|Year : 2021 | Volume
| Issue : 3 | Page : 269-271
Unusual presentation of posttransplant renal artery stenosis - A case report
Sashi Kiran Annavarajula1, B Suryaprakash2, D Kashinatham2, Pawan Poddar3
1 Department of Nephrology, Yashoda Hospital, Hyderabad, Telangana, India
2 Department of Urology, Yashoda Hospital, Hyderabad, Telangana, India
3 Department of Cardiology, Yashoda Hospital, Hyderabad, Telangana, India
|Date of Submission||21-Sep-2020|
|Date of Decision||10-Jan-2021|
|Date of Acceptance||07-Feb-2021|
|Date of Web Publication||30-Sep-2021|
Dr. Sashi Kiran Annavarajula
Departments of Nephrology, Yashoda Hospital, Hyderabad - 500 039, Telangana
Source of Support: None, Conflict of Interest: None
Transplant renal artery stenosis (TRAS) is a well-recognized and potentially treatable cause of early graft dysfunction. Recognition of TRAS can sometimes be difficult, and the presentation may mimic acute allograft rejection. A high index of suspicion along with arteriography is crucial in early recognition and management.
Keywords: Angioplasty, magnetic resonance angiogram, transplant renal artery stenosis
|How to cite this article:|
Annavarajula SK, Suryaprakash B, Kashinatham D, Poddar P. Unusual presentation of posttransplant renal artery stenosis - A case report. Indian J Transplant 2021;15:269-71
|How to cite this URL:|
Annavarajula SK, Suryaprakash B, Kashinatham D, Poddar P. Unusual presentation of posttransplant renal artery stenosis - A case report. Indian J Transplant [serial online] 2021 [cited 2022 Jan 26];15:269-71. Available from: https://www.ijtonline.in/text.asp?2021/15/3/269/327384
| Introduction|| |
Early renal allograft dysfunction following a living-related renal transplant is rare. In instances where this happens, the presentation can sometimes be perplexing and difficult to diagnose. We present here a patient with early graft dysfunction who posed a diagnostic challenge.
| Case Report|| |
A 53-year-old gentleman who developed end stage renal disease due to progression of IgA nephropathy underwent a living-related renal transplantation. The kidney donor was his sister and they had a 3/6 HLA match. Induction was with basiliximab and methylprednisolone. The graft kidney had a single renal artery, and it was anastomosed to the internal iliac artery of the recipient end to end. He had profound hypotension during the surgery and needed two inotropes for the next 36 h. There was a delayed graft function, but he did not need dialysis. Hypersensitivity to basiliximab was considered the cause of hypotension after carefully ruling out all the other possibilities. Hence, the second dose of basiliximab was skipped. The graft function was stable till the 7th postoperative day (POD).
An increase in the serum creatinine from 2.3 to 2.6 mg/dl along with a decrease in urine output occurred on the 8th POD. Renal biopsy was performed and the trough level of tacrolimus was estimated. The renal biopsy was opined as borderline T-cell–mediated rejection (TCMS) [Figure 1] and the trough level of tacrolimus was 6.24 mcg/l. The dose of tacrolimus was increased by 1 mg/day, and he was also administered methylprednisolone 500 mg/day for 3 days. The urine output progressively decreased and he became anuric by the 13th POD. His serum creatinine had worsened to 6 mg/dl. In-between, he needed two sessions of hemodialysis on the 10th and 12th POD. He also had worsening of hypertension and hyperkalemia. A second renal biopsy was performed and trough level of tacrolimus was estimated. This renal biopsy was suspicious of calcineurin inhibitor toxicity with no evidence of rejection. Donor-specific antibodies (DSAs) were not detected. The trough level of tacrolimus was 12.4 mcg/l. The dose of tacrolimus was reduced by 0.5 mg/day. The next day, his urine output increased to 500 ml/day. His serum creatinine started to decrease and reached 1.3 mg/dl by the 22nd POD. Despite this, his urine output remained low, his hypertension had worsened, and he had a weight gain of 12 kg. His urine revealed 1+ protein and no red blood cells. Cytomegalovirus was undetectable by quantitative DNA PCR estimation. At this juncture, renal artery stenosis (RAS) was suspected. Doppler examination of the renal artery was opined as normal and magnetic resonance angiogram was suspicious of RAS [Figure 2]. Since the suspicion for RAS was high, he was subjected to renal arteriography. The arteriography revealed significant stenosis of the renal artery at the anastomotic site [Figure 3]. Angioplasty and stent placement were performed. This resulted in gross diuresis. His edema and hypertension disappeared over the next 48 h. Now at 11 months posttransplant, he is normotensive and his serum creatinine is 0.8 mg/dl.
| Discussion|| |
We present here a patient who developed early transplant renal artery stenosis (TRAS) and anuria. TRAS is a potentially curable cause of early allograft dysfunction which manifests between 3 months and 2 years after transplant and can sometimes present as anuria. The incidence of this complication varies between 1% and 23%, though the incidence of functionally significant TRAS occurs in about 12% of patients. End-to-end anastomosis has a threefold greater risk of stenosis than an end-to-side anastomosis.
There are several features that are interesting in our patient. The first and noteworthy was the development of anuria when the dose of tacrolimus was increased to achieve the therapeutic levels. Tacrolimus is known to cause vasoconstriction but rarely causes anuria in an adult who has undergone renal transplant since calcineurin-induced nephrotoxicity is predominantly nonoliguric.
Second, the renal biopsy (performed twice in this patient) did not show hyperplasia of the juxtaglomerular apparatus but rather showed features of tubulituis, suggestive of borderline TCMS prompting us to increase the dose of tacrolimus. Acute rejection can cause endothelial proliferation, and this may mimic TRAS. There was no evidence of rejection in the second biopsy despite worsening of oliguria and graft function and this prompted us to suspect TRAS.
Third, Doppler ultrasonography which has a very good accuracy in detecting RAS but is operator dependent failed to detect TRAS in our patient. Repeated Doppler examination did not reveal peak systolic velocity or resistive index which could suggest TRAS. Parvus et tardus pattern was conspicuously absent. Magnetic resonance imaging, which is known to have a high false-positive rate, was suggestive of stenosis. Since the suspicion of TRAS was high, an arteriography was performed.
| Conclusion|| |
The present patient serves as an illustrative example of the difficulties one can encounter in diagnosing early allograft kidney dysfunction. Since acute rejection is an important cause, the diagnostic uncertainty can sometimes make us to perform a renal biopsy when noninvasive diagnostic modalities are inconclusive. A high index of suspicion of TRAS and early therapeutic intervention would provide an excellent result.
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 understand that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.
Dr. Ravikanth J, Radiologist, and Dr. Sarika, Pathologist, were acknowledged.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3]