Development Of Kidney Disease Research Articles

Effect of individualized nutrition interventions on clinical outcomes of pregnant women with gestational diabetes mellitus.

Gestational diabetes mellitus (GDM) can lead to excessive pregnancy weight gain (PWG), abnormal glucolipid metabolism, and delayed lactation. Therefore, it is necessary to provide appropriate and effective interventions for pregnant women with GDM. To clarify the effects of individualized nutrition interventions on PWG, glucolipid metabolism, and lactation in pregnant women with GDM. The study population consisted of 410 pregnant women with GDM who received treatment at the Northern Jiangsu People's Hospital of Jiangsu Province and Yangzhou Maternal and Child Health Hospital between December 2020 and December 2022, including 200 who received routine in-terventions [control (Con) group] and 210 who received individualized nutrition interventions [research (Res) group]. Data on PWG, glucolipid metabolism [total cholesterol, (TC); triglycerides (TGs); fasting blood glucose (FPG); glycosylated hemoglobin (HbA1c)], lactation time, perinatal complications (cesarean section, premature rupture of membranes, postpartum hemorrhage, and pregnancy-induced hypertension), and neonatal adverse events (premature infants, fetal macrosomia, hypo-glycemia, and respiratory distress syndrome) were collected for comparative analysis. The data revealed markedly lower PWG in the Res group vs the Con group, as well as markedly reduced TG, TC, FPG and HbA1c levels after the intervention that were lower than those in the Con group. In addition, obviously earlier lactation and statistically lower incidences of perinatal complications and neonatal adverse events were observed in the Res group. Individualized nutrition interventions can reduce PWG in pregnant women with GDM, improve their glucolipid metabolism, and promote early lactation, which deserves clinical promotion.

Effects of insulin aspart and metformin on gestational diabetes mellitus and inflammatory markers

Diabetes mellitus is one of the most common causes of chronic kidney disease. Kidney involvement in patients with diabetes has a wide spectrum of clinical presentations ranging from asymptomatic to overt proteinuria and kidney failure. The development of kidney disease in diabetes is associated with structural changes in multiple kidney compartments, such as the vascular system and glomeruli. Glomerular alterations include thickening of the glomerular basement membrane, loss of podocytes, and segmental mesangiolysis, which may lead to microaneurysms and the development of pathognomonic Kimmelstiel-Wilson nodules. Beyond lesions directly related to diabetes, awareness of the possible coexistence of nondiabetic kidney disease in patients with diabetes is increasing. These nondiabetic lesions include focal segmental glomerulosclerosis, IgA nephropathy, and other primary or secondary renal disorders. Differential diagnosis of these conditions is crucial in guiding clinical management and therapeutic approaches. However, the relationship between diabetes and the kidney is bidirectional; thus, new-onset diabetes may also occur as a complication of the treatment in patients with renal diseases. Here, we review the complex and multifaceted correlation between diabetes and kidney diseases and discuss clinical presentation and course, differential diagnosis, and therapeutic opportunities offered by novel drugs.

Multifaceted relationship between diabetes and kidney diseases: Beyond diabetes.

Diabetes mellitus is one of the most common causes of chronic kidney disease. Kidney involvement in patients with diabetes has a wide spectrum of clinical presentations ranging from asymptomatic to overt proteinuria and kidney failure. The development of kidney disease in diabetes is associated with structural changes in multiple kidney compartments, such as the vascular system and glomeruli. Glomerular alterations include thickening of the glomerular basement membrane, loss of podocytes, and segmental mesangiolysis, which may lead to microaneurysms and the development of pathognomonic Kimmelstiel-Wilson nodules. Beyond lesions directly related to diabetes, awareness of the possible coexistence of nondiabetic kidney disease in patients with diabetes is increasing. These nondiabetic lesions include focal segmental glomerulosclerosis, IgA nephropathy, and other primary or secondary renal disorders. Differential diagnosis of these conditions is crucial in guiding clinical management and therapeutic approaches. However, the relationship between diabetes and the kidney is bidirectional; thus, new-onset diabetes may also occur as a complication of the treatment in patients with renal diseases. Here, we review the complex and multifaceted correlation between diabetes and kidney diseases and discuss clinical presentation and course, differential diagnosis, and therapeutic oppor-tunities offered by novel drugs.

