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Plasma levels of angiopoietin-2 are increased in patients with chronic kidney disease (CKD). Moreover, mouse models of progressive kidney disease also demonstrate increased angiopoietin-2 in both plasmas and kidneys. The role of dysregulated angiopoietins in the progression of kidney disease has not been thoroughly investigated. Here, we found in a cohort of 319 patients with CKD that plasma angiopoietin-2 and angiopoietin-2/angiopoietin-1 ratios were positively associated with the development of kidney failure. In mice with progressive kidney disease induced by either ureteral obstruction or ischemia-reperfusion injury, overexpression of human angiopoietin-1 in the kidney tubules not only reduced macrophage infiltration in the initial stage post-injury but also attenuated endothelial cell apoptosis, microvascular rarefaction, and fibrosis in the advanced disease stage. Notably, angiopoietin-1 attenuated chemokine C-C motif ligand 2 (CCL2) expression in the endothelial cells of the fibrosing kidneys, and these protective effects led to attenuation of functional impairment. Mechanistically, angiopoietin-1 reduced CCL2-activated macrophage migration and protected endothelial cells against cell apoptosis induced by angiopoietin-2 and Wnt ligands. Based on this, we applied L1-10, an angiopoietin-2 inhibitor, to the mouse models of progressive kidney disease and found inhibitory effects on macrophage infiltration, microvascular rarefaction, and fibrosis. Thus, we defined the detrimental impact of increased angiopoietin-2 on kidney survival of patients with CKD which appears highlighted by angiopoietin-2 induced endothelial CCL2-activated macrophage infiltration and endothelial cell apoptosis in their kidneys undergoing fibrosis., (Copyright © 2022 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.)

Objective: The aim of this retrospective observational study was to determine the efficacy of carbetocin in reducing blood loss and primary postpartum hemorrhage (PPH) in vaginal and cesarean deliveries in a tertiary hospital in Taiwan., Materials and Methods: Eligible gravid women (27-41 weeks) with available data were categorized into those treated prophylactically with and without carbetocin. The primary outcome was blood loss and incidence of primary PPH as measured by intrapartum/intraoperative and postpartum (recovery room) blood loss., Results: A total of 1069 deliveries were evaluated. Maternal age (∼31 years of age), body mass index (∼27 kg/m 2 ) and parity (∼1.4) were similar among those treated with and without carbetocin for both vaginal and cesarean deliveries. The majority [749/1069 (70.1%)] of deliveries were vaginal; a similar proportion of women undergoing vaginal [221/749 (29.5%)] and cesarean [110/320 (34.4%)] deliveries received prophylactic carbetocin for prevention of PPH. Among vaginal deliveries, there was no significant difference in intrapartum (p = 0.083) or postpartum (p = 0.925) blood loss, or incidence of PPH (p = 0.092) between women with versus without carbetocin prophylaxis. However, there was a significant reduction in the intraoperative and total blood loss among cesarean deliveries with versus without carbetocin prophylaxis (p < 0.001). The incidence of PPH was higher [84/320 (26.3%)] among cesarean than among vaginal deliveries [62/749 (8.3%)], but was significantly lower among cesarean deliveries with [18 (16.36%)] versus without [66 (30.45%); p = 0.003] carbetocin prophylaxis., Conclusion: In Taiwan, prophylactic use of carbetocin resulted in significantly less blood loss and incidence of PPH in cesarean than in vaginal deliveries., (Copyright © 2016. Published by Elsevier B.V.)

