摘要:

Morphological and immunohistochemical studies using the anti-macrophage monoclonal antibody RbM2 were performed in cholesterol-fed rabbits. From the beginning of the experiment, the levels of lipoproteins showed the pattern of familial type III hyperlipoproteinemia patients, and glomerular endothelial and mesangial cells had lipid deposits. By the 3rd week, RbM2-positive cells appeared in the capillary lumina. These cells became larger and increased in number after the 8th week. Although they had become very large and had increased noticeably by the 20th week, few sclerotic glomeruli were observed. We could hardly detect any proliferation of or foamy changes in the mesangial cells, and monocyte/macrophages showed no proliferative capacity within the glomeruli. These findings suggest that hyperlipidemia alone did not cause proliferation or foam transformation of the mesangial cells. The glomerular macrophages, probably derived from circulating monocytes, did not induce a glomerular injury under the short-term hyperlipidemic conditions of these experiments.

ISSN:1660-8151    

DOI:10.1159/000188310

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

In this study, we compared the cellular functions of cultured glomerular mesangial cells (MC) from spontaneously hypertensive rats (SHR) and from normotensive Wistar-Kyoto rats (WKY) in response to the growth factors insulin-like growth factor I (IGF-I) and platelet-derived growth factor (PDGF). IGF-I and PDGF at a concentration above 2 ng/ml and a combination of both tested growth factors exerted a highly elevated growth response of SHR MC versus WKY MC. The total RNA synthesis induced by IGF-I and PDGF was increased in SHR MC as compared with WKY MC, while the overall protein synthesis showed no differences between both strains. Analysis of cell-associated fibro-nectin accumulation and incorporation of proline into collagenous proteins revealed an enhanced basal and PDGF-stimulated matrix formation of SHR MC which was not dependent on the increased production of autocrine matrix-stimulatory mediators by SHR MC. Changes of cytosolic free calcium – [Ca2+]i -could not be correlated with the enhanced responsiveness of SHR MC to the tested growth factors. The described differences of cellular functions between SHR and WKY MC may contribute to pronounced glomerular alterations such as glomerulosclerosis seen in primary and secondary forms of hypertensio

ISSN:1660-8151    

DOI:10.1159/000188311

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

The human nephrotic syndrome is accompanied by important alterations of the coagulation system related proteins. The purpose of the present study was to examine the activity of coagulation- and fibrinolysis-related proteins in plasma and urine of control and puromycin aminonucleoside injected rats on days 2 (prenephrotic stage) and 10 (nephrotic stage). We measured the prothrombin time (PT), the activated partial thromboplastin time (aPTT), and the activities of (1) the coagulation factors (CFs) I, II, V, and VII-XII; (2) the inhibitor of coagulation antithrombin III (ATIII), and (3) the component of the fibrinolytic system α2-antiplasmin (α2-APL). PT and aPTT and the activities of CF, ATIII, and α2-APL were not measurable in the urine of control and puromycin aminonucleoside injected rats on day 2. On this same day, plasma ATIII and CF VIII decreased. On day 10 (1) PT and aPTT decreased in plasma and were not measurable in urine; (2), plasma CFs I, II, V, VII, VIII, X, and XI increased; (3), plasma ATIII decreased; (4), plasma CFs IX and XII and α2-APL did not change, and (5) ATIII and CFs II, VII, VIII, IX, X, XI, and XII, but not CFs I and V and α2-APL, appeared in urine on day 10. ATIII deficiency was secondary probably to the urinary losses; however, the plasma activity of CFs II, VII, VIII, X, and XI increased and that of CFs IX and XII remained unchanged in spite of their urinary losses which suggests that other mechanisms such as deranged catabolism and altered hepatic synthesis may be involved. This model may be useful to study the pathophysiology of the abnormalities of coagulation in humans with nephrotic synd

ISSN:1660-8151    

DOI:10.1159/000188312

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

Two patients on maintenance hemodialysis after terminal renal failure due to nephrotic syndrome and biopsy-proven focal-segmental glomerulosclerosis received three cadaver renal allografts. Immediate recurrence of nephrotic syndrome was observed. In two transplants immunosuppression consisted of ciclosporin A and low-dose steroids. One patient was unsuccessfully treated with immunoadsorption after the second transplant. All grafts were lost because of uncontrolled nephrotic syndrome. Renal allograft biopsy specimens showed findings indicating recurrence of the original disease.

ISSN:1660-8151    

DOI:10.1159/000188313

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

We report on a 45-year-old female who presented with end-stage renal disease due to Wegener’s granulomatosis limited to the kidneys. Ultrasonography and computed tomography revealed a masslike expansion involving the upper pole of an otherwise small right kidney. Histopathology of a nephrectomy specimen revealed cystic dilatation of renal tubules and active lesions of Wegener’s granulomatosis in the upper pole. The lower part of the kidney showed atrophic changes. Wegener’s granulomatosis presenting as a renal mass is extremely rare. Only 3 cases have been previously reported in the literature. Wegener’s granulomatosis only limited to the kidney is also rare. A brief review of 23 previously reported cases who initially presented with renal disease is presented. All but 2 patients subsequently manifested extrarenal lesions. Our patient continues to be free of any extrarenal involvement 18 months following presentation, although subsequent development of extrarenal lesions cannot be ru

ISSN:1660-8151    

DOI:10.1159/000188314

出版商:S. Karger AG    

年代:1994

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000188317

出版商:S. Karger AG    

年代:1994

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000188318

出版商:S. Karger AG    

年代:1994

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000188328

出版商:S. Karger AG    

年代:1994

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000188319

出版商:S. Karger AG    

年代:1994

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000188320

出版商:S. Karger AG    

年代:1994

数据来源: Karger