INTRODUCTION: Lower extremity deep venous thrombosis (DVT) with severe iliac vein stenosis is common and can lead to significant morbidity and mortality. Treatment options are limited, and the safety and effectiveness of...INTRODUCTION: Lower extremity deep venous thrombosis (DVT) with severe iliac vein stenosis is common and can lead to significant morbidity and mortality. Treatment options are limited, and the safety and effectiveness of stent implantation are unclear. This study evaluated stent implantation for treating this condition. MATERIAL AND METHODS: This observational clinical study analyzed data from DVT patients who underwent stent implantation at Changxing People's Hospital, Zhejiang, China, between 2017 and 2022. Patients who received stent implantation comprised the experimental group, while those who did not formed the control group. All patients underwent thrombus aspiration and/or stent implantation, and outcomes were compared between the two groups during follow-up. RESULTS: In this study, in 60 cases the procedures were completed with no significant changes in hemoglobin, hematoma formation, thrombolytic time, or bleeding complications ( > 0.05). The stent group demonstrated a higher thrombolytic rate and lower limb swelling ( < 0.05). During a mean follow-up of 15.2 ±5.8 months, 1 stent patient developed DVT and another had stenosis, while the control group had 3 DVT recurrences and 5 iliac vein occlusions. The stent group had a higher deep vein patency rate and lower iliac vein occlusion rate ( = 0.01), with similar DVT recurrence rates ( = 0.34). Additionally, the stent group had higher Chronic Venous Insufficiency Questionnaire (CIVIQ) ( = 2.54, = 0.01) and lower CEAP scores ( = 3.72, < 0.01). CONCLUSIONS: Our study suggests that stent implantation is an effective and safe treatment option for DVT with severe iliac vein stenosis.
INTRODUCTION: Studies in beta thalassaemia major (β-TM) patients have shown that the responses of HIF2α, hepcidin, and ferroportin molecules to high iron levels are impaired. In recent years, studies conducted in patient...INTRODUCTION: Studies in beta thalassaemia major (β-TM) patients have shown that the responses of HIF2α, hepcidin, and ferroportin molecules to high iron levels are impaired. In recent years, studies conducted in patients with iron deficiency anaemia have investigated the relationship between ghrelin hormone and iron metabolism. In this study, we aimed to contribute to the aetiopathogenesis of this disease by examining the changes in ghrelin hormone levels in patients with β-TM. MATERIAL AND METHODS: Fifty-two β-TM and 23 controls were included in our study. Blood counts, routine biochemical parameters, HIF2α, hepcidin, and ghrelin levels were studied in blood samples taken from the volunteers. RESULTS: Erythrocyte indexes, serum bilirubin, iron, unsaturated iron binding capacity, total iron binding capacity, and ferritin levels showed significant differences between the 2 groups ( < 0.05). There was no significant difference between 2 groups for serum HIF2α and hepcidin levels. When the 2 groups were compared, ghrelin levels were found to be significantly higher in the patients ( < 0.05). When the correlation between parameters was examined in all subjects, a weak positive correlation was found between ghrelin and HIF2α ( = 0.263) ( < 0.05), and a significant positive correlation was found between ghrelin and ferritin ( = 0.417) ( < 0.05). CONCLUSIONS: Our study showed that there is a positive correlation between ghrelin and ferritin levels. Elevated ghrelin levels in patients with β-TM may play an important role in regulating impaired iron metabolism. Molecular level studies are needed to determine synthesis pathways.
