scholarly journals Inflammation and Oxidative Stress in Obesity-Related Glomerulopathy

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Jinhua Tang ◽  
Haidong Yan ◽  
Shougang Zhuang
Keyword(s):  
Oxidative Stress ◽  
Cell Function ◽  
Kidney Injury ◽  
Biologically Active ◽  
Renal Diseases ◽  
Low Grade ◽  
Chronic Oxidative Stress ◽  
Stage Renal Disease ◽  
End Stage ◽  
And Oxidative Stress

Obesity-related glomerulopathy is an increasing cause of end-stage renal disease. Obesity has been considered a state of chronic low-grade systemic inflammation and chronic oxidative stress. Augmented inflammation in adipose and kidney tissues promotes the progression of kidney damage in obesity. Adipose tissue, which is accumulated in obesity, is a key endocrine organ that produces multiple biologically active molecules, including leptin, adiponectin, resistin, that affect inflammation, and subsequent deregulation of cell function in renal glomeruli that leads to pathological changes. Oxidative stress is also associated with obesity-related renal diseases and may trigger the initiation or progression of renal damage in obesity. In this paper, we focus on inflammation and oxidative stress in the progression of obesity-related glomerulopathy and possible interventions to prevent kidney injury in obesity.

Renal medicine

2021 ◽  
pp. 353-382
Author(s):  
Gopesh K. Modi ◽  
Vivekanand Jha
Keyword(s):  
Kidney Disease ◽  
Renal Disease ◽  
Rapidly Progressive Glomerulonephritis ◽  
Kidney Injury ◽  
Renal Stones ◽  
Renal Diseases ◽  
Acute Glomerulonephritis ◽  
Glomerular Diseases ◽  
Stage Renal Disease ◽  
End Stage

Assessing renal function, Urinalysis, Proteinuria, Hematuria, Chyluria, Imaging in renal disease, Kidney biopsy, Acute Kidney Injury (AKI), Chronic Kidney Disease (CKD), Diabetic Nephropathy, End Stage Renal Disease and Dialysis, Kidney Transplantation, Glomerular diseases, Acute glomerulonephritis, Urinary schistosomiasis (bilharzia), Infections and Kidney Disease, Rapidly Progressive glomerulonephritis, Tubulointerstitial Disease, Urinary Tract Infection, Vesico-ureteric reflux, Renal Stones, Renal Disease in Pregnancy, Renal Artery Stenosis, Renal Mass, Inherited Renal Diseases

scholarly journals Serum Prolidase Activity and Oxidative Stress in Diabetic Nephropathy and End Stage Renal Disease: A Correlative Study with Glucose and Creatinine

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Akhilesh Kumar Verma ◽  
Subhash Chandra ◽  
Rana Gopal Singh ◽  
Tej Bali Singh ◽  
Shalabh Srivastava ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Nephropathy ◽  
Blood Glucose ◽  
Renal Disease ◽  
Serum Creatinine ◽  
End Stage Renal Disease ◽  
Prolidase Activity ◽  
Stage Renal Disease ◽  
End Stage ◽  
And Oxidative Stress

Association of oxidative stress and serum prolidase activity (SPA) has been reported in many chronic diseases. The study was aimed at evaluating the correlation of glucose and creatinine to SPA and oxidative stress in patients with diabetic nephropathy (DN) and end stage renal disease (ESRD) concerned with T2DM. 50 healthy volunteers, 50 patients with T2DM, 86 patients with DN, and 43 patients with ESRD were considered as control-1, control-2, case-1, and case-2, respectively. Blood glucose, creatinine, SPA, total oxidant status (TOS), total antioxidant status (TAS), and oxidative stress index (OSI) were measured by colorimetric tests. SPA, TOS, and OSI were significantly increased in case-1 and case-2 than control-1 and control-2, while TAS was significantly decreased(P<0.001). Blood glucose was linearly correlated to SPA, TOS, TAS, and OSI in control-2, case-1 and case-2(P<0.001). Serum creatinine was linearly correlated with SPA, TOS, TAS and OSI in control-2 and case-1(P<0.001). In case-2, serum creatinine was significantly correlated with SPA only(P<0.001). Thus, the study concluded that SPA and oxidative stress significantly correlated with blood glucose and creatinine. SPA, TOS, TAS, and OSI can be used as biomarkers for diagnosis of kidney damage.

