are normal when the other kidney is not affected. External pressure to kidney parenchyma results in renin-angiotensin-aldosterone activation and hyper-tension.¹⁰ This situation causes increased serum creatinine levels in renal transplant patients. Our patient had hypertension postoperatively, but this was not resistant hypertension. Furthermore, our patient was hypertensive preoperatively, so we believed that the subcapsular hematoma was not the cause of hypertension in this patient. Decreased urinary output between postoperative hours 10 and 36 might have been due to pressure of the hematoma on kidney parenchyma. Increased urinary flow after hour 36 suggests that rupture of the hematoma occurred at that time.

Intervention for subcapsular hematoma after kidney transplant is controversial. Salgado and colleagues preferred nonoperative follow-up for a subcapsular hematoma that covered two-thirds of the kidney surface after a living-donor transplant. They observed rapid worsening of renal function and signs of pressure to kidney parenchyma early after surgery. In the subsequent days, spontaneous resolution of the hematoma was detected using Doppler ultrasonography.⁴

Risk of perinephric hematoma after transplant kidney biopsy is between 0.7% and 30%.^10,11 Chung and coworkers performed emergency capsulotomy in 4 cases for subcapsular hematomas that developed after transplant graft kidney biopsies. They reported that renal function normalized in 3 cases, but graft loss occurred in 1 case due to acute rejection.¹ Maurya and associates performed surgical decompression of a subcapsular hematoma that developed after graft biopsy because of worsening of renal function.¹² Our patient had partial worsening of renal function, so we decided to follow the patient nonoperatively with close hemodynamic and renal function evaluation. Surgical decompression and renal hemostasis were performed due to signs of renal capsule rupture. Increased urinary output and decreased serum creatinine levels were observed after reoperation. Serum creatinine level was 1.87 mg/dL when the patient was discharged. Serum creatinine level was higher than expected at discharge, possibly the result of renal parenchymal damage due to acute tubular necrosis.

In summary, intervention for subcapsular hema-toma of the transplanted kidney is controversial. Capsulotomy should be considered for treatment of increased pressure to the graft, risk of permanent damage, and risk of graft loss.

Volume: 15 Issue: 3 June 2017

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