INTRODUCTION: This study aimed to investigate the relationship between serum cytokine levels, particularly interleukin 6 (IL-6), and diabetic nephropathy (DN) in patients with type 1 (T1D) and type 2 diabetes (T2D). MATE...INTRODUCTION: This study aimed to investigate the relationship between serum cytokine levels, particularly interleukin 6 (IL-6), and diabetic nephropathy (DN) in patients with type 1 (T1D) and type 2 diabetes (T2D). MATERIAL AND METHODS: A cross-sectional study was conducted among 200 patients diagnosed with either T1D or T2D from January 2022 to December 2023 at the Endocrinology and Diabetes Department of Madinah Hospital, Saudi Arabia. RESULTS: A total of 200 individuals with T1D ( = 100) or T2D ( = 100) were enrolled in this research. Male patients (54%) and those aged 30-50 (67.5%) dominated the cohort. About 50% had diabetes for less than 10 years, and 49.5% were overweight. 63.5% ( = 117) had a reduced glomerular filtration rate (GFR), whereas 46% ( = 92) had albuminuria. T1D patients were mostly normal weight, while T2D patients were overweight or obese. Both diabetes types had identical kidney damage stages. T1D patients were more likely to have moderately elevated albuminuria (53% vs. 37%, < 0.05) than T2D individuals. T1D patients had considerably lower serum cytokine levels than T2D patients. IL-6 levels were moderately correlated with fasting blood glucose (FBG) ( = -0.318, < 0.01) and HbA ( = -0.319, < 0.01) in T1D patients. IL-6 had a modest correlation with renal dysfunction markers including GFR and urine albumin-creatinine ratio (UACR) ( = -0.250, < 0.05 and = 0.338, < 0.001, respectively). In T1D patients there was a weak but significant correlation between GFR and IL6. CONCLUSIONS: Lower serum IL-6 levels in T1D patients are linked to delayed onset of kidney damage. The pro-inflammatory role of IL-6 may contribute to the development of DN in T1D patients, as indicated by its association with albuminuria and renal function markers. Further research is warranted to explore IL-6 as a potential therapeutic target in diabetic nephropathy.
INTRODUCTION: Congenital heart anomalies (CHAs) remain a significant global health issue for children, evidenced by persistent disparities in healthcare access across different socio-demographic index (SDI) regions and g...INTRODUCTION: Congenital heart anomalies (CHAs) remain a significant global health issue for children, evidenced by persistent disparities in healthcare access across different socio-demographic index (SDI) regions and genders, despite slight decreases in prevalence. MATERIAL AND METHODS: This cross-sectional study used the Global Burden of Disease 2021 dataset to analyze CHAs in children aged 0-14 from 204 countries. Data analysis was performed using R software, incorporating global mapping, Joinpoint regression, and estimation of annual percent changes and rates, stratified by age, sex, and SDI. RESULTS: A total of 218,909,652 children, including 113,892,505 (52.03%) males and 105,017,147 (47.97%) females, were included in the analysis. From 1990 to 2021, the global prevalence of CHAs in children decreased by 4.294% (95% uncertainty interval [UI], -5.696-2.695%). Over three decades, CHA-associated deaths decreased from 497,979 (95% UI: 282,166-642,052) to 222,415 (95% UI: 181,359-275,182). The global mortality rate decreased from 28.633 (95% UI: 16.224-36.918) to 11.055 (95% UI: 9.014-13.678) per 100,000 population, while the prevalence rate changed from 377.257 cases per 100,000 in 1990 to 361.060 cases per 100,000 in 2021. Among the five SDI regions, the low SDI region had the highest CHA-associated mortality rate in 2021. CONCLUSIONS: The study highlights the persistent global challenge of CHAs, particularly in low-SDI regions. It underscores the need for targeted public health interventions to reduce disparities and improve health outcomes globally.
INTRODUCTION: Hypertensive heart disease (HHD) has emerged as a significant global public health concern, with the increasing prevalence of high body mass index (HBMI) contributing to its growing burden. This study aimed...INTRODUCTION: Hypertensive heart disease (HHD) has emerged as a significant global public health concern, with the increasing prevalence of high body mass index (HBMI) contributing to its growing burden. This study aimed to evaluate trends in HHD mortality attributable to HBMI from 1990 to 2021 and projections up to 2040. MATERIAL AND METHODS: Data on HHD mortality attributable to HBMI were obtained from the Global Burden of Diseases (GBD) 2021 database. Temporal trends in the burden of HHD attributable to HBMI were analyzed using generalized linear models to calculate the estimated annual percentage change (EAPC) in age-standardized mortality rates (ASMR) and age-standardized disability-adjusted life-year (DALY) rates (ASDR) from 1990 to 2021. A linked-point regression model, based on a linear statistical framework, was employed to evaluate these trends. Additionally, the burden of HHD attributable to HBMI was further analyzed by disaggregating contributions from population size, age structure, and epidemiologic changes. Cross-national