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The phagocytic capacity of the glomerular mesangial cells in 42 rats was inhibited by the prolonged injection of PVA. Morphometric evaluation of electron microscopic sections showed that this treatment leads to an accelerated thickening of the lamina densa of the glomerular basement membrane and of the mesangial matrix (early glomerulosclerosis). This suggests that a disturbance of lysosomal degradation can lead to glomerulosclerosis, and that the possibility of mesangial dysfunction should always be considered as a possible factor in the pathogenesis of all types of diffuse glomerulosclerosis.
Virchows Arch B Cell Pathol Incl Mol Pathol 1979
PMID:Diffuse glomerulosclerosis--a dysfunction of the mesangium? A morphometric study of the rat's kidney. 4 14

Insulin-like growth factors (IGFs) and their binding proteins are implicated in the growth regulation of the kidney during embryogenesis and differentiation. Recent evidence also suggests that IGFs play a role in kidney physiology (glomerular filtration rate, renal plasma flow) and pathology (diabetic renal hypertrophy, nephritis, glomerulosclerosis, kidney tumours, chronic renal failure). This review focuses on the biology of IGFs at the molecular, protein and receptor levels and considers their importance in renal physiology and pathology. The current data demonstrate a central role for the IGFs in the mediation of a wide variety of effects on renal growth, function and malignancy.
Virchows Arch B Cell Pathol Incl Mol Pathol 1992
PMID:The role of insulin-like growth factors and IGF-binding proteins in the physiological and pathological processes of the kidney. 127 87

Renal biopsies (n = 45) from patients with various forms of glomerulonephritis (GN), comprising mesangial IgA-GN (n = 25), focal glomerular sclerosis (n = 13) and acute GN (n = 7), were examined by double staining immunocytochemistry (APAAP, streptavidin-peroxidase) using unconjugated monoclonal antibodies (Ab) against--(i) the CD1b antigen expressed on dendritic cells (DCs), (ii) the invariant chain (Ii), and (iii) biotin-conjugated Ab against HLA-DR. In normal control kidneys (n = 7) without interstitial inflammation, CD1b-positive DCs were not detected. Glomerular endothelial cells and a few cells in mesangial areas showed double staining with the Ab against HLA-DR in Ii. In GN without active interstitial inflammation (n = 9), CD1b-positive DCs were not found. In biopsies with interstitial inflammation (n = 36) CD1b-positive DCs were found interspersed among other inflammatory cells. In seven of the biopsies showing IgA-GN DCs were seen in the vicinity of those glomeruli that exhibited either crescents or glomerular sclerosis with splitting of Bowman's capsule. In proximal tubular epithelial cells de novo expression of HLA-DR/Ii-chain was only seen when DCs were present. We conclude that in different forms of GN: (i) CD1b-positive DCs play an important role in the development of interstitial inflammation, and (ii) their presence may be related to the de novo coexpression of HLA-DR/Ii in tubular epithelial cells, possibly mediated through the production of interferon gamma and other cytokines.
Virchows Arch B Cell Pathol Incl Mol Pathol 1992
PMID:Dendritic cells in glomerulonephritis. 128 Aug 85

Characteristic pathological changes in the glomeruli in diabetic nephropathy include expansion of the mesangial matrix and thickening of the glomerular basement membrane (GBM). Using an acellular digestion technique combined with scanning electron microscopy, the three-dimensional ultrastructural changes in glomerular extracellular matrices were studied in rats with diabetic glomerulopathy. Diabetes was induced by the intravenous injection of streptozotocin and morphological analyses were performed 3, 6 and 11 months after the injection. Expansion of mesangial area and GBM thickening became evident with time. After treatment with the series of detergents, all cellular components were completely removed leaving the extracellular matrices intact. In normal controls, the mesangial matrix appeared as fenestrated septa with oval or round stomata between the glomerular capillaries. In diabetic glomerulopathy, expansion of mesangial matrix and narrowing of the mesangial fenestrae were observed. These changes in the mesangial matrices seem to play a vital role in the progression of glomerulosclerosis in rat diabetes. A subendothelial thin layer of the GBM was continuous with the mesangial matrix. One cause of GBM thickening in streptozotocin diabetes may be expansion of the mesangial matrix into the peripheral GBM.
Virchows Arch B Cell Pathol Incl Mol Pathol 1992
PMID:Glomerular extracellular matrices in rat diabetic glomerulopathy by scanning electron microscopy. 135 71

