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  • 1
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Aims:  This retrospective study defined the clinical features and outcome of antineutrophil cytoplasmic antibody-associated glomerulonephritis in 18 seropositive Taiwanese patients (11 male, seven female; median age 64 years; range 21–82 years) with biopsy-proven pauci-immune necrotizing crescentic glomerulonephritis.Results:  Fourteen patients had a diagnosis of systemic vasculitis including 10 with microscopic polyangiitis and four with Wegener's granulomatosis; the remaining four had only glomerulonephritis. At onset, 100% of the systemic vasculitis patients had pulmonary lesions with or without haemoptysis, and 29% presented with seizure in the absence of a defined brain lesion. Median serum creatinine concentration was 362.4 µmol/L (range 61.9–857.5 µmol/L) and dialysis therapy was needed in six patients. During follow up (median 16.5 months; range 2–72 months), treatment included cyclophosphamide and corticosteroids (n = 8) or corticosteroids alone (n = 7). In some patients, treatment improved (n = 4) or stabilized (n = 4) renal function. But chronic dialysis was needed in the other 10 patients. Follow-up death occurred because of sepsis (n = 3) and haemorrhage (n = 2). Patient survival rates were 78% (1 year) and 72% (5 years). Renal survival rates were 56 and 39% at 1 and 5 years, respectively. Of the candidate clinical and pathological parameters, chronic glomerular lesions in renal biopsy were the only determinant of poor renal outcome (P = 0.006).Conclusion:  Antineutrophil cytoplasmic antibody-associated glomerulonephritis should be considered in nephritic patients with extrarenal manifestations, especially pulmonary infiltrate, unexplained seizure, and fever of an unknown origin in Taiwanese patients. Renal biopsy should be performed before initiating immunosuppressive therapy because the most common cause of mortality was sepsis.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Nephrology 7 (2002), S. 0 
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: SUMMARY: Peritoneal fibrosing syndrome (PFS) is composed of a wide spectrum of peritoneal alterations observed in patients under peritoneal dialysis (PD). Long-term peritoneal exposure to unphysiological PD solutions and recurrent bacterial peritonitis had been claimed as the most common causes predisposing to the development of PFS in a PD population. With the advances in molecular research, physicians and pathologists recognized that peritoneal injury and the accompanied accumulation of extracellular matrix (ECM) within the peritoneum are key events leading to PFS. Bioincompatible solution and it's related products, inflammatory mediators, growth factors as well as cytokines in the peritoneal cavity are contributing factors. Therapeutic strategies antagonizing these mediators and/or their downstream intracellular signalling pathways with either drug molecules or gene transfer may have potential for the prevention or treatment of PFS.
    Type of Medium: Electronic Resource
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  • 3
    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:  The peritoneal mesothelial cell is a critical component of the peritoneal membrane. The intraperitoneal use of several antibiotics to treat bacterial peritonitis is current clinical practice. Our previous study showed that cephalothin (CPL) and cefotaxime (CFT) have cytotoxic effects on human peritoneal mesothelial cells (HPMC), however, the exact mechanism of cytotoxicity has not been elucidated. In the present study, flow cytometry, TdT-mediated dUTP nick-end labelling (TUNEL) staining and electron microscopy were used to detect the apoptosis of HPMCs. Immunofluorescent staining was used to evaluate the cytochrome c distribution pattern. Western blotting was used to assess apoptotic signalling proteins. We found that CPL (0.5 mg/mL) and CFT (1 mg/mL) induced apoptosis of HPMCs, whereas cefazolin (0.5 mg/mL) and ceftriaxone (0.5 mg/mL) failed to induce apoptosis of HPMCs. While the DNA content of CFT- or CPL-treated cells was reduced, as determined by flow cytometry, cefazolin and ceftriaxone had no such effect. The CFT- or CPL-treated cells displayed the features of apoptosis both under the electron microscope and by using TUNEL staining. However, cefazolin and ceftriaxone produced the same result as the medium controls. Furthermore, CFT and CPL increased the expression of Bax and p53, and caused the translocation of cytochrome c from the mitochondria to the cytoplasm. The HPMC treated by CFT but not by CPL induced the cleavage of procaspase-3 to form active caspase-3. In conclusion, cefotaxime and cephalothin induce apoptosis of HPMCs in vitro. Signal transduction may be through the mitochondrial pathway.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 23 (1996), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. We have studied the role of kallikrein (KK) in the maintenance of renal function in chronic hypoxic rats (high altitude; HA), compared with control rats kept at sea level (SL). Hypoxia was induced by placing female Wistar rats (198-290 g) in an altitude chamber (5500m) 15 h/day for 4 weeks. Experiments were also conducted to study the interaction of KK with renal nerve activity and endothelin (ET), two parameters previously shown to be altered in this model.2. It was found that renal cortex tissue KK activity (TKA) was not significantly different in 10 SL and 10 HA rats. However, the urinary KK activity (UKA) was reduced nearly to half (from 35.2±4.6 to 18.5±1.7 pkat/min) in HA rats after 4 weeks of chronic hypoxia.3. Acute renal denervated diuresis was accompanied by a significant increase in UKA (from 9±2 to 14±2 pkat/min in HA and denervated HA rats, respectively; P 〈 0.05) in HA rats. Intrarenal arterial pretreatment of aprotinin reduced the denervated diuresis.4. Endothelin (600 ng/kg per h) reduced urine flow, sodium and potassium excretion in the ipsilateral kidney in another 10 SL and 10 HA rats. The extent of the drop of these parameters was significantly less in HA rats. Urinary KK activity was correlated significantly with the measured renal functional parameters (r ranging from 0.472 to 0.612) in SL rats, but was insignificant in HA rats (r ranging from 0.032 to 0.192).5. We have demonstrated that chronic exposure to hypoxia decreases urinary KK excretion and that KK is involved in acute renal denervated diuresis generated in these animals. The present study suggests that KK plays a partial role in the maintenance of renal function in chronic hypoxic rats.
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  • 5
    Electronic Resource
    Electronic Resource
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 9 (2004), S. 0 
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: SUMMARY:  Almost all forms of chronic kidney disease progressing to end-stage kidney failure are characterized by diffuse fibrosis, a final common pathway converging from multiple pathogenetic networks regardless of the initial injury. Four principal interventions including glycaemic and blood pressure control, dietary protein restriction, and angiotensin II blockade have been proven to slow progression of diabetic and/or non-diabetic chronic kidney disease. However, the ultimate solution to halt disease progression in the long term is still pending. Because of the pathogenetic complexity of kidney disease, multidrug intervention with the least side-effects should, without doubt, be the next step to stop kidney disease progression. Animal and cellular studies have demonstrated the rationale for pentoxifylline (i.e. its effects against cell proliferation, inflammation, and extracellular matrix accumulation) in the treatment of chronic kidney disease induced by immune- or non-immune-mediated mechanisms. Limited human studies have proven its efficacy in reducing proteinuria in patients with diabetes receiving angiotensin-converting enzyme inhibitors, and in patients with nephrotic syndrome refractory to conventional immunosuppressive therapy. Moreover, monotherapy with pentoxifylline markedly reduces proteinuria in patients with membranous nephropathy. Further studies are required to examine whether pentoxifylline can improve the renal outcome in patients receiving interventions with proven efficacy.
    Type of Medium: Electronic Resource
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