Increase in the number of patients diagnosed using the new classification of hypertensive disorders of pregnancy in Japan.

AIM: This study aimed to examine how the number of patients diagnosed with pre-eclampsia increased according to the Japanese classification of hypertensive disorders of pregnancy (HDP) that was revised in 2018. The effect of new classification on perinatal outcomes was also analyzed. METHODS: We enrolled 181 women with HDP who delivered at Hokkaido University Hospital between February 2011 and December 2017. All women were reclassified on the basis of the new classification, in which proteinuria was not required to diagnose pre-eclampsia in patients with maternal organ damage. The number and reasons of reclassification and the admission rate to the neonatal intensive care unit (NICU) and gestational age (GA) at the onset of HDP and at delivery were analyzed. RESULTS: In this cohort, 17 (9.4%) of 181 women with HDP were reclassified. Low platelet count (41.2%) and uteroplacental dysfunction (41.2%) were the two main causes for reclassification. GA at the onset of HDP (33.6 [29.9-36.1] weeks vs 37.4 [35.7-38.4] weeks; P < 0.001) and at delivery (35.9 [32.4-37.3] weeks vs 38.1 [37.3-39.6] weeks; P < 0.001) were significantly earlier in women with reclassification than women without reclassification. The NICU admission rate was higher in women with reclassification than women without reclassification (70.6% vs 20.4%; P < 0.001). CONCLUSION: Almost 10% of pregnant women were newly diagnosed with pre-eclampsia as per the new Japanese classification of HDP. Women with reclassification as pre-eclampsia had a greater risk of preterm delivery and NICU admission than those who were not reclassified.

Post-partum podocyturia following pre-eclamptic pregnancy.

AIM: Urine podocin mRNA expression and urine podocin : nephrin mRNA expression ratio (PNR) increase with increasing proteinuria during pregnancy complicated with pre-eclampsia (PE). This suggests that urine podocytes with reduced nephrin mRNA expression are abundant in pathological podocyturia. The aim of this study was therefore to determine post-partum changes in podocyturia and PNR in relation to proteinuria after pre-eclampsia (PE). METHODS: A total of 137 peripartum urine specimens, consisting of 72 and 65 from 24 and 30 women with PE and normotensive control pregnancies (NCP), respectively, were studied. Determination of urine protein and creatinine concentration and quantitative analysis of podocyte-specific podocin and nephrin mRNA expression were carried out using reverse transcription-polymerase chain reaction in pelleted urine samples. Podocyturia was monitored via urine podocin mRNA expression. Podocyturia and proteinuria were normalized by urine creatinine concentration. RESULTS: Podocyturia and urine PNR decreased with decreasing proteinuria as well as with increasing time after delivery in the urine from PE women. In physiological proteinuria (i.e. protein : creatinine ratio [P/Cr] 0.005-0.1 mg/mg), however, both podocyturia and PNR were significantly greater in the urine from PE women compared with NPC women, although P/Cr was similar between the groups (median, 0.037 mg/mg for PE vs 0.029 mg/mg for NCP). CONCLUSIONS: Podocyturia decreases with decreasing proteinuria in PE women after childbirth. In PE women, however, pathological podocyturia consisting of podocytes with decreased nephrin mRNA expression persisted even after proteinuria decreased to a level similar to that in NCP women.

Serum placental growth factor and soluble fms-like tyrosine kinase 1 at mid-gestation in healthy women: Association with small-for-gestational-age neonates.

AIM: This study was performed to determine the associations between serum placental growth factor (PlGF) and soluble fms-like tyrosine kinase 1 (sFlt-1) levels at mid-gestation with the risk of small-for-gestational-age (SGA) neonates born at gestational week (GW) ≥ 36 in healthy women. METHODS: PlGF and sFlt-1 concentrations were determined at GW 24-27 in 183 women with births at GW ≥ 36, but without gestational diabetes mellitus and hypertension. RESULTS: Thirteen (7.1%) SGA neonates were born. Median (range) GW at blood sampling was similar between women with and without SGA (25 [24-25] and 24 [24-27], respectively, P = 0.671). Pre-pregnancy body mass index (BMI) and PlGF levels were significantly lower in women with than without SGA, while sFlt-1 levels and sFlt-1 : PlGF ratio (sFlt-1/PlGF) did not differ significantly between the two groups. PlGF and sFlt-1/PlGF, but not BMI or sFlt-1, showed significant correlations with birthweight z-score; the correlation was positive for PlGF and negative for sFlt-1/PlGF. Women with PlGF level < 10th percentile and those with sFlt-1/PlGF level > 90th percentile showed significantly increased risk of SGA compared to those with respective counterpart characteristics; relative risk was 3.8 (95% confidence interval, 1.3-11.3; 21% [4/19] vs 5.5% [9/164]) for PlGF and 7.9 (95% confidence interval, 3.0-20.8, 33.3% [6/18] vs 4.2% [7/165]) for sFlt-1/PlGF. CONCLUSION: Maternal PlGF and sFlt-1/PlGF determined during GW 24-27 were associated with the risk of SGA neonates born at GW ≥ 36, even in women with uncomplicated pregnancies.

Maternal bradycardia occurring prior to onset of HELLP syndrome in a woman with pre-eclampsia.

A 36-year-old nulliparous woman developed pre-eclampsia at gestational week (GW) 28-6/7 Cardiac status was checked regularly. Heart rate of 93 beats per minute (bpm) with left atrial diameter (LAD) of 35 mm, left ventricular hypertrophy and inferior vena cava diameter (IVCD) of 8 mm at GW 32-0/7 decreased to 48 bpm with an expanded IVCD to 25 mm, dilated left atrium (LAD to 39 mm), increased pulmonary arterial pressure, increased systemic vascular resistance (approximate 3000 dyn s/cm5) and biphasic intrarenal venous flow pattern 3.5 hours prior to childbirth at GW 32-3/7 Epigastralgia, tachycardia (160 bpm) and marked hypertension (201/111 mm Hg) occurring 2 hours after echocardiography necessitated caesarean section, with subsequent development of HELLP syndrome. Acute fluid shift from the splanchnic vasculature to central vasculature may have occurred causing HELLP syndrome as a result from vasospasm associated with sympathetic hyperactivity. The cause of bradycardia prior to tachycardia remains unclear.