Antibody-mediated rejection presenting as allograft hydronephrosis

Abstract

An 18-year-old boy underwent living-donor renal transplantation. His mother was the donor. The patient was started on tacrolimus (0.1 mg/kg/d), prednisolone (20 mg/d) and azathioprine (2 mg/kg/d), after initial 3 days of I.V. methyl prednisolone (15 mg/kg/d), as immunosuppressive regimen. Six months after transplantation, he presented with fever that had occurred for two days. There was no history of dysuria, altered urine colour, pyuria or edema. Serum creatinine increased from 1.0 mg/dl to 1.9?2.8?3.7 mg/dl over the next 3 days. On the day of admission, serum tacrolimus levels, blood and urine cultures, and search for polyoma virus were ordered. A Doppler ultrasound of the renal allograft artery revealed a resistive index of 0.9 and hydronephrosis, which had not been present on any of the previous ultrasound exams. A CT scan of the abdomen, with an empty urinary bladder, confirmed hydronephrosis of the allograft, with possible pelvic ureteric junction obstruction (Fig. 1). Blood clots, a technically poor ureteral implantation and ureteral are common causes of obstruction in the early post operative phase, whereas periureteral fibrosis, lymphocele and calculi are possible causes in the late post-operative phase. On the same day, the renal transplant surgeon reviewed the operation protocol notes and confirmed that an antireflux procedure, the Lich reimplantation, had indeed been performed. The radionuclide micturition cystography did not reveal vesicoureteral reflux. Ureteric stenosis due to polyoma virus–associated nephropathy (PVAN) was provisionally diagnosed. However, it is known that PVAN typically induces stenosis in the distal rather than the proximal part of the ureter [1, 2]. On day two, the polyoma virus DNA was found to be negative in both urine and blood. Blood and urine cultures were also sterile. Serum tacrolimus levels were found to be 1.8 ng/l. Circulating donor-specific antibodies determination was unfortunately not available in our hospital. The allograft biopsy was done, under ultrasound guidance, and it revealed neutrophils in the capillaries and in the interstitium, diffuse acute tubular injury and C4d positivity in peritubular capillaries. PVAN may be differentiated from acute antibody-mediated rejection (AMR), but not from acute cellular rejection, by the presence of mononuclear and plasma cell infiltration. After renal transplantation, the ureter receives its entire blood supply from the ureteral branch of the renal artery [3]. Acute rejection involves both the kidney and the ureter, and the resulting edema and possible secondary ischaemia may also lead to ureteral obstruction [3]. In an animal model, Hricak et al. [4], found significant alterations in the ureteral dynamics during rejection, as shown by the progressive decrease in electrical activity of the ureteral muscle on electromyography and the reduced G. Swarnalatha R. Ram (&) B. H. Santosh Pai V. Ramesh K. V. Dakshinamurty Nizam’s Institute of Medical Sciences, Punjagutta, Hyderabad 082, India e-mail: ram_5_1999@yahoo.com