inequalities in this burden were quantified using standard health equity methodologies recommended by the World Health Organization (WHO). Finally, changes in the burden of HHD attributable to HBMI were projected to 2040. RESULTS: From 1990 to 2021, the global ASMR for HHD attributable to HBMI increased from 6.83 to 7.21, with an EAPC value of 0.33 for the ASMR. ASDR increased from 144.72 to 147.33, with an EAPC value of 0.15 for ASDR. Particularly severe ASMR and ASDR were observed in most countries in Africa and in a few countries along the Mediterranean coast. In contrast, most developed countries in North America, Europe, and Australia presented lower ASMR and ASDR. When the overall trend was divided into subsections, at the end of the study period, ASMR and ASDR for HHD attributable to HBMI showed a downward trend. By dividing the regions by sociodemographic index (SDI), middle SDI had the greatest fluctuation in ASMR and ASDR, and low SDI showed an increasing trend in ASMR and ASDR at the final joinpoint. Decomposition analyses found that population growth and aging were the main factors driving changes in the burden of death due to HHD attributable to HBMI. Cross-country inequality analyses showed that high SDI countries bear a disproportionate share of the burden of deaths due to HHD attributable to HBMI and that SDI-related inequality has increased over time. Global trends in ASMR and ASDR for HHD attributable to HBMI are projected to show gradual and moderate increases from 2022 to 2040, but the number of deaths and DALYs will continue to increase. CONCLUSIONS: From 1990 to 2021, the burden of HHD attributable to HBMI increased globally, with developing countries and low SDI regions bearing a relatively large burden of disease. Furthermore, this burden is expected to continue to increase until 2040. Therefore, more targeted prevention approaches should be established to mitigate this growing trend.
INTRODUCTION: This study aimed to provide genetic evidence linking drinking habits of different beverages (DHDB) to sleep disorder liability (SDL), potentially informing clinical treatments to improve lifestyle factors....INTRODUCTION: This study aimed to provide genetic evidence linking drinking habits of different beverages (DHDB) to sleep disorder liability (SDL), potentially informing clinical treatments to improve lifestyle factors. MATERIAL AND METHODS: A two-sample Mendelian randomization (MR) method was employed to explore the genetic associations between DHDB and SDL. The DHDB variables studied encompassed alcohol intake (ALI), alcohol intake frequency (ALF), high-frequency drinking with meals (HAL), tea intake (TEAI), coffee intake (COFI), and red wine intake (RWI). The SDL variables analyzed were insomnia (INS), inhibit excitability (IE), and sleep duration (SD). RESULTS: The MR analysis identified genetic links between ALI and INS, ALF and IE, ALF and SD, HAL and INS, HAL and IE, HAL and SD, TEAI and IE, TEAI and SD, and COFI and IE ( (inverse variance weighting - IVW) < 0.05). Nonetheless, no significant genetic links were detected between ALI and IE, ALI and SD, ALF and INS, TEAI and INS, COFI and INS, COFI and SD, RWI and INS, RWI and IE, or RWI and SD ( (IVW) > 0.05). CONCLUSIONS: Alcohol intake may elevate insomnia risk without affecting daytime sleepiness or sleep duration. Frequent alcohol consumption may lead to daytime sleepiness and reduced sleep duration but not insomnia. Alcohol with meals might reduce insomnia and daytime sleepiness while improving sleep duration. Tea appears unlinked to insomnia and may reduce daytime drowsiness. Coffee may alleviate daytime drowsiness without causing insomnia, and red wine shows no significant association with sleep disorders. Reverse MR suggests potential links between sleep disorders and alcohol or caffeine intake.
INTRODUCTION: Withaferin-A (WA) derived from natural products can inhibit the growth and metastasis of colorectal cancer (CRC) and . MATERIAL AND METHODS: WA effects on colorectal cancer cells were studied using HCT116...INTRODUCTION: Withaferin-A (WA) derived from natural products can inhibit the growth and metastasis of colorectal cancer (CRC) and . MATERIAL AND METHODS: WA effects on colorectal cancer cells were studied using HCT116 and SW480 lines. we used shRNA knockdown, plasmid overexpression, viability, proliferation, colony, migration, and invasion assays. And Xenograft and metastasis mouse models evaluated tumor growth and toxicity. Molecular analysis used qRT-PCR, Western blot, IHC, immunoprecipitation, and RNA sequencing. RESULTS: Transcriptome analysis showed WA suppressed EMT, HSP90, and HIF-1α in CRC. WA inhibited HSP90, HIF-1α, E-cadherin, and their interaction. HIF-1α knockdown reduced CRC migration, invasion, and lung metastasis. 17-AAG similarly inhibited HSP90/HIF-1α and metastasis. HSP90 overexpression rescued HIF-1α expression, binding, and migratory ability in HIF-1α knockdown cells. CONCLUSIONS: These findings indicate that WA inhibits CRC's growth, migration, and invasion by inhibiting the HSP90/HIF-1α/EMT axis. And showed that WA could be a potential therapeutic agent for CRC.
