Risk Of Chronic Kidney Disease Research Articles

Mannose and glycine: Metabolites with potentially causal implications in chronic kidney disease pathogenesis.

Chronic Kidney Disease (CKD) represents a global health challenge, with its etiology and underlying mechanisms yet to be fully elucidated. Integrating genomics with metabolomics can offer insights into the putatively causal relationships between serum metabolites and CKD. Utilizing bidirectional Mendelian Randomization (MR), we assessed the putatively causal associations between 486 serum metabolites and CKD. Genetic data for these metabolites were sourced from comprehensive genome-wide association studies, and CKD data were obtained from the CKDGen Consortium. Our analysis identified four metabolites with a robust association with CKD risk, of which mannose and glycine showed the most reliable causal relationships. Pathway analysis spotlighted five significant metabolic pathways, notably including "Methionine Metabolism" and "Arginine and Proline Metabolism", as key contributors to CKD pathogenesis. This study underscores the potential of certain serum metabolites as biomarkers for CKD and illuminates pivotal metabolic pathways in CKD's pathogenesis. Our findings lay the groundwork for potential therapeutic interventions and warrant further research for validation.

Gonadal dysfunction in women with diabetes mellitus.

It is well known that both type 1 and type 2 diabetes mellitus (DM) are related to increased risk for cardiovascular (CV) and chronic kidney disease (CKD). However, besides these prominently presented complications, DM has also been associated with reproductive dysfunctions. It seems that these disorders are met in up to 40% of women with DM and consist of delayed menarche, all types of menstrual disorders, such as amenorrhea, oligomenorrhea, menstrual irregularity, as well as menorrhagia, infertility, characteristics of polycystic ovary syndrome (PCOS) and early (or rarely late) menopause. In type 1 DM (T1DM), insulin treatment, although it has reduced the rates of insulinopenic-induced hypogonadotropic hypogonadism, an entity commonly presented in many women with the disease in the past decades, when it is used in excess it can also promote hyperandrogenism. Regarding type 2 DM (T2DM), insulin resistance (IR) and hyperinsulinemia have mainly been implicated in the pathogenesis of reproductive dysfunctions, as insulin can act as gonadotropin on the theca cells of the ovary and can lead to hyperandrogenism and inhibition of proper ovulation. This review aims to detail the reproductive dysfunctions associated with DM and provide scientific data to enlighten the underlying pathogenetic mechanisms.

Higher potassium intake is associated with a lower risk of chronic kidney disease: population-based prospective study

BackgroundHigh-potassium intake is associated with a lower risk of cardiovascular disease. However, the association between potassium intake and the development of chronic kidney disease (CKD) remains unclear. ObjectiveThe objective of this study was to investigate whether potassium intake is associated with outcomes of incident CKD. MethodsThis is a population-based prospective observational cohort study from the UK Biobank cohort between 2006 and 2010. We included 317,162 participants without CKD from the UK Biobank cohort. The main predictor was spot urine potassium-to-creatinine ratio (KCR). The primary outcome was incident CKD, which was defined by the International Classification of Disease 10 codes or Operating Procedure Codes Supplement 4 codes. ResultsAt baseline, individuals with higher KCR had lower blood pressure, body mass index, and inflammation, and were less likely to have diabetes and hypertension. During a median follow-up of 11.9 y, primary outcome events occurred in 15,246 (4.8%) participants. In the cause-specific model, the adjusted hazard ratio (aHR) per 1-standard deviation increase in KCR for incident CKD was 0.90 [95% confidence interval (CI): 0.89, 0.92]. Compared with quartile 1 of KCR, the aHRs (95% CIs) for quartiles 2–4 were 0.98 (0.94, 1.02), 0.90 (0.86, 0.95), and 0.80 (0.76, 0.84), respectively. In sensitivity analysis with different definitions of CKD, the results were similar. In addition, further analysis with dietary potassium intake also showed a negatively graded association with the primary outcome. ConclusionsHigher urinary potassium excretion and intake were associated with a lower risk of incident CKD.

