scholarly journals Functional Evaluation of Early Renal Interstitial Fibrosis in Patients with Chronic Kidney Disease Using Diffusion-Weighted and BOLD MR Imaging: Preliminary Experience

2013 ◽  
Vol 03 (04) ◽  
pp. 51-56
Author(s):  
颖华 邬
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Mr Imaging ◽  
Interstitial Fibrosis ◽  
Functional Evaluation ◽  
Renal Interstitial Fibrosis ◽  
Diffusion Weighted

scholarly journals Shen Shuai II Recipe Attenuates Renal Interstitial Fibrosis by Improving Hypoxia via the IL-1β/c-Myc Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Liuyi Yang ◽  
Meng Wang ◽  
Yuan Zhou ◽  
Jing Yang ◽  
Chaoyang Ye ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Renal Failure ◽  
Renal Function ◽  
Chronic Renal Failure ◽  
Kidney Disease ◽  
Protein Expression ◽  
Interstitial Fibrosis ◽  
Renal Interstitial Fibrosis ◽  
Related Factors

Background. Renal interstitial fibrosis is a pathological manifestation of progression of chronic kidney disease induced by various factors. Shen Shuai II Recipe (SSR) has been used in clinical practice for more than 20 years, and clinical studies have confirmed that SSR significantly improves the renal function of patients with chronic kidney disease. However, the specific mechanisms underlying its efficacy require further research. This study aims to explore the influencing factors of renal interstitial fibrosis in the context of hypoxia via the IL-1β/c-Myc pathway and the potential molecular mechanisms of SSR intervention in vivo and in vitro. Methods. A rat model of chronic renal failure was developed by performing 5/6 (ablation/infarction, A/I) surgery on randomly selected, male Sprague Dawley rats. Thirty-six successfully modeled rats were randomly divided into three groups: 5/6 (A/I), 5/6 (A/I) + SSR, and 5/6 (A/I) + losartan. Another 12 rats were used as the sham group. After 8 weeks of the corresponding intervention, renal function, liver function, and protein expression of renal-fibrosis-related factors, HIF-1α, IL-1β, and c-Myc, were detected. In vitro analysis was performed using hypoxia-induced rat renal tubular epithelial cells (NRK-52E) and IL-1β-stimulated rat renal interstitial fibroblasts (NRK-49F). IL-1β concentration in the culture medium and IL-1β protein expression in hypoxic NRK-52E treated with different concentrations of SSR were investigated. Furthermore, we also studied the changes in protein expression of c-Myc and fibrosis-related factors after c-Myc gene silencing in IL-1β-stimulated NRK-49F treated with SSR. Results. Shen Shuai II Recipe significantly reduced RIF and downregulated the expression of HIF-1α, c-Myc, and IL-1β proteins in 5/6 (A/I) rats with chronic renal failure. It also inhibited IL-1β secretion from NRK-52E induced by hypoxia, which in turn inhibited fibroblast activation mediated by the IL-1β/c-Myc pathway, and finally reduced the overproduction of the extracellular matrix. Conclusion. The renoprotective effects of SSR in rats with chronic renal failure may be related to its inhibition of hypoxia via the IL-1β/c-Myc pathway. Thus, SSR is a potentially effective drug for delaying the progression of renal interstitial fibrosis.

scholarly journals Lithium-Associated Kidney Microcysts

2008 ◽  
Vol 8 ◽  
pp. 828-829 ◽  
Author(s):  
Jennifer Tuazon ◽  
David Casalino ◽  
Ehteshamuddin Syed ◽  
Daniel Batlle
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Mr Imaging ◽  
Interstitial Fibrosis ◽  
Renal Cysts ◽  
Lithium Therapy ◽  
Tubular Atrophy ◽  
Advanced Chronic Kidney Disease ◽  
Tubulointerstitial Nephropathy

Long-term lithium therapy is associated with impairment in concentrating ability and, occasionally, progression to advanced chronic kidney disease from tubulointerstitial nephropathy. Biopsy findings in patients with lithium-induced chronic tubulointerstitial nephropathy include tubular atrophy and interstitial fibrosis interspersed with tubular cysts and dilatations. Recent studies have shown that cysts are seen in 33––62.5% of the patients undergoing lithium therapy. MR imaging is highly capable of defining renal morphological features and has been demonstrated to be superior to US and CT scan for the visualization of small renal cysts. The microcysts are found in both cortex and medulla, particularly in the regions with extensive atrophy and fibrosis, and can be multiple and bilateral. They tend to be sparse and do not normally exceed 1–2 mm in diameter. The renal microcysts in the image here reported are subtle, but consistent with lithium-induced chronic nephropathy. An MRI of the kidneys provides noninvasive evidence that strengthens the diagnosis of lithium-induced nephropathy.