The purpose of the study was to investigate the development of microangiopathic complications in North African sand rats with diabetes induced by a long-term standard laboratory diet. Hyperinsulinaemic rats, whether non-diabetic obese or diabetic, developed capillary basement membrane (CBM) thickening in the skin; in insulin-dependent animals, this change was diffuse. Many PAS positive areas were demonstrated in skeletal muscle and myocardium, together with evidence of microangiopathy; the primary myocardial lesion in insulin-dependent disease was ischaemic fibrosis. The kidney was also affected with marked basement membrane thickening in Bowman's capsule and glomerular capillaries; glomerulosclerosis and tubular changes were found in insulin-dependent disease. No evidence of diabetic retinopathy was found, and there was a high incidence of cataract.
Cell Mol Biol 1991
PMID:Diabetes mellitus in sand rats (Psammomys obesus): microangiopathy during development of the diabetic syndrome. 174

Although chronic progressive nephropathy and proteinuria are well-known to affect old laboratory rats, the occurrence of tubular metaplasia of Bowman's capsule (TM) in aging rats has received little attention. We report here that old (24-26 months) male, but not female Sprague-Dawley rats show a high incidence of TM which is significantly (P less than 0.01) correlated with the levels of glomerular sclerosis and intracellular deposits of iron in the tubular epithelium. The incidence of these changes was not correlated with serum testosterone levels, which showed a significant age-related reduction in males. The reported findings suggest that the aging male Sprague-Dawley rat is a useful animal model to investigate the pathogenesis of TM and related morphologic changes in hematuric humans.
Virchows Arch B Cell Pathol Incl Mol Pathol 1990
PMID:Sex-related incidence of tubular metaplasia in Bowman's capsule of aging rats. 197 35

Twenty-three nonobese KK mice with abnormal tolerance to glucose, hyperinsulinemia with insulin resistance and human diabetic-like nephropathy were treated with either saline (12 mice) or glipizide, an oral hypoglycemic compound, 1 mg/kg, (11 mice) from 120 to 360 days of age. These mice develop significant increases in mesangial volume and matrix by 40 days of age. Oral glucose tolerance (OGTT), glucosyltransferase and N-acetyl-beta-glucosaminidase (enzymes involved in synthesis and degradation of kidney glycoproteins, respectively) in the kidney and serum, 24-hr proteinuria, and light microscopy studies of the kidney were performed. Glipizide-treated mice improved their OGTT. There was no difference in body weight; however, a 16% decrease (P less than 0.05) in kidney weight was observed in glipizide-treated mice. Both enzymes were significantly increased in the kidneys of mice treated with glipizide. No difference in serum enzymes was found between the two groups of mice. About 58% of the saline-treated mice had moderate glomerulosclerosis. By contrast, only 27% of glipizide-treated mice had moderate glomerulosclerosis. Also, a significant decrease in proteinuria was found in glipizide-treated mice. These data suggest that glipizide improves glucose metabolism, decreases kidney size, prevents kidney glycoprotein and mesangial matrix accumulation, and reduces proteinuria in type II diabetic KK mice. This indicates that good glycemic control prevents further progression of established diabetic nephropathy in animals.
Exp Mol Pathol 1990 Oct
PMID:Diabetic microangiopathy in KK mice. VI. Effect of glycemic control on renal glycoprotein metabolism and established glomerulosclerosis. 214 55

The histopathology of the acute and chronic kidney reaction to low-frequency nonionizing electromagnetic radiation was evaluated in New Zealand white rabbits treated with multiple exposure to 27.12-MHz radiofrequencies. At the end of treatment, the animals exhibited focal tubular necrosis and focal and segmental glomerular sclerosis which in a few months evolved into a membranous nephropathy. The latter was characterized by a diffuse, granular localization of rabbit gamma-globulin and complement in most glomeruli and by electron-dense deposits in the subepithelial zone of the glomerular capillary walls, suggesting that these glomerular changes are induced by the localization of antigen-antibody complexes. The data obtained provide strong evidence for the potential nephrotoxicity of radiofrequency radiation and indicate that these nonionizing types of radiation may be capable of eliciting autoimmune phenomena that are likely responsible for the evolution of renal disease in rabbits.
Exp Mol Pathol 1988 Aug
PMID:Effects of radiofrequency radiation on rabbit kidney: a morphological and immunological study. 339 66