Gut microbiome supplementation as therapy for metabolic syndrome.

The gut microbiome is defined as an ecological community of commensal symbiotic and pathogenic microorganisms that exist in our body. Gut microbiome dysbiosis is a condition of dysregulated and disrupted intestinal bacterial homeostasis, and recent evidence has shown that dysbiosis is related to chronic inflammation, insulin resistance, cardiovascular diseases (CVD), type 2 diabetes mellitus (T2DM), and obesity. It is well known that obesity, T2DM and CVD are caused or worsened by multiple factors like genetic predisposition, environmental factors, unhealthy high calorie diets, and sedentary lifestyle. However, recent evidence from human and mouse models suggest that the gut microbiome is also an active player in the modulation of metabolic syndrome, a set of risk factors including obesity, hyperglycemia, and dyslipidemia that increase the risk for CVD, T2DM, and other diseases. Current research aims to identify treatments to increase the number of beneficial microbiota in the gut microbiome in order to modulate metabolic syndrome by reducing chronic inflammation and insulin resistance. There is increasing interest in supplements, classified as prebiotics, probiotics, synbiotics, or postbiotics, and their effect on the gut microbiome and metabolic syndrome. In this review article, we have summarized current research on these supplements that are available to improve the abundance of beneficial gut microbiota and to reduce the harmful ones in patients with metabolic syndrome.

Partners in diabetes epidemic: A global perspective.

There is a recent increase in the worldwide prevalence of both obesity and diabetes. In this review we assessed insulin signaling, genetics, environment, lipid metabolism dysfunction and mitochondria as the major determinants in diabetes and to identify the potential mechanism of gut microbiota in diabetes diseases. We searched relevant articles, which have key information from laboratory experiments, epidemiological evidence, clinical trials, experimental models, meta-analysis and review articles, in PubMed, MEDLINE, EMBASE, Google scholars and Cochrane Controlled Trial Database. We selected 144 full-length articles that met our inclusion and exclusion criteria for complete assessment. We have briefly discussed these associations, challenges, and the need for further research to manage and treat diabetes more efficiently. Diabetes involves the complex network of physiological dysfunction that can be attributed to insulin signaling, genetics, environment, obesity, mitochondria and stress. In recent years, there are intriguing findings regarding gut microbiome as the important regulator of diabetes. Valid approaches are necessary for speeding medical advances but we should find a solution sooner given the burden of the metabolic disorder - What we need is a collaborative venture that may involve laboratories both in academia and industries for the scientific progress and its application for the diabetes control.

Establishment and evaluation of a risk prediction model for gestational diabetes mellitus.

Gestational diabetes mellitus (GDM) is a condition characterized by high blood sugar levels during pregnancy. The prevalence of GDM is on the rise globally, and this trend is particularly evident in China, which has emerged as a significant issue impacting the well-being of expectant mothers and their fetuses. Identifying and addressing GDM in a timely manner is crucial for maintaining the health of both expectant mothers and their developing fetuses. Therefore, this study aims to establish a risk prediction model for GDM and explore the effects of serum ferritin, blood glucose, and body mass index (BMI) on the occurrence of GDM. To develop a risk prediction model to analyze factors leading to GDM, and evaluate its efficiency for early prevention. The clinical data of 406 pregnant women who underwent routine prenatal examination in Fujian Maternity and Child Health Hospital from April 2020 to December 2022 were retrospectively analyzed. According to whether GDM occurred, they were divided into two groups to analyze the related factors affecting GDM. Then, according to the weight of the relevant risk factors, the training set and the verification set were divided at a ratio of 7:3. Subsequently, a risk prediction model was established using logistic regression and random forest models, and the model was evaluated and verified. Pre-pregnancy BMI, previous history of GDM or macrosomia, hypertension, hemoglobin (Hb) level, triglyceride level, family history of diabetes, serum ferritin, and fasting blood glucose levels during early pregnancy were de-termined. These factors were found to have a significant impact on the development of GDM (P < 0.05). According to the nomogram model's prediction of GDM in pregnancy, the area under the curve (AUC) was determined to be 0.883 [95% confidence interval (CI): 0.846-0.921], and the sensitivity and specificity were 74.1% and 87.6%, respectively. The top five variables in the random forest model for predicting the occurrence of GDM were serum ferritin, fasting blood glucose in early pregnancy, pre-pregnancy BMI, Hb level and triglyceride level. The random forest model achieved an AUC of 0.950 (95%CI: 0.927-0.973), the sensitivity was 84.8%, and the specificity was 91.4%. The Delong test showed that the AUC value of the random forest model was higher than that of the decision tree model (P < 0.05). The random forest model is superior to the nomogram model in predicting the risk of GDM. This method is helpful for early diagnosis and appropriate intervention of GDM.

