摘要:

The effects of uninephrectomy on the function and structure of the remnant kidney were assessed in rats with Adriamycin-induced nephrosis, 12 weeks after the injection of Adriamycin. The kidney volume of Adriamycin-treated uninephrectomized rats (NX-AD) was 2.3 times that of sham-operated, Adriamycin-treated animals (SH-AD; p < 0.001). The marked renal enlargement in NX-AD animals was due to the development of large tubular cysts. Following uninephrectomy, the fractional volume of tubular lumen almost doubled (NX-AD, 0.33 ± 0.02; SH-AD, 0.17 ± 0.02; p < 0.001) and the absolute volume of tubular lumen increased more than fourfold (NX-AD, 0.51 ± 0.08 ml; SH-AD, 0.12 ± 0.02 ml; p 40,000 μm2) was 5.8 ± 1.1% in NX-AD and 0.7 ± 0.2% in SH-AD groups (p < 0.001). The fractional volume of interstitial fibrosis in NX-AD animals was larger than in SH-AD (0.09 ± 0.02 versus 0.04 ± 0.01%, p < 0.05). As opposed to the worsening of tubulointerstitial disease, single-kidney glomerular filtration rate, fractional protein clearance, glomerular volume and the extent of glomerular sclerosis did not differ significantly in NX-AD as compared to SH-AD groups. This study shows that uninephrectomy in rats with Adriamycin nephrosis worsens interstitial nephrosis and aggravates the formation of tubular cysts, leading to a macrocystic kidney disease. These changes are not associated with an increase in glomerular s

ISSN:1660-8151    

DOI:10.1159/000187798

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

The mesangium is centrally located in the glomerulus and plays an important role in the microcirculation within the glomerulus. In order to reveal the role of the mesangial matrix in the microcirculation, the movement of native anionic ferritin into the juxtaglomerular region was tracked following the intravenous injection of ferritin into rats. The three-dimensional ultrastructures of the mesangial matrix and juxtaglomerular apparatus were studied by conventional scanning and high-resolution scanning electron microscopy after removal of the cellular components. Many ferritin particles were observed from the glomerular capillary to the mesangial matrix, in the mesangial matrix of the juxtaglomerular apparatus and in the tubular lumen of the macula densa after the injection of ferritin. Secretion of macromolecules from the distal tubules seems to be one of the exits from the juxtaglomerular zone. The mesangial matrix was continous from the vascular pole to the periphery like a branching tree. The intraglomerular mesangial matrix was continuous to the extraglomerular mesangial matrix in the juxtaglomerular region. The mesangial matrix appeared to consist of a polygonal meshwork structure of thin fibrils and pores with high-resolution scanning electron microscopy. The thinnest fiber was approximately 6-nm wide, and the pore size was averaged 20 nm in diameter. We were able to demonstrate the meshwork structure of the mesangial matrix, thus giving the morphological basis of the mesangial matrix to serve as mesangial pathway from the intraglomerular to the extraglomerular mesangial matrix.

ISSN:1660-8151    

DOI:10.1159/000187799

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

We examined the ultrastructure of the bovine glomerular basement membrane (GBM) and tubular basement membrane (TBM) using ultra-high-resolution scanning electron microscopy after conductive staining without metal coating. Purified basement membranes (BMs) were obtained by sonication and acellular BMs by detergent treatments. Purified GBMs (PGBMs) and acellular GBMs (AGBMs) showed similar meshwork structures composed of regular round or oval pores and branching strands. Pore diameters were 10.2 ± 2.4 nm (mean ± SD) in PGBMs and 9.8 ± 3.1 nm in AGBMs. Purified TBMs (PTBMs) and acellular TBMs (ATBMs) exhibited heterogeneous meshwork structures in which compact meshes in the cristae were combined with coarse meshes in the invaginations on the epithelial surfaces. Pore diameters were 12.6 ± 5.2 nm in PTBMs and 11.4 ± 4.0 nm in ATBMs which were significantly larger than those in GBMs. The width of the strands ranged from 3 to 15 nm in all BMs. A 4 M guanidine hydrochloride extraction of the acellular BMs revealed large polygonal networks in the invaginations of the TBM and twisted strands which were considered to be type IV collagen fibrils. Ultra-high-resolution scanning electron microscopy and conductive staining were useful for the study of three-dimensional architectures of BMs and revealed heterogeneous meshwork structures in the GBM and TBM which were probably caused by a different ratio of the major compon

