Images--pT3a clear-cell renal cell carcinoma in a renal allograft managed effectively with open partial nephrectomy.
Primary renal cell carcinoma (RCC) post-kidney transplantation can occur in either the native kidney(s) or renal allograft, although their occurrence is significantly rarer in the latter. Immunosuppressive therapy is known to increase the incidence of various malignancies in patients on these regimens due to their effects on the immune system and its role in anti-cancer immune surveillance. (1) Neoplasms can develop as the result of accidental transplantation from donor with undetected primary cancer, recurrence or undiagnosed metastases, or de novo. As well, these tumours tend to be more aggressive, confer a poor prognosis, and are associated with a higher rate of recurrence than the same tumours in the general population.
We present a case of a large pT3a clear-cell RCC found incidentally in a renal allograft.
A 49-year-old male is referred for further evaluation of an incidentally noted solid renal mass of the left iliac fossa renal allograft found on routine ultrasound in June of 2017. The patient denied any flank, abdominal or pelvic pain. No voiding dysfunction or gross hematuria. He underwent renal transplant from a deceased donor in 1997 for end-stage renal disease (ESRD) secondary to focal segmental glomerulosclerosis (FSGS). His serum creatinine had remained stable at 170 [micro]mol/L. In 2007, he was diagnosed with an 8.4 cm renal cell carcinoma of his right native kidney and underwent radical nephrectomy for a pT2 clear cell renal cell carcinoma (RCC), Fuhrman nuclear grade 4 tumour with negative surgical margins. There had been no evidence of local or distant recurrence since.
Routine renal ultrasound revealed a 4.9cm lobulated solid mass with internal vascularity involving the upper pole of the allograft. Computed Tomography (CT) scan was used to further characterize the mass. This demonstrated a 5.4 cm x 4.1 cm x 4.2 cm solid enhancing lesion of the upper pole with 50% endophytic component, and close approximation to the renal hilar fat. The renal vein and external iliac vein were patent. No local lymphadenopathy or metastatic disease was appreciated. A chest radiograph was normal. His serum creatinine was stable at 173 [micro]mol/L with eGFR 36 mL/min/1.73[m.sup.2] indicating moderate renal impairment.
The patient subsequently underwent an uneventful CT-guided percutaneous biopsy of the renal mass. Histopathology demonstrated Clear Cell Renal Cell Carcinoma (RCC), Fuhrman nuclear grade 2. He was planned for open left partial nephrectomy of the transplant kidney with all benefits, risks and potential complications reviewed.
In October 2017, the patient underwent an uneventful open left renal allograft partial nephrectomy for a 5.4cm mass extending deep into the renal sinus fat. The kidney and associated tumour were identified. Dissection was performed around the renal artery and vein until control of the renal hilum was achieved. He received 12.5g of intravenous Mannitol. Following en bloc clamping of the renal hilar vessels, the mass was excised in completion. The tumour extended quite deep into the kidney and sinus fat in the interpolar region. Deep margin on histopathology was negative for tumour. Following complete excision, the defect was repaired in multiple layers. Vascular clamps were removed and hemostasis was controlled. A Jackson-Pratt surgical drain was placed and secured. Blood loss was about 200ml and cold ischemic time was about 20 minutes.
At follow up, final surgical histopathology demonstrated pT3a clear cell RCC, Fuhrman nuclear grade 2 (pT3aN0M0). Renal sinus fat was involved with tumour. The surgical margins were negative. No evidence of acute graft rejection was present. He had evidence of urine leak from the surgical defect and was discharged home with Jackson-Pratt drain and Foley catheter on resumption of a regular diet and uninhibited mobilization. Post-operatively, his serum creatinine climbed to 266 [micro]mol/L and he continued to have elevated output from his drain. He was readmitted to hospital and arranged for cystoscopy and left retrograde pyelography, which confirmed urine extravasation from an interpolar calyx. A double-J ureteric stent was placed along with a urethral catheter. Immediately, drain outputs subsided. The patient was discharged home with catheter in place. His drain was removed a few days later. The stent was removed via cystoscopy at 4 weeks post-operatively. On follow up renal ultrasound in July 2018, there is no evidence of local tumour recurrence or other solid organ metastasis. His chest radiograph is clear. His serum creatinine has stabilized at 212 [micro]mol/L with eGFR 31 mL/min/1.73[m.sup.2] and he remains dialysis free 11 months post partial nephrectomy.
In a recent systematic review, Boissier et al reported on the recurrence of RCC in patients with ESRD undergoing renal transplantation following prior management for RCC and found that 5-16% of RCC cases in renal allografts were stage pT3. Clear cell RCC represented the main histological subtype. Cancer specific survival ranged from 75-100% at 5-years. Tumour recurrence was similar between those patients managed with transplantation and those who remained on dialysis. Prognostic factors for recurrence included stage, Fuhrman grade, histological subtype, and solid/cystic component of the initial tumour. (4)
The development of renal cell carcinoma in the renal allograft is a rare event and poses a dilemma for the managing Urologist. Aggressive management with transplant nephrectomy would necessitate a return to hemodialysis while a conservative nephron-sparing approach presents the risk of tumour recurrence in the setting of ongoing immunosuppression. Indeed, nephron-sparing surgery (NSS) with partial nephrectomy has been demonstrated as a safe and effective option for patients presenting with localized tumours without impairing graft function. Ribal et al. in their review of three patients with tumour in the renal allograft undergoing partial nephrectomy, all were managed successfully with this nephron sparing approach and were tumour free at follow up ranging from 0.5 to 6 months. (5) In the case we have presented, a pT3a tumour was managed effectively via a nephron sparing approach demonstrating its safety and effectiveness in managing these tumours.
(1.) Karczewski, M., Czapiewski, W., & Karczewski, J. Urologic de novo malignancies after kidney transplantation: A single center experience. Transplantation Proceedings, 2012. 44(5),1293-97.
(2.) Penn, I., & Staezl, T. E. Malignant tumors arising de novo In immunosuppressed organ transplant recipients. Transplantation, 1972. 14(4), 407-17.
(3.) Bieniasz, M., Chmura, A., Kwapisz, M., et al. Renal tumor in allogeneic kidney transplant recipient. Transplantation Proceedings. 2016, 48(5), 1849-54.
(4.) Boissier, R., Hevia, V., Bruins, H. M., et al. The risk of tumour recurrence in patients undergoing renal transplantation for end-stage renal disease after previous treatment for a urological cancer: A Systematic review. European Urology, 2018. 73(1), 94-108.
(5.) Ribal, M., Rodriguez, F., Musquera, M., et al. Nephron-sparing surgery for renal tumor: A choice of treatment in an allograft kidney. Transplantation Proceedings. 2006. 38(5), 1359-62.
Figures and Tables
Jas Singh (1); Rachel Wong (2); Rahul K. Bansal
(1) Section of Urology, Department of Surgery, University of Manitoba, Winnipeg, MB, Canada; (2) Max Rady College of Medicine, University of Manitoba, Winnipeg, MB, Canada
Caption: Fig. 1. Contrast-Enhanced CT (CECT) with axial (A) and coronal (B) imaging illustrating a 5.4cm enhancing solid lesion arising from the upper pole of the left iliac fossa renal allograft.
Please Note: Illustration(s) are not available due to copyright restrictions.
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|Title Annotation:||Images in Urology|
|Author:||Singh, Jas; Wong, Rachel; Bansal, Rahul K.|
|Publication:||Canadian Urological Association Journal (CUAJ)|
|Date:||Jun 27, 2019|
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