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Purpose: The effects of augmenter of liver regeneration (ALR) on the acute kidney injury (AKI) rats were investigated by measuring the inflammatory response associated with transcription factor nuclear factory (NF-κB) pathway., Methods: The model of AKI rats was established by occluded the renal pedicles for 60 min and then released. After that, animals were treated with ALR (100 or 200 μg/kg). All rats were killed at different time points (24, 48, 72 h). Renal function and kidney histological changes were measured. The apoptosis of tubular cells was evaluated by TdT-mediated dUTP nick end labeling assay. Cytokines and chemokines were assessed by immunohistochemistry, enzyme-linked immunosorbent assay and real-time polymerase chain reaction (RT-PCR). The NF-κB p65 protein was analyzed by immunohistochemistry and RT-PCR, respectively., Results: Ischemia reperfusion induced tubular cells necrosis and apoptosis, and ALR can significantly reduce this damages. The productions of MCP-1, IL-1β and IL-6 were lower in the group of ALR treatment, especially in the high-dose group. The inflammatory infiltrates were lower in the rats with administration of ALR. ALR mediated the level of cytokines and chemokines through inhibited the activation of NF-κB., Conclusion: ALR can improve renal function and inhibit the expression of inflammatory factors. This protects against renal ischemia reperfusion injury, which may be associated with preventing NF-κB activation in rats.

Background: Conversion from calcineurin inhibitor (CNI) to mTOR inhibitors may reduce and even halt the progression of chronic allograft dysfunction (CAD) which is the most important cause of renal allograft loss. We aimed to investigate the effects of conversion from CNI to everolimus on parameters of fibrosis, inflammation, glomerulotubular damage and vascular functions in renal transplant recipients., Methods: Fifteen stable renal transplant recipients who were under CNI treatment (male/female 13/2, mean age 41 ± 10 years) were enrolled and switched to everolimus. Serum and urinary transforming growth factor-β (TGF-β), urinary neutrophil gelatinase-associated lipocalin (NGAL) and monocyte chemoattractant protein-1 (MCP-1) were measured as markers of fibrosis, tubular damage and inflammation. As parameters of vascular functions, pulse wave velocity (PWV), augmentation index (AIx), serum asymmetric dimethyl-arginine and fibroblast growth factor-23 (FGF-23) were measured. All these measurements were repeated at the 3rd month of conversion., Results: Estimated GFR (52 ± 7-57 ± 11 ml/min/l.73 m(2), p = 0.02) (was increased after conversion to everolimus. However, serum uric acid levels were significantly decreased (6.21 ± 1.21-5.50 ± 1.39 mg/dL, p = 0.01). Serum TGF-β levels (8727 ± 2897-1943 ± 365 pg/mL, p = 0.03) and urinary NGAL levels (26 ± 10-12 ± 2 ng/mg creatinine, p = 0.05) were significantly decreased. However, urinary MCP-1, FGF-23, PWV and AIx did not change. Urinary TGF-β was associated with urinary NGAL (r = 0.62, p = 0.01), urinary MCP-1 (r = 0.68, p = 0.005) and proteinuria (r = 0.50, p = 0.05)., Conclusion: Conversion from CNI to everolimus resulted in significant decreases of serum TGF-β and urinary NGAL which may represent less fibrosis and tubular damage. Association of urinary TGF-β with NGAL and MCP-1 suggests that tubular damage, fibrosis and inflammation may act together for progression of CAD.

In a previous study, we demonstrated the benefit of tonsillectomy for early recovery from Henoch-Schönlein purpura (HSP) nephritis (HSPN), suggesting the pathological role of tonsils in HSP (Inoue et al., Clin Nephrol 67:298-305, 2007). In this study, we evaluated the efficacy of extensive eradication of infectious foci directly connected to the tonsils, including those involved in oral as well as ear, nose, and throat (ENT) diseases, in reducing the nephropathy in HSP. For this purpose, we examined the focal points of infection in 40 newly diagnosed HSP patients. After these focal points of infection had been identified, they were extensively eradicated; when the clinical course was intractable, we also considered tonsillectomy. After administering such therapy to HSP patients, we prospectively followed them up for 0.6 to 8 years. The identified focal infections included dental caries in 28 (70%), apical periodontitis in 21 (53%), rhinosinusitis in 19 (48%), tonsillitis in five (13%), and otitis media in four (10%) of the 40 patients. Seventeen patients (43%) had more than two simultaneous infectious foci, whereas, in five (13%), no infectious focus was found. In 32 patients, antimicrobial treatment with concurrent dental and/or ENT therapy resulted in a complete cure without development of HSPN or recurrent attacks. In eight patients, we performed tonsillectomy-adenotonsillectomy to treat their clinical symptoms, including aggravated purpura and recurrent attacks of HSP or HSPN. All patients were completely cured. The overall incidence of HSPN was only three out of the 40 patients (8%). Oral and ENT diseases were found with high percentages in HSP patients. Early and extensive treatment for these lesions and tonsillectomy-adenotonsillectomy for intractable cases may prevent the complication of HSPN, contributing to the early curing of HSP.

Background: Henoch-Schönlein purpura (HSP) is a systemic, small vessel vasculitis, which is very common among pediatric population. Findings of previous reports addressing the preventive effect of corticosteroid treatment in HSP nephritis have been inconsistent. The aim of this study was to determine whether corticosteroid therapy was effective in preventing Henoch-Schönlein nephritis., Methods: The medical records of 216 children with HSP, seen in 2 tertiary care pediatric nephrology centers, were reviewed retrospectively. The effect of corticosteroid therapy on preventing nephritis was assessed in 157 patients who had no evidence of nephritis at the initial urinalysis. The treatment group (n=61) had received oral corticosteroids for gastrointestinal symptoms and/or arthritis. The dosage of prednisone was 1 mg/kg per day for 1-2 weeks, with weaning over a week. We compared the rate of renal involvement during follow-up between the groups who were treated with corticosteroids and not., Results: Nephritis developed in 17 of the 61 (27.8%) corticosteroid-treated patients and 18 of the 96 (18.7%) untreated patients during follow-up., Conclusion: There was no evidence that corticosteroids reduced the risk of renal involvement in HSP, and these results do not support the use of corticosteroids in early HSP to prevent renal injury.

Background: Hypertension causes an inflammatory response in the kidney. Many studies have demonstrated that activation of the renal renin-angiotensin system, and therefore an increase in local angiotensin II (AngII) production, participates in the renal inflammatory cell recruitment. Our aim was to investigate the role of AngII blockade in hypertension-induced inflammatory response., Methods: To replicate chronic hypertension with renal disease, we used a model of spontaneously hypertensive rats with unilateral nephrectomy (UNX-SHR). These animals were studied for 48 weeks. We investigated the effect of long-term treatment with an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin II type 1 (AT1 ) antagonist, 2 strategies currently used in humans, on renal proinflammatory parameters., Results: UNX-SHR rats presented elevated renal inflammatory cell infiltration and up-regulation of proinflammatory factors, including activation of nuclear factor chi B (NF-chi B) and related genes. Both ACE inhibition and AT 1 blockade decreased the number of inflammatory cells as well as the up-regulation of proinflammatory factors in the kidney., Conclusions: These results suggest that either AT 1 blockade or ACE inhibition can stop the renal inflammatory process in chronic hypertension-associated inflammatory response.