Role of glycolysis in diabetic atherosclerosis.

Diabetes mellitus is a kind of typical metabolic disorder characterized by elevated blood sugar levels. Atherosclerosis (AS) is one of the most common complications of diabetes. Modern lifestyles and trends that promote overconsumption and unhealthy practices have contributed to an increase in the annual incidence of diabetic AS worldwide, which has created a heavy burden on society. Several studies have shown the significant effects of glycolysis-related changes on the occurrence and development of diabetic AS, which may serve as novel thera-peutic targets for diabetic AS in the future. Glycolysis is an important metabolic pathway that generates energy in various cells of the blood vessel wall. In particular, it plays a vital role in the physiological and pathological activities of the three important cells, Endothelial cells, macrophages and vascular smooth muscle cells. There are lots of similar mechanisms underlying diabetic and common AS, the former is more complex. In this article, we describe the role and mechanism underlying glycolysis in diabetic AS, as well as the therapeutic targets, such as trained immunity, microRNAs, gut microbiota, and associated drugs, with the aim to provide some new perspectives and potentially feasible programs for the treatment of diabetic AS in the foreseeable future.

Integrated proteome and malonylome analyses reveal the potential meaning of TLN1 and ACTB in end-stage renal disease

BackgroundEnd-stage renal disease (ESRD) is a condition that is characterized by the loss of kidney function. ESRD patients suffer from various endothelial dysfunctions, inflammation, and immune system defects. Lysine malonylation (Kmal) is a recently discovered post-translational modification (PTM). Although Kmal has the ability to regulate a wide range of biological processes in various organisms, its specific role in ESRD is limited.MethodsIn this study, the affinity enrichment and liquid chromatography-tandem mass spectrometry (LC-MS/MS) techniques have been used to create the first global proteome and malonyl proteome (malonylome) profiles of peripheral blood mononuclear cells (PBMCs) from twenty patients with ESRD and eighty-one controls.ResultsOn analysis, 793 differentially expressed proteins (DEPs) and 12 differentially malonylated proteins (DMPs) with 16 Kmal sites were identified. The Rap1 signaling pathway and platelet activation pathway were found to be important in the development of chronic kidney disease (CKD), as were DMPs TLN1 and ACTB, as well as one malonylated site. One conserved Kmal motif was also discovered.ConclusionsThese findings provided the first report on the Kmal profile in ESRD, which could be useful in understanding the potential role of lysine malonylation modification in the development of ESRD.

Super-Resolution Ultrasound Imaging of Renal Vascular Alterations in Zucker Diabetic Fatty Rats during the Development of Diabetic Kidney Disease.

Individuals with diabetes at risk of developing diabetic kidney disease (DKD) are challenging to identify using currently available clinical methods. Prognostic accuracy and initiation of treatment could be improved by a quantification of the renal microvascular rarefaction and the increased vascular tortuosity during the development of DKD. Super-resolution ultrasound (SRUS) imaging is an in vivo technique capable of visualizing blood vessels at sizes below 75 µm. This preclinical study aimed to investigate the alterations in renal blood vessels' density and tortuosity in a type 2 diabetes rat model, Zucker diabetic fatty (ZDF) rats, as a prediction of DKD. Lean age-matched Zucker rats were used as controls. A total of 36 rats were studied, subdivided into ages of 12, 22, and 40 weeks. Measured albuminuria indicated the early stage of DKD, and the SRUS was compared with the ex vivo micro-computed tomography (µCT) of the same kidneys. Assessed using the SRUS imaging, a significantly decreased cortical vascular density was detected in the ZDF rats from 22 weeks of age compared to the healthy controls, concomitant with a significantly increased albuminuria. Already by week 12, a trend towards a decreased cortical vascular density was found prior to the increased albuminuria. The quantified vascular density in µCT corresponded with the in vivo SRUS imaging, presenting a consistently lower vascular density in the ZDF rats. Regarding vessel tortuosity, an overall trend towards an increased tortuosity was present in the ZDF rats. SRUS shows promise for becoming an additional tool for monitoring and prognosing DKD. In the future, large-scale animal studies and human trials are needed for confirmation.