Evaluating Osteoporosis in Chronic Kidney Disease: Both Bone Quantity and Quality Matter.

Bone strength is determined not only by bone quantity [bone mineral density (BMD)] but also by bone quality, including matrix composition, collagen fiber arrangement, microarchitecture, geometry, mineralization, and bone turnover, among others. These aspects influence elasticity, the load-bearing and repair capacity of bone, and microcrack propagation and are thus key to fractures and their avoidance. In chronic kidney disease (CKD)-associated osteoporosis, factors traditionally associated with a lower bone mass (advanced age or hypogonadism) often coexist with non-traditional factors specific to CKD (uremic toxins or renal osteodystrophy, among others), which will have an impact on bone quality. The gold standard for measuring BMD is dual-energy X-ray absorptiometry, which is widely accepted in the general population and is also capable of predicting fracture risk in CKD. Nevertheless, a significant number of fractures occur in the absence of densitometric World Health Organization (WHO) criteria for osteoporosis, suggesting that methods that also evaluate bone quality need to be considered in order to achieve a comprehensive assessment of fracture risk. The techniques for measuring bone quality are limited by their high cost or invasive nature, which has prevented their implementation in clinical practice. A bone biopsy, high-resolution peripheral quantitative computed tomography, and impact microindentation are some of the methods established to assess bone quality. Herein, we review the current evidence in the literature with the aim of exploring the factors that affect both bone quality and bone quantity in CKD and describing available techniques to assess them.

Glomerular hyperfiltration as a therapeutic target for CKD.

The global burden of chronic kidney disease (CKD) is high and increasing. Early diagnosis and intervention are key to improve outcomes. Single nephron glomerular hyperfiltration is an early pathophysiologic manifestation of CKD that may result in absolute glomerular hyperfiltration, i.e. a high glomerular filtration rate (GFR) or be associated with normal or low GFR because of nephron loss (relative glomerular hyperfiltration). Even though compensatory glomerular hyperfiltration may contribute to maintain kidney function after loss of kidney mass, the associated increased glomerular capillary pressure and glomerular and podocyte size drive podocyte loss, albuminuria and proximal tubular overload, contributing to CKD progression. In this regard, all kidney protective drugs in clinical use so far, from renin-angiotensin system blockers to mineralocorticoid receptor blockers to sodium-glucose cotransporter-2 inhibitors to tolvaptan, induced an early dip in glomerular filtration that is thought to represent reversal of hyperfiltration. As glomerular hyperfiltration may be present early in the course of kidney disease, its recognition may provide an effective intervention window that may predates current criteria based on high albuminuria or loss of GFR. Nevertheless, there is no diagnostic method with high sensitivity and specificity to identify single nephron glomerular hyperfiltration, except when it leads to obvious absolute glomerular hyperfiltration, as observed in the early stages of diabetic kidney disease when nephron mass is still preserved. We now review the concept of glomerular hyperfiltration as an indicator of CKD risk, including definitions, challenges in diagnosis and evaluation, underlying pathophysiological mechanisms, potential therapeutic approaches and unanswered questions.

Ambient PM2.5 components and prevalence of chronic kidney disease: a nationwide cross-sectional survey in China.

