Mesangial immune injury, hypertension, and progressive glomerular damage in DahI rats. Hypertension frequently accompanies chronic glomerulonephritis. Mesangial injury and glomerulosclerosis are com-mon in glomerulonephritis and are often harbingers of progressive glomerular destruction. Thus, in a model of mesangial immune injury we studied the relationship between hypertension, mesangial injury, and glomeruloscierosis. We induced mesangial ferritin-antiferritin immune complex disease (FTC) in DahI salt-sensitive (S) and salt-resistant (R) rats. S and R rats with FTC were fed chow containing 0.3% NaCl until 14 weeks of age and then switched to 8.0% NaCI chow until 28 weeks of age. Groups of control S and R rats (no FTC) were either fed 0.3% NaCI for 28 weeks or switched to 8.0% NaCI chow at 14 weeks of age. Blood pressure, serum creatinine, urinary protein, and glomerular injury (assessed by semiquantitative morphometric analysis) were determined at 14 and 28 weeks of age.(1) R rats with or without F1C did not develop hypertension; mesangial injury was minimal.(2) At 14 weeks of age, only S FTC rats developed hypertension, proteinuria, significant mesangial expansion and early glomerulosclerosis.(3) At 28 weeks of age, proteinuria, mesangial expansion, and glomerulosclerosis were significantly more severe in hypertensive S rats with FIC than in those without FTC. These studies show that despite a normal salt intake, mesangial injury hastened the onset of hypertension, but only in rats genetically predisposed to hypertension (S F1C at 14 weeks). High dietary salt further aggravated hypertension, which, in turn, magnified both mesangial injury and glornerulosclerosis. Clinically, the different rates of progression of human glomerulonephritis associated with hypertension may be in part dependent on similar mechanisms.

Atteinte immune mésangiale, hypertension, et alteration glomerulaire progressive chez des rats DahI. L'hypertension accompagne souvent les glomérulonéphrites chroniques. Une atteinte mesangiale et une glomerulosclérose sont courantes lors des glomerulonéphrites et souvent annoncent une destruction glomerulaire progressive. Ainsi, dans un modèle d'atteinte immune mésangiale, nous avons étudié les relations entre hypertension, lesions mesangiales, et glomerulosclerose. Nous avons induit une maladie mésangiale a complexes immuns ferritine-antiferritine (FTC) chez des rats DahI sensibles (5) ou résistants (R) au sel. Les rats S et R atteints de FIC ant recu un régime contenant 0, 3% de NaCljusqu'a l'age de 14 semaines, puis mis a un régime a 8, 0% de NaCl jusqu'a l'age de 28 semaines. Des groupes contrôles de rats S et R (sans FTC) ont été nourris soit avec 0, 3% de NaCl pendant 28 semaines, soit passes au régime avec 8, 0% de NaC1 a partir de l'âge de 14 semaines. La pression sanguine, Ia créatininémie, Ia protéinurie, et les lesions glomérulaires (ddterminées par une analyse