Page kidney: A cause of acute renal allograft dysfunction

ABSTRACT

Page kidney is a rare but reversible cause of secondary hypertension due to renin–angiotensin–aldosterone system activation from external renal parenchymal compression. We report acase of a 30-year-old male renal transplant recipient who developed oliguria and refractory hypertension in the early postoperative period. Imaging revealed a spontaneous subcapsular hematoma causing graft compression. Surgical capsulotomy with hematoma evacuation was performed. The patient had an uneventful recovery, with stable graft function at 1-year follow-up. This case highlights the importance of early recognition and timely surgical intervention to prevent irreversible graft dysfunction in posttransplant Page kidney.

INTRODUCTION

Page kidney is a potentially reversible form of secondary hypertension resulting from external compression of the renal parenchyma by a mass effect, such as subcapsular hematomas, urinomas, cysts, or tumors.[1] It was first described by Irving Page in 1939, who demonstrated that wrapping canine kidneys in cellophane resulted in hypertension. The pathophysiology involves hypoperfusion of renal tissue, activating the renin–angiotensin–aldosterone system (RAAS), leading to systemic hypertension.[2]

In renal transplant recipients, the Page kidney can threaten graft survival and patient outcomes. Prompt recognition and intervention are crucial due to limited diagnostic consensus and therapeutic guidelines. We report a case of Page kidney resulting from a spontaneous subcapsular hematoma that occurred shortly after renal transplantation, which was effectively treated with prompt surgical intervention.

CASE REPORT

A 30-year-old male with end-stage renal disease, on hemodialysis for 1 year and no history of anticoagulation, underwent an ABO-compatible living-related donor kidney transplant in the right iliac fossa. Donor nephrectomy was uneventful, with an intact renal capsule. Intraoperatively, the graft demonstrated good perfusion without anastomotic bleeding, and immediate diuresis was noted. Postoperatively, the patient remained hemodynamically stable with an average urine output of 100 mL/h. He received standard immunosuppression, including tacrolimus, mycophenolic acid, and methylprednisolone. A baseline Doppler ultrasound on postoperative day (POD) 1 confirmed normal graft perfusion. As per institutional protocol, follow-up Doppler ultrasound of the renal graft is performed based on changes in clinical parameters such as decreased urine output, rising serum creatinine levels, new-onset or worsening hypertension, or hemodynamic instability. He was recovering uneventfully up to POD 3. Although the serum creatinine remained slightly elevated (around 2 mg/dL) during the initial recovery phase, it was considered acceptable due to stable urine output, hemodynamic stability, and a downward trend in daily creatinine levels.

On POD 4, the patient developed uncontrolled hypertension despite intravenous nitroglycerin infusion, oral labetalol, and diuretics. Urine output decreased to 30 mL/h. Laboratory evaluation revealed a 2 g/dL drop in hemoglobin and a rise in serum creatinine from 2.1 to 4.6 mg/dL. Notably, a single dose of intravenous enalapril led to a significant drop in blood pressure, which raised suspicion for Page kidney. An emergency bedside Doppler ultrasonography showed a 20–30 cc subcapsular collection compressing the renal cortex, with an elevated resistive index (0.90–0.94). There was no evidence of rejection, renal vein thrombosis, or arterial stenosis. A noncontrast computed tomography of kidneys, ureters, and bladder confirmed a hyperdense subcapsular hematoma (50–55 HU), measuring 2.6 cm in thickness and approximately 30 cc in volume [Figure 1]. Given worsening clinical parameters and imaging findings, the patient was taken for urgent surgical exploration after obtaining informed consent.

Figure 1.

Noncontrast computed tomography kidneys, ureters, and bladder image of subcapsular hematoma. Here arrow head pointing towards subcapsular hematoma arround graft kidney

The transplanted kidney was approached via the previous Gibson incision. Old clots were evacuated, and a 4-cm subcapsular hematoma was identified at the posterolateral aspect of the kidney. Complete decortication was necessary to evacuate the hematoma. Diffuse oozing of blood was managed using fibrin glue (octyl cyanoacrylate), oxidized regenerated cellulose mesh wrapping, and porcine gelatin sponges for hemostasis [Figure 2]. Intraoperatively, urine output increased immediately after decompression, reaching 100–150 mL/h. Hemostasis was satisfactory, so no surgical drains were placed. Placement of a surgical drain may cause further bleeding in a decorticated kidney due to mechanical trauma. The wound was closed in layers.

Figure 2.

Oxidized cellulose mesh wrapping of kidney

The patient demonstrated a remarkable recovery, with stabilized blood pressure and restored urine output. He was discharged on the 6^th POD with stable graft function and improved clinical condition. At 1-year follow-up, the patient maintained stable graft function without recurrence.

DISCUSSION

As per the literature, the first case of Page kidney in a renal transplant patient was reported in 1976 as “pseudo-rejection” by Cromie et al.,[3] as it resembles renal allograft rejection. Page phenomenon is an external compression of renal parenchyma due to mass effect from a variety of etiologies, causing hypoperfusion and microvascular ischemia in the kidney. This stimulates RAAS and causes hypertension.[1,2] The most common causes are iatrogenic, trauma, spontaneous, and postoperative bleeding.[4] The diagnosis is suspected on renal allograft Doppler ultrasound findings of absent arterial diastolic flow, a raised arterial resistive index with evidence of a perirenal allograft collection suggestive of extrinsic compression of renal parenchyma with subsequent cortical ischemia. Different management options in such cases are conservative management with antihypertensives and waiting for spontaneous resolution, percutaneous drainage, surgical decortication (capsulotomy/capsulectomy), and graft nephrectomy.[5]

It is worth noting that the care of a Page kidney in a renal transplant recipient differs from Page kidney in the native kidney because of a single functioning precious renal unit and ongoing immunosuppression. Improved blood pressure control with RAAS inhibitors (such as the ACE inhibitor enalapril, as observed in our case) compared to other antihypertensive agents may serve as a diagnostic clue for Page kidney in such scenarios.

In our case, the main etiology behind the Page kidney was a spontaneous idiopathic subcapsular hematoma. Because of uncontrolled hypertension with severe oliguria, we had opted for prompt surgical intervention, and we had succeeded in saving the renal allograft. We recommend avoiding complete surgical decortication (capsulectomy) and instead opting for capsulotomy when feasible. However, this was not possible in our case because the renal capsule was already fully detached due to the presence of a large subcapsular hematoma. In such cases, topical fibrin sealants (octyl cyanoacrylate glue) and complete wrapping of the kidney with oxidized cellulose mesh are good options to consider in case of diffuse parenchymal bleeding.

CONCLUSION

Page kidney should be suspected in transplant recipients with unexplained hypertension and oliguria, especially when traditional antihypertensives fail but RAAS inhibitors provide benefit. Early surgical intervention, including decompression and the use of hemostatic agents, may be lifesaving and graft-preserving. This case highlights the importance of prompt recognition and individualized management to ensure favorable outcomes in transplant-related Page kidney.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.