Chronic kidney disease (CKD) is a global public health concern, and accumulating evidence has indicated that air pollution increases the odds of CKD. However, a limited number of studies have examined the long-term effects of ambient fine particulate matter (PM2.5) components on the risk of CKD among general population; thus, major knowledge gaps remain. Using data from a nationwide representative cross-sectional survey in China and a validated PM2.5 composition dataset, we established generalized linear models to quantify the association between five major components of PM2.5 and CKD prevalence. There were significant associations between long-term exposure to three PM2.5 components [including black carbon (BC), sulfate (SO42-), organic matter (OM)] and increased odds of CKD prevalence. Along with an interquartile range (IQR) increment in BC (3.3 μg/m3), SO42- (9.7 μg/m3), and OM (16.2 μg/m3) at a 4-year moving average, the odds ratios (ORs) for CKD prevalence were 1.28 (95% CI 1.07, 1.54), 1.23 (95% CI 1.03, 1.45), and 1.23 (95% CI 1.02, 1.47), respectively. We did not detect any significant association of the other two PM2.5 components [nitrate (NO3-) or ammonium (NH4+)] with CKD prevalence. Stratified analyses revealed no differences (P ≥ 0.05) in the effect estimates of subgroups based on administrative region, sex, age, and other demographic characteristics. For instance, along with an IQR increment in BC at a 4-year moving average, the ORs of CKD prevalence among males and females were 1.30 (95% CI 0.98, 1.73) and 1.29 (95% CI 1.01, 1.65), respectively. The odds of CKD were generally higher with increasing PM2.5 composition concentration. Our study demonstrated that long-term exposure to specific PM2.5 components including BC, SO42-, and OM increased CKD risk in the general population. This study could provide new insights into source-directed PM2.5 control and CKD prevention.

Mitochondrial genetic variation and risk of chronic kidney disease and acute kidney injury in UK Biobank participants

Experimental models suggest an important role for mitochondrial dysfunction in the pathogenesis of chronic kidney disease (CKD) and acute kidney injury (AKI), but little is known regarding the impact of common mitochondrial genetic variation on kidney health. We sought to evaluate associations of inherited mitochondrial DNA (mtDNA) variation with risk of CKD and AKI in a large population-based cohort. We categorized UK Biobank participants who self-identified as white into eight distinct mtDNA haplotypes, which were previously identified based on their associations with phenotypes associated with mitochondrial DNA copy number, a measure of mitochondrial function. We used linear and logistic regression models to evaluate associations of these mtDNA haplotypes with estimated glomerular filtration rate by serum creatinine and cystatin C (eGFRCr-CysC, N = 362,802), prevalent (N = 416 cases) and incident (N = 405 cases) end-stage kidney disease (ESKD), AKI defined by diagnostic codes (N = 14,170 cases), and urine albumin/creatinine ratio (ACR, N = 114,662). The mean age was 57 ± 8 years and the mean eGFR was 90 ± 14 ml/min/1.73 m2. MtDNA haplotype was significantly associated with eGFR (p = 2.8E−12), but not with prevalent ESKD (p = 5.9E−2), incident ESKD (p = 0.93), AKI (p = 0.26), or urine ACR (p = 0.54). The association of mtDNA haplotype with eGFR remained significant after adjustment for diabetes mellitus and hypertension (p = 1.2E−10). When compared to the reference haplotype, mtDNA haplotypes I (β = 0.402, standard error (SE) = 0.111; p = 2.7E−4), IV (β = 0.430, SE = 0.073; p = 4.2E−9), and V (β = 0.233, SE = 0.050; p = 2.7E−6) were each associated with higher eGFR. Among self-identified white UK Biobank participants, mtDNA haplotype was associated with eGFR, but not with ESKD, AKI or albuminuria.

Plasma Levels of Polyunsaturated Fatty Acids and Adverse Kidney Outcomes

Many studies have reported polyunsaturated fatty acids (PUFA) as significant predictors of cardiovascular disease, but little is known about the relationship between PUFA levels and chronic kidney disease (CKD). This study explored this relationship among individuals with and without CKD. Prospective observational cohort study. 78,950 participants without CKD (cohort 1) and 7,233 participants with CKD (cohort 2) in the UK Biobank Study with PUFA levels measured between 2007 and 2010. Percentage of plasma PUFA, omega-3 fatty acid (FA), omega-6 FA, docosahexaenoic acid (DHA), and linoleic acid relative to total fatty acid. Incident CKD for cohort 1 and incident kidney failure requiring replacement therapy (KFRT) for cohort 2. Cox proportional hazards regression analyses, including a cause-specific competing risk model. In cohort 1, individuals with higher quartiles of plasma PUFA levels had healthier lifestyles and fewer comorbidities. During 841,007 person-years of follow-up (median 11.9 years), incident CKD occurred in 4.5% of participants (incidence rate, 39.1 per 10,000 person-years). For incident CKD in cohort 1, the adjusted cause-specific hazard ratios (HR) (95% CIs) for quartiles 2, 3, and 4 were 0.83 (0.75-0.92), 0.85 (0.76-0.96), 0.71 (0.62-0.82), respectively, compared with quartile 1. This inverse relationship was consistently observed for all PUFA types. In cohort 2, although, total PUFA levels were not associated with KFRT, higher PUFA subtype levels of DHA were associated with a lower risk of KFRT. Observational design and limited generalizability to individuals with higher disease severity; no data on eicosapentaenoic acid. Among individuals without CKD, higher plasma PUFA levels and all four PUFA components were associated with a lower risk of incident CKD. In individuals with CKD, only the omega-3 component of PUFA, DHA, was associated with a lower risk of KFRT.

