254 Urinary C-Reactive Protein in Small for Gestational Age Neonates

Abstract

Background: C reactive protein (CRP) has been found in amniotic fluid (AF) and fetal urine. Elevated levels of AF-CRP have been associated with preterm birth and neonatal infection. Increased AF-CRP levels have been found at the time of genetic amniocentesis in cases which developed preeclampsia later in gestation. The aim of this study was to explore whether small for gestational age neonates (SGA) excrete more CRP.

Methods: Consecutive newborns admitted to the NICU were included in the study. SGA was defined as a birth weight below the 10th percentile. SGA neonates exposed to placental insufficiency leading to intrauterine growth restriction (IUGR), defined as abdominal circumference below the 5th percentile at prenatal sonography, were analysed separately. Each SGA/IUGR infant was matched for gestational age to an appropriate for gestational age (AGA) neonate. Neonates with infectious morbidity at delivery were excluded. Urine samples were obtained in the first week of life using sterile cotton flock. After centrifugation of the flock, CRP was collected in sterile tubes and sent immediately to the laboratory. Urinary CRP was measured with a commercially available ELISA kit. The sensitivity of the assay was below 10%. The urinary CRP values were normalized for the urinary creatinine content of every single probe. Spearman rank correlation and Mann Whitney test were used for statistical purposes.

Results: Urinary CRP was measured in 21 SGA and 21 control infants. Clinical and laboratory results are presented in the table.

Table 1

Serum CRP values were below the detection limit (<3mg/l) in 66.7% (14/21) and 76.2% (16/21) of cases and controls, respectively. Including only IUGR infants in the analysis, the difference in urinary CRP between cases and controls [92.1 (2–544.9) vs. 3.1 (0.2–114.5); p<0.05] remained statistically significant.

Conclusion: SGA and IUGR infants excrete in the urine more CRP than AGA infants. This difference may be explained either by a prerenal mechanisms due to hypoperfusion during placental insufficiency or increased stimulation of renal CRP production by circulating pro-inflammatory cytokines.

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