Renal Biopsy for Diagnosis in Kidney Disease: Indication, Technique, and Safety.

Renal biopsies are the gold standard for diagnosis, staging, and prognosis of underlying parenchymal kidney disease. This article provides an overview of the current indications and highlights ways to reduce bleeding complications in order to achieve optimal diagnostic yield with minimal risk to the patient. Novel indications have emerged from the increasing use of new molecularly targeted oncologic therapies in recent years, which often induce immune-mediated renal disease. On the other hand, the detection of specific antibodies against target antigens on podocytes in the sera of patients with new-onset nephrotic syndrome has now relativized the indication for biopsy in membranous nephropathy. The use of semi-automatic spring-loaded biopsy devices and real-time ultrasound considerably declined the complication rate and is the current standard. Percutaneous renal biopsies are overall a safe procedure if contraindications are considered. A coagulation disorder needs to be excluded beforehand, and an elevated blood pressure must be reduced to the normotensive range with medications. A laparoscopic approach or a radiology interventional procedure through the internal jugular vein may be considered for obtaining a kidney tissue sample if there is an urgent indication and a bleeding tendency cannot be adequately corrected. Major bleeding after a percutaneous renal biopsy can usually be managed with selective arterial embolization of the injured renal vessel. The use of a 16-gauge needle is the most reasonable compromise between diagnostic benefit and risk of complication. In the routine diagnostic, the biopsy specimen is examined with light microscopy, immunohistochemistry, and electron microscopy. Combination with modern molecular pathology techniques will contribute to more precise insights into the development and progression of kidney disease, which will likely refine future treatments in nephrology.

A - 160 Cognition over Time in Chronic sTBI with Non-Neurologic Comorbidities in Residential NeuroRehab.

Traumatic brain injury has been associated with increased risk of many comorbid neurologic and non-neurologic disorders (Masel & DeWitt, 2010). There is scant literature, however, to describe serial assessment of cognitive changes associated with comorbid non-neurologic disorders and sequelae in patients with chronic, severe traumatic brain injury (sTBI). A 60-year-old, right-handed, White male sustained an sTBI at age 15 secondary to a motor vehicle collision and subsequently developed behavioral and substance use problems, before being placed in a long-term residential neurorehabilitation program. He later developed kidney disease, believed to be the result of long-term use of anti-epileptic drugs (AEDs) that were prescribed to control seizures that developed following his brain injury. He continued to experience seizures, despite taking AEDs. Staff at his residential program reported concerns of declines in cognition and daily functioning over the past three years. Compared to results from two previous evaluations performed approximately four and six years prior, he demonstrated reductions in attention and working memory, processing speed, executive functioning, auditory and reading comprehension, and functional living skills. Expressive language, memory, and visuospatial skills were generally consistent with previous evaluations. Due to significant reductions across multiple cognitive domains, and multiple potential contributing factors, including ongoing seizures, late-stage kidney disease, and a possible superimposed neurodegenerative disorder, it was recommended that the patient continue to undergo serial neurocognitive testing to monitor for further decline and provide etiological clarification. The results were used by his therapists, residential program staff, and neurology providers to inform his treatment planning and care.

Association between Fiber Intake and Risk of Incident Chronic Kidney Disease: The UK Biobank Study.

