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  • 1
    Electronic Resource
    Electronic Resource
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 8 (2003), S. 0 
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: SUMMARY:  Intraglomerular deposition of low-density lipoprotein (LDL) and oxidized LDL has been described in various human glomerular diseases. Yet it is not clear whether esterified cholesterol (EC) and unesterified cholesterol (UC) carried in LDL are mobilized from deposited LDL particles or accumulate in the diseased human glomeruli, particularly in the segmentally sclerotic lesions. To address this issue, frozen sections of renal biopsies were first immunostained to localize apolipoprotein B (apo B) and then oil red O (ORO) stained to colocalize neutral lipids. By using 124 ORO-positive biopsies and nine ORO-negative ones, UC was visualized directly with filipin staining, and EC was visualized after its enzymatic hydrolysis and staining with filipin. Seventy-seven biopsies (58%) showed filipin staining of accumulated EC and/or UC in the glomeruli. Of these, 11 showed heavy filipin staining for both EC and UC in the segmentally sclerotic lesions. In a group with UC deposits in the sclerotic segments, the percentage of the glomeruli affected by sclerosis and the intensity of filipin fluorescence for UC were significantly higher than biopsies with only mesangial UC deposits. Most filipin-positive biopsies showed apo B staining mainly in the mesangium. Yet in the sclerotic segments, apo B staining was rarely noted. Accumulated apo B-stained lipoprotein was not coincident with ORO-stained lipid in the diseased glomeruli. These results suggest that both EC and UC accumulate in the sclerotic glomerular segments as the glomerular lesions are advanced, and that these EC and UC appear to be derived from altered LDL with progressive loss of apo B.
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  • 2
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: SUMMARY: The role of platelet-derived growth factor (PDGF) and transforming growth factor-β1 (TGF-β1) in relation to mesangial matrix expansion and progressive glomerulosclerosis in IgA nephropathy (IgAN) is not clearly defined. Expression of PDGF B, TGF-β1, and extracellular matrix proteins in glomeruli was assessed by immunohistochemistry in 42 biopsies with IgAN and six renal biopsies with no detectable abnormalities. the mRNA expression of PDGF B, TGF-β1, α1(IV) collagen, laminin B1 and fibronectin genes was further evaluated by in situ hybridization in 25 biopsies with IgAN and six controls. In IgAN, the intensity of immunostaining for PDGF B, type IV collagen, laminin and fibronectin, but not for TGF-β1, was increased in the mesangium compared with controls. the immunoreactivity of PDGF B was closely correlated with that of type IV collagen and laminin. the number of PDGF B mRNA-, α1(IV) collagen mRNA-, laminin B1 mRNA-, and TGF-β1 mRNA-expressing cells/glomerular section, but not the number of fibronectin mRNA-expressing cells, was increased in IgAN compared with controls. the number of PDGF B mRNA-expressing cells correlated significantly with the percentage of glomerulosclerosis. In the cellular lesions of focal segmental glomerulosclerosis (FSGS), expression of TGF-β1 protein and mRNA was markedly increased in visceral glomerular epithelial cells (GEC). These results suggest that PDGF B mainly overproduced by mesangial cells may cause mesangial matrix expansion, whereas TGF-β1 produced by GEC may be related to the formation of FSGS in IgAN. Thus, PDGF B and TGF-β1 may play differential roles in the pathogenesis of renal fibrosis and the progression of IgAN.
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  • 3
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: SUMMARY: The pathogenetic mechanisms of IgA nephropathy are diverse and are not yet clearly elucidated. We believe pro-inflammatory cytokines, Th1/Th2, and chemokines would be involved in the pathogenetic pathways and would affect the functional and histological consequences of IgA nephropathy. By using semiquantitative reverse transcriptase–polymerase chain reactions (RT-PCR), we measured the level of intrarenal gene expression of various cytokines and chemokines in 61 renal core biopsy specimens confirmed as IgA nephropathy. And, by using immunohistochemistry (IHC), the degree of expression and the location of various cytokines and chemokines in renal tissues in 29 of the above patients were attempted to be determined. In RT-PCR, the γ-interferon (IFN-γ)/interleukin-10 (IL-10) ratio was higher in patients with renal dysfunction than in those with normal renal function. The levels of pro-inflammatory cytokine gene transcripts (tumor necrosis factor-α (TNF-α), IL-1β) were high in patients with significant proteinuria. In patients with severe glomerular sclerosis, the ratio of IFN-γ/IL-10 gene transcripts was high. The level of IL-10 gene transcript was related to the severity of tubular atrophy and interstitial fibrosis. The extent of intrarenal arteriolar lesions correlated with the expression of the IL-8 gene transcript. The degree of IgA deposition in glomeruli was related to the expression of IL-15 and IL-6. In IHC, TNF-α, IFN-γ and IL-2 were immunostained dominantly in the mesangial region, but not in the tubulointerstitial region. In contrast, positive reactions for IL-10 were observed primarily in tubules. Significant reactions for IL-8 were noted in the periarteriolar and arteriolar areas. The results of RT-PCR and IHC showed positive relationships, but these were not statistically significant. This study suggests that pro-inflammatory, Th1/Th2 cytokines and chemokines are involved in the specific processes of inflammation and immunological injury in IgA nephropathy.