Branched-chain amino acid levels are inversely associated with incident and prevalent chronic kidney disease in people with type 2 diabetes.

To investigate the association of plasma metabolites with incident and prevalent chronic kidney disease (CKD) in people with type 2 diabetes and establish whether this association is causal. The Hoorn Diabetes Care System cohort is a large prospective cohort consisting of individuals with type 2 diabetes from the northwest part of the Netherlands. In this cohort we assessed the association of baseline plasma levels of 172 metabolites with incident (Ntotal = 462/Ncase = 81) and prevalent (Ntotal = 1247/Ncase = 120) CKD using logistic regression. Additionally, replication in the UK Biobank, body mass index (BMI) mediation and causality of the association with Mendelian randomization was performed. Elevated levels of total and individual branched-chain amino acids (BCAAs)-valine, leucine and isoleucine-were associated with an increased risk of incident CKD, but with reduced odds of prevalent CKD, where BMI was identified as an effect modifier. The observed inverse effects were replicated in the UK Biobank. Mendelian randomization analysis did not provide evidence for a causal relationship between BCAAs and prevalent CKD. Our study shows the intricate relationship between plasma BCAA levels and CKD in individuals with type 2 diabetes. While an association exists, its manifestation varies based on disease status and BMI, with no definitive evidence supporting a causal link between BCAAs and prevalent CKD.

Abstract WP159: Chronic Kidney Disease and Risk of Intracerebral Hemorrhage: The Role of Hypertension as a Mediator

Introduction: Chronic kidney disease (CKD) is a well-established risk factor for spontaneous intracerebral hemorrhage (ICH). However, the biological pathway underlying this association remains unclear. We therefore conducted a phenome-wide association study (PheWAS) to assess for mediators of the association between CKD and ICH risk. Methods: We conducted a PheWAS using data from the UK Biobank (UKB), a large cohort study that enrolled over 500,000 Britons aged 40-69. We first developed a polygenic risk score that contained 27 independent (r2 <0.1) genetic risk variants known to be associated with CKD at genome-wide significant levels (p<5x10 -8 ). We subsequently tested for associations between this CKD genetic risk score and the 1,840 disease phenotypes available through the UKB baseline assessment. We used a Bonferroni corrected p<2.7x10 -5 as our threshold for significance. For all phenotypes that reached statistical significance in the PheWAS, we obtained summary results from previously published genome-wide association studies and implemented multivariable Mendelian Randomization (MR) to evaluate the proportion of the total effect of CKD on ICH risk mediated through these phenotypes. The indirect effect of CKD on ICH risk via mediators was calculated by subtracting the direct effect of CKD obtained from multivariable MR from the total effect of CKD obtained from univariable MR. Results: Excluding renal-related diseases, hypertension was the only significant phenotype in the PheWAS (p=3.2x10 -21 ). Genetically determined CKD was associated with a total increase in ICH risk of 38% in univariable MR (OR 1.38; 95% CI 1.12-1.71; p=0.002). This association was reduced to a 19% increase in ICH risk after adjusting for hypertension in multivariable MR (OR 1.19; 95% CI 1.03-1.39; p=0.021). The proportion of the total effect of CKD on ICH risk mediated through hypertension was estimated to be 55%. Conclusions: Hypertension accounts for approximately 55% of the total effect of CKD on ICH risk in genetic analyses. This aligns with existing knowledge that CKD worsens hypertension by causing renal retention of sodium and increased sympathetic activity. Further studies are needed to identify other pathways that mediate the remaining effect of CKD on ICH risk.

