Limited data exist about Clostridium difficile colitis (CDC) in solid organ transplant patients. Between 1/1/99 and 12/31/02, 600 kidney and 102 pancreas-kidney allograft recipients were transplanted. Thirty-nine (5.5%) of these patients had CDC on the basis of clinical and laboratory findings. Of these 39 patients, 35 have information available for review. CDC developed at a median of 30 days after transplantation, and the patients undergoing pancreas-kidney transplantation had a slightly higher incidence of CDC than recipients of kidney alone (7.8% vs. 4.5%, P> 0.05). All but one patient presented with diarrhea. Twenty-four patients (64.9%) were diagnosed in the hospital, and CDC occurred during first hospitalization in 14 patients (40%). Treatment was with oral metronidazole (M) in 33 patients (94%)and M + oral vancomycin (M + V) in 2 patients. Eight patients had recurrent CDC, which occurred at a median of 30 days (range 15-314) after the first episode. Two patients (5.7%) developed fulminant CDC, presented with toxic megacolon, and underwent colectomy. One of them died; the other patient survived after colectomy. CDC should be considered as a diagnosis in transplant patients with history of diarrhea after antibiotic use, and should be treated aggressively before the infection becomes complicated. KeywordsClostridium difficile; kidney; pancreas; kidney; transplantation Infections are the leading cause of morbidity and mortality in the early post-transplant period. More than 80% of recipients suffer at least one episode of infection in the first year (1,2). The occurrence of infectious complications is closely related to immunosuppressive treatment, including induction, maintenance, and the treatment of acute rejection.Although, many viral and bacterial opportunistic infections are well known in kidney and pancreas-kidney allograft recipients, Clostridium difficile colitis (CDC) is a less frequently described gastrointestinal infection in these patients. Clostridium difficile (CD) is one of the most common hospital-acquired (nosocomial) infections causing antibiotic-associated colitis (3). CDC has been defined as the existence of diarrhea and CD toxin in the stool.In this study, we identified our patients with CDC after kidney and pancreas-kidney transplantation and report the clinical presentation, timing of infection, risk factors, recurrence, and treatment. We also report two patients with fulminant CDC (FCDC) after kidney transplantation.

Alemtuzumab has been used in off-label studies of solid organ transplantation. We extend our report of the first 200 consecutive living donor solitary kidney transplantations under alemtuzumab pretreatment with tacrolimus monotherapy and subsequent spaced weaning to 3 years of follow-up. We focused especially on the causes of recipient death and graft loss, and the characteristics of rejection. The actuarial 1-, 2-and 3-year patient and graft survivals were 99.0% and 98.0%, 96.4% and 90.8% and 93.3% and 86.3%, respectively. The cumulative incidence of acute cellular rejection (ACR) at the following months was 2% ≤6, 9.0% ≤12, 16.5% ≤18, 19.5% ≤24, 23.5% ≤30, 24.0% ≤36 and 25% ≤42. The mean serum creatinine (mg/dL) and glomerular filtration rate (mL/min/1.73 m 2 ) at 1 and 3 years were 1.4 ± 0.6 and 58.7 ± 21.6 and 1.5 ± 0.7 and 54.9 ± 20.9, respectively. Fifty (25%) recipients had a total of 89 episodes of ACR. About 88.7% of ACR episodes were Banff 1, and of those, 82% were steroid-sensitive. Nine (4.5%) recipients had antibodymediated rejection (AMR). About 76.5% were weaned but only 46% are currently on spaced dose (qod or less) tacrolimus monotherapy, and 94.4% remained steroidfree from the time of transplantation. Infectious complications were uncommon. This experience suggests the 3-year efficacy of this approach.

Knowledge of polyomavirus BK (BKV) genomic diversity has greatly expanded. The implications of BKV DNA sequence variation for the performance of molecular diagnostic assays is not well studied. We analyzed 184 publically available VP-1 sequences encompassing the BKV genomic region targeted by an in-house quantitative hydrolysis probe-based PCR assay. A perfect match with the PCR primers and probe was seen in 81 sequences. One Dun and 13 variant prototype oligonucleotides were synthesized as artificial targets to determine how they affected the performance of PCR. The sensitivity of detection of BKV in the PCR assay was a function of the viral genotype. Prototype 1 (BKV Dun) could be reliably detected at concentrations as low as 10 copies/l. However, consistent detection of all BKV variants was possible only at concentrations of 10,000 copies/l or higher. For BKV prototypes with 2 or more mismatches (representing genotype IV, genotype II, and genotype 1c strains), the calculated viral loads were 0.57 to 3.26% of the expected values. In conclusion, variant BKV strains lower the sensitivity of detection and may have a substantial effect on quantitation of the viral load. Physicians need to be cognizant of these effects when interpreting the results of quantitative PCR testing in transplant recipients, particularly if there is a discrepancy between the clinical impression and the measured viral load.Polyomavirus BK (BKV) has become an important pathogen in kidney transplant patients. Immunosuppression given to prevent acute rejection triggers BK viruria in 10 to 60%, viremia in 5 to 30%, and biopsy-proven viral nephropathy in 1 to 10% of patients (8,10,11). Initial graft loss rates associated with BKV nephropathy were very high but have now dropped to Ͻ25%. This success has been attributed to intensive viral monitoring followed by preemptive reduction in immunosuppression (1,14). In a recent survey that had an overall response rate of 55.5%, 173 of 200 (86.5%) kidney transplant centers reported screening for BKV in blood by quantitative PCR, while 111 of 202 (55.5%) performed viral screening in urine (2). In the latter category, 90% of respondents preferred PCR screening to urine cytology. While cytology is a useful modality to screen for viral nephropathy in low-resource settings, it is less sensitive than quantitative PCR for detecting viral replication prior to the onset of clinical nephropathy. In addition, it cannot differentiate BKV infection from infection by the related polyomavirus JC, which causes significant graft dysfunction at a substantially lower frequency.Current quantitative PCR assays were developed several years ago using BKV Dun or similar genotype I strains as reference sequences for the design of primers and probes. However, our knowledge of BKV genomic diversity has expanded enormously (6,7,12,16). PCR-based diagnostic and treatment algorithms must be reevaluated to take into account newly discovered BKV single-nucleotide polymorphisms. One approach to define the potential extent of this probl...

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Chronic allograft nephropathy (CAN) is a major indication for initiation of sirolimus (SRL) in renal transplantation (TX) to prevent deterioration of renal function. We evaluated whether the CAN score at time of sirolimus rescue (SRL-R) predicts renal allograft function. CAN score is the sum of the following 4 categories: glomerulopathy (cg, 0-3), interstitial fibrosis (ci, 0-3), tubular atrophy (ct, 0-3), and vasculopathy (cv, 0-3).