title: Pregnancy aggravates proteinuria in subclinical glomerulonephritis in the rat.
abstract: Because subclinical renal disease may be aggravated during pregnancy--as reflected in the occurrence of proteinuria, for example--we investigated whether a subclinical glomerulonephritis (SG) in the non-pregnant rat (passive Heymann nephritis), a condition without proteinuria, is aggravated when the animals become pregnant and, if so, whether this is associated with a glomerular inflammatory reaction. SG was induced in non-pregnant rats 8 days before pregnancy. On day -1, part of the group of rats became pregnant. Three experiments were performed. In experiment 1, 4-hour urine albumin excretions and blood pressure (tail cuff) were measured. In experiment 2, the glomerular filtration rate (GFR) was measured with the chromium 51-labeled ethylenediaminetetraacetic acid method, while in experiment 3, parameters characteristic of a glomerular inflammation were studied. Experiment 1 revealed that non-pregnant rats with SG did not exhibit proteinuria. However, after the rats became pregnant, a significant proteinuria occurred, without an increase in systolic blood pressure. Experiment 2 revealed that the GFR did not increase in pregnant rats with SG, while experiment 3 showed that only pregnant animals exhibited a significant glomerular inflammation; this glomerular inflammation was characterized by intraglomerular influx of polymorphonuclear cells and monocytes. The results suggest that an SG in the rat may flare up during pregnancy. This exacerbation is characterized by proteinuria and coincides with a glomerular inflammatory reaction. It is suggested that proteinuria and the glomerular inflammatory reaction are causally related and promoted by the pregnant condition.
authors.affiliation: Department of Obstetrics and Gynecology, University of Groningen, The Netherlands.
authors.forename: M M
authors.initials: MM
authors.lastname: Faas
authors.forename: W W
authors.initials: WW
authors.lastname: Bakker
authors.forename: R T
authors.initials: RT
authors.lastname: Poelman
authors.forename: G A
authors.initials: GA
authors.lastname: Schuiling
mesh_terms: D000419:Albuminuria / Q000150:complications; D000818:Animals; D001794:Blood Pressure; D004195:Disease Models, Animal; D005260:Female; D005919:Glomerular Filtration Rate; D005921:Glomerulonephritis / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D007249:Inflammation / Q000473:pathology; D039041:Integrin alpha4beta1; D016023:Integrins / Q000378:metabolism; D016169:Lymphocyte Function-Associated Antigen-1 / Q000378:metabolism; D016177:Macrophage-1 Antigen / Q000378:metabolism; D009000:Monocytes / Q000276:immunology / Q000473:pathology; D009504:Neutrophils / Q000276:immunology / Q000473:pathology; D011247:Pregnancy; D011248:Pregnancy Complications / Q000473:pathology / Q000503:physiopathology; D011507:Proteinuria / Q000150:complications*; D051381:Rats; D017208:Rats, Wistar; D016201:Receptors, Lymphocyte Homing / Q000378:metabolism
chemical_list: D039041:Integrin alpha4beta1; D016023:Integrins; D016169:Lymphocyte Function-Associated Antigen-1; D016177:Macrophage-1 Antigen; D016201:Receptors, Lymphocyte Homing