An Overview of Chronic Kidney Disease Pathophysiology: The Impact of Gut Dysbiosis and Oral Disease DOI Creative Commons
Serena Altamura, Davide Pietropaoli, Francesca Lombardi

et al.

Biomedicines, Journal Year: 2023, Volume and Issue: 11(11), P. 3033 - 3033

Published: Nov. 12, 2023

Chronic kidney disease (CKD) is a severe condition and significant public health issue worldwide, carrying the burden of an increased risk cardiovascular events mortality. The traditional factors that promote onset progression CKD are cardiometabolic like hypertension diabetes, but non-traditional contributors escalating. Moreover, gut dysbiosis, inflammation, impaired immune response emerging as crucial mechanisms in pathology. microbiome exert reciprocal influence commonly referred to "the gut-kidney axis" through induction metabolic, immunological, endocrine alterations. Periodontal diseases strictly involved axis for their impact on microbiota composition metabolic immunological alterations occurring reciprocally affecting both conditions. This review aims provide overview dynamic biological interconnections between oral status, gut, renal pathophysiology, spotlighting oral-gut-kidney raising whether periodontal can be modifiers CKD. By doing so, we try offer new insights into therapeutic strategies may enhance clinical trajectory patients, ultimately advancing our quest improved patient outcomes well-being.

Language: Английский

Chronic kidney disease and cardiovascular risk: epidemiology, mechanisms, and prevention DOI
Ron T. Gansevoort, Ricardo Correa‐Rotter, Brenda R. Hemmelgarn

et al.

The Lancet, Journal Year: 2013, Volume and Issue: 382(9889), P. 339 - 352

Published: May 31, 2013

Language: Английский

Citations

1948

Kidney lipid dysmetabolism and lipid droplet accumulation in chronic kidney disease DOI
Alla Mitrofanova, Sandra Merscher, Alessia Fornoni

et al.

Nature Reviews Nephrology, Journal Year: 2023, Volume and Issue: 19(10), P. 629 - 645

Published: July 27, 2023

Language: Английский

Citations

118

Long-term kidney outcomes of semaglutide in obesity and cardiovascular disease in the SELECT trial DOI Creative Commons
Helen M. Colhoun, Ildiko Lingvay, Paul Brown

et al.

Nature Medicine, Journal Year: 2024, Volume and Issue: 30(7), P. 2058 - 2066

Published: May 25, 2024

Abstract The SELECT trial previously reported a 20% reduction in major adverse cardiovascular events with semaglutide ( n = 8,803) versus placebo 8,801) patients overweight/obesity and established disease, without diabetes. In the present study, we examined effect of once-weekly 2.4 mg on kidney outcomes trial. incidence pre-specified main composite endpoint (death from initiation chronic replacement therapy, onset persistent estimated glomerular filtration rate (eGFR) < 15 ml min −1 1.73 m − 2 , ≥50% eGFR or macroalbuminuria) was lower (1.8%) (2.2%): hazard ratio (HR) 0.78; 95% confidence interval (CI) 0.63, 0.96; P 0.02. treatment benefit at 104 weeks for 0.75 (95% CI 0.43, 1.06; 0.001) overall 2.19 1.00, 3.38; baseline <60 . These results suggest individuals overweight/obesity, ClinicalTrials.gov identifier: NCT03574597

Language: Английский

Citations

66

Semaglutide in patients with overweight or obesity and chronic kidney disease without diabetes: a randomized double-blind placebo-controlled clinical trial DOI
Ellen M. Apperloo, José Luis Górriz, María José Soler

et al.

Nature Medicine, Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 25, 2024

Language: Английский

Citations

19

Growth-Dependent Podocyte Failure Causes Glomerulosclerosis DOI Open Access

Akihiro Fukuda,

Mahboob A. Chowdhury,

Madhusudan Venkatareddy

et al.

Journal of the American Society of Nephrology, Journal Year: 2012, Volume and Issue: 23(8), P. 1351 - 1363

Published: July 6, 2012

Podocyte depletion leads to glomerulosclerosis, but whether an impaired capacity of podocytes respond hypertrophic stress also causes glomerulosclerosis is unknown. We generated transgenic Fischer 344 rats that express a dominant negative AA-4E-BP1 transgene driven by the podocin promoter; member mammalian target rapamycin complex 1 (mTORC1) pathway, 4E-BP1 modulates cap-dependent translation, which key determinant cell’s response nutrients and growth factors. rat expressed had normal kidney histology protein excretion at 100 g body weight developed ESRD 12 months. Proteinuria were linearly related both increasing dose. Uni-nephrectomy reduced proteinuria first 40%–50%. The initial histologic manifestation disease was appearance bare areas glomerular basement membrane from pulling apart podocyte foot processes, followed adhesions Bowman capsule. Morphometric analysis confirmed mismatch between tuft volume total (number × size) per in relation gain nephrectomy. did not develop if dietary calorie restriction prevented enlargement. In summary, failure match signaling through mTORC1 pathway can trigger proteinuria, progression ESRD. Reducing may be useful adjunctive therapies slow or prevent

Language: Английский

Citations

159

Potential Association between Breakfast Skipping and Concomitant Late-Night-Dinner Eating with Metabolic Syndrome and Proteinuria in the Japanese Population DOI Creative Commons

Ayano Kutsuma,

Kei Nakajima,

Kaname Suwa

et al.

