Pilot study on the effect of flavonoids on arterial stiffness and oxidative stress in chronic kidney disease

BACKGROUND Flavonoids,the main class of polyphenols,exhibit antioxidant and antihypertensive properties.AIM To prospectively investigate the impact of flavonoids on arterial stiffness in patients with chronic kidney disease(CKD)stagesⅠ-Ⅳ.METHODS In this prospective,single-arm study,CKD patients with arterial hypertension and diabetes mellitus were enrolled.Baseline demographic,clinical,and laboratory variables were recorded.Patients received daily treatment with a phenol-rich dietary supplement for 3 months.Blood pressure,arterial stiffness(carotidfemoral pulse wave velocity,central pulse pressure),and oxidative stress markers(protein carbonyls,total phenolic compound,total antioxidant capacity)were measured at baseline and at study end.RESULTS Sixteen patients(mean age:62.5 years,87.5%male)completed the study.Following intervention,peripheral systolic blood pressure decreased significantly by 14 mmHg(P<0.001).Carotid-femoral pulse wave velocity decreased from 8.9 m/s(baseline)to 8.2 m/s(study end)(P<0.001),and central pulse pressure improved from 59 mmHg to 48 mmHg(P=0.003).Flavonoids also reduced oxidative stress markers including protein carbonyls(P<0.001),total phenolic compound(P=0.001),and total antioxidant capacity(P=0.013).CONCLUSION Flavonoid supplementation in CKD patients shows promise in improving blood pressure,arterial stiffness,and oxidative stress markers.

Interplay between metabolic dysfunction-associated fatty liver disease and chronic kidney disease:Epidemiology,pathophysiologic mechanisms,and treatment considerations

The recently proposed nomenclature change from non-alcoholic fatty liver disease to metabolic dysfunction-associated fatty liver disease(MAFLD)has resulted in the reappraisal of epidemiological trends and associations with other chronic diseases.In this context,MAFLD appears to be tightly linked to incident chronic kidney disease(CKD).This association may be attributed to multiple shared risk factors including type 2 diabetes mellitus,arterial hypertension,obesity,dyslipidemia,and insulin resistance.Moreover,similarities in their molecular pathophysiologic mechanisms can be detected,since inflammation,oxidative stress,fibrosis,and gut dysbiosis are highly prevalent in these pathologic states.At the same time,lines of evidence suggest a genetic predisposition to MAFLD due to gene polymorphisms,such as the PNPLA3 rs738409 G allele polymorphism,which may also propagate renal dysfunction.Concerning their management,available treatment considerations for obesity(bariatric surgery)and novel antidiabetic agents(glucagon-like peptide 1 receptor agonists,sodiumglucose co-transporter 2 inhibitors)appear beneficial in preclinical and clinical studies of MAFLD and CKD modeling.Moreover,alternative approaches such as melatonin supplementation,farnesoid X receptor agonists,and gut microbiota modulation may represent attractive options in the future.With a look to the future,additional adequately sized studies are required,focusing on preventing renal complications in patients with MAFLD and the appropriate management of individuals with concomitant MAFLD and CKD.