Association between renal iron accumulation and renal interstitial fibrosis in a rat model of chronic kidney disease

2015 ◽  
Vol 38 (7) ◽  
pp. 463-470 ◽  
Author(s):  
Yoshiro Naito ◽  
Aya Fujii ◽  
Hisashi Sawada ◽  
Makiko Oboshi ◽  
Toshihiro Iwasaku ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Rat Model ◽  
Interstitial Fibrosis ◽  
Iron Accumulation ◽  
Renal Interstitial Fibrosis

scholarly journals TDAG51 induces renal interstitial fibrosis through modulation of TGF-β receptor 1 in chronic kidney disease

2021 ◽  
Vol 12 (10) ◽  
Author(s):  
Rachel E. Carlisle ◽  
Zahraa Mohammed-Ali ◽  
Chao Lu ◽  
Tamana Yousof ◽  
Victor Tat ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Er Stress ◽  
Interstitial Fibrosis ◽  
Health Concern ◽  
Tubular Damage ◽  
Wild Type ◽  
Renal Interstitial Fibrosis ◽  
Β Receptor ◽  
Dependent Mechanism

AbstractChronic kidney disease (CKD) is characterized by the gradual loss of renal function and is a major public health concern. Risk factors for CKD include hypertension and proteinuria, both of which are associated with endoplasmic reticulum (ER) stress. ER stress-induced TDAG51 protein expression is increased at an early time point in mice with CKD. Based on these findings, wild-type and TDAG51 knock-out (TDKO) mice were used in an angiotensin II/deoxycorticosterone acetate/salt model of CKD. Both wild-type and TDKO mice developed hypertension, increased proteinuria and albuminuria, glomerular injury, and tubular damage. However, TDKO mice were protected from apoptosis and renal interstitial fibrosis. Human proximal tubular cells were used to demonstrate that TDAG51 expression induces apoptosis through a CHOP-dependent mechanism. Further, a mouse model of intrinsic acute kidney injury demonstrated that CHOP is required for ER stress-mediated apoptosis. Renal fibroblasts were used to demonstrate that TGF-β induces collagen production through an IRE1-dependent mechanism; cells treated with a TGF-β receptor 1 inhibitor prevented XBP1 splicing, a downstream consequence of IRE1 activation. Interestingly, TDKO mice express significantly less TGF-β receptor 1, thus, preventing TGF-β-mediated XBP1 splicing. In conclusion, TDAG51 induces apoptosis in the kidney through a CHOP-dependent mechanism, while contributing to renal interstitial fibrosis through a TGF-β-IRE1-XBP1 pathway.

Inhibition of CTCF-regulated miRNA-185-5p mitigates renal interstitial fibrosis of chronic kidney disease

Epigenomics ◽  
2021 ◽  
Author(s):  
Jiajun Zhou ◽  
Han Zhou ◽  
Yong Liu ◽  
Caixin Liu
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Mouse Model ◽  
Ureteral Obstruction ◽  
Interstitial Fibrosis ◽  
Unilateral Ureteral Obstruction ◽  
Renal Interstitial Fibrosis ◽  
Underlying Mechanisms

Aim: The present study aimed to elucidate the effect of CTCF on renal interstitial fibrosis in chronic kidney disease (CKD) and underlying mechanisms. Materials & methods: We measured NPHS2 expression and investigated its function in a unilateral ureteral obstruction-induced mouse model of CKD. Results: NPHS2 was poorly expressed in CKD mice. miR-185-5p targeted NPHS2 and reduced its expression, leading to increased α-SMA and COL I/III expression, increased renal interstitial fibrosis area and elevated phosphorylated vasodilator-stimulated phosphoprotein/vasodilator-stimulated phosphoprotein ratio. Cotreatment with CTCF downregulated miR-185-5p expression and abolished its effects in the CKD model. Conclusion: CTCF suppressed miR-185-5p and upregulated its target NPHS2, with a net effect of alleviating renal interstitial fibrosis in CKD.

Diffusion-weighted MR imaging of kidneys in patients with chronic kidney disease: initial study

2009 ◽  
Vol 20 (4) ◽  
pp. 978-983 ◽  
Author(s):  
Xueqin Xu ◽  
Wenqiang Fang ◽  
Huawei Ling ◽  
Weimin Chai ◽  
Kemin Chen
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Mr Imaging ◽  
Initial Study ◽  
Diffusion Weighted

scholarly journals Pomolic Acid Ameliorates Fibroblast Activation and Renal Interstitial Fibrosis through Inhibition of SMAD-STAT Signaling Pathways

Molecules ◽  
2018 ◽  
Vol 23 (9) ◽  
pp. 2236 ◽  
Author(s):  
Ji-Hyun Park ◽  
Kyung Jang ◽  
Hyun An ◽  
Jung-Yeon Kim ◽  
Mi-Gyeong Gwon ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Interstitial Fibrosis ◽  
Fibroblast Cells ◽  
Potential Candidate ◽  
Renal Interstitial Fibrosis ◽  
Fibroblast Activation ◽  
Pomolic Acid ◽  
Kidney Fibroblast ◽  
Tgf Β1

Fibrosis is a common pathological feature in most kinds of chronic kidney disease. Transforming growth factor β1 (TGF-β1) signaling is the master pathway regulating kidney fibrosis pathogenesis, in which mothers against decapentaplegic homolog 3 (SMAD3) with signal transducer and activator of transcription 3 (STAT3) act as the integrator of various pro-fibrosis signals. We examine the effects of pomolic acid (PA) on mice with unilateral ureteral obstruction (UUO) and TGF-β1 stimulated kidney fibroblast cells. UUO mice were observed severe tubular atrophy, and tubulointerstitial fibrosis and extracellular matrix (ECM) deposition at seven days postoperatively. However, PA-treated UUO mice demonstrated only moderate injury, minimal fibrosis, and larger reductions in the expression of ECM protein and epithelial-mesenchymal transition (EMT) progress. PA inhibited the SMAD-STAT phosphorylation in UUO mice. PA effects were also confirmed in TGF-β1 stimulated kidney fibroblast cells. In this study, we first demonstrated that PA ameliorates fibroblast activation and renal interstitial fibrosis. Our results indicate that PA may be useful as a potential candidate in the prevention of chronic kidney disease.

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