Multiprofessional Approach for Chronic Kidney Disease (CKD) Risk Reduction and Prophylaxis in the Kushiro Medical Area

Chronic kidney disease (CKD) is closely related to disorders of various organs of the body and is also a factor in increasing social security costs such as medical costs for dialysis. Multiprofessional public health associations in Kushiro City jointly manage CKD-targeted action as "Kushiro CKD network" composed of medical/dental physicians, nurses, nutritionists and pharmacists. Pharmacists have played a central role in affixing a CKD sticker to a patient's medicine notebook when the patient's estimated glomerular filtration rate (eGFR) <45 mL/min/1.73 m2, in order to highlight the risk of CKD for those patients and related medical staff. There are many drugs that require dose reduction considering for renal function, but we had found cases where renal function was not monitored and pharmaceutical dispensation adjusted before the CKD network started. Therefore, we took this opportunity to investigate the impact of CKD stickers on pharmacists' work. During the period from August 2018 to August 2021, about 3200 CKD stickers were affixed by pharmacists, and about 4500 cases of decreased renal function were detected at pharmacies. In addition, there were 334 cases in which renal function deterioration was identified by the CKD stickers and led to further inquiries, of which 265 cases, or about 80%, resulted in prescription changes. Based on these results, it is considered that CKD stickers are effective method for pharmacies understand renal function deterioration and conduct appropriate prescription reviews. Finally, and perhaps most importantly, the use of CKD stickers can help assure that patients with renal impairment care treated with appropriate medication doses.

Relationship Between Lipoprotein(a), Renal Function Indicators, and Chronic Kidney Disease: Evidence From a Large Prospective Cohort Study.

Chronic kidney disease (CKD) poses a significant global public health challenge. While lipoprotein(a) (Lp[a]) has been established as a significant factor in cardiovascular disease, its connection to CKD risk remains a topic of debate. Existing evidence indicates diverse risks of kidney disease among individuals with various renal function indicators, even when within the normal range. This study aims to investigate the joint associations between different renal function indicators and Lp(a) regarding the risks of incident CKD in the general population. The analysis involved a cohort of 329,415 participants without prior CKD who were enrolled in the UK Biobank between 2006 and 2010. The participants, with an average age of 56 (SD 8.1) years, included 154,298/329,415 (46.84%) males. At baseline, Lp(a) levels were measured using an immunoturbidimetric assay and classified into 2 groups: low (<75 nmol/L) and high (≥75 nmol/L). To assess participants' baseline renal function, we used the baseline urine albumin-to-creatinine ratio (UACR) and estimated glomerular filtration rate (eGFR). The relationship between Lp(a), renal function indicators, and the risk of CKD was evaluated using multivariable Cox regression models. These models were adjusted for various factors, including sociodemographic variables, lifestyle factors, comorbidities, and laboratory measures. A total of 6003 incident CKD events were documented over a median follow-up period of 12.5 years. The association between elevated Lp(a) levels and CKD risk did not achieve statistical significance among all participants, with a hazard ratio (HR) of 1.05 and a 95% CI ranging from 0.98 to 1.13 (P=.16). However, a notable interaction was identified between Lp(a) and UACR in relation to CKD risk (P for interaction=.04), whereas no significant interaction was observed between Lp(a) and eGFR (P for interaction=.96). When compared with the reference group with low Lp(a) and low-normal UACR (<10 mg/g), the group with high Lp(a) and low-normal UACR exhibited a nonsignificant association with CKD risk (HR 0.98, 95% CI 0.90-1.08; P=.74). By contrast, both the low Lp(a) and high-normal UACR (≥10 mg/g) group (HR 1.16, 95% CI 1.08-1.24; P<.001) and the high Lp(a) and high-normal UACR group (HR 1.32, 95% CI 1.19-1.46; P<.001) demonstrated significant associations with increased CKD risks. In individuals with high-normal UACR, elevated Lp(a) was linked to a significant increase in CKD risk, with an HR of 1.14 and a 95% CI ranging from 1.03 to 1.26 (P=.01). Subgroup analyses and sensitivity analyses consistently produced results that were largely in line with the main findings. The analysis revealed a significant interaction between Lp(a) and UACR in relation to CKD risk. This implies that Lp(a) may act as a risk factor for CKD even when considering UACR. Our findings have the potential to provide valuable insights into the assessment and prevention of CKD, emphasizing the combined impact of Lp(a) and UACR from a public health perspective within the general population. This could contribute to enhancing public awareness regarding the management of Lp(a) for the prevention of CKD.