scholarly journals Dietary Antioxidant Supplements and Uric Acid in Chronic Kidney Disease: A Review

Nutrients ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1911 ◽  
Author(s):  
Stefanos Roumeliotis ◽  
Athanasios Roumeliotis ◽  
Evangelia Dounousi ◽  
Theodoros Eleftheriadis ◽  
Vassilios Liakopoulos
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Uric Acid ◽  
Kidney Disease ◽  
Serum Levels ◽  
Maintenance Hemodialysis ◽  
Antioxidant Supplements ◽  
Stage Renal Disease ◽  
End Stage ◽  
And Oxidative Stress

Increased serum levels of uric acid have been associated with the onset and development of chronic kidney disease (CKD), cardiovascular disease, and mortality, through several molecular pathogenetic mechanisms, such as inflammation and oxidative stress. Oxidative stress is present even in the early stages of CKD, progresses parallelly with the deterioration of kidney function, and is even more exacerbated in end-stage renal disease patients undergoing maintenance hemodialysis. Although acting in the plasma as an antioxidant, once uric acid enters the intracellular environment; it behaves as a powerful pro-oxidant. Exogenous intake of antioxidants has been repeatedly shown to prevent inflammation, atherosclerosis and oxidative stress in CKD patients. Moreover, certain antioxidants have been proposed to exert uric acid-lowering properties. This review aims to present the available data regarding the effects of antioxidant supplements on both oxidative stress and uric acid serum levels, in a population particularly susceptible to oxidative damage such as CKD patients.

P0123THE IMPORTANCE OF PPAR-ALPHA IN AKI TO CKD TRANSITION IN NEPHROPATHY INDUCED BY FOLIC ACID

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Gabriel Estrela ◽  
Adriano Arruda ◽  
Leandro Freitas-Lima ◽  
Jonatan Barrera-Chimal ◽  
Ronaldo Araujo
Keyword(s):  
Folic Acid ◽  
Chronic Phase ◽  
Kidney Injury ◽  
Tnf Alpha ◽  
Renal Diseases ◽  
Tubular Injury ◽  
Ppar Alpha ◽  
Beneficial Effects ◽  
Stage Renal Disease ◽  
End Stage

Abstract Background and Aims PPAR-alpha is a nuclear receptor which plays major role in the regulation of lipid metabolism, activation of PPAR-alpha has been shown to have beneficial effects in renal diseases. Acute kidney injury (AKI), even if followed by renal recovery, is a risk factor for the future development of chronic kidney disease (CKD) and end-stage renal disease (ESRD). Our main objective was to determine the importance of PPAR-alpha in AKI to CKD transition in folic acid induced nephropathy. Method Male C57/Bl6 and PPARKO (C57Bl6 background) mice were divided in 4 groups, Control, Folic Acid, Gemfibrozil + Folic Acid and PPARKO + Folic Acid. Animals has been treated with single dose of Folic Acid (250mg/kg i.p) and Gemfibrozil (150mg/kg gavage) euthanized after 48 hours for AKI assessment and 28 days for CKD. Renal parameters, histology, real time PCR were performed to investigate renal injury, inflammation and fibrosis. Results After 48 hours of folic acid inducing AKI, PPARKO mice showed decreased urea levels (Folic Acid: 178,9±25,2 PPARKO: 92,4±15,5), less tubular injury (Folic Acid: 0,61±0,05 PPARKO: 0,21±0,03), lower mRNA expression of NGAL (Folic Acid; 32,2±7,67 PPARKO 3,74±1,71), KIM-1 (Folic Acid: 671,8±170,2 PPARKO: 43,4±29,7) and TNF-alpha (Folic Acid: 2,81±0,58 PPARKO: 0,67±0,14), while PPAR-alpha activation with gemfibrozil showed to have no effects in AKI. After 28 days of folic acid inducing CKD. PPARKO showed same levels of injury than folic acid alone treated mice, however PPAR-alpha activation with gemfibrozil decreased urea levels (Folic Acid: 79,2±3,2 Gemfibrozil: 46,1±3,8), showed less tubulointerstitial fibrosis (Folic Acid: 0,60±0,05 Gemfibrozil: 0,18±0,02) and lower urine protein/creatinine ratio (Folic Acid: 5,48±0,58 Gemfibrozil: 2,53±0,12), Conclusion PPAR-alpha deletion protects against AKI induced by folic acid but did not showed protection in chronic phase, in the other hand ppar-alpha activation with gemfibrozil did not protect in AKI but show to be effective in CKD.