Objective: We describe a prenatal molecular diagnosis of hypochondroplasia (HCH) in a pregnancy not at risk of HCH and review the literature on prenatal diagnosis of HCH., Case Report: A 28-year-old primigravid woman was referred for genetic counseling at 30 weeks of gestation because of short-limbed dwarfism in the fetus. The woman had a body height of 152 cm. Her husband had a body height of 180 cm. Level II ultrasound showed a normal amount of amniotic fluid and a singleton fetus with fetal biometry equivalent to 30 weeks except for short limbs. Fetal biometry measurements were as follows: biparietal diameter = 7.38 cm (30 weeks); head circumference = 28.14 cm (30 weeks); abdominal circumference (AC) = 24.64 cm (30 weeks); femur length (FL) = 3.97 cm (<5th centile); FL/AC ratio = 0.161 (normal > 0.18); humerus = 3.64 cm (<5th centile); radius = 3.49 cm (30 weeks); ulna = 3.76 cm (<5(th) centile); tibia = 3.67 cm (<5th centile); and fibula = 3.72 cm (<5th centile). The digits and craniofacial appearance were normal. A tentative diagnosis of achondroplasia (ACH) was made. DNA testing for the FGFR3 gene and whole-genome array comparative genomic hybridization (aCGH) analysis were performed using cord blood DNA obtained by cordocentesis. FGFR3 mutation analysis revealed a de novo heterozygous c.833A > G, TAC > TGC transversion in exon 7 leading to a p.Tyr278Cys (Y278C) mutation in the FGFR3 protein. aCGH analysis revealed no genomic imbalance in cord blood. After delivery, the fetus had short limbs, a narrow thorax, brachydactyly, and relative macrocephaly. Cytogenetic analysis of cultured placental cells revealed a karyotype of 46,XX., Conclusion: Prenatal diagnosis of abnormal ultrasound findings suspicious of ACH should include a differential diagnosis of HCH by molecular analysis of FGFR3., (Copyright © 2013. Published by Elsevier B.V.)

Objective: Fetal intracranial hemorrhage (ICH) in utero is a rare complication of pregnancy associated with subsequent neurological sequelae or fetal death., Case Report: A 34-year-old woman with Crohn's disease presented at 36 weeks' gestation due to decreased fetal movement. Fetal heart-rate tracing indicated poor beat-to-beat variability. In addition, a Doppler ultrasonography suggested a prenatal stroke with evidences of ICH, reverse-end diastolic velocity of the middle cerebral artery, and a persistent distended bladder. A nonaggressive treatment option was chosen after counseling about the unfavorable prognosis. However, 22 hours after her admission, intrauterine fetal death occurred., Conclusion: Fetal ICH in utero might be a rare yet lethal complication of Crohn's disease in pregnancy., (Copyright © 2013. Published by Elsevier B.V.)

Objective: To present a rare case of fetal nonfamilial proximal femoral focal deficiency (PFFD) diagnosed as early as 21 weeks' gestation., Case Report: A 32-year-old woman was referred to our hospital at 21 weeks' gestation. An ultrasound examination revealed isolated unilateral short femur (right femur = 27.3 mm and left femur = 37.9 mm). The measurements of all the remaining long bones were within the normal range. The facial profile was unremarkable. Results of amniocentesis revealed a normal 46,XX female karyotype. A follow-up ultrasound 2 weeks later demonstrated further discrepancy in femoral length. A diagnosis of PFFD was made. The parents were well informed about the treatment options and after counseling they decided to terminate the pregnancy. A postmortem X-ray examination confirmed the diagnosis of PFFD., Conclusion: We have to measure both sides of extremities according to the ultrasound scan guidelines so as not to overlook any possible case of skeletal dysplasia. An advanced three-dimensional (3D) and 4D ultrasound evaluation of the bony structures and carefully observing the range of mention of the affect limbs will provide proper information to formulate a further therapeutic plan., (Copyright © 2013. Published by Elsevier B.V.)

Objective: To present intensive intrauterine treatment of recurrent early onset fetal erythroblastosis due to anti-M alloimmunization., Case Report: A 33-year-old woman, gravid 3, para 1, had anti-M IgG antibody, which caused alloimmunization of her previous pregnancies. This time she visited our hospital for intensive intervention. No evidence of fetal hydrops was found during ultrasound examination at 12 weeks of gestation. Plasmapheresis was given from 17 weeks of gestation but fetal erythroblastosis still developed 1 week later. Two intraperitoneal transfusions and one intracardiac transfusion were given within three days but fetal erythroblastosis still progressed to fetal bradycardia and occasional asystole. Epinephrine resuscitation could only temporarily improve the fetal heart rate and fetal death was inevitable., Conclusion: Serial measurements of fetal middle cerebral artery peak systolic velocities, advanced plasmapheresis, intrauterine blood transfusion, and, if needed, intravenous immunoglobulin supplement, may be the appropriate treatment for early onset fetal erythroblastosis resulting from alloimmunization., (Copyright © 2012. Published by Elsevier B.V.)