Scientifica, Journal Year: 2014, Volume and Issue: 2014, P. 1 - 9

Published: Jan. 1, 2014

Skipping breakfast is considered to be an unhealthy eating habit linked predispositions obesity and type 2 diabetes. Because dinner late at night can elicit subsequent skipping, we investigated if skipping concomitant with late-night-dinner (LNDE) was associated metabolic syndrome (MetS) proteinuria in the general Japanese population. We examined self-reported habitual LNDE, MetS (modified ATP-III criteria), a cross-sectional study of 60,800 adults aged 20–75 years. A total 14,068 subjects (23.1%) skipped breakfast, whom approximately half (52.8%) alone (without LNDE). The percentages who showed J-shaped relationship body mass index (BMI). Multivariate logistic regression analysis that LNDE (n= 6,645) significantly proteinuria, even after adjusting for relevant confounders (odds ratio (95% CI), 1.17 (1.08–1.28),P=0.0003, 1.37 (1.24–1.52),P<0.0001, resp.). were not respectively. In conclusion, may represent poorer behavior than alone, MetS, asymptomatic obesity, low weight

Language: Английский

Citations

133

Obesity Associated Hypertension: New Insights into Mechanism DOI Creative Commons
Young Sun Kang

Electrolytes & Blood Pressure, Journal Year: 2013, Volume and Issue: 11(2), P. 46 - 46

Published: Jan. 1, 2013

With excess nutrition, the burden of obesity is a growing problem worldwide. The imbalance between energy intake and expenditure leads to variable disorders as all major risk factors for cardiovascular disease. There are many hypothetical mechanisms explain obesity-associated hypertension. Activation RAAS key contributing factor in obesity. Particularly, adipose tissue plays crucial role dysfunction obesity-induced inflammation. phenotypic changes adipocytes occur into hypertrophy an inflammatory response autocrine paracrine manner impair adipocyte function, including insulin signaling pathway. Adipose produce secretes several molecules such leptin, resistin, adiponectin, visfatin, well cytokines TNF-α, IL-6, MCP-1, IL-1. These adipokines stimulated via intracellular pathways that regulate inflammation tissue. Inflammation oxidative stress important interact with microvascular endothelium Increased resistance raises blood pressure. Therefore, regulatory link perivascular adipokine synthesis provided mechanism

Language: Английский

Citations

122

Hesperidin protects against cyclophosphamide-induced hepatotoxicity by upregulation of PPARγ and abrogation of oxidative stress and inflammation DOI
Ayman M. Mahmoud

Canadian Journal of Physiology and Pharmacology, Journal Year: 2014, Volume and Issue: 92(9), P. 717 - 724

Published: June 16, 2014

The most important reason for the non-approval and withdrawal of drugs by Food Drug Administration is hepatotoxicity. Therefore, this study was undertaken to evaluate protective effects hesperidin against cyclophosphamide (CYP)-induced hepatotoxicity in Wistar rats. rats received a single intraperitoneal dose CYP 200 mg/kg body mass, followed treatment with hesperidin, orally, at doses 25 50 11 consecutive days. induced hepatic damage, as evidenced significantly elevated levels serum pro-inflammatory cytokines, transaminases, liver lipid peroxidation, nitric oxide. As consequence, there reduced glutathione content, activities antioxidant enzymes superoxide dismutase, catalase, peroxidase, were markedly reduced. In addition, administration considerable downregulation peroxisome proliferator activated receptor gamma (PPARγ) upregulation nuclear factor-kappa B (NF-κB) inducible oxide synthase (iNOS) mRNA expression. Hesperidin, dose-dependent manner, rejuvenated altered markers an almost normal state. conclusion, showed potent effect CYP-induced oxidative stress inflammation leading suggests that exerts its through PPARγ expression abrogation stress.

Language: Английский

Citations

116

Steatotic liver disease, MASLD and risk of chronic kidney disease DOI Creative Commons
Josh Bilson, Alessandro Mantovani, Christopher D. Byrne

et al.

Diabetes & Metabolism, Journal Year: 2023, Volume and Issue: 50(1), P. 101506 - 101506

Published: Dec. 21, 2023

With the rising tide of fatty liver disease related to metabolic dysfunction worldwide, association this common with chronic kidney (CKD) has become increasingly evident. In 2020, more inclusive term dysfunction-associated (MAFLD) was proposed replace old nonalcoholic (NAFLD). 2023, a modified Delphi process led by three large pan-national associations. There consensus change nomenclature and definition include presence at least one five cardiometabolic risk factors as diagnostic criteria. The name chosen NAFLD steatotic (MASLD). from MAFLD then MASLD resulted in reappraisal epidemiological trends associations developing CKD. observed between MAFLD/MASLD CKD our understanding that can be an epiphenomenon linked underlying support notion individuals are substantially higher incident than those without MASLD. This narrative review provides overview literature on (a) evolution criteria for diagnosing highly prevalent disease, (b) evidence linking CKD, (c) mechanisms which (and strongly MASLD) may increase (d) potential drug treatments benefit both

Language: Английский

Citations

35

Temporal trends in prevalence and disability of chronic kidney disease caused by specific etiologies: an analysis of the Global Burden of Disease Study 2019 DOI
Qing Xin, Junyi Jiang, Chunlei Yuan

et al.

Journal of Nephrology, Journal Year: 2024, Volume and Issue: 37(3), P. 723 - 737

Published: March 21, 2024

Language: Английский

Citations

9