Effect of Renal Transplantation on Biomarkers of Inflammation and Oxidative Stress in End-Stage Renal Disease Patients

2005 ◽  
Vol 79 (8) ◽  
pp. 914-919 ◽  
Author(s):  
Edith M. Simmons ◽  
Anthony Langone ◽  
M Tugrul Sezer ◽  
John P. Vella ◽  
Peter Recupero ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Renal Transplantation ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Stage Renal Disease ◽  
End Stage ◽  
And Oxidative Stress

Chronic tubulointerstitial nephritis

2018 ◽  
Author(s):  
Adalbert Schiller ◽  
Adrian Covic ◽  
Liviu Segall
Keyword(s):  
Renal Tubular Acidosis ◽  
Urinary Tract Obstruction ◽  
Clinical Manifestations ◽  
Renal Diseases ◽  
Low Grade ◽  
Tubular Atrophy ◽  
Interstitial Inflammation ◽  
Renal Tubular ◽  
Stage Renal Disease ◽  
End Stage

Chronic tubulointerstitial nephropathies (CTINs) are a group of renal diseases, characterized by variable interstitial inflammation and fibrosis and tubular atrophy, and a slow course towards end-stage renal disease (ESRD). The causes of CTIN are numerous, including nephrotoxic drugs and chemicals, infections, autoimmune diseases, obstructive uropathies, and metabolic disorders. Taken together, CTIN are responsible for less than 10% of all ESRD cases requiring renal replacement therapy. The clinical manifestations of CTIN typically comprise low-grade proteinuria, leucocyturia, and variably reduced glomerular filtration rate (GFR), whereas the blood pressure is usually normal or moderately increased. Tubular abnormalities are common, including type 2 (proximal) renal tubular acidosis, Fanconi syndrome, nephrogenic diabetes insipidus, and type 1 (distal) renal tubular acidosis, with hypokalaemia and nephrolithiasis. Radiology exams reveal shrunken kidneys, sometimes with irregular outlines. A renal biopsy is often required for the diagnosis of CTIN and its aetiology. The treatment of CTIN mainly involves discontinuation of exposure to nephrotoxins and specific therapy of renal infections, urinary tract obstruction, or underlying systemic diseases. Agents like ACE inhibitors and pirfenidone, which might reduce interstitial inflammation and fibrosis, are still under clinical evaluation.

scholarly journals Resveratrol Supplementation Protects Against Nicotine-Induced Kidney Injury

2019 ◽  
Vol 16 (22) ◽  
pp. 4445 ◽  
Author(s):  
Ramalingam ◽  
Santhanathas ◽  
Shaukat Ali ◽  
Zainalabidin
Keyword(s):  
Oxidative Stress ◽  
Angiotensin Ii ◽  
Prolonged Exposure ◽  
Kidney Injury ◽  
Receptor Blocker ◽  
Renal Diseases ◽  
Angiotensin Ii Receptor Blocker ◽  
Type I ◽  
Sprague Dawley ◽  
And Oxidative Stress

Prolonged exposure to nicotine accelerates onset and progression of renal diseases in habitual cigarette smokers. Exposure to nicotine, either via active or passive smoking is strongly shown to enhance renal oxidative stress and augment kidney failure in various animal models. In this study, we investigated the effects of resveratrol supplementation on nicotine-induced kidney injury and oxidative stress in a rat model. Male Sprague-Dawley rats were given nicotine (0.6 mg/kg, i.p.) alone or in combination with either resveratrol (8 mg/kg, i.p.), or angiotensin II type I receptor blocker, irbesartan (10 mg/kg, p.o.) for 28 days. Upon completion of treatment, kidneys were investigated for changes in structure, kidney injury markers and oxidative stress. Administration of nicotine alone for 28 days resulted in significant renal impairment as shown by marked increase in plasma creatinine, blood urea nitrogen (BUN) and oxidative stress. Co-administration with resveratrol however successfully attenuated these changes, with a concomitant increase in renal antioxidants such as glutathione similar to the conventionally used angiotensin II receptor blocker, irbesartan. These data altogether suggest that targeting renal oxidative stress with resveratrol could alleviate nicotine-induced renal injury. Antioxidants may be clinically important for management of renal function in habitual smokers.

