Immune and Inflammatory Role in Renal Disease

Imig, John D.; Ryan, Michael J.

doi:10.1002/cphy.c120028

Cited by 293 publications

(240 citation statements)

References 283 publications

(411 reference statements)

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“…It is believed that phlegm stagnation implicates the renal microcirculation system, qi stagnation, stasis and pathogenic factor accumulation into turbidity toxins and that the toxins damage the renal microcirculation system (4). Damage to the renal microcirculation system is considered the most important pathogenesis factor of DN, which is a condition associated with the production of various inflammatory factors, including MCP-1 and NF-κB (34). The essence of stasis refers to thrombosis or embolism complications in the kidney, which is the typical pathology of DN in traditional Chinese medicine and its symptoms include a change in renal hemodynamics and involves mesangial cell proliferation and extracellular matrix accumulation (34).…”

Section: Discussionmentioning

confidence: 99%

“…Damage to the renal microcirculation system is considered the most important pathogenesis factor of DN, which is a condition associated with the production of various inflammatory factors, including MCP-1 and NF-κB (34). The essence of stasis refers to thrombosis or embolism complications in the kidney, which is the typical pathology of DN in traditional Chinese medicine and its symptoms include a change in renal hemodynamics and involves mesangial cell proliferation and extracellular matrix accumulation (34). This may lead to the onset of glomerulosclerosis in patients with DN (34).…”

Section: Discussionmentioning

confidence: 99%

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Tangshen formula improves inflammation in renal tissue of diabetic nephropathy through SIRT1/NF-κB pathway

Zhang

Gao

et al. 2017

Exp Ther Med

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Abstract. The present study investigated the mechanism underlying the anti-inflammatory effects of Tangshen formula (TS) in Sprague Dawley (SD) rats with diabetic nephropathy (DN). A rat model of DN was established by intraperitoneal injection of 1% (40 mg/kg) streptozotocin and administration of a high fat and glucose diet. Subsequently, SD rats were randomly divided into six groups (n=8): A DN group, a valsartan group, a high-dose TS group, a middle-dose TS group, a low-dose TS group and a control group with normal SD rats. Once rats received their allocated treatment for 12 weeks, body weight and kidney weight were recorded, and fasting blood glucose, ratio of urinary protein, β 2 -MG and creatinine clearance rate were determined. Furthermore, hemodynamic indices, including plasma viscosity and whole blood reduction viscosity were detected. Immunohistochemistry was used to detect the infiltration of macrophages in the kidneys of rats. Reverse transcription-quantitative polymerase chain reaction and western blotting were performed to investigate the activation; mRNA and protein expression levels of monocyte chemoattractant protein-1 (MCP-1), macrophage migration inhibitory factor (MIF), nuclear factor-κB (NF-κB) and sirtuin-1 (SIRT1) in each group. In comparison with the DN group, each biochemical indicator of rats in the high-dose TS group was significantly decreased (P<0.05). Blood viscosity in each treatment group was significantly decreased when compared with the DN group (P<0.01). Hematoxylin and eosin staining indicated that the infiltration of macrophages was significantly decreased in the high-dose TS group when compared with the DN group (P<0.01). mRNA and protein expression levels of MCP-1 and MIF in the high-dose TS group were significantly decreased when compared with the DN group (P<0.05). In the treatment groups, SITR1 mRNA expression levels were significantly increased, whereas the mRNA expression levels of NF-κB were significantly decreased (P<0.01). Western blotting results indicated a significant decrease in the protein expression levels of acetylated NF-κB in the treatment groups when compared with the DN group (P<0.01) and the propensity of protein expression of the other inflammatory factors were consistent with the mRNA findings. The results of the high-dose TS group were similar to those of the valsartan group. The present study indicates that TS was able to activate SITR1, which lead to NF-κB deacetylation, thus reducing the release of inflammatory factors and decreasing the severity of diabetic nephropathy.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Tangshen formula improves inflammation in renal tissue of diabetic nephropathy through SIRT1/NF-κB pathway

Zhang

Gao

et al. 2017

Exp Ther Med

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“…Unresolved inflammation characterized by leukocyte infiltration is considered to be a main factor contributing to renal fibrosis (Figure 1) [23–25,28,29]. Infiltrated leukocytes excrete various pro-fibrotic growth factors and cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, and IL-6, which promote the proliferation of myofibroblasts (Figure 1) [29,30].…”

Section: Mechanisms Of Renal Fibrosismentioning

confidence: 99%

“…Infiltrated leukocytes excrete various pro-fibrotic growth factors and cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, and IL-6, which promote the proliferation of myofibroblasts (Figure 1) [29,30]. Levels of these cytokines in plasma have been shown to increase in patients with CKD [31,32].…”

Section: Mechanisms Of Renal Fibrosismentioning

confidence: 99%

Nano-sized carriers in gene therapy for renal fibrosisin vivo

Miyazawa

Hirai

Ookawara

et al. 2017

Nano Reviews & Experiments

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Renal fibrosis is the final common pathway leading to end-stage renal failure regardless of underlying initial nephropathies. No specific therapy has been established for renal fibrosis. Gene therapy is a promising strategy for the treatment of renal fibrosis. Nano-sized carriers including viral vectors and non-viral vectors have been shown to enhance the delivery and treatment effects of gene therapy for renal fibrosis in vivo. This review focuses on the mechanisms of renal fibrosis and the in vivo technologies and methodologies of nano-sized carriers in gene therapy for renal fibrosis. RESPONSIBLE EDITOR Alexander Seifalian Director of Nanotechnology & Regenerative Medicine Ltd., The London BioScience Innovation Centre, London, UNITED KINGDOM

