ABSTRACT
To examine the effect of T lymphocyte deficiency on the course of immune complex nephritis, we studied renal function and structure in Swiss albino nude and non-nude mice following injection of heterologous protein. Four groups of 22 mice each (two nude and two non-nude) received either apoferritin 2 mg or saline daily for 10 weeks. Nude mice were maintained in a gnotobiotic environment. Non-nude mice receiving apoferritin developed proteinuria and had increased cellularity within glomeruli compared to either nude mice receiving apoferritin or to control groups (p less than 0.05). Of 22 non-nude mice receiving apoferritin, 16 had glomerular immune deposits by electron and immunofluorescent microscopy while 9 of 22 counterpart nude mice receiving apoferritin had such deposits. Non-nude mice more commonly showed membraneous deposits. Nude and non-nude mice receiving saline had no glomerular deposits. These preliminary data suggest that T lymphocytes may play a significant role in the development of immune complex nephritis.
Subject(s)
Disease Models, Animal , Immune Complex Diseases/immunology , Mice, Nude/immunology , Nephritis/immunology , Animals , Antigen-Antibody Complex , Immunity, Cellular , Kidney/ultrastructure , Male , Mice , Nephritis/pathology , T-Lymphocytes/immunologyABSTRACT
In order to study the effects of the protein moiety independent of the protein-iron complex in the development of ferritin-induced glomerulonephritis, we compared the effects of ferritin, equimolar amounts of apoferritin, and equimolar amounts of iron dextran in Swiss albino mice. The results were compared to both saline-injected and non-injected controls. Ferritin resulted in a glomerulonephritis associated with predominantly mesangial deposition of immune complexes. Tubulo-interstitial changes occurred as well. Iron dextran resulted in similar but less severe tubulo-interstitial changes and evoked no glomerular alterations. Apoferritin resulted in an immune complex glomerulonephritis usually associated with membranous deposits. No tubular or interstitial changes occurred. Proteinuria developed in animals receiving apoferritin. Since the protein-iron complex caused tubular and interstitial damage, apoferritin may provide a more suitable model of immune-complex-mediated glomerulonephritis.
Subject(s)
Antigen-Antibody Complex , Apoferritins , Ferritins , Glomerulonephritis/immunology , Animals , Disease Models, Animal , Ferritins/analogs & derivatives , Glomerulonephritis/chemically induced , Glomerulonephritis/pathology , Iron-Dextran Complex , Male , Mice , Microscopy, Electron , Proteinuria/chemically induced , Sodium ChlorideABSTRACT
To assess the possibility that non-aminoglycoside antibiotics may adversely affect the nephrotoxicity of the new semisynthetic aminoglycoside netilmicin, we gave ampicillin, carbenicillin, methicillin, cefamandole, and clindamycin, either singly or in combination with netilmicin, at two dose concentrations in rats. Results were compared as to the effect of netilmicin given singly and to saline-injected and noninjected controls. Antibiotic combinations resulted in no greater nephrotoxicity than did netilmicin alone. Netilmicin concentrations in renal tissue were high, and these levels were not consistently affected by the other drugs. The data suggest that in rats the nephrotoxicity of netilmicin is not affected adversely by the presence of non-aminoglycoside antibiotics.
