Preeclampsia, HELLP Syndrome, and Postpartum Renal Failure with Thin Basement Membrane Nephropathy: Case Report and a Brief Review of Postpartum Renal Failure.

A 36-year-old primigravida female from a birthing center was referred for elevated blood pressure to the hospital two days after normal spontaneous vaginal delivery with nausea, vomiting, and diarrhea. During this two-day period, she was experiencing persistent vaginal bleeding and lower abdominal pains for which she took six doses of 600 mg ibuprofen. Further laboratory evaluation reflected leukocytosis, anemia, thrombocytopenia, elevation of liver enzymes, and renal failure with hyperkalemia requiring emergent hemodialysis once in the Medical Intensive Care Unit (MICU). She was diagnosed with HELLP syndrome with underlying preeclampsia. A week later, due to hypertension controlled with medications and nonoliguric renal failure with no active urine sediments, a renal biopsy was indicated to direct management. The renal biopsy supported the diagnosis of diffuse severe acute tubulointerstitial nephritis with hypereosinophilia and thin basement membrane nephropathy (see figures). She was subsequently treated with high-dose steroids which resulted in the normalization of blood pressures and renal function returning to baseline. We report the first case of acute tubulointerstitial nephritis in an individual with thin basement membrane nephropathy secondary to postpartum complications.

Patterning of sexually dimorphic neurogenesis in the caenorhabditis elegans ventral cord by Hox and TALE homeodomain transcription factors.

BACKGROUND: Reproduction in animals requires development of distinct neurons in each sex. In C. elegans, most ventral cord neurons (VCNs) are present in both sexes, with the exception of six hermaphrodite-specific neurons (VCs) and nine pairs of male-specific neurons (CAs and CPs) that arise from analogous precursor cells. How are the activities of sexual regulators and mediators of neuronal survival, division, and fate coordinated to generate sex-specificity in VCNs? RESULTS: To address this, we have developed a toolkit of VCN markers that allows us to examine sex-specific neurogenesis, asymmetric fates of daughters of a neuroblast division, and regional specification on the anteroposterior axis. Here, we describe the roles of the Hox transcription factors LIN-39 and MAB-5 in promoting survival, differentiation, and regionalization of VCNs. We also find that the TALE class homeodomain proteins CEH-20 and UNC-62 contribute to specification of neurotransmitter fate in males. Furthermore, we identify that VCN sex is determined during the L1 larval stage. CONCLUSIONS: These findings, combined with future analyses made possible by the suite of VCN markers described here, will elucidate how Hox-mediated cell fate decisions and sex determination intersect to influence development of neuronal sex differences.