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“…KBH progresyonunda etkili olduğu iyi bilinen diğer önemli patofizyolojik mekanizmalardan biri inflamasyondur (8,9). NS ile inflamasyonun ilişkili olduğunda dair az da olsa bazı çalışmalar mevcuttur (10,11).…”

Section: Gereç Ve Yöntemlerunclassified

Effects of the Clinical and Biochemical Features of Patients with Treatment-Resistant Primary Nephrotic Syndrome on Renal Survival

Bilgin¹,

Özkök²,

Köstek³

et al. 2017

Turk Neph Dial Transpl

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ÖzAMAÇ: Nefrotik sendrom (NS), sıklıkla kronik böbrek hastalığına (KBH) ilerleyen heterojen hastalık gruplarını içerir. Tedaviye direnç, NS hastalarında önemli bir problemdir ve böbrek sağkalımını olumsuz etkiler. Çalışmamızda, tedaviye dirençli primer NS hastalarının klinik ve laboratuvar özelliklerinin böbrek sağkalımı üzerine etkileri araştırılmıştır. GEREÇ ve YÖNTEMLER:2000-2015 tarihleri arasında primer NS tanısı ile takip edilen 1305 hasta değerlendirildi. Tedaviye rağmen 3.5g/gün üzerinde proteinürisi devam eden 50 hasta (E/K:32/18, ortalama yaş:50±16) çalışmaya dahil edildi.BULGULAR: NS etiyolojilerine göre hasta sayıları şu şekilde dağılıyordu: membranöz nefropati (MN), 19 (%38); fokal segmental glomerüloskleroz (FSGS), 16 (%32); IgA nefropatisi (IgAN), 8 (%16); membranoproliferatif glomerülonefrit (MPGN),7 (%14). En düşük bazal GFR değerleri IgAN'de saptandı [37 (23-57) mL/dak]. Gruplar GFR'de yıllık düşüş hızlarına (∆GFR/yıl) göre karşılaştırıldığında, gruplar arasında anlamlı fark saptanmadı. FSGS hastalarında bazal proteinüri miktarları ne kadar fazla ise ∆GFR/yıl da o kadar fazla idi (r=-0.51, p=0.04). MPGN hastalarında ise bazal C-reaktif-protein (CRP) ile ∆GFR/yıl ters koreleydi (r=-0.75, p=0.04). Sigara, hiperlipidemi, siklofosfamid, kalsinörin inhibitörü veya steroid kullanımının ∆GFR/yıl'a herhangi bir etkisi saptanmadı. SONUÇ:Tedaviye cevapsız primer NS'un en sık nedeni MN olarak saptandı. Glomerülonefrit tiplerinin yıllık GFR düşüş hızlarının benzer olduğu saptandı. Bu hasta grubunda verilen tedavilerin renal sağkalım üzerine herhangi bir etkisi saptanamadı. FSGS'de proteinüri, MPGN'de ise CRP, KBH progresyonunu predikte edebilir.ANAhTAR SÖzcükLER: Nefrotik sendrom, Proteinüri, Tedaviye direnç, Glomerülonefrit, Kronik böbrek hastalığı ABSTRAcT OBJEcTIVE: Nephrotic syndrome (NS) is commonly associated with progression of chronic kidney disease (CKD). Resistance to treatment is an important problem that is a poor prognostic factor for progression of CKD. Herein, we aimed to investigate the effects of clinical and biochemical parameters on renal survival in patients with treatment-resistant primary NS. MATERIAL and METhODS:A total of 1305 NS cases who were followed were evaluated. Fifty primary NS patients (M/F: 32/18, mean age: 50±16) who had persistent proteinuria>3.5g/day despite treatment were included.RESULTS: NS etiologies were as follows: membranous nephropathy (MN), 19 (38%); focal segmental glomerulosclerosis (FSGS), 16 (32%); IgA nephropathy (IgAN), 8 (16%) and membranoproliferative glomerulonephritis (MPGN), 7 (14%). Baseline GFR values were significantly lower in patients with ) mL/min]. Annual rate of decline in GFR levels (∆GFR/year) was not different between the groups. Proteinuria was significantly associated with ∆GFR/year in patients with FSGS (r=-0.51, p=0.04). Baseline C-reactive-protein (CRP) levels were found to be correlated with ∆GFR/year in the MPGN group (r=-0.75,p=0.04). Smoking, hyperlipidemia and treatment had no effect on ΔGFR/years. cONcLUSION: MN was the most fre...

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Immune and Inflammatory Role in Renal Disease

Cited by 293 publications

References 283 publications

Tangshen formula improves inflammation in renal tissue of diabetic nephropathy through SIRT1/NF-κB pathway

Tangshen formula improves inflammation in renal tissue of diabetic nephropathy through SIRT1/NF-κB pathway

Nano-sized carriers in gene therapy for renal fibrosisin vivo

Effects of the Clinical and Biochemical Features of Patients with Treatment-Resistant Primary Nephrotic Syndrome on Renal Survival

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