ISSN:1660-8151    

DOI:10.1159/000187800

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

Antiendothelial cell antibodies and increased von Willebrand factor (vWF) levels are observed in many renal diseases. We studied renal morphology after administration of rabbit anti-human factor VIII-von Willebrand factor (FVIII-vWFc) γ-globulin (IgG) in rats. Isolated perfusion of normal rat kidney with the antibodies disclosed rabbit IgG along glomerular endothelium and in mesangial areas. Systemic administration resulted in an identical antibody distribution. C3 deposits and few electron dense deposits were transiently noted. After 1 week the mesangial deposition of rabbit IgG had increased significantly, most likely reflecting increased release of vWF by the endothelium. Thereafter, the deposits gradually relocated into mesangial stalk and into the glomerular vascular pole, and they had vanished after 6 weeks. Except for a mild influx of leukocytes, no renal injury occurred. In conclusion, although FVIII-vWFc antibodies cause mesangial immune deposits, antibodies against other endothelial antigens are apparently needed to inflict renal damage

ISSN:1660-8151    

DOI:10.1159/000187801

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

Inner medullary blood flow has been found to remain nearly unchanged during postischemic renal failure, despite a severely disturbed perfusion in the outer medulla. In order to elucidate this discrepancy, rats were subjected to 1 h left renal artery occlusion and 1 h reflow. The blood plasma was then labeled by dye-conjugated globulin for 1 min. The in vivo indicator distribution was histologically analyzed, especially in the medullary vascular bundles. The filling there was observed along a section plane positioned through the inner stripe along the long and the short axis of the organ. Vessels centrally located within the bundles were more labeled than those in the periphery of the bundles. In addition, the degree of filling on the whole was almost twice as high in the tissue near the renal sinus as in the central area. At the same time, filling defects in the renal papilla were restricted mostly to the center of that tissue. The observations support the assumption that differences in blood flow obstruction exist within each bundle. They also show that perfusion defects of the outer medulla occur more readily in the center of the organ, thus allowing blood to enter the inner medulla via vascular bundles located marginally, adjacent to the renal sinus of the kidney.

ISSN:1660-8151    

DOI:10.1159/000187802

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

Progressive hereditary nephropathy is described in 6 members of a single family. Renal biopsies, performed in 3 patients, revealed tubular atrophy, interstitial fibrosis, and lymphomonocytic infiltration associated with severe vascular lesions. These features were disproportionately serious when related to age, arterial pressure, and renal function. Similar familial nephropathy has been reported in the literature, generally in association with gout or asymptomatic hyperuricemia. The patients described here had normal blood concentrations of uric acid. It is proposed that the members of the present group of patients are suffering from the same interstitial nephropathy as that described in the literature and that the hyperuricemia found by other investigators is coincidental and does not play a pathogenetic role.

ISSN:1660-8151    

DOI:10.1159/000187803

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

The association of a spondyloepiphyseal dysplasia and disproportionate short stature with focal glomerular sclerosis is reported in two girls. Renal disease manifested by proteinuria at the age of 2.5 and 11 years, leading to treatment-resistant nephrotic syndrome over 15 and 45 months, respectively. One patient went into end-stage renal failure shortly after nephrotic syndrome developed, the other died from sepsis. The association of spondyloepiphyseal dysplasia and focal glomerular sclerosis with nephrotic syndrome may represent a distinct disease entity.

ISSN:1660-8151    

DOI:10.1159/000187804

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

Gallstone disease was detected in 28% of 119 patients on regular dialysis treatment. The disease was silent in 82% of the patients. Stones were radiolucent in 88% of the cases, radioopaque in 8% and mixed in 4%. Among 49 variables considered, increasing age was the only variable that correlated significantly with increasing prevalence of gallstone disease. Since no relationships were found between gallstones and age or modes of dialysis, it is conceivable that some mechanism(s) linked with the preexisting chronic nephropathy might have been involved in the development of cholelithiasis. End-stage renal disease could be another so far unrecognized risk factor for cholelithiasis.

ISSN:1660-8151    

DOI:10.1159/000187805

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

Abnormalities in plasma amino acid profiles have been reported in severe uraemia and dialysis patients and may be a consequence of altered protein metabolism in the presence of metabolic acidosis. We studied plasma amino acid profiles in 7 control subjects [GFR 92.7 ± (SEM) 14.5 ml/min/1.73 m2] and 7 elderly patients with renal failure (GFR 16.5 ± 1.3 ml/min/1.73 m2). Uraemic patients had significantly reduced plasma levels of valine, tyrosine, phenylalanine, tryptophan and elevated histidine compared to controls. There was no correlation between arterial pH or bicarbonate and plasma amino acid level

ISSN:1660-8151    

DOI:10.1159/000187806

出版商:S. Karger AG    

年代:1994

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000187807

出版商:S. Karger AG    

年代:1994

数据来源: Karger