REVIEW OF THE PHYTOTHERAPY FOR NEPHROLITHIASIS

Nephrolithiasis (kidney stone) cases have a prevalence ranging from 1% to 13%. The disease not only hampers kidney function but also elevates the risk of chronic kidney diseases. The pathophysiology of nephrolithiasis is closely linked to elevated concentrations of calcium, oxalate, and/or uric acid in the urine. Pharmacotherapy to manage nephrolithiasis includes thiazide diuretics, allopurinol, citrate supplements, and alpha-blockers that have been prescribed to relieve symptoms. In addition, there is growing interest in exploring the potential of phytotherapy. This review aims to identify suitable phytotherapy approaches by examining relevant articles on nephrolithiasis. The research methodology involved searching PubMed articles using the keywords of (("Plant Extracts") AND ("Nephrolithiasis")) OR ("Ureterolithiasis"). The articles obtained from the initial search were n =123. 2 authors screened articles for their eligibility. The inclusion criteria were limited to articles written in English, topics related to nephrolithiasis and not other kidney diseases, the botanical names of the plants and the method of extraction are clearly described, complete studies with clear descriptions regarding the methods and results, not synthetic drugs, and not involving medical instruments or laser to remove the stones. Articles included in the review were n = 17. Water and hydro-alcohol were the solvents used to extract the plants. Twenty-two plants have confirmed their anti-nephrolithiasis activity, and nine articles described the assay by in vivo study, two by in vitro study, three by both in vitro and in vivo study, and only one article mentioned a study in humans by a randomized-control trial on a mixture of herbs. It is concluded that Rhizoma alismatis, Poria cocos, Polyporus umbellatus, Atractylodis macrocephalae, and Cinnamomi Cassiae prepared as a mixture in the Wu-Ling-San formula have a potential therapeutic effect on nephrolithiasis, as this formula has been studied in humans.

Predictive Analysis in Nephrology: Evaluating Machine Learning Models for Chronic Kidney Disease Prediction

Abstract: In the realm of healthcare, early detection and accurate diagnosis are critical for effective treatment, especially for diseases that are often undiagnosed until later stages. This research presents an Automated Classification System focused on Chronic Kidney Disease (CKD), a prevalent condition frequently undetected in its early stages. Leveraging advanced machine learning techniques, the study aims to overcome the traditional reliance on doctors' intuition and experience by providing a data-driven approach for CKD diagnosis. Utilizing a comprehensive dataset, the research explores various data pre-processing methods, including innovative approaches for handling missing values and data integrity, which surpass the conventional mean and mode-based imputation methods prevalent in existing literature. Through exploratory data analysis and the application of diverse machine learning algorithms, the study seeks to identify the most effective model for predicting CKD risk. The findings of this research have significant implications for enhancing clinical decisions, offering a path towards more accessible, efficient, and accurate diagnosis of Chronic Kidney Disease, ultimately contributing to improved patient outcomes and healthcare practices

Early detection of the risk of chronic kidney disease based on eating and drinking behaviors in Kendari City Indonesia

Early detection of the risk of chronic kidney disease based on eating and drinking behaviors in Kendari City Indonesia

Prediction of the risk of 3-year chronic kidney disease among elderly people: a community-based cohort study