Dietary fiber intake is associated with a lower risk of diabetes, cardiovascular disease, and cancer. However, it is unknown whether dietary fiber has a beneficial effect on preventing the development of chronic kidney disease (CKD). Using the UK Biobank prospective cohort, 110,412 participants who completed at least one dietary questionnaire and had an estimated glomerular filtration rate ≥60 mL/min/1.73 m2, urinary albumin-to-creatinine ratio <30 mg/g, and no history of CKD were included. The primary exposure was total dietary fiber density, calculated by dividing the absolute amount of daily total fiber intake by total energy intake (g/1,000 kcal). We separately examined soluble and insoluble fiber densities as additional predictors. The primary outcome was incident CKD based on diagnosis codes. A total of 3,507 (3.2%) participants developed incident CKD during a median follow-up of 9.9 years. In a multivariable cause-specific model, the adjusted hazard ratios (aHRs; 95% confidence intervals [CIs]) for incident CKD were 0.85 (0.77-0.94), 0.78 (0.70-0.86), and 0.76 (0.68-0.86), respectively, for the second, third, and highest quartiles of dietary fiber density (reference: lowest quartile). In a continuous model, the aHR for each +∆1.0g/1,000 kcal increase in dietary fiber density was 0.97 (95% CI, 0.95-0.99). This pattern of associations was similar for both soluble and insoluble fiber densities and did not differ across subgroups of sex, age, body mass index, hypertension, diabetes, smoking, and inflammation. Increased fiber intake was associated with a lower risk of CKD in this large well-characterized cohort.

Obesity as a risk factor for chronic kidney disease: a contemporary view on the problem. Review

The review article is devoted to an actual clinical problem of participation of obesity in development and progression of chronic kidney disease (CKD). Some pathogenic links due to which a negative renal effect of obesity is mediated including in particular, dyslipidemia (DLP), endothelial dysfunction (ED) of renal vessels, activation of renin‑angiotensin‑aldosterone system (RAAS), arterial hypertension (AH), a production of adipose tissue mediators with renal injuring properties such as leptin, tumor necrosis factor‑α, interleukines 1,6,8 are discussed. The data about the main factors of progression of renal damage associated with obesity included insulin resistance (IR), hyperinsulinemia, DLP, systemic and renal hemodynamic disorders caused by activation of RAAS (AH, intraglomerular hypertension) are given. The role of metabolic syndrome and its components in pathogenesis of CKD as well as a role of diabetes mellitus (DM) frequently combined with obesity in development of diabetic kidney disease (diabetic nephropathy) is generalized. Among adipokines a special attention in the present review is paid for pathogenic role of leptin and adiponektin in obesity with its conditions promoted renal damage. The participation of resistance to leptin in the pathogenesis of CKD through such links as IR, ED, oxidative stress and inflammation is discussed. The role of ED and glomerular hyperfiltration in pathogenesis of microalbuminuria is elucidated. The significance of injury of kidney tubular cell structures so called podocytes in pathogenesis of CKD in obesity is uncovered. The clinical significance of early revealing of renal pathology as well as body weight, glycemia level, arterial blood pressure control and following of healthy mode of life in reduction of risk development of CKD associated with obesity, DM and other metabolic disorders is generalized. It’s emphasized that evaluation of lipid and carbohydrate exchange parameters, serum leptin level, IR indices is considered to be perspective for diagnostics of renal damage in obesity.

MircroRNA-92b as a negative regulator of the TGF-β signaling by targeting the type I receptor

Transforming growth factor β1 (TGFβ1) has been identified as a major pathogenic factor underlying the development of chronic kidney disease (CKD). This study investigated the role of miR-92b-3p in the progression of renal fibrosis in unilateral ureteral occlusion (UUO) and unilateral ischemia-reperfusion injury (uIRI) mouse models, as well as explored its underlying mechanisms in human proximal tubular epithelial (HK2) cells. We found that renal fibrosis increased in UUO mice after miR-92b knockout, while it reduced in miR-92b overexpressing mice. MiR-92b knockout aggravated renal fibrosis in uIRI mice. RNA-sequencing analysis, the luciferase reporter assay, qPCR analysis, and western blotting confirmed that miR-92b-3p directly targeted TGF-β receptor 1, thereby ameliorating renal fibrosis by suppressing the TGF-β signaling pathway. Furthermore, we found that TGF-β suppressed miR-92b transcription through Snail family transcriptional repressors 1 and 2. Our results suggest that miR-92b-3p may serve as a novel therapeutic for mitigating fibrosis in CKD.