Heparins blunt the development of glomerulosclerosis in several disease models in the rat and this protective effect may be related to suppression of glomerular cell proliferation. In this study the direct effect of heparins on another key event in glomerulosclerosis, extracellular matrix (ECM) deposition, was examined. Standard heparin (hep) and non-anticoagulant N-desulfated acetylated heparin (DSA-hep) significantly reduced the fibronectin content in the conditioned media of subconfluent, confluent, and supraconfluent rat glomerular mesangial cells (MCs) in culture, as assessed by a sandwich ELISA technique. Both heparins significantly increased the amount of cell-associated fibronectin in sparse and subconfluent MCs. DSA-hep, but not hep, increased the fibronectin content of ECM formed by confluent and supraconfluent MCs. Using 3H-proline pulse-labeling, Hep and DSA-hep were found to significantly decrease cell-associated collagen in subconfluent but not in confluent MCs. No effects were seen on newly synthesized collagen secreted into the culture medium. Neither hep nor DSA-hep affected total protein synthesis, studied by metabolic labeling with 35S-methionine. High resolution 2-D electrophoresis (molecular weight range, 120 to 10 Kd; isoelectric interval, 5.0 to 7.0) revealed one particular intracellular protein (molecular weight 54 Kd, pI 5.91) which was consistently overexpressed in hep. Both heparins affected an identical set of another 19 different intracellular MC proteins (over-/underexpression or shift to higher molecular weights). In conclusion, the present data demonstrate the profound direct metabolic effects of hep and DSA-hep.(ABSTRACT TRUNCATED AT 250 WORDS)
Virchows Arch B Cell Pathol Incl Mol Pathol 1993
PMID:Heparins modulate extracellular matrix and protein synthesis of cultured rat mesangial cells. 809 75

The effects of hypercholesterolemia on both the initial and chronic phases of rat nephrotoxic serum (NTS) nephritis have been investigated. Injury during the initial phase of NTS nephritis in hypercholesterolemic rats maintained on a cholesterol-supplemented diet (Group 2) was characterized by segmentally accentuated accumulations of vacuolated cells with lipid droplets (foam cells) in the glomeruli, while the kidneys of rats fed a standard diet (Group 1) revealed only mild intracapillary cell proliferation. Immunoelectron microscopy showed that the foam cells observed in Group 2 rats were largely derived from macrophages. The glomerular macrophage number, defined by the number of ED1-positive cells per glomerulus, was significantly higher in Group 2 than in Group 1 animals at days 5-6 (3.4 +/- 1.4 in Group 1 against 6.3 +/- 1.0 in Group 2; p < 0.01) as well as at days 21-28 (5.5 +/- 2.6 in Group 1 against 10.9 +/- 2.8 in Group 2; p < 0.01). In contrast, the numbers of OX19-positive T-lymphocytes and OX33-positive B-lymphocytes were similar in both groups. In the chronic phase of NTS nephritis at week 20, semiquantitative evaluation of the glomerular lesions disclosed more severe focal segmental glomerulosclerosis (FSGS) in Group 2 compared with Group 1 animals (glomerular injury score: 14 +/- 10 in Group 1 against 73 +/- 17 in Group 2; p < 0.01). Accumulations of lipid and foam cells were invariably seen in the sclerotic foci of Group 2 animals. The results indicate that hypercholesterolemia played an important role in the accelerated development of FSGS in rat NTS nephritis.(ABSTRACT TRUNCATED AT 250 WORDS)
Virchows Arch B Cell Pathol Incl Mol Pathol 1993
PMID:Effects of hypercholesterolemia on initial and chronic phases of rat nephrotoxic serum nephritis: development of focal segmental glomerulosclerosis, analogous to atherosclerosis. 822 Aug 24


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