Triplet Pregnancy in a Diabetic Mother With Kidney Transplant: Case Report and Review of the Literature.

Triplet and higher-order multiple pregnancies can carry increased fetal and maternal complications. Reports of triplet pregnancies after kidney transplant are scarce and have been associated with perinatal complications. Presence of diabetes in such cases worsens both fetal and maternal outcomes. Here, we present a triplet pregnancy in a kidney transplant recipient with diabetes. We also reviewed the literature for causes, prevalence, and outcomes in association with chronic kidney disease, kidney transplant, and diabetes mellitus. The patient, a 31-year-female who received a living-donor kidney transplant, had a first-time pregnancy 6 years after transplant. Pregnancy was complicated by gestational diabetes, preeclampsia, and miscarriage. She continued to have postpartum-impaired glucose tolerance. She became pregnant again after 6 months but required insulin therapy during her third trimester. Pregnancy was terminated by cesarean section for a viable small boy. Two years later, she had triplet pregnancy after ovulation induction with clomiphene. Glycemic control was maintained using intensive insulin therapy guided by frequent home blood glucose monitoring (HbA1c was 5.8% at 22 wk). Both gynecologic care and nephrologic care were carried out through outpatient follow-up. Pregnancy was complicated by hypertension and mild renal dysfunction without proteinuria and ended in elective premature cesarean section at 32 weeks of gestation. She had 3 male babies with low birth weights (1320, 1380, 1275 g), with the largest baby developing sepsis and requiring an intensive care unit stay and then incubator for 49 days. The other 2 required incubators for 36 days. Their weights after 22 months were 9, 16, and 11 kg. The mother is now normotensive with normal renal function and impaired glucose tolerance. Care of diabetic kidney recipients with triplet pregnancy constitutes a special challenge requiring a multispecialty skilled team to ensure the best outcome.

Active management versus minimization of immunosuppressives of BK virus-associated nephropathy after a kidney transplant.

OBJECTIVES: Thus far, there is no active treatment for BK virus-associated nephropathy after a kidney transplant that has proven to be effective. We sought to assess the effectiveness of treatment with leflunomide, intravenous immunoglobulin, and ciprofloxacin on graft outcome after 1 year compared with a historical group treated with reduced immunosuppressive medications strategy. MATERIALS AND METHODS: Group 1 (n = 19) was composed of kidney transplant recipients with twice positive BK virus-polymerase chain reaction in urine and blood who underwent graft biopsy to confirm BK virus-associated nephropathy. Once BK virus-associated nephropathy was diagnosed, antimetabolite (mycophenolate mofetil or azathioprine) was changed to leflunomide, and intravenous immunoglobulin and oral ciprofloxacin were given. Group 2 (n = 14) was composed of BK virus-associated nephropathy patients treated conventionally with reduced immunosuppressive medications. RESULTS: Thirty-three patients were treated, 23 were males (70%), there were 15 were deceased donors (45.5%), 15 were diabetics (45.5%), mean human leukocyte antigen mismatches were 3.76, seven had a zero DR mismatch (21.2%), and 8 were CW7 negative (24.2%). All patients received induction therapy (thymoglobulin in 22 [66.6%]), 7 had delayed graft function (21.2%) and 18 received antirejection therapy before receiving BK virusassociated nephropathy diagnosis (52.9%). Maintenance immunosuppression was prednisolone and mycophenolate mofetil (2 g/d) in 31 patients (94%), and tacrolimus in 13 (39.4%). Tacrolimus was given to 12 patients in group 1 (63.1%), while sirolimus was given to 7 patients in group 2 (50%). One graft was lost in each group by the end of the study, and 1 patient died with functioning graft in group 2. CONCLUSIONS: No significant difference existed in 1-year graft outcomes between treatment of BK virus-associated nephropathy by reduction of immunosuppressive medications or actively by leflunomide, intravenous immunoglobulin, and ciprofloxacin.

Late acute antibody mediated rejection after nine years of renal transplantation.

Acute antibody mediated rejection (AMR) is rarely reported as a long-term com-plication of renal transplantation, and it can present on top of another chronic pathology affecting the graft. A 45-year-old gentleman with chronic kidney disease due to unknown etiology received renal transplantation from his sister with 4 HLA mismatches. He received antithymocte globulin induction therapy and was maintained on steroids, azathioprine (AZA) and cyclosporine A (CsA). Up to eight years post-transplantation he was clinically and biochemically stable. He lost follow-up for about one year, and then presented with nephritic nephrotic syndrome and rise of serum creatinine (SCr.) to 210 µmol/L. Graft biopsy revealed picture suggestive of acute AMR on top of de novo membranoprolipherative glomerulonephritis (MPGN) with focal crescent formation, diffuse immune complex deposition and peritubular capillaries C4d positivity. Anti-HLA donor specific antibodies were highly positive for B and T cells class I and class II. The patient was treated with intravenous immunoglobulin, plasma exchange and anti-CD20 (rituximab). AZA was changed to mycophenolate mofetil and CsA to tacrolimus. He had partial response, but SCr. continued at 220 µmol/L.