Constrictive pericarditis is easily overlooked and can lead to severe problems in hemodynamics and end-organ perfusion, in our patient leading to 98 days of anuria after living kidney transplantation. This was completely reversible after pericardectomy. A 43-year-old female caucasian patient received a living kidney donation from her mother. She had developed end-stage renal disease 2 years prior due to nephrotic syndrome linked to graft-versus-host disease after allogenic stem-cell transplantation for aplastic anemia. The graft showed insufficient function already in the early postoperative phase. Dialysis was paused after surgery, but the patient developed hypervolemia with ascites and edema in the lower extremities. Doppler ultrasonography showed scarce perfusion, with intrarenal arterial waveforms without end-diastolic flow. The venous perfusion profiles showed pulsatile retrograde flow. There was no identifiable reason for a primary vascular perfusion problem on ultrasonography or transplant kidney angiography. Kidney transplant biopsy revealed no rejection but extensive acute tubular necrosis. Three weeks after transplantation, the patient developed an acute anuric graft failure caused by severe cardiac decompensation. Echocardiography revealed a previously unnoticed constrictive pericarditis, which could be confirmed in a cardio computed tomography scan. The constrictive pericarditis had not been apparent on previous x-rays, computed tomography scans, or echocardiographies, including those for transplantation evaluation. Conservative management of the constrictive pericarditis was not successful and the graft remained anuric. Eventually, the patient underwent pericardectomy 16 weeks after kidney transplantation. Shortly after surgery, the graft started urine production again, which significantly increased within a few days. The clearance improved and 2 weeks later, the patient was free from dialysis. This case illustrates that special attention should be given to the pericardium during transplant evaluation, especially for patients who previously underwent stem-cell transplantations, chemotherapy or radiation.

中文翻译：

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缩窄性心包炎后的心包切除术导致无尿肾移植 98 天后移植肾功能开始：病例报告。

缩窄性心包炎很容易被忽视，可导致血流动力学和终末器官灌注出现严重问题，导致活体肾移植后 98 天无尿。这在心包切除术后完全可逆。一名 43 岁的白人女性患者接受了她母亲的活体肾脏捐赠。由于再生障碍性贫血的同种异体干细胞移植后与移植物抗宿主病相关的肾病综合征，她在 2 年前发展为终末期肾病。移植物在术后早期就显示出功能不足。手术后暂停透析，但患者出现血容量过多伴腹水和下肢水肿。多普勒超声显示灌注不足，肾内动脉波形无舒张末期血流。静脉灌注曲线显示脉动逆行血流。在超声检查或移植肾血管造影中，没有可识别的原发性血管灌注问题的原因。肾移植活检显示无排斥反应，但有广泛的急性肾小管坏死。移植后三周，患者出现严重心脏失代偿引起的急性无尿移植物衰竭。超声心动图显示先前未被注意到的缩窄性心包炎，这可以在心脏计算机断层扫描中得到证实。缩窄性心包炎在之前的 X 射线、计算机断层扫描或超声心动图（包括用于移植评估的那些）中并不明显。缩窄性心包炎的保守治疗没有成功，移植物仍然无尿。最终，患者在肾移植后 16 周接受了心包切除术。手术后不久，移植物再次开始产生尿液，并在几天内显着增加。清除率改善，2 周后，患者不再需要透析。该病例说明在移植评估过程中应特别注意心包，特别是对于以前接受过干细胞移植、化疗或放疗的患者。