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Background. Due to the shortage of deceased donors ABO-incompatible (ABOi) living kidney transplantation has become a popular alternative to deceased kidney transplantation. In recent years, recipient desensitization with a combination of anti-CD20 treatment (rituximab), antigen-specific immunoadsorptions (IA) and intravenous immunoglobulin (IVIG), led to promising short-term and intermediate-term results. However, little is known about the impact of this intensified desensitization protocol on the risk of surgical and infectious complications.Methods. We retrospectively analysed 21 consecutive recipients who underwent ABOi renal transplantation. Pre-transplant desensitization included administration of rituximab (375 mg/m2), mycophenolate mofetil (MMF), tacrolimus and prednisolone 4 weeks prior of scheduled transplantation as well as IA and IVIG. Forty-seven patients who underwent ABO-compatible (ABOc) renal transplantation served as the control group. Medical records and electronic databases were reviewed for patient and graft survival, renal function, rate of rejections, viral and bacterial infections as well as for surgical complications (SCs) post-transplantation.Results. All patients showed an immediate graft function. During a mean follow-up of 15.7 ± 8.3 months (interquartile range 11.9) patient survival was 95 and 98% in the ABOi and ABOc group, respectively. Allograft survival and function, as assessed by serum creatinine levels and calculated glomerular filtration rate at 1 year, did not differ between ABOi and ABOc recipients. Furthermore, the rate of biopsy-proven acute rejections was comparable between the two groups. However, there was a trend towards more SCs within the ABOi group (29 versus 11%, non-significant). In addition, the rate of viral infections including cytomegalovirus, Herpes simplex virus, Varicella zoster virus and polyoma virus was significantly increased among the ABOi recipients (50 versus 21%; P = 0.038) despite comparable tacrolimus trough levels and MMF and steroid doses.Conclusions. Our results, in line with the extended experience of other groups, demonstrate favourable short-term allograft survival and function after ABOi renal transplantation after desensitization with antigen-specific IA, IVIG and rituximab. However, the intensified desensitization was associated with an increased risk of infectious complications. This observation prompted us to briefly escalate the desensitization protocol in ABOi kidney recipients in our centre. [ABSTRACT FROM PUBLISHER]

Risk factors for chronic allograft nephropathy after renal transplantation: A protocol biopsy study.Background.Chronic allograft nephropathy (CAN) leads to chronic allograft dysfunction and loss. Regular renal transplant biopsies may be useful to find risk factors for CAN.Methods.We carried out 688 protocol biopsies in 258 patients at 6, 12, and 26 weeks after renal transplantation. Patients with signs of CAN in the biopsy 3 (N= 70, CAN group), and those without (N= 120, non-CAN group), were compared.Results.Chronic tubulointerstitial changes increased from biopsy 1 to 3 (5% vs. 37%,P<0.0001). Fifty-six of 190 patients had acute rejection within 6 months (30%), 33 of which were found in protocol biopsies (17%). On univariate analysis, the CAN group had CAN more often at biopsy 2 than the non-CAN group (23% vs. 4%,P<0.0001), had a lower calculated creatinine clearance at biopsy 1 and 2 (49.4± 25.8 vs. 57± 20.2 mL/min,P= 0.01; 47.3± 21.2 vs. 57.9± 19.5 mL/min,P= 0.001, respectively), had a living donor less often than a brain dead donor (7% vs. 18%,P= 0.045), had a longer cold ischemia time (17.4± 7 vs. 14.9± 8.1 hours,P= 0.04), and had arterionephrosclerosis more often (24% vs. 12%,P= 0.02). On multivariate analysis, the differences in CAN at biopsy 2 (P= 0.001) and lower GFR at biopsy 2 (P= 0.002) were confirmed; in addition, nephrocalcinosis (P= 0.006) and acute rejection (P= 0.046) were found to occur more often.Conclusion.Chronic tubulointerstitial changes develop early after renal transplantation and are associated with reduced kidney function. Risk factors for CAN are arterionephrosclerosis (donor-related), nephrocalcinosis (related to preexisting hyperparathyroidism), a long cold-ischemia time (ischemia-perfusion-related), and acute rejection. Renal functional decline precedes morphologic changes of CAN, expressed as tubular atrophy and interstitial fibrosis. [ABSTRACT FROM AUTHOR]

SUMMARY: The case of a 48-year-old female patient who underwent renal transplantation because of an end-stage renal disease after membranous glomerulonephritis (WHO class V) in systemic lupus erythematosus (SLE) is presented. The patient lost one cadaveric allograft immediately after transplantation because of renal vein thrombosis, presumably caused by anti-Cardiolipin antibodies. A second cadaveric allograft showed a stable function for several years before slowly deteriorating. An abrupt increase of serum creatinine led to the suspicion of a final episode of acute rejection. A biopsy was performed, which showed an overlap of rejection and recurrent lupus nephritis in an advanced chronically damaged allograft. The lupus nephritis recurred as the same WHO class V as in the native kidney, but without significant predictive clinical or serological signs of SLE activity. The case presented and a review of the literature indicate that the frequency of recurrent lupus nephritis might be underestimated, and earlier surveillance biopsies in transplanted SLE patients should be considered. [ABSTRACT FROM AUTHOR]