Subcapsular hematoma following kidney transplantation is an uncommon but serious complication that can compromise graft perfusion and function. The hematoma exerts extrinsic pressure on the graft parenchyma, leading to decreased renal perfusion and activation of the renin–angiotensin–aldosterone system—a condition known as the Page kidney phenomenon.(1,2) Without early recognition and intervention, this can result in irreversible graft loss. The causes of post-transplant subcapsular hematoma include surgical trauma, coagulation abnormalities, biopsy-related injury, and delayed bleeding from capsular vessels.(2) The clinical presentation is often non-specific, manifesting as graft tenderness, decreased urine output, or rising serum creatinine. Therefore, imaging modalities—particularly duplex ultrasound—are indispensable for timely diagnosis.

Ultrasound provides a non-invasive, bedside, and readily available means of assessing graft morphology and perfusion. Doppler parameters such as resistive index (RI) offer valuable clues regarding vascular compromise.(3) Despite these advantages, reports highlighting the diagnostic utility of ultrasound in detecting subcapsular hematoma after ABO-incompatible transplantation remain limited. We herein describe a case in which ultrasound findings were crucial in guiding immediate surgical intervention and salvaging graft function.

A 42-year-old woman with a 20-year history of diabetes mellitus and hypertension was admitted for living donor kidney transplantation. One year prior, she had been diagnosed with chronic kidney disease stage 5 and initiated hemodialysis. The donor was her 21-year-old daughter, who was healthy with no notable past medical history. The transplantation was ABO-incompatible (recipient: O+, donor: B+). Preoperative immunologic evaluation showed negative crossmatch results and a panel-reactive antibody (PRA) level of 0% for class I and 26% for class II. The isoagglutinin initial titer was 1:128 and decreased to 1:8 immediately before surgery after four-time plasmapheresis. The donor left kidney was transplanted into the recipient’s right iliac fossa. Vascular anastomoses were performed between the graft renal artery and the recipient’s internal iliac artery, and between the graft renal vein and the external iliac vein. Immediate urine output was noted following reperfusion. The ureteroneocystostomy was performed using the Lich-Gregoir technique. Minor oozing was observed around the anastomosis site, and a drain was placed. The early postoperative course was uneventful. 5-day after the transplant, the patient reported mild tenderness over the graft site, and her urine output abruptly decreased. Serum creatinine rose from 1.4 to 2.8 mg/dL within 12 hours. Doppler ultrasound demonstrated a crescent-shaped, hypoechoic collection beneath the graft capsule compressing the renal parenchyma, consistent with a subcapsular hematoma. The resistive index of the segmental arteries was elevated to 0.9-1.0, suggesting significant vascular compression and impaired perfusion—findings compatible with Page kidney (Fig. 1).

Given these findings, emergency surgical exploration was undertaken. Intraoperatively, an approximately 8-cm subcapsular hematoma was identified along the lateral surface of the graft (Fig. 2). A 3-cm incision was made in the capsule, and unlooping was performed to release the hematoma and decompress the parenchyma. Small oozing areas from the renal cortex were coagulated using bipolar electrocauterization. The capsule was left partially open to prevent re-accumulation.

Following hematoma evacuation, urine output improved immediately. Serum creatinine levels declined to 1.3 mg/dL within 48 hours. Doppler ultrasound performed after the surgery showed no further hematoma accumulation, the RI value was measured within the normal range of 0-75-0.77, and vascularity also improved (Fig. 3). The patient’s recovery was uneventful, and she was discharged on postoperative day 14 with stable graft function.

Subcapsular hematoma after kidney transplantation is an uncommon event, with reported incidence rates ranging from 0.2% to 6% depending on the diagnostic criteria and population studied.(4) The condition is clinically important because the rigid renal capsule can transmit even minor bleeding into significant parenchymal compression, leading to decreased perfusion and the Page kidney phenomenon.(1) Unfortunately, we have not found any studies on the incidence or risk factors of subcapsular hematoma in ABO incompatible kidney transplantation.

The diagnosis of subcapsular hematoma can be difficult based on clinical findings alone. Pain, tenderness, and oliguria are nonspecific and may mimic acute rejection or vascular thrombosis.(5) Doppler ultrasound remains the first-line imaging modality for evaluating early post-transplant complications owing to its noninvasive, bedside availability and lack of nephrotoxic contrast.(1,6,7) In subcapsular hematoma, B-mode ultrasound typically demonstrates a crescentic or lenticular hypoechoic or mixed-echoic collection conforming to the contour of the graft, with the renal capsule acting as a distinct echogenic line separating the hematoma from perinephric fat.(8) With time, the echogenicity may evolve from hyperechoic (acute clot) to hypoechoic (subacute liquefied phase).(4) Color Doppler reveals decreased or absent parenchymal perfusion in the compressed region, and spectral Doppler shows an elevated resistive index (RI), often exceeding 0.9, due to downstream vascular impedance.(3,6) These hemodynamic findings are key differentiators from other causes of graft dysfunction. In our patient, Doppler findings of elevated RI (>0.9) along with a compressive hypoechoic rim strongly suggested subcapsular hematoma before confirmation at surgery.

It is important to distinguish subcapsular hematoma from perinephric (peri-graft) hematoma, as their clinical implications and management differentiation. A subcapsular hematoma lies beneath the renal capsule and directly compresses the parenchyma, whereas a perinephric hematoma is outside the capsule, displacing but not compressing the kidney. Also, in subcapsular hematoma, the graft surface appears flattened or indented due to pressure effect, while in perinephric hematoma the renal contour remains convex. Moreover, intraparenchymal arterial flow is reduced with high RI in subcapsular hematoma, whereas perinephric collections usually preserve parenchymal perfusion. Finally, only the subcapsular type is typically associated with Page kidney physiology and requires urgent decompression when hemodynamically significant.(3,5-7)

Other postoperative complications that can reduce graft perfusion include renal vein thrombosis, ureteral obstruction, and acute rejection. In renal vein thrombosis, Doppler ultrasound typically shows reversed diastolic flow, whereas in rejection, there is increased echogenicity and parenchymal swelling without capsular compression.(3,6) Therefore, distinguishing subcapsular hematoma using ultrasound is both feasible and crucial for clinical decision-making.

The management strategy depends on the hematoma size and hemodynamic impact. Small, non-compressive hematomas may be managed conservatively with close monitoring.(4,5,8) However, large hematomas causing decreased urine output or high RI require urgent decompression, as delayed treatment can result in irreversible ischemic injury.(8) In our case, prompt recognition by ultrasound led to timely surgical evacuation and complete graft function recovery—highlighting its clinical usefulness not just diagnostically, but therapeutically.

Subcapsular hematoma after kidney transplantation, though rare, should be considered in cases of graft tenderness or sudden oliguria. Ultrasound examination, particularly with Doppler assessment, provides rapid, noninvasive, and accurate detection of this complication. Early diagnosis followed by appropriate surgical management can result in complete graft recovery. This case illustrates the vital clinical role of ultrasound in post-transplant care, especially for early detection of potentially reversible causes of graft dysfunction.

This paper was supported by Fund of Jeonbuk National University School of Medicine and Hospital.