Chronic Kidney Disease as Oxidative Stress- and Inflammatory-Mediated Cardiovascular Disease

Antioxidants, Journal Year: 2020, Volume and Issue: 9(8), P. 752 - 752

Published: Aug. 14, 2020

Generating reactive oxygen species (ROS) is necessary for both physiology and pathology. An imbalance between endogenous oxidants antioxidants causes oxidative stress, contributing to vascular dysfunction. The ROS-induced activation of transcription factors proinflammatory genes increases inflammation. This phenomenon crucial importance in patients with chronic kidney disease (CKD), because atherosclerosis one the critical their cardiovascular (CVD) increased mortality. effect ROS disrupts excretory function each section nephron. It prevents maintenance intra-systemic homeostasis leads accumulation metabolic products. Renal regulatory mechanisms, such as tubular glomerular feedback, myogenic reflex supplying arteriole, renin-angiotensin-aldosterone system, are also affected. makes it impossible compensate water-electrolyte acid-base disturbances, which progress further mechanism positive leading a intensification stress. As result, progression CKD observed, spectrum complications malnutrition, calcium phosphate abnormalities, atherosclerosis, anemia. review aimed show role stress inflammation renal impairment, particular emphasis on its influence most common disturbances that accompany CKD.

Language: Английский

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The Effects of High-Protein Diets on Kidney Health and Longevity

Journal of the American Society of Nephrology, Journal Year: 2020, Volume and Issue: 31(8), P. 1667 - 1679

Published: July 15, 2020

Although high-protein diets continue to be popular for weight loss and type 2 diabetes, evidence suggests that worsening renal function may occur in individuals with-and perhaps without-impaired kidney function. High dietary protein intake can cause intraglomerular hypertension, which result hyperfiltration, glomerular injury, proteinuria. It is possible long-term high lead

Language: Английский

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Endothelial Cell Dysfunction and Increased Cardiovascular Risk in Patients With Chronic Kidney Disease

Circulation Research, Journal Year: 2023, Volume and Issue: 132(8), P. 970 - 992

Published: April 13, 2023

The endothelium is considered to be the gatekeeper of vessel wall, maintaining and regulating vascular integrity. In patients with chronic kidney disease, protective endothelial cell functions are impaired due proinflammatory, prothrombotic uremic environment caused by decline in function, adding increase cardiovascular complications this vulnerable patient population. review, we discuss functioning healthy conditions contribution dysfunction disease. Further, summarize phenotypic changes disease relation risk We also review mechanisms that underlie consider potential pharmacological interventions can ameliorate health.

Language: Английский

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Plant-Based Diets for Kidney Disease: A Guide for Clinicians

American Journal of Kidney Diseases, Journal Year: 2020, Volume and Issue: 77(2), P. 287 - 296

Published: Oct. 16, 2020

Language: Английский

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Calcium phosphate microcrystals in the renal tubular fluid accelerate chronic kidney disease progression

Journal of Clinical Investigation, Journal Year: 2021, Volume and Issue: 131(16)

Published: June 29, 2021

The Western pattern diet is rich not only in fat and calories but also phosphate. negative effects of excessive calorie intake on health are widely known, the potential harms phosphate poorly recognized. Here, we show mechanism by which dietary damages kidney. When was relative to number functioning nephrons, circulating levels FGF23, a hormone that increases excretion per nephron, were increased maintain homeostasis. FGF23 suppressed reabsorption renal tubules thus raised concentration tubule fluid. Once it exceeded threshold, microscopic particles containing calcium crystals appeared lumen, damaged cells through binding TLR4 expressed them. Persistent damage induced interstitial fibrosis, reduced further boosted trigger deterioration spiral leading progressive nephron loss. In humans, progression chronic kidney disease (CKD) ensued when serum 53 pg/mL. present study identified tubular fluid as an effective therapeutic target decelerate loss during course aging CKD progression.

Language: Английский

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The therapeutic importance of acid-base balance

Biochemical Pharmacology, Journal Year: 2020, Volume and Issue: 183, P. 114278 - 114278

Published: Oct. 9, 2020

Language: Английский

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Dual-Targeting Glycol Chitosan/Heparin-Decorated Polypyrrole Nanoparticle for Augmented Photothermal Thrombolytic Therapy

ACS Applied Materials & Interfaces, Journal Year: 2021, Volume and Issue: 13(8), P. 10287 - 10300