Objective We conducted a community-based cohort study to predict the 3-year occurrence of chronic kidney disease (CKD) among population aged ≥60 years. Method Participants were selected from two communities through randomized cluster sampling in Jiading District of Shanghai, China. The two communities were randomly divided into a development cohort (n = 12012) and a validation cohort (n = 6248) with a 3-year follow-up. Logistic regression analysis was used to determine the independent predictors. A nomogram was established to predict the occurrence of CKD within 3 years. The area under the curve (AUC), the calibration curve and decision curve analysis (DCA) curve were used to evaluate the model. Result At baseline, participants in development cohort and validation cohort were with the mean age of 68.24 ± 5.87 and 67.68 ± 5.26 years old, respectively. During 3 years, 1516 (12.6%) and 544 (8.9%) new cases developed CKD in the development and validation cohorts, respectively. Nine variables (age, systolic blood pressure, body mass index, exercise, previous hypertension, triglycerides, fasting plasma glucose, glycated hemoglobin and serum creatinine) were included in the prediction model. The AUC value was 0.742 [95% confidence interval (CI), 0.728–0.756] in the development cohort and 0.881(95%CI, 0.867–0.895) in the validation cohort, respectively. The calibration curves and DCA curves demonstrate an effective predictive model. Conclusion Our nomogram model is a simple, reasonable and reliable tool for predicting the risk of 3-year CKD in community-dwelling elderly people, which is helpful for timely intervention and reducing the incidence of CKD.

Risk Prediction and Management of Chronic Kidney Disease in People Living with Type 2 Diabetes Mellitus.

People with type 2 diabetes mellitus have increased risk of chronic kidney disease and atherosclerotic cardiovascular disease. Improved care delivery and implementation of guideline-directed medical therapy have contributed to the declining incidence of atherosclerotic cardiovascular disease in high-income countries. By contrast, the global incidence of chronic kidney disease and associated mortality is either plateaued or increased, leading to escalating direct and indirect medical costs. Given limited resources, better risk stratification approaches to identify people at risk of rapid progression to end-stage kidney disease can reduce therapeutic inertia, facilitate timely interventions and identify the need for early nephrologist referral. Among people with chronic kidney disease G3a and beyond, the kidney failure risk equations (KFRE) have been externally validated and outperformed other risk prediction models. The KFRE can also guide the timing of preparation for kidney replacement therapy with improved healthcare resources planning and may prevent multiple complications and premature mortality among people with chronic kidney disease with and without type 2 diabetes mellitus. The present review summarizes the evidence of KFRE to date and call for future research to validate and evaluate its impact on cardiovascular and mortality outcomes, as well as healthcare resource utilization in multiethnic populations and different healthcare settings.

Prevalence and assessment of risk factors of chronic kidney disease in the ASIR region of Saudi Arabia

Introduction: Chronic kidney disease (CKD) is a major health concern in Saudi Arabia. The prevalence of CKD and associated risk factors in Saudi Arabia’s general population are not efficiently studied. The goal of this research is to determine the prevalence rate of CKD in the ASIR region and its associated epidemiological risk factors. Methodology: This is a cross-sectional study that used a comprehensive direct questionnaire to collect data on CKD prevalence and risk factors in the ASIR region of Saudi Arabia. The study was carried out in different age groups. Demographic characteristics, presence of CKD, and associated factors such as a history of acute kidney disease, obstructive sleep apnea, family history, history of non-steroid anti-inflammatory drugs (NSAID), smoking status, comorbidities, and history of periodontal diseases were asked. The survey tool was validated through a pilot study, and a statistical p-value of 0.05 was considered significant. Results: A total of 967 participants were included in the study, with a CKD prevalence rate of 1.9%. Gender, history of acute kidney disease, obstructive sleep apnea, family history of kidney disease, smoking, diabetes, peptic ulcer disease, hypertension and hyperlipidemia were commonly found to be associated with CKD. A binary logistic regression model was carried out to assess the risk factors for CKD. Gender, history of acute kidney disease, family history of kidney disease, obstructive sleep apnea, smoking status, peptic ulcer, diabetes, hypertension, hyperlipidemia, hypertension and diabetes, two or more comorbidities and NSAID use had an increased risk of CKD. Conclusion: Gender, history of acute kidney disease, obstructive sleep apnea, family history, smoking, diabetes, hypertension, peptic ulcer, hyperlipidemia, multi-comorbidity, and use of NSAIDs are all associated with an increased risk of CKD. The prevalence of CKD in this study is comparatively lower when compared to other regions in Saudi Arabia.