The role of glycosaminoglycans in blood pressure regulation.

Essential hypertension (HT) is the global health problem and is a major risk factor for the development of cardiovascular and kidney disease. High salt intake has been associated with HT and impaired kidney sodium excretion is considered to be a major mechanism for the development of HT. Although kidney has a very important role in regulation of BP, this traditional view of BP regulation was challenged by recent findings suggesting that nonosmotic tissue sodium deposition is very important for BP regulation. This new paradigm indicates that sodium can be stored and deposited nonosmotically in the interstitium without water retention and without increased BP. One of the major determinants of this deposition is glycosaminoglycans (GAGs). By binding to GAGs found in the endothelial surface layer (ESL) which contains glycocalyx, sodium is osmotically inactivated and not induce concurrent water retention. Thus, GAGs has important function for homeostatic BP and sodium regulation. In the current review, we summarized the role of GAGs in ESL and BP regulation.

A Combined Biomarker That Includes Plasma Fibroblast Growth Factor 23, Erythropoietin, and Klotho Predicts Short- and Long-Term Morbimortality and Development of Chronic Kidney Disease in Critical Care Patients with Sepsis: A Prospective Cohort.

Acute Kidney Injury (AKI) is a frequent complication in intensive care unit (ICU) patients that increases mortality and chronic kidney disease (CKD) development. AKI is associated with elevated plasma fibroblast growth factor 23 (FGF23), which can be modulated by erythropoietin (EPO) and Klotho. We aimed to evaluate whether a combined biomarker that includes these molecules predicted short-/long-term outcomes. We performed a prospective cohort of ICU patients with sepsis and previously normal renal function. They were followed during their inpatient stay and for one year after admission. We measured plasma FGF23, EPO, and Klotho levels at admission and calculated a combined biomarker (FEK). A total of 164 patients were recruited. Of these, 50 (30.5%) had AKI at admission, and 55 (33.5%) developed AKI within 48 h. Patients with AKI at admission and those who developed AKI within 48 h had 12- and 5-fold higher FEK values than non-AKI patients, respectively. Additionally, patients with higher FEK values had increased 1-year mortality (41.9% vs. 18.6%, p = 0.003) and CKD progression (26.2% vs. 8.3%, p = 0.023). Our data suggest that the FEK indicator predicts the risk of AKI, short-/long-term mortality, and CKD progression in ICU patients with sepsis. This new indicator can improve clinical outcome prediction and guide early therapeutic strategies.

Chronic Kidney Disease Risk in Living Kidney Transplant Donors: A Long-Term Follow-Up Study

Background: Living kidney donors (LKD) may experience some untoward consequences following donation such as development of chronic kidney disease (CKD). In this study, we aimed to investigate the rate of development of CKD and factors affecting the development of CKD in LKDs during long-term follow-up from a center in Turkey. Methods: This study was a retrospective analysis of LKDs followed between January 2000 and December 2017. Pre-transplant and post-transplant clinical data of the 338 LKDs were recorded and compared. Factors affecting the development of stage 3 and later stages of CKD were analyzed. Results: Majority of the donors were females (64.2%), and the median age of all donors was 47 (39–54) years. Stage 3 CKD developed in 50 donors during the median follow-up of 71 months. Older age at the time of transplantation and a low pre-transplant estimated glomerular filtration rate (eGFR) were determined as the factors affecting the development of stage 3 CKD (p < 0.001, p < 0.001). The receiver operating characteristic analysis showed that the cut-off age for the development of stage 3 CKD was 50.5 years. Newly diagnosed hypertension was detected in 57 patients (16.8%) after the transplantation. While hypertension was seen at a rate of 42% in those with an eGFR <60 mL/min/1.73 m², it was detected at 19.4% in the group with an eGFR >60 mL/min/1.73 m² (p < 0.001). Conclusion: These results reveal that being a LKD is associated with the development of CKD and hypertension. Age and eGFR values at the time of transplantation were the determinants for the development of CKD.

