MYSTERY IN THE TRANSPLANT URETER: A RARE CASE OF POST-TRANSPLANT CALCIFICATION

Introduction:

Post-renal mechanical complications in kidney transplant recipients often involve the transplant ureter, with common issues like ureteral stenosis arising from ischemia or BK virus infection. Although rare, calcification in the transplant ureter can occur. This calcification may result from nephrolithiasis, which can be donor-derived or, in rare cases, develop de novo without metabolic abnormalities. Additionally, encrustation calcification in the ureter wall can happen due to trauma or infection by urease-producing organisms such as Corynebacterium urealyticum.

Methods:

A 64-year-old female with a history of Roux-en-Y gastric bypass and CKD following AKI from septic shock 5 years ago progressed to ESRD, requiring a deceased donor kidney transplant. An aortic cuff was used to connect two upper pole and one lower pole renal artery. Her intraoperative course was complicated by poor kidney perfusion, which improved with intraoperative heparin and arteriotomy, though perfusion through the small lower pole artery remained suboptimal. A ureteral stent was placed and removed 15 days post-transplant. Her immediate post-transplant course was uncomplicated, with a discharge creatinine of 1.3 mg/dl (eGFR 42). Two months later, she presented with increased creatinine (2.75 mg/dl). CT revealed hydroureteronephrosis with a 3.1 cm calcification in the distal transplant ureter (no stone in the donor’s kidney at transplant). Ureteroscopy confirmed intraluminal calcification with ureter stenosis on retrograde pyelogram. A Double J stent was placed for urinary drainage. Labs showed calcium 9.6 mg/dl, phosphorus 2.5 mg/dl, PTH 205 pg/ml (secondary to renal failure), serum oxalate 1.8 mcmol/L (improved from 49.5 pre-transplant), urine oxalate 20.2 mg/24 hours, urine pH 6.7, and a negative 24-hour urine culture. Ultimately, the transplant ureter was transected and ligated, and the renal pelvis was connected to the right native ureter to bypass the distal stenotic transplant ureter.

Results:

De novo calcification in the transplant ureter is very rare. It could result from ureterolithiasis or calcification in the wall of the ureter. The exact mechanism of calcification in our patient is unknown, but possible mechanisms include: 1. mucosal injury and ischemia: dystrophic calcification from stent-related mucosal injury and ischemic damage, with migration upon stent removal. 2. metabolic factors: hyperparathyroidism and potential enteric hyperoxaluria from gastric bypass, increasing calcium oxalate supersaturation (the urine oxalate level may have been lower than actual in our patient in the setting of reduced GFR during AKI). 3. infection and trauma: infection by urease-producing organisms and trauma from a foreign body, leading to encrusting calcification. The negative culture might not have detected Corynebacterium urealyticum. 4. combination of the above mechanisms.

Conclusions:

De novo calcification in transplant ureters can arise from various causes. Identifying the precise etiology and mechanism is crucial for effective treatment and preventing recurrence. Treatment options include ureter reconstruction, connecting the ureter to the bladder or native ureter, or lithotripsy to break down the calcification.

I have no potential conflict of interest to disclose.

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