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At least 73 records · Page 4Linked to original sources
PubMed1983

Acute arterial fibrinoid deposition and ischaemic parenchymal damage of the kidney. Pathogenic factors in the development of malignant hypertension.

The development and evolution of hypertensive vascular lesions affecting the arterial supply of (a) the kidney and (b) organs other than the kidney were studied in rats developing either malignant (MHY) or benign (BHY) hypertension 3, 6, 9 and 12 days after aortic ligation between the renal arteries. Vascular disease evolved into two distinct patterns which suggested acute renal damage to be the determinant for the development of either the malignant or benign form of hypertension. Three days after aortic ligation MHY and BHY animals showed widespread fibrinoid deposition in vascular territories above the aortic ligature. However, in MHYs these lesions were much more severe and, in the kidney, they were accompanied by the development of focal parenchymal atrophy, microinfarcts and hyalin droplet degeneration of cells of the Bowman capsule. The degree of renal damage correlated with elevations in blood urea nitrogen (BUN) and plasma creatinine; however, there was no correlation with rises in blood pressure, plasma renin activity (PRA), aldosterone or corticosterone which were similarly elevated in 3-day MHY and 3-day BHY animals. Between 6 and 12 days a marked clearance of fibrinoid took place in all organ beds of BHYs, but in the non-renal vasculature of MHY animals fibrinoid remained prominent and served as the central core for necrotising arterial lesions. In the kidney of MHYs some reduction in the fibrinoid content was observed, but the parenchymal damage perpetuating from the earlier stages had exacerbated leading to collagen deposition and a marked increase in the collagen concentration of the renal cortex. These features were accompanied by further elevations in PRA and corticosteroids and a progressive deterioration of renal function. By contrast, in 12-day BHY animals, despite sustained hypertension, PRA and corticosteroids were falling from their previously higher levels and normal renal function was maintained. These studies warrant inference that extensive parenchymal damage of the kidney due in part to severe arterial fibrinoid deposition is one of the initial events in the development of malignant hypertension.

Aldosterone↗
PubMed1985

Cationic dyes reveal proteoglycans on the surface of epithelial and endothelial kidney cells.

The glomerular epithelial cells of the rat kidney fixed by vascular perfusion with an aldehyde solution containing either safranine O or alcian blue (and 0.3 M MgCl2) display filaments which are located close to the outer surface of the plasma membrane. These filaments are similar to those revealed by the same methods in the laminae rarae of the glomerular basement membrane. Alcian blue (and MgCl2) further demonstrates the presence of anionic sites inside the endothelial cell pores of the glomerular and peritubular capillaries, on the luminal surface of endothelial cells of large renal vessels and along the basolateral surface of the epithelial cells of the Bowman capsule and of the proximal convoluted tubule.

Alcian Blue↗
PubMed2005

Effectiveness of bombesin and Saccharomyces boulardii against the translocation of Candida albicans in the digestive tract in immunosuppressed rats.

PURPOSE: We investigated the effects of bombesin on disseminated candidiasis, and compared the effectiveness of bombesin with Saccharomyces boulardii against Candida albicans translocation from the gastrointestinal tract in immunosuppressed rats. METHODS: Sixty rats were divided into five groups of 12. Group 1 was given only a laboratory pellet diet and water during the experiments; the other four groups were orally inoculated with C. albicans; and groups 3, 4, and 5 were also given prednisolone intraperitoneally. The treatment groups consisted of group 4, given S. boulardii orally, and group 5, given bombesin subcutaneously. The rats were killed after 10 days, and the large bowel, liver, spleen, and kidneys were removed for microbiological and histopathological examination. Blood samples were taken to measure tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1beta) levels, and the results were compared. RESULTS: The number of translocated C. albicans colonies from the gastrointestinal tract and the serum TNF-alpha and IL-beta levels were significantly lower in groups 4 and 5 than in group 3 (P < 0.05). Histological analysis revealed that the bombesin-treated group (group 5) had significantly less mucosal ulceration and submucosal inflammation in the large bowel, less inflammation and necrosis in the liver, and less inflammation of the Bowman capsules in the kidney than the S. boulardii-treated group (group 4) (P < 0.05). CONCLUSIONS: These findings show that both S. boulardii and bombesin inhibit the translocation of C. albicans from the gastrointestinal tract, although mucosal ulceration, submucosal inflammation in the large bowel, and dissemination in the liver and kidneys were significantly less severe in the bombesin-treated immunosuppressed rats.

Analysis of Variance↗
PubMed1980

Tubular basement membrane antibody-induced interstitial nephritis in systemic lupus erythematosus.

Interstitial nephritis characterized by linear staining for human immunoglobulin G (IgG) along the tubular basement membrane of proximal renal tubules is described in a child with systemic lupus erythematosus (SLE). Autoantibodies reacting with the tubular basement membrane of the proximal renal tubules and Bowman capsule of glomeruli were present in serum. The autoantibodies were specific and could be absorbed with a normal human renal cortical fraction. The findings suggest that in addition to the well-known, immune complex-mediated injury, autoantibody-induced interstitial nephritis can also rarely occur in SLE.

Antibody Specificity↗
PubMed1997

Localisation of tissue kallikrein in the kidney of black African women with early onset pre-eclampsia: a pilot study.

