'GA-gestational age; 2BW-birthweight; -'Newborn malformations; 4Graft loss within 2 years of delivery; ^International survey and NTPR data; "Only livebirths reported; 'Neonatal deaths excluded from analysis; 8NR-not reported; ®1 kidney and 1 pancreas loss in 2 different recipients;101 kidney and 1 pancreas/kidney loss in 2 different recipients.


Toma et al reported that the 57 babies born to mothers on azathioprine had a significantly higher mean birthweight (2567 ± 491.1 gms) than the 94 babies born to mothers on CsA (2252 ± 629.2 gms). There were no congenital anomalies in either group. In this survey of 143 transplant units, graft function deteriorated in 20% of patients after delivery, with graft loss in approximately 10% of the pa-tients.9 In an analysis of NTPR data on female renal recipients, significant differences between CsA and non-CsA (azathioprine, steroids) recipients were noted for birthweight (CsA group lower, p=0.003) and drug-treated hypertension (CsA group higher, p=0.0001). When the data were analyzed using a multivariate analysis of all renal recipients, the most significant predictors of lower birthweight in newborns were maternal hypertension (p=0.0073), serum creatinine (> 1.5 mg/dL, p=0.0439), and diabetes mellitus (p=0.05). There were no specific patterns of malformation noted in the offspring of either recipient group (CsA vs. non-CsA) with a lower incidence of complications in the newborn of CsA-recipients. Neonatal death rates were 0.9% in the CsA-based recipients and 2.4% in the non-CsA-based recipients.10

As there are more extensive data available regarding renal transplant recipients and pregnancy, there have been efforts to identify predictors of adverse maternal and fetal outcomes as well as to determine whether pregnancy has long-term effects on graft function. Two well-designed case studies showed no significant effect on graft function when a group of pregnant women was compared to nonpregnant controls.11,12 A longer-term follow-up of one of these studies, however, did suggest that a minor deleterious effect might result.13 A retrospective case control study from the EDTA suggested that pregnancy rarely if ever has a deleterious effect on graft function.14 NTPR data have shown a minor increase in serum creatinine post-partum when compared to prepregnancy levels.

A report from the National Transplant Database Pregnancy Register from the U.K. has recently shown that pregnancy success, defined as a livebirth and survival after at least a 24 weeks gestation, was significantly related to the serum creatinine level measured within 3 months prior to conception (p=0.04).15

Variables affecting post-partum graft loss were analyzed in female recipients from NTPR data.16 Forty recipients whose graft failed any time after pregnancy were compared to 81 randomly selected recipients who did not experience a graft loss; all were on CsA-based regimens. In an analysis using a Cox proportional hazards model, those recipients with a prepregnancy serum creatinine > 2.5 mg/ dL were approximately 3 times more likely to experience graft loss than recipients with a prepregnancy serum creatinine < 1.5 mg/dL. An increase in serum creatinine during pregnancy was also associated with an increased risk of graft loss. In a recent single center analysis of 33 pregnancies in 29 female renal recipients, all recipients with prepregnancy serum creatinine > 200mmol/l had progression of renal impairment and required renal replacement therapy within 2 years of delivery.17 The authors also suggested that no evidence of chronic rejection before pregnancy and proteinuria < 1 gm/day allowed for a good obstetric outcome. In another single center study, 0.3 gms per day of urine protein loss prior to pregnancy was

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