Immunosuppression (IS) is often withdrawn in patients with end stage renal disease secondary to a failed renal allograft, and this can lead to an accelerated loss of residual renal function (RRF). As maintenance of RRF appears to provide a survival benefit to peritoneal dialysis (PD) patients, it is not clear whether this benefit of maintaining RRF in failed allograft patients returning to PD outweigh the risks of maintaining IS. A 49 year-old Caucasian male developed progressive allograft failure nine years after living-donor renal transplantation. Hemodialysis was initiated via tunneled dialysis catheter (TDC) and IS was gradually withdrawn. Two weeks after IS withdrawal he developed a febrile illness, which necessitate removal of the TDC and conversion to PD. He was maintained on small dose of tacrolimus (1 mg/d) and prednisone (5 mg/d). Currently (1 year later) he is doing exceedingly well on cycler-assisted PD. Residual urine output ranges between 600-1200 mL/d. Total weekly Kt/V achieved 1.82. RRF remained well preserved in this patient with failed renal allograft with minimal immunosuppressive therapy. This strategy will need further study in well-defined cohorts of PD patients with failed allografts and residual RRF to determine efficacy and safety.

Data from the United States Renal Data System revealed that the number of patients with a failed transplanted kidney in the United States has increased over the past few years[1]. The management of those patients with a failed transplant involves two major decisions: optimal management of immunosuppression (IS) and whether or not to perform graft nephrectomy. While there might be a survival advantage in maintaining dialysis patients on long-term immunosuppressive therapy after allograft failure[2], immunotherapy comes with its own risks, which include increased susceptibility to infections and cancers[3,4]. This case report and review of the literature illustrates the fact that not all dialysis patients with allograft dysfunction are created equally and that different cohorts deserve further study regarding the benefits of maintenance of low dose IS after declared allograft failure.

A 49-year-old Caucasian male with past medical history of hypertension was diagnosed with end stage renal disease (ESRD) and was started on peritoneal dialysis (PD) in 2001. One year later he had living-donor renal transplantation, after which he maintained fair allograft function with new baseline creatinine around 1.8-2.2 mg/dL. His initial immunosuppressive therapy included tacrolimus, mycophenolate mofetil (MMF) and prednisone. His medications were adjusted over the next few months and he was maintained on tacrolimus 3 mg twice daily, MMF 500 mg twice daily, and prednisone 5 mg/d. 3 mo after his transplant, he had a biopsy-proven type IIA acute rejection, which responded well to treatment with steroids.

He presented to the transplant clinic on September 13, 2010 for a routine visit with elevated serum creatinine of 3.2 mg/dL compared to creatinine of 1.8 mg/dL one year prior to that. Further testing revealed nephrotic range proteinuria of around 3 g by a spot urine analysis. The patient has been compliant with his immunosuppressive medications and has no major change in his medical, surgical, and social history. The patient was admitted to the hospital and underwent a diagnostic percutaneous ultrasound guided renal biopsy (Figure 1). Histopathologic examination of the tissue confirm the presence of focal segmental glomerulosclerosis as evidenced by involvement of approximately 50% of the glomeruli with segmental lesions and some of the glomeruli had total global glomerulosclerosis. There was also associated interstitial fibrosis and tubular atrophy. Immunofluorescence studies were consistent with a diagnosis of focal segmental glomerulosclerosis with 2+ staining for IgG and a segmental distribution, 2+ staining of IgM and a segmental distribution, negative staining for IgA and 2+ staining for kappa and lambda light chains. The patient had one area of questionable crescent formation on a single glomerulus but the biopsy was unrevealing otherwise for any other disease process. There was no evidence of transplant rejection or antibody mediated rejection as the patient had a negative C4d immunofluorescence. His medications were adjusted where his prednisone dose was increased to 60 mg/d and lisinopril was resumed to reduce proteinuria.

Open in New Tab   Full Size Figure   Download Figure

Figure 1 Patient was admitted to the hospital and underwent a diagnostic percutaneous ultrasound guided renal biopsy (HE stain, ×100). Hematoxylin and eosin (A) and periodic acid-Schiff stains of the kidney biopsy specimens (light microscopy) (B) showing the histopathology examination of the kidney, which tissue confirm the presence of focal segmental glomerulosclerosis as evidenced by involvement of approximately 50% of the glomeruli with segmental lesions and some of the glomeruli had total global glomerulosclerosis. There was also associated interstitial fibrosis and tubular atrophy.

His creatinine worsened gradually over the next five months. He was readmitted to the hospital in February 2011 with herpes zoster involving his eye and was treated with ganciclovir and local erythromycin ointment. The serum creatinine was 5.02 mg/dL at the time of admission and 5.42 mg/dL at the time of discharge. It was clear that the patient was experiencing progressive renal allograft failure and the options of dialysis were explained to the patient.

Few days after his discharge, he was readmitted to the hospital for evaluation of pneumonia and was treated with antibiotics. During that hospitalization his renal function continues to worsen with associated oliguria and clinical uremia that required initiation of dialysis. Tunneled dialysis catheter (TDC) was placed and the patient was discharged in stable condition. He remained oliguric with minimal urine output and he continued hemodialysis via TDC. In the interim, he also had a PD catheter placed. MMF was discontinued but he was maintained on low dose of tacrolimus (1 mg twice daily). Two months later he was re-admitted to the hospital with suspected sepsis and associated TDC infection. He was treated with antibiotics, stress dose steroids and removal of the hemodialysis catheter. During the hospitalization he had increased urine output up to 1.0-1.5 L per 24 h. However, he continued to be dialysis dependent with elevated creatinine around 7-8 mg/dL. At that point of time, PD was initiated and we opted to continue his tacrolimus at 1 mg daily (serum levels not measurable) and prednisone 5 mg daily. Currently (1 year later) he is doing exceedingly well on cycler-assisted PD regimens of 10 L exchanged over 8 h. Residual urine output ranges between 600-1200 mL/d. Total weekly Kt/V achieved 1.82 (dialysate: 1.30; endogenous: 0.51) and global creatinine clearance 64.8 L/wk per 1.73 m² (dialysate: 39.3; endogenous: 25.4). A renal scan confirmed that all endogenous renal function is originating from the partially functioning renal allograft. Furthermore, his albumin remained stable at 4 g/dL and hemoglobin well controlled (11.6 g/dL) on darbopotein-alfa 12.5 mg/wk. He is currently awaiting another renal transplant and has an arteriovenous fistula in place.