Response to Steroids Is Not Completely Protective Against the Development of Progressive Kidney Disease in Collapsing Focal Segmental Glomerulosclerosis

Response to Steroids Is Not Completely Protective Against the Development of Progressive Kidney Disease in Collapsing Focal Segmental Glomerulosclerosis

Association of metabolic syndrome and chronic kidney disease.

The prevalence of kidney disease is increasing rapidly worldwide, reflecting rising rates of obesity, diabetes, and associated metabolic syndrome (MetS). Chronic kidney disease and related comorbidities such as obesity, diabetes, and hypertension place a significant financial burden on healthcare systems. Despite the widespread use of RAAS inhibitors, intensive blood pressure and glycemic control, and newer therapeutic options consisting of sodium/glucose cotransporter-2 (SGLT-2) inhibitors or glucagon-like peptide-1 (GLP-1) receptor agonists, a significant risk of progression to end-stage renal disease remains in the high-risk obese and diabetic population. The MetS is a cluster of cardiovascular risk factors that adversely affect the development and progression of chronic kidney failure. According to the criteria of the World Health Organization, it is defined by visceral adiposity, impaired glucose tolerance or insulin resistance, atherogenic dyslipidemia, raised blood pressure, and microalbuminuria with a albumin-to-creatinine ratio ≥30 mg/g. At molecular level MetS is marked by a proinflammatory state and increased oxidative stress leading to various pathophysiological changes causing endothelial dysfunction and a hypercoagulable state. Because the kidney is a highly vascularized organ, it is especially susceptible for those microvascular changes. Therefore, the MetS and its individual components are associated with the premature development, acceleration, and progression of chronic kidney disease. Therefore, it is becoming increasingly important to elucidate the underlying mechanisms of MetS-associated chronic kidney disease in order to develop new strategies for preventing and slowing the progression of renal disease. In this review, we will elucidate (i) the renal structural, hemodynamic, and metabolic changes that occur in obesity and obesity-related kidney injury; (ii) the clinicopathological characteristics of obesity-related kidney injury, primarily focusing on obesity-associated glomerulopathy; (iii) the potential additional factors or predisposing factors that may turn patients more susceptible to renal structural or functional compensatory failure and subsequent injury.

Association of Chronic Kidney Disease With Dietary Inflammatory Index in Adults Aged 50 Years and Older: Dose-Response Analysis of a Nationally Representative Population-Based Study

ObjectiveDietary inflammatory index (DII) is associated with systemic inflammatory markers, which have been linked to the development of chronic kidney disease (CKD). However, epidemiological studies on the association of DII scores with CKD are sparse. This study aimed to quantitatively assess the dose-response relationship of DII scores with the prevalence of CKD. MethodsAdults (≥50 years) from the 2007–2018 National Health and Nutrition Examination Survey (N=12,090) were included. DII scores were calculated based on 27 nutritional parameters. The outcome of interest is the prevalence of CKD 3-5 stages, which is defined as estimated glomerular filtration rate <60 mL/min/1.73 m2. The non-linear dose-response relationship of DII scores with the prevalence of CKD stages 3–5 was assessed with restricted cubic splines. Stratified analyses were conducted by age, sex and race/ethnicity. Covariates included age, sex, body mass index, race/ethnicity, educational, ratio of family income to poverty, smoking, physical activity, hypertension, diabetes, and daily intakes of total plain water, sodium and energy. ResultsThe weighted prevalence of CKD stages 3–5 was 14.77%. The relationship of DII scores with CKD stages 3–5 was linear, and the odds ratios (95% confidence intervals) of CKD stages 3–5 were 0.68 (0.51-0.84) for -2 (DII score), 0.83 (0.74-0.93) for -1, 1.00 for 0 (reference value), 1.20 (1.07-1.32) for 1, 1.41 (1.16-1.66) for 2, 1.63 (1.28-1.98) for 3, 1.84 (1.34-2.34) for 4, and 2.08 (1.30-2.86) for 5. The linear relationship pattern of DII scores with CKD stages 3–5 was observed in stratified analyses by age, sex and race/ethnicity, respectively. ConclusionsHigher DII scores were independently and linearly associated with the odds of CKD stages 3–5, which deserves to be confirmed in further prospective cohort studies.