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  • 4
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: SUMMARY: The role of platelet-derived growth factor (PDGF) and transforming growth factor-β1 (TGF-β1) in relation to mesangial matrix expansion and progressive glomerulosclerosis in IgA nephropathy (IgAN) is not clearly defined. Expression of PDGF B, TGF-β1, and extracellular matrix proteins in glomeruli was assessed by immunohistochemistry in 42 biopsies with IgAN and six renal biopsies with no detectable abnormalities. The mRNA expression of PDGF B, TGF-β1, α1(IV) collagen, laminin B1 and fibronectin genes was further evaluated by in situ hybridization in 25 biopsies with IgAN and six controls. In IgAN, the intensity of immunostaining for PDGF B, type IV collagen, laminin and fibronectin, but not for TGF-β1, was increased in the mesangium compared with controls. The immunoreactivity of PDGF B was closely correlated with that of type IV collagen and laminin. The number of PDGF B mRNA-, α1(IV) collagen mRNA-, laminin B1 mRNA-, and TGF-β1 mRNA-expressing cells/glomerular section, but not the number of fibronectin mRNA-expressing cells, was increased in IgAN compared with controls. The number of PDGF B mRNA-expressing cells correlated significantly with the percentage of glomerulosclerosis. In the cellular lesions of focal segmental glomerulosclerosis (FSGS), expression of TGF-β1 protein and mRNA was markedly increased in visceral glomerular epithelial cells (GEC). These results suggest that PDGF B mainly overproduced by mesangial cells may cause mesangial matrix expansion, whereas TGF-β1 produced by GEC may be related to the formation of FSGS in IgAN. Thus, PDGF B and TGF-β1 may play differential roles in the pathogenesis of renal fibrosis and the progression of IgAN.
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  • 5
    ISSN: 1432-198X
    Keywords: Key words: Morphometry ; Mean glomerular volume ; Mesangial volume ; Focal segmental glomerulosclerosis ; Age
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Studies have suggested that glomerular size increases in childhood minimal lesion with age or growth. To examine whether mean glomerular volume (MGV) of pediatric patients with focal segmental glomerulosclerosis (FSGS) also increases with age and whether FSGS by itself can contribute to glomerular hypertrophy, we studied 67 children (40 boys, 27 girls) with primary FSGS and 95 children (68 boys, 27 girls) with minimal lesion by morphometry. FSGS patients had segmental sclerosis affecting 17.1%±14.8% of the glomeruli. The percentage of segmental glomerulosclerosis was not related to age. MGV increased with age in the FSGS patients (r 2 = 0.36, P 〈0.001) and in the minimal lesion patients (r 2 = 0.37, P 〈0.001). MGV of children with FSGS is significantly larger than that of the minimal lesion group [(14.8±5.7) × 105μm3 vs. (12.1±3.7) × 105μm3, P 〈0.001]. Multiple regression estimates suggest that the FSGS lesion affects MGV independently (P 〈0.001). The volume density of mesangium and the volume density of cortical interstitium were significantly greater in the FSGS patients than in the minimal lesion patients (P 〈0.001). These results indicate that MGV of pediatric FSGS patients increases with age and that the FSGS lesion itself may cause glomerular hypertrophy, possibly via mesangial expansion. Thus, glomerular hypertrophy in childhood minimal lesion may be an indicator of FSGS that is undetected because of the problem of sampling.
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  • 6
    ISSN: 1432-198X
    Keywords: Childhood renal disease ; Renal biopsy ; Korea
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Between June 1975 and March 1987, 662 renal biopsies were performed in 657 children at Seoul National University Children's Hospital. Nephrotic syndrome was the most indication for renal biopsy and accounted for 62% of all cases. Of these, 57% showed minimal change lesions and 21% showed focal segmental glomerular sclerosis. Nephropathy, associated with Australia-antigenpositive hepatitis, was the most prominent cause of secondary nephrotic syndrome, and of these patients membranous nephropathy was found in 86%. Diffuse proliferative glomerulonephritis was found in 60% of patients with acute nephritic syndrome. Fifty-eight percent of children with haematuria were found to have either IgA nephropathy or Henoch-Schönlein nephritis. Fifteen children with acute renal failure were biopsied, 2 of whom had haemorrhagic fever.
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  • 7
    ISSN: 1432-198X
    Keywords: Key words MELAS syndrome ; Alport syndrome ; Focal segmental glomerulosclerosis ; Hearing loss ; Diabetes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Several cases of hereditary glomerulopathy associated with an A to G transition at position 3243 in mitochondrial DNA, which is known to be associated with most cases of MELAS syndrome (myopathy, encephalopathy, lactic acidosis, and stroke-like episodes), have been recently reported. These patients share the characteristics of hereditary progressive glomerular disease and hearing loss with Alport syndrome. We therefore screened 27 patients with kidney disease clinically mimicking Alport syndrome for the presence of the 3243 mitochondrial mutation, and found one girl with the mutation and a positive family history. Her clinical features were very similar to those of all cases reported to date. An absence of hematuria, severe kidney involvement in a female, pathological changes of focal segmental glomerulosclerosis with no basket-weave change of the glomerular capillary wall, and the frequent association of steroid-induced diabetes are the major features that distinguish this condition from Alport syndrome. Careful neurological examination may detect neuromuscular symptoms compatible with mitochondrial cytopathies. In conclusion, progressive glomerulopathy should be included in the broad spectrum of mitochondrial cytopathies, especially in cases of MELAS syndrome. This mutation should also be included in the etiologies of secondary focal segmental glomerulosclerosis and in the differential diagnosis of Alport syndrome.
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