INTRODUCTION: Uric acid (UA) is the end product of the metabolism of purine compounds. There is overwhelming evidence linking hyperuricaemia (high levels of UA) and cerebrovascular diseases, but the effect of high levels...INTRODUCTION: Uric acid (UA) is the end product of the metabolism of purine compounds. There is overwhelming evidence linking hyperuricaemia (high levels of UA) and cerebrovascular diseases, but the effect of high levels of UA on cerebral vessels is not fully understood. The aim of this research is to clarify how UA affects the endothelin (ET) receptor in rat cerebral arteries and the related mechanism. MATERIAL AND METHODS: In an setting, segments of rat cerebral arteries ( = 12) were exposed to high levels of UA, either alone or in conjunction with MAPK pathway inhibitors. ET agonists were used to induce contractions that were then measured with a myograph. ET receptor expression was measured using RT-PCR ( = 6), western blot ( = 3), or immunohistochemistry ( = 3) to quantify mRNA and protein levels. RESULTS: The study revealed that high levels of UA notably increase ET and ET receptor-induced contractions and boosted the expression of ET receptors in cerebral arteries when compared to fresh or cultured alone, suggesting that UA enhances ET and ET receptors. Additionally, the up-regulation of ET receptors induced by UA was inhibited by the p38 inhibitor SB203580, the JNK inhibitor SP600125, and the ERK1/2 inhibitor U0126. SB203580 significantly blocked the increase in ET receptor-mediated contractions induced by UA and the upregulation of ET receptor. Neither SP600125 nor U0126 had such an effect. CONCLUSIONS: High levels of UA stimulate the up-regulation of ET receptors in rat cerebral arteries through MAPK pathways. This study may offer novel perspectives on hyperuricaemia-associated cerebrovascular diseases.
Banach M, Fronczek M, Goc A
… +12 more, Lejawa M, Boniewska-Bernacka E, Osadnik T, Pańczyszyn A, Strzelczyk JK, Pawlas N, Gierlotka M, Goławski M, Krystek K, Gach A, Osadnik K, Jóźwiak J
INTRODUCTION: Telomere length is a cellular aging marker and correlates with various cardiovascular disease (CVD) risk factors. The current study assessed the association between obesity, metabolic syndrome (MetS), and t...INTRODUCTION: Telomere length is a cellular aging marker and correlates with various cardiovascular disease (CVD) risk factors. The current study assessed the association between obesity, metabolic syndrome (MetS), and telomere length. MATERIAL AND METHODS: The LIPIDOGRAM&LIPIDOGEN2015 study was conducted in primary care in 2015-2016. Patients recruited to the LIPIDOGEN2015 cohort ( = 1788) were a random subset of patients of the LIPIDOGRAM2015 ( = 13,724) study. For the aims of this analysis, the recruited patients were divided into four groups based on the presence of MetS: healthy slim (HS), metabolically healthy obese (MHO), non-obese with MetS (NOMS), and metabolically unhealthy obese (MUO). Relative telomere length (RTL) was measured using quantitative polymerase chain reaction (qPCR). RESULTS: 1516 patients (85% of the total group; 59.7% female, mean age 50.3 years) were included in the final analyses. Increases in body mass index (BMI), waist circumference, prevalence of diabetes mellitus, hypertension, dyslipidemia, and history of myocardial infarction moving from HS to MUO were observed. The MUO group exhibited the highest triglyceride and lowest high-density lipoprotein (HDL-C) levels. In the univariate regression analyses, NOMS ( = 0.038) and MUO ( = 0.003) were associated with significantly decreased RTL. After adjusting for age, gender, education, smoking, place of residence, and myocardial infarction, the association was no longer statistically significant. CONCLUSIONS: Despite the lack of statistical significance in the multivariate analysis, the univariate results suggest that both MUO and NOMS phenotypes contribute to the shortening of telomere length. These results may also indicate that MetS, irrespectively of obesity occurrence, is responsible for the shortened lifespan.
