Recurrent membranous lupus nephritis after renal transplantation: a case report and review of the literature.

Recurrent lupus nephritis in transplanted kidneys is rare. To the best of our knowledge, we report only the second case of recurrent membranous lupus nephritis in an allograft 8 years after transplantation. Unlike the first case, our patient received a transplant from a living-related donor rather than a cadaver. Disease "burn-out," the use of immunosuppressive drugs, and treatment of recurrence as rejection have all been offered as possible explanations for the rarity of recurrence. The majority of cases represent recurrence of the proliferative lesions, although a variety of histologic patterns and transformations have been reported.

Phorbol ester, prolactin, and relaxin cause translocation of protein kinase C from cytosol to membranes in human endometrial cells.

Incubation of endometrial cells with 100 nM 12-O-tetradecanoylphorbol 13-acetate (TPA) for 2, 5, 10 and 30 min decreased cytosolic protein kinase C (PKC) activity to 80%, 68%, 66%, and 72% of the control values, while membrane-associated PKC increased to 116%, 168%, 154% and 134% of the control values, respectively. Long-term incubation of cells with TPA resulted in a loss in total PKC activity. Treatment of secretory endometrial cells with prolactin (100 ng/ml) decreased cytosolic PKC to 64% (10 min) and 72% (20 min) while membrane PKC increased to 133% (10 min) and 158% (20 min) compared to control values. Relaxin (100 ng/ml) also caused translocation of PKC in secretory endometrium. Neither hormone induced PKC translocation in proliferative endometrium. In intact endometrial cells TPA stimulated the phosphorylation of an 80 kDa protein. Cytosolic protein phosphorylation in the presence of EGTA resulted in phosphorylation of proteins of 68 kDa and 19 kDa which was increased by prolactin. Upon activation by calcium and phosphatidylserine, PKC phosphorylated a protein of 39 kDa, and prolactin did not further enhance its phosphorylation. The present results indicate that TPA induces an intracellular translocation and down-regulation of PKC. The translocation of PKC by prolactin and relaxin suggests an involvement of this enzyme in the action of these hormones in human endometrium.

Umbilical vessels endothelium and vascular reactivity.

In vitro preparations of isolated umbilical vessels are ideal for the study of vasoactive substances. These vessels display vascular reactivity in response to numerous substances, although the mechanism of action of many of these agents is unknown. The present study was undertaken to study the role of the endothelium in the vasoactivity of these preparations, and to examine their cellular integrity. Umbilical artery and vein were studied using conventional isometric techniques, and using high power light microscopy. We found that umbilical vessel rings had no relaxant response to agents believed to release endothelium-derived relaxant factor (EDRF). Mechanical and chemical treatment to remove endothelium did not significantly alter vascular response to known contractile agonists. Cellular morphology is well maintained in ring preparations. Finally, mechanical rubbing of the intima of these rings is more reliable in endothelium removal, as compared to chemical removal with the detergent saponin.