Successful treatment of spontaneous kidney graft decapsulation 18 years after renal transplantation: a case report

Sir,

The detection of a perirenal fluid collection causing graft dysfunctions is common in the early postoperative phase after renal transplantation. These are typically lymphoceles, urinomas, abscesses and haematomas, and treatment is well established. Perirenal fluid collection causing acute or sub-acute renal failure several years after engraftment is unusual. A rare, but potentially treatable condition is acute spontaneous decapsulation of the kidney graft. We hereby present a case of spontaneous decapsulation and rapid decline of renal function 18 years after engraftment.

A 41-year-old Caucasian male with end-stage renal failure was diagnosed in 1989 with chronic glomerulonephritis (not biopsy verified) and received a renal transplant in 1990 at age 23, from his HLA-identical 21-year-old brother (CMV+ to +, PRA−). There were no rejections or other early complications. Graft function remained steady over the next 18 years with s-creatinine 100–120 μmol/L. Immunosuppression consisted of CsA (125 mg b.i.d., C₀ target level 75–125), prednisolone (5 mg × 1/day) and azathioprine (75 mg/day, 6-TGN target 100). In 2003, an ultrasound of the renal graft and in 2005 a CT scan of the abdomen was done with normal findings regarding the graft.

During a routine control at the local hospital s-creatinine had increased from a stable value (100–120 μmol/L) to 150 μmol/L. The development of chronic allograft nephropathy was suspected. Azathioprine was replaced by mycophenolate mofetil (MMF; 750 mg b.i.d.), and an ultrasound-guided renal biopsy was planned. The day after switch from azathioprine to MMF, the patient experienced a sudden onset of severe pain, and swelling in the graft was localized. S-creatinine at admission had further increased to 201 μmol/L.

A CT scan of the abdomen revealed a large fluid collection (>1 L) encasing the renal graft (Figure 1). A pigtail catheter was placed within the cavity. On the first day, 800 ml of yellow-coloured fluid was drained out and analysis showed an albumin content of 9 g/L, creatinine level 102 μmol/L, WBC < 0.1 × 10⁹/L and lactate dehydrogenase 68 U/L. Ultrasound/Doppler examination of the graft (after drainage) demonstrated normal parenchyma, renal pelvis and flow pattern. A renal biopsy was not performed. His symptoms resolved and s-creatinine normalized.

Fig. 1.

A CT Scan of the abdomen revealed a fluid collection (A) encasing the renal graft (B).

However, fluid secretion through the pigtail catheter persisted, at the level of 100–200 mL/day. A laparoscopic exploration was therefore performed after 1 week. Perioperatively, a huge cyst encapsulating the kidney graft was noted. A fenestration to the peritoneal cavity was easily performed by making a 3-inch window in the anterior/cranial wall of the cyst. The kidney surface was described as intensely red and ‘bare’—well in conjunction with the CT finding of renal decapsulation. Three months after the procedure, the renal allograft was functioning remarkably well with s-creatinine 95 μmol/L.

Discussion

Late spontaneous decapsulation of a kidney graft is a rare event [1–5]. The pathophysiology behind spontaneous decapsulation of kidney transplants remains unclear. Case reports indicate, however, that they all share some common clinical features; the late occurrence (4–12 years post-Tx); subcapsular localization; lymphatic biochemistry; large fluid volume and persisting secretion after drainage.

Several treatment options have been described. Koena et al. reported the first two cases in 1979 [1]. They tried to develop a new capsule and drainage by a LeVeen shunt, but failed. Both patients ended up with a graftectomy. In 1982, marsupialization was successfully used for the first time by Nghiem et al. [2]. According to Brown et al. [3] diuretics solved the problem.

The choice of therapy must depend on the patient's clinical presentation. In our case, the accumulation of fluid leads to pressure on the kidney and rapid deterioration of graft function. The biochemical composition of the fluid indicated lymphatic or transudative character.

He was switched from azathioprine to mycophenolate mofetil, but that was after s-creatinine had started to rise. To our knowledge, this is the latest post-Tx time point for spontaneous decapsulation reported in the literature. This is a rare complication, but with a deleterious effect on kidney function, if not detected and treated adequately. The exact cause of the late, spontaneous decapsulation remains obscure. But the incident seems to be inherent to transplanted kidneys, and the progressive tissue weakening possibly caused by the immunosuppressive therapy could be a contributing factor for the tissue disruption.

Conflict of interest statement. None declared.