INTRODUCTION: Metabolic dysfunction related steatotic liver disease (MASLD) is a long-term liver disease. Oxidative stress plays a key role in MASLD. The oxidative balance score (OBS) measures oxidative and reactive stre...INTRODUCTION: Metabolic dysfunction related steatotic liver disease (MASLD) is a long-term liver disease. Oxidative stress plays a key role in MASLD. The oxidative balance score (OBS) measures oxidative and reactive stress, but its relationship with MASLD and fibrosis remains unclear. MATERIAL AND METHODS: The National Health and Nutrition Examination Survey records from 1999 to 2018 were used in this study. We used weighted multivariate logistic regression, subgroup studies, and restricted cubic spline regression to examine the associations between OBS and MASLD and fibrosis. Sensitivity studies were conducted to evaluate the robustness of the results. RESULTS: A total of 12,272 people enrolled in the study. There was a strong negative relationship between OBS and MASLD, and all -values for interactions were less than 0.05. After adjusting for potential confounders, people with higher OBS had a lower risk of MASLD (OR = 0.37, 95% CI (0.27-0.51), for trend < 0.001). Then, the stratified studies showed that lifestyle OBS was significantly associated with MASLD in both men and women, but dietary OBS was only significantly associated with MASLD in men (OR = 0.95, 95% CI (0.93, 0.98), < 0.001). Finally, lifestyle OBS showed a strong association with MASLD-related fibrosis (OR = 0.37, 95% CI (0.24, 0.56), for trend < 0.0001). In the subgroup studies, the findings remained consistent. CONCLUSIONS: OBS was associated with a lower risk of MASLD, and lifestyle OBS showed strong protective effects against MASLD and fibrosis. Because of this, people who have MASLD and fibrosis should focus on researching and looking into antioxidant treatment that is based on dietary and lifestyle, with particular emphasis on lifestyle factors.
INTRODUCTION: Multiple studies have indicated that immune cells play a significant role in the occurrence and development of membranous nephropathy (MN). However, the causal relationship between the two has not been full...INTRODUCTION: Multiple studies have indicated that immune cells play a significant role in the occurrence and development of membranous nephropathy (MN). However, the causal relationship between the two has not been fully established. To further investigate this, we employed a Mendelian randomization (MR) study design. MATERIAL AND METHODS: Genetic instrumental variables for immune cells were sourced from an extensive genome-wide association study (GWAS). MN summary statistics, involving 2,150 cases and 5,829 controls, were obtained from a separate GWAS. The primary analysis employed the inverse-variance weighted (IVW) method. To explore reverse causation, a reverse MR analysis was undertaken. Rigorous sensitivity analyses were conducted to ensure the resilience and reliability of the study's findings. RESULTS: We identified eight immunophenotypes associated with a reduced risk of MN, and all of them were protective factors for MN. The sensitivity analyses consistently yielded similar results for these immune traits. In the reverse MR analysis, we did not observe any statistically significant associations between MN and these eight immunophenotypes. CONCLUSIONS: Our study, utilizing genetic approaches, provides evidence for a causal relationship between immune cells and MN, which has implications for clinical diagnosis and treatment. Further comprehensive investigations are needed to explore the detailed mechanisms underlying the impact of immune cells on MN.
INTRODUCTION: The aim of this study was to investigate the association between the systemic inflammation response index (SIRI) and all-cause and cardiovascular disease (CVD) mortality in maintenance hemodialysis (MHD) pa...INTRODUCTION: The aim of this study was to investigate the association between the systemic inflammation response index (SIRI) and all-cause and cardiovascular disease (CVD) mortality in maintenance hemodialysis (MHD) patients. MATERIAL AND METHODS: 371 MHD patients were included in this retrospective study. Time-dependent receiver operating characteristic (ROC) curve analysis was used to evaluate the predictive value of SIRI. Patients were categorized into two groups based on the median SIRI value. Kaplan-Meier survival analysis was used to compare the difference in survival rate. Cox regression analysis was used to analyze all-cause and CVD mortality risk factors, and nomograms were developed. RESULTS: The average age of the patients was 60.71 ±15.34 years, and the median follow-up was 42 months. 157 patients died. SIRI had predictive value for all-cause and CVD mortality. The AUC of the SIRI to predict all-cause mortality was 0.698, 0.664, 0.713, and 0.900 at 1, 3, 5, and 10 years, respectively. For CVD mortality, the AUC of the SIRI was 0.678, 0.667, 0.717, and 0.906 at 1, 3, 5, and 10 years, respectively. Kaplan-Meier survival analysis showed that patients with high SIRI values had a significantly lower survival rate. Multivariate Cox regression analysis showed that SIRI > 1.88 was an independent risk factor for all-cause and CVD mortality. CONCLUSIONS: SIRI can independently predict all-cause and CVD mortality in MHD patients, which has important value for prognosis.