Increased renal production of vasodilator mediators like kinins would counteract the vasospasm of pre-eclampsia. This study examines the cellular localisation of tissue kallikrein (TK), the potent kinin forming enzyme within the nephron of patients with early onset pre-eclampsia. Using the peroxidase-antiperoxidase immunoenzyme complex, TK was immunolocalised in the principal cells of the distal connecting tubule and the cortical collecting duct cells of the distal nephron of control tissue. Moderate reactivity was observed in the epithelial cells lining the Bowmans capsule. In early onset pre-eclampsia, TK was additionally localised in the proximal tubule cells, however, the intensity of reactivity was reduced when compared to that of the distal tubule cells. In patients with hypertension of pregnancy, the occurrence of TK in the proximal tubule suggests either gene induction or emiocytosis of TK.

Adolescent↗
PubMed2002

Expression of hsp 90 in the human kidney and in proximal tubule cells exposed to heat, sodium arsenite and cadmium chloride.

The expression of heat shock protein (hsp) 90alpha and beta mRNA and protein were determined in the human kidney and in human proximal tubule (HPT) cells exposed to lethal and sub-lethal concentrations of Cd(+2) under both acute and extended conditions of exposure. Using immunohistochemical analysis, it was demonstrated that hsp 90 was widely distributed in the human adult and fetal kidney. Moderate to strong staining was observed in the straight portions of the distal and proximal tubules, the distal convoluted tubule, the collecting ducts and the parietal epithelium of Bowmans capsule in the glomerulus. Moderate staining was observed in the proximal convoluted tubule of the cortex and the thick loops of Henle within the medulla. In addition, the fetal kidney demonstrated strong staining of the blastema, the 'S-shaped' bodies, and the developing glomeruli. Analysis of hsp 90alpha and beta mRNA expression in total RNA isolated from in situ microdissected proximal tubules or HPT cells demonstrated similar expression levels of both the alpha and beta isoforms in this tubule segment. It was demonstrated that HPT cells exhibited the classic heat shock response when subjected to a physical (heat) or chemical stress (NaAsO(2)). Heat stress, elevated temperature at 42.5 degrees C for 1 h, caused a modest increase in both hsp 90alpha and beta mRNA and protein. Similar results were obtained when the cells were subjected to a classic chemical stress of exposure to 100 microM NaAsO(2) for 4 h. In contrast, acute exposure of HPT cells to 53.4 microM CdCl(2) for 4 h resulted in no consistent increase in hsp 90alpha and beta mRNA or protein. Chronic exposure to Cd(+2) likewise failed to increase either hsp 90 mRNA or protein expression, even at concentrations of Cd(+2) that were lethal to the cells during the time course. This study shows that the HPT has a high basal expression of hsp 90, which is not induced by Cd(+2) exposure.

Arsenites↗
PubMed1997

A histopathological study of liver and kidney in male Wistar rats treated with subtoxic doses of t-butyl alcohol and trichloroacetic acid.

Tertiary butyl alcohol and trichloroacetic acid are known to be contaminants in drinking water. In order to evaluate the interactive toxicity of t-butyl alcohol with trichloroacetic acid, young male Wistar rats were dosed through water at a dose level of t-butyl alcohol (TBA)-0.5% (v/v), trichloroacetic acid (TCA)-25 ppm and a combined dose of TBA + TCA (0.5% v/v TBA-25 ppm TCA) for a period of 10 weeks ad libitum and were maintained on normal diet. The control animals received plain water and normal diet. The liver and kidney histology was undertaken to see whether subtoxic administration of TBA and TCA individually as well as combined administration for a period of 10 weeks would bring about any histological alterations. It was observed that TBA, TCA and TBA + TCA caused histological alterations in the liver such as centrilobular necrosis, vacuolation in hepatocytes and loss of hepatic architecture. TBA and TBA + TCA caused periportal proliferation and lymphocytic infiltration. Hypertrophy of hepatocytes in the periportal area was a characteristic feature in the liver of TCA treated rats. Moreover, in the histology of the kidney, in the three treated groups, degeneration of renal tubules, with syncitial arrangements of the nucleus of renal tubular epithelial cells was evident. In addition to this, degeneration of the basement membrane of the Bowmans capsule, diffused glomeruli and vacuolation of glomeruli was also evident in the three treated rat kidneys. Renal tubular proliferation in certain areas was also evident in certain areas of the kidney in TCA treated rats. The results indicate that, TBA and TCA do bring about alterations in histology of liver and kidney, but on combined administration, do not show enhanced toxicity in the form of increased hepatic and renal injury.

Animals↗
PubMed1986

Effect of age and diabetes on type IV collagen and laminin in human kidney cortex.

Specific radioimmunoassays for the 7-S domain of type IV collagen and the fragment P1 of laminin were used to quantify these basement membrane proteins in human kidney cortex at different ages and in some patients with diabetes mellitus. The antigens were solubilized by treating the tissue samples with the proteolytic enzymes collagenase, trypsin and pepsin. Total collagen content (as indicated by hydroxyproline concentration) increased with age, and the proportion of the collagen that could be solubilized by any enzyme treatment decreased. The type IV collagen concentration increased significantly with age, whereas the laminin concentration tended to decrease. In the one case of a type I diabetic the amounts of both antigens exceeded those in the age matched controls. In four type II diabetics the results were comparable with those for other aged cases. The distribution of the proteins was studied using the peroxidase-antiperoxidase method. The staining intensity and thickness of both antigens increased with age in the mesangium and Bowmans capsules, the change in type IV collagen staining being more evident. In diabetic patients these changes were more pronounced and other basement membranes appeared thicker in the stainings. These results indicate that basement membrane material accumulates in the kidney cortex during aging and that an alteration takes place in the composition of the basement membranes, the proportion of type IV collagen increasing and that of laminin decreasing.

Adolescent↗