scholarly journals Cell-free DNA as a marker for the outcome of end-stage renal disease patients on haemodialysis

2020 ◽  
Author(s):  
Susana Coimbra ◽  
Susana Rocha ◽  
Henrique Nascimento ◽  
Maria João Valente ◽  
Cristina Catarino ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
End Stage Renal Disease ◽  
Stress Markers ◽  
Free Dna ◽  
All Cause Mortality ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients ◽  
And Oxidative Stress

Abstract Background DNA damage and inflammation are common in end-stage renal disease (ESRD). Our aim was to evaluate the levels of circulating cell-free DNA (cfDNA) and the relationship with inflammation, anaemia, oxidative stress and haemostatic disturbances in ESRD patients on dialysis. By performing a 1-year follow-up study, we also aimed to evaluate the predictive value of cfDNA for the outcome of ESRD patients. Methods A total of 289 ESRD patients on dialysis were enrolled in the study: we evaluated cfDNA, haemogram, serum iron, hepcidin, inflammatory and oxidative stress markers, and haemostasis. Events and causes of deaths were recorded throughout the follow-up period. Results ESRD patients, as compared with controls, presented significantly higher levels of cfDNA, hepcidin, and inflammatory and oxidative stress markers, and significantly lower values of iron and anaemia-related haemogram parameters. The all-cause mortality rate was 9.7%; compared with alive patients, deceased patients (n = 28) were older and presented significantly higher values of inflammatory markers and of cfDNA, which was almost 2-fold higher. Furthermore, cfDNA was the best predictor of all-cause mortality and cardiovascular mortality in ESRD patients, in both unadjusted and adjusted models for basic confounding factors in dialysis. Conclusions Our data show cfDNA to be a valuable predictive marker of prognosis in ESRD patients on dialysis treatment; high levels of cfDNA were associated with a poor outcome.

Inflammation and Oxidative Stress in End-Stage Renal Disease Patients Treated with Hemodialysis or Peritoneal Dialysis

2009 ◽  
Vol 32 (12) ◽  
pp. 872-882 ◽  
Author(s):  
Vassilis Filiopoulos ◽  
Dimitrios Hadjiyannakos ◽  
Lambrini Takouli ◽  
Polixeni Metaxaki ◽  
Vasilis Sideris ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Peritoneal Dialysis ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Stage Renal Disease ◽  
End Stage ◽  
And Oxidative Stress

scholarly journals Oxidative Stress and Acute Kidney Injury in Critical Illness: Pathophysiologic Mechanisms—Biomarkers—Interventions, and Future Perspectives

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Paraskevi Pavlakou ◽  
Vassilios Liakopoulos ◽  
Theodoros Eleftheriadis ◽  
Michael Mitsis ◽  
Evangelia Dounousi
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Stress Generation ◽  
Clinical Settings ◽  
Future Perspectives ◽  
Icu Patients ◽  
Stage Renal Disease ◽  
End Stage ◽  
Pathophysiologic Mechanisms

Acute kidney injury (AKI) is a multifactorial entity that occurs in a variety of clinical settings. Although AKI is not a usual reason for intensive care unit (ICU) admission, it often complicates critically ill patients’ clinical course requiring renal replacement therapy progressing sometimes to end-stage renal disease and increasing mortality. The causes of AKI in the group of ICU patients are further complicated from damaged metabolic state, systemic inflammation, sepsis, and hemodynamic dysregulations, leading to an imbalance that generates oxidative stress response. Abundant experimental and to a less extent clinical data support the important role of oxidative stress-related mechanisms in the injury phase of AKI. The purpose of this article is to present the main pathophysiologic mechanisms of AKI in ICU patients focusing on the different aspects of oxidative stress generation, the available evidence of interventional measures for AKI prevention, biomarkers used in a clinical setting, and future perspectives in oxidative stress regulation.

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