INTRODUCTION: The relationship between the inflammatory response (IR) and osteoporosis (OP) has been the subject of extensive research; however, their genetic link remains unclear. This study used IR-related genes as ins...INTRODUCTION: The relationship between the inflammatory response (IR) and osteoporosis (OP) has been the subject of extensive research; however, their genetic link remains unclear. This study used IR-related genes as instrumental variables (IVs) to represent IR, while summary data of OP served as the outcome to explore their genetic relationship. MATERIAL AND METHODS: IR-related genes were retrieved from the GeneCards database. OP transcriptome datasets were collected from the Gene Expression Omnibus (GEO) database and meta-analyzed to identify differentially expressed genes (DEGs) related to IR in OP. Genetic proxy instruments for IR-related genes were derived from studies of corresponding gene expression ( = 31,684) and DNA methylation ( = 1,980) quantitative trait loci (eQTLs and mQTLs), respectively. Aggregated data for OP (1,351 OP cases and 209,313 controls) were extracted from the largest genome-wide association study (GWAS) of OP. We integrated QTL data with OP GWAS data to estimate their genetic associations using summary data-based Mendelian randomization analysis (SMR). Additionally, Bayesian colocalization analysis was employed to reveal the potential relationships between IR gene expression and inflammatory factors, as well as various hormones. Finally, to further validate whether the statistical evidence provided in GWAS comprised true-positive findings, a replication study (1,955 cases and 278,169 controls) was conducted here through genotype-phenotype associations. RESULTS: A meta-analysis of four datasets identified 115 IR-related DEGs in OP out of 612 IR-related genes. Through SMR analysis, we found that the expression levels of two IR-related genes were associated with OP risk. Specifically, elevated gene expression levels of FAS (odds ratio (OR) = 1.094; 95% confidence interval (CI) = 0.892-1.341; false discovery rate (FDR) = 0.034) increased the risk of OP. Conversely, increased expression levels of CHUK decreased the risk of OP (OR = 0.518; 95% CI = 0.424-0.637; FDR = 0.039). Colocalization analysis identified potential interactions between the FAS gene and estradiol (PP.H4 = 0.95) as well as interleukin-1α (IL-1α) (PP.H4 = 0.65). Potential interactions were also observed between the CHUK gene and growth hormone (PP.H4 = 0.59) as well as macrophage inflammatory protein-1α (MIP-1α) (PP.H4 = 0.62). In addition, consistent results were observed in the replication study, further demonstrating the reliability of our findings. CONCLUSIONS: This multi-omics integration study revealed a genetic link between IR and OP, as represented by IR-related genes, and provided new insights into the potential pathogenic mechanisms of OP. Additionally, these identified candidate genes offer avenues for future targeted functional studies aimed at developing appropriate therapeutic interventions and preventing OP.
Obesity significantly contributes to the development and progression of chronic kidney disease (CKD) by inducing metabolic and hemodynamic disturbances that drive gene dysregulation, inflammation, fibrosis, and renal str...Obesity significantly contributes to the development and progression of chronic kidney disease (CKD) by inducing metabolic and hemodynamic disturbances that drive gene dysregulation, inflammation, fibrosis, and renal structural injury. Key molecular mediators include genetic polymorphisms - such as AGT rs699, ACE I/D, LEP ENSSNP5824596, and FTO rs17817449 - and epigenetic regulators like microRNAs (e.g., miR-21, miR-192) and long non-coding RNAs (e.g., ANRIL, HOTAIR). These alterations affect signaling cascades such as TGF-β/Smad3, NF-κB, and AMPK, accelerating renal damage in obese individuals. Despite advances, reliable biomarkers and therapeutic targets remain scarce. This review integrates current evidence on the genetic and epigenetic basis of obesity-related CKD, offering a framework for early detection and precision medicine.