|Year : 2022 | Volume
| Issue : 2 | Page : 230-233
Lessons learnt from progressive vascular calcification in a renal transplant recipient
Urmila Anandh1, Ritesh Kumar2, G Ramesh3
1 Department of Nephrology, Yashoda Hospitals, Secunderabad, Telangana, India
2 Department of Radiology, Yashoda Hospitals, Secunderabad, Telangana, India
3 Department of Cardiology, Yashoda Hospitals, Secunderabad, Telangana, India
|Date of Submission||14-May-2021|
|Date of Acceptance||17-Oct-2021|
|Date of Web Publication||30-Jun-2022|
Dr. Ritesh Kumar
Department of Radiology, Yashoda Hospitals, Alexander Road, Secunderabad, Telangana
Source of Support: None, Conflict of Interest: None
Chronic kidney disease − mineral bone disorder is a common complication in patients with renal failure. Vascular calcification is the part of this clinical syndrome and progresses over the years. A successful renal transplantation ameliorates the uremic milieu and retards the progression of vascular calcification. In some cases, the vascular calcification is progressive even after transplantation leading to undesirable complications. We describe a case of renal allograft recipient who developed renal allograft dysfunction secondary to his progressive vascular disease. His extensive vessel calcification was missed in routine investigations. This case illustrates the need for dedicated evaluation of vascular calcification in high-risk patients undergoing renal transplantation.
Keywords: Allograft artery stenosis, aortic calcification, heart failure, renal transplant
|How to cite this article:|
Anandh U, Kumar R, Ramesh G. Lessons learnt from progressive vascular calcification in a renal transplant recipient. Indian J Transplant 2022;16:230-3
|How to cite this URL:|
Anandh U, Kumar R, Ramesh G. Lessons learnt from progressive vascular calcification in a renal transplant recipient. Indian J Transplant [serial online] 2022 [cited 2023 Feb 5];16:230-3. Available from: https://www.ijtonline.in/text.asp?2022/16/2/230/349367
| Introduction|| |
Long-standing renal failure predisposes to medial arterial calcification. This lesion is pathophysiologically distinct from that of the intimal calcification noted in atherosclerosis., Vascular calcification is an important manifestation of altered mineral metabolism in long-standing hemodialysis patients and is an important predictor of overall mortality., It is commonly believed that vascular calcification regresses following kidney transplantation with the improvement of the uremic milieu. Other studies have reported conflicting results., As in hemodialysis patients, persistence and or progression of vascular calcification in kidney transplant recipients (KTRs) have an impact on cardiovascular mortality. We report a KTR whose vascular calcification was not evaluated during his pretransplantation evaluation leading to unfortunate consequences.
| Case Report|| |
A 50-year-old male was referred for renal transplantation at our center. He was on dialysis for 6 months in a different center. He gave a history of long-standing diabetes and hypertension. He came to know of his kidney disease 2 years back on a routine evaluation and was on conservative management for the same. His transplant workup revealed the presence of triple-vessel disease on coronary angiogram. The cardiologist felt that he could go ahead with his transplantation and have coronary artery bypass grafting surgery at a later date (as there were no evidence of critical stenosis) when his renal functions were stable. His pretransplantation investigations are given in [Table 1].
|Table 1: Pretransplant laboratory and radiological investigations in our hospital|
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He underwent a spousal transplantation 10 months back. His postoperative period was uneventful, and his discharge creatinine was 1.2 mg/dl. A routine allograft Doppler showed normal blood flow to the allograft with normal resistivity indices. His follow-ups for the next 4 months were uneventful and his renal functions stayed stable. On the 5th month posttransplant, he developed worsening hypertension and his serum creatinine increased to 2.4 mg/dl. His other investigations were essentially normal with a normal liver function test, normal calcium, and normal phosphorus levels. His Parathormone levels were at 114 pg/ml. A Doppler evaluation of the allograft showed high systolic velocities at the anastomosis and tardus parvus pattern in the segmental renal arteries. This was suggestive of allograft renal artery stenosis. A magnetic resonance angiography confirmed the presence of allograft renal artery stenosis [Figure 1]. He underwent stenting of the allograft artery stenosis. Poststenting ultrasound showed reduction of the peak systolic velocity at the anastomotic site with normal segmental artery waveforms and acceleration times (<70 ms) [Figure 2]. With the successful stenting, the serum creatinine also normalized to 1.1 mg/dl. His follow-up investigations after a month showed a rising serum creatinine (2.5 mg/dl) and the presence of pedal edema and ascites. There were no skin changes suggestive of athero-embolic disease. Urinary eosinophils were not detected. His liver functions were normal, and the Doppler showed normal flows at the anastomotic site but a diffuse reduction of blood flow throughout the allograft. A biopsy was not possible as he was on dual anti-platelets. A computed tomography (CT) of the abdomen was done which showed extensive calcification of the aorta [Figure 3]. The pretransplant evaluation for the vessels was limited to an iliac vessel Doppler, and the aortic calcification was completely missed. The echocardiography showed stable ejection fraction. The urinary fractional excretion of sodium was <1. A repeat Doppler at this time showed reversal of diastolic flow all the way up to the common iliac artery. It was felt that the progressive allograft dysfunction and fluid retention were because of the prerenal state secondary to reduced pulsatile blood flow from the calcified aorta. The patient was put on salt restricted diet and diuretics. His CABG was deferred because of his clinical condition. Over the next 2 months, he had progressive fluid retention and passed away with congestive heart failure.
|Figure 1: Magnetic resonance angiogram showing stenosis at the anastomotic site|
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|Figure 2: Ultrasound Doppler with normalised peak systolic velocities at the anastomotic site postallograft renal artery stenosis|
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|Figure 3: Computed tomography abdomen showing extensive abdominal aorta calcification|
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| Discussion|| |
Screening for cardiovascular disease is one of the most important evaluations in prospective KTR. Screening is often limited to coronary artery disease (CAD) and occasionally uncovers significant disease necessitating treatment., The emphasis on CAD evaluation pretransplant is reflective of its significance vis-à-vis posttransplant mortality. However, the presence of untreated significant CAD does not completely explain posttransplant cardiovascular mortality. The presence of vascular calcification is actually not only suggestive of significant CAD but also of ongoing inflammation. Despite its significance, the evaluation of vascular calcification is not advised routinely. The only investigation which is done is the iliofemoral Doppler.
We have presented a case earlier wherein iliofemoral Doppler did not accurately detect vascular calcification and the surgical team had difficulty during anastomosis. This case also illustrates the pitfalls of a negative iliofemoral Doppler. A CT scan of the abdomen showing extensive aortic calcification might have alerted us about progressive allograft vascular compromise. Not only that, the presence of extensive vascular calcification in a high-risk transplant candidate might have changed our decision regarding transplantation.
| Conclusions|| |
High-risk transplant recipients should not only be evaluated for atherosclerotic cardiovascular disease, but abdominal vascular calcification should also be looked into. Extensive vascular calcification can hinder surgical anastomosis. In extensive cases of aortic calcification, the physician should be aware of risk of excessive cardiovascular mortality. Aortic vascular stiffness may also have an impact on allograft perfusion.
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 identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3]