Impaired kidney function and the risk of all-cause mortality and cardiovascular disease among Chinese hypertensive adults: Using three different equations to estimate the glomerular filtration rate

ObjectivesWe aimed to seek accurate assessments of the glomerular filtration rate (GFR) in a Chinese hypertensive population to identify individuals at high risk for chronic kidney disease (CKD) progression. Then, the risk of cardiovascular disease (CVD) and all-cause death due to kidney injury were further investigated under appropriate GFR-estimation equations. MethodsIn this prospective follow-up cohort study of 10,171 hypertensive patients, we compared the discrimination power of a trio of GFR-estimation equations using Harrell's C-index, measuring the model fit by calculating the Akaike information criterion. Univariate and multivariable logistic regression analyses were respectively used to calculate the hazard ratio (HR) and 95% confidence interval [CI] values for CKD progression. In addition, we also assessed the risk of CVD and all-cause death with impaired renal function using multivariable-adjusted Cox regression models. ResultsThe Modification of Diet in Renal Disease (MDRD) equation showed the highest C-index range for the predicted probability of CKD progression in the fully adjusted model. During MDRD analysis, a low eGFR (60–89 mL/min/1.73m2 or < 60 mL/min/1.73m2) was an independent risk factor for CVD, especially stroke (1.28 [95% CI, 1.05–1.55] and 1.89 [95% CI, 1.08–3.31]), as well as all-cause mortality (1.28 [95% CI, 1.09–1.50] and 1.68 [95% CI, 1.01–2.78]). ConclusionsThe MDRD equation seems to be more suitable for screening CKD progression in Chinese hypertensive populations, targeting potential risk factors for effective prevention to reduce renal impairment so as to further limit CVD morbidity and mortality.

Uric acid level in Chronic Kidney Disease patients and its association with other established CKD risk factors

Introduction: Chronic Kidney Disease (CKD) is a rising global health concern with increased cardiovascular risks. Hyperuricemia, linked to CKD and related conditions, warrants investigation. Objectives: This study examines the uric acid in different stages of CKD and the association between uric acid levels and established CKD risk factors. Methodology: A hospital-based prospective cross-sectional study was conducted at Birat Medical College Teaching Hospital from 10 June 2023 to 30 August 2023. We enrolled 90 patients with non-dialytic chronic kidney disease (CKD) by complete enumeration sampling method. Ethical approval was obtained from the institutional review committee of the college. Written informed consent was obtained from each participant. Data was collected by means of a self developed questionnaire. Blood samples were obtained for estimation of serum creatinine and uric acid level and recorded in Microsoft excel sheet and analyzed by using SPSS software version 23. Results: Hyperuricemia was seen in 33(36.7%) ranging from 3.5-12 mg/dl with an average uric acid level of 6.38 mg/dl and a standard deviation of 1.43 mg/dl of total 90 patients. The mean serum uric acid level was highest in stage 2 CKD which includes 6.88±2.10 ranging from 4.3-12 mg/dl. CKD patients with a history of alcohol intake had increased risk of hyperuricemia and it was statistically significant (p value 0.005). Different stages of CKD (p value: 0.70), age groups, (p value 0.17), gender(P value 0.082), diabetes(p value 0.954), hypertension(p value 0.364), other CVDs(p value 0.649)and anemia(p value 0.0602)had no statistical significant association with hyperuricemia. Conclusion: In conclusion, hyperuricemia prevalence was observed in CKD patients, with the highest levels in stage 2 CKD. Notably, alcohol intake significantly correlated with hyperuricemia, while other studied factors did not show significant associations.