Published: Feb. 21, 2021

Near-infrared (NIR)-light-modulated photothermal thrombolysis has been investigated to overcome the hemorrhage danger posed by clinical clot-busting substances. A long-standing issue in thrombosis fibrinolytics is lack of lesion-specific therapy, which should not be ignored. Herein, a novel therapy using disintegration fibrin clot was explored through dual-targeting glycol chitosan/heparin-decorated polypyrrole nanoparticles (GCS-PPY-H NPs) enhance thrombus delivery and thrombolytic therapeutic efficacy. GCS-PPY-H NPs can target acidic/P-selectin high-expression inflammatory endothelial cells/thrombus sites for initiating lesion-site-specific hyperthermia NIR irradiation. significant clot-clearance rate achieved with dual-targeting/modality vivo. The molecular level mechanisms developed nanoformulations interface properties were determined multiple surface specific analytical techniques, such as particle size distribution, zeta potential, electron microscopy, Fourier-transform infrared spectroscopy (FTIR), wavelength absorbance, photothermal, immunofluorescence, histology. Owing augmented swift treatment time, systematic effectively applied thrombolysis. This approach possesses promising future treatment.

Language: Английский

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Kidney metabolism and acid–base control: back to the basics

Pflügers Archiv - European Journal of Physiology, Journal Year: 2022, Volume and Issue: 474(8), P. 919 - 934

Published: May 5, 2022

Kidneys are central in the regulation of multiple physiological functions, such as removal metabolic wastes and toxins, maintenance electrolyte fluid balance, control pH homeostasis. In addition, kidneys participate systemic gluconeogenesis production or activation hormones. Acid-base conditions influence all these functions concomitantly. Healthy properly coordinate a series responses face acute chronic acid-base disorders. However, injured have reduced capacity to adapt challenges. Chronic kidney disease patients an example individuals typically exposed progressive acidosis. Their organisms undergo alterations that brake large detrimental changes homeostasis several parameters, but may also operate further drivers damage. disorders lead not only mechanisms involved balance maintenance, they affect other tightly wired it. this review article, we explore basic renal activities show how interconnected cell energy metabolism important intracellular activities. These intertwined relationships been investigated for more than century, modern conceptual organization events is lacking. We propose indissociably interacts with pathways drive progression disease, inflammation metabolism, independent etiology.

Language: Английский

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Modifiable Lifestyle Behaviors and CKD Progression: A Narrative Review

Kidney360, Journal Year: 2022, Volume and Issue: 3(4), P. 752 - 778

Published: Jan. 18, 2022

Living a healthy lifestyle is one of the safest and most cost-effective ways to improve one’s quality life prevent and/or manage chronic disease. As such, current CKD management guidelines recommend that patients adhere diet, perform ≥150 minutes per week physical activity, their body weight, abstain from tobacco use, limit alcohol. However, there are limited studies investigate relationship between these factors progression among people with established CKD. In this narrative review, we examine reported frequencies health behavior engagement individuals non–dialysis-dependent existing literature examines influences weight management, alcohol consumption, use on CKD, as measured by decline in GFR, incident ESKD, or elevated proteinuria albuminuria Many available length follow-up small sample sizes, meta-analyses were because sparse had heterogeneous classifications behaviors referent groups progression. Further research should be done determine optimal methods assess better understand levels at which needed slow progression, effect combining multiple important clinical outcomes develop effective techniques for change. Despite lack evidence efficacy large trials ability maintaining remains cornerstone given undisputed benefits cardiovascular health, BP control, survival.

Language: Английский

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Effects of Short-Term Potassium Chloride Supplementation in Patients with CKD

Journal of the American Society of Nephrology, Journal Year: 2022, Volume and Issue: 33(9), P. 1779 - 1789

Published: May 24, 2022

Observational studies suggest that adequate dietary potassium intake (90-120 mmol/day) may be renoprotective, but the effects of increasing and risk hyperkalemia are unknown.This is a prespecified analysis run-in phase clinical trial in which 191 patients (age 68±11 years, 74% males, 86% European ancestry, eGFR 31±9 ml/min per 1.73 m2, 83% renin-angiotensin system inhibitors, 38% diabetes) were treated with 40 mmol chloride (KCl) day for 2 weeks.KCl supplementation significantly increased urinary excretion (72±24 to 107±29 mmol/day), plasma (4.3±0.5 4.7±0.6 mmol/L), aldosterone (281 [198-431] 351 [241-494] ng/L), had no significant effect on sodium excretion, renin, BP, eGFR, or albuminuria. Furthermore, KCl (104±3 105±4 mmol/L) reduced bicarbonate (24.5±3.4 23.7±3.5 urine pH (all P<0.001), did not change ammonium excretion. In total, 21 participants (11%) developed (plasma 5.9±0.4 mmol/L). They older higher baseline potassium.In CKD stage G3b-4, recommended levels raises by 0.4 mmol/L. This result those potassium. Longer-term should address whether cardiorenal protection outweighs hyperkalemia.Clinical number: NCT03253172.

Language: Английский

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