Chronic Kidney Disease Factors Research Articles

Causative Factors of Chronic Kidney Disease in Patiens with Hemodialysis Therapy

Chronic kidney disease (CKD) is a pathological process with various etiologies, causing decreased kidney function progressively and irreversibly. The prevalence of CKD in the last ten years has increased. Causative factors of CKD vary highly in each countries around the world. Hemodialysis is still the primary kidney therapy besides peritoneal dialysis and kidney transplantation. This study aims to discover the causative factors of chronic kidney disease in patients with hemodialysis therapy at the Medan Rasyida Kidney Specialty Hospital in 2019. The design of this research is a descriptive method, the respondents were 307 chronic kidney disease patients with hemodialysis therapy taken by total sampling. The most common factors causing chronic kidney disease in patients with hemodialysis therapy were hypertension (59.6%), diabetes mellitus (32.2%), obstructive nephropathy (2.6%), and gout nephropathy (2.3%), polycystic kidney (2.0%) and glomerulonephritis (1.3%). Hypertension is the most common cause of CKD in Medan Rasyida Kidney Hospital in 2019.

Air Pollution Alleviation During COVID-19 Pandemic is Associated with Renal Function Decline in Stage 5 CKD Patients.

IntroductionAir pollution is a novel environmental risk factor for chronic kidney disease (CKD). Air quality improved during COVID-19 lockdowns; however, the effects of these lockdowns on PM2.5 concentrations and renal function remain unclear.MethodsWe conducted a retrospective cohort study to compare air pollution and estimated glomerular filtration rate (eGFR) decline in patients with stage 5 CKD between a year-long period of lockdown (2020; n = 724) and a similar period before lockdown (2019, n = 758).ResultsCompared with 2019, a 17.5% reduction in the average PM2.5 concentration (from 17.36% to 14.32%; P < 0.001) and a 45.1% reduction (from 20.56% to 11.25%; P < 0.001) in cumulative days with PM2.5 concentration >35 μg/m3 were noted in 2020. Moreover, a 93% reduction in PM2.5 air quality index >150 per station-day (from 0.43% to 0.03%) was observed in 2020. From 2019 to 2020, the yearly incidence of eGFR decline ≥5 mL/min/1.73 m2 decreased by 33.7% (24.6% vs 16.3%; P < 0.001). Similarly, the proportion of patients who started undergoing regular dialysis also decreased by 32.7% in 2020 (from 20.8% to 14.0%; P = 0.001).ConclusionOur findings suggest that fewer events of renal function decline during the COVID-19 pandemic may be associated with a decline in PM2.5 concentrations, supporting the global strategy of reducing air pollution to prevent CKD progression.

Association between metabolic phenotype and urinary albumin‐creatinine ratio in Chinese community adults: A cross‐sectional study

BackgroundUrinary albumin‐creatinine ratio (UACR) is a sensitive marker of kidney injury. This study analyzed the prevalence of different metabolic phenotypes and investigated their relationship with UACR in Chinese community adults.MethodsThis study involved 33 303 participants over 40 years old from seven centers across China. They were stratified into six groups according to their body mass index (BMI) and metabolic status: metabolically healthy normal weight (MHNW), metabolically healthy overweight (MHOW), metabolically healthy obesity (MHO), metabolically unhealthy normal weight (MUNW), metabolically unhealthy overweight (MUOW), and metabolically unhealthy obesity (MUO). Increased albuminuria was defined as a UACR ≥30 mg/g.ResultsThe percentages of MHNW, MHOW, MHO, MUNW, MUOW, and MUO were 27.6%, 15.9%, 4.1%, 19.8%, 22.5%, and 9.6%, respectively. Multiple logistic regression analysis showed that the MHO group (odds ratio [OR] 1.205; 95% CI, 1.081‐1.343), MUNW group (OR 1.232; 95% CI, 1.021‐1.486), MUOW group (OR 1.447; 95% CI, 1.303‐1.607), and MUO group (OR 1.912; 95% CI, 1.680‐2.176) were at higher risk of increased albuminuria compared to the MHNW group. Subgroup analysis indicated that the risk of increased albuminuria was further elevated among regular smokers in men aged 40 to 55 years old with abdominal obesity.ConclusionsAmong Chinese community adults, increased albuminuria was associated with increased BMI whether metabolism was normal or not, and those with abnormal metabolism were at greater risk of increased albuminuria than those with normal metabolism. These findings suggest that overweight or obesity or metabolic abnormalities are risk factors for chronic kidney disease.

Quality of life in older patients with obesity and chronic kidney disease

Background and Aims : Obesity is a risk factor for chronic kidney disease (CKD). The aim of this study was to investigate quality of life and psychological status in older patients with СKD and obesity.

Impact of Hypertension on Chronic Kidney Disease Patients

Hypertension is a progressive cardiovascular syndrome arising from complex and interrelated etiologies, characterized by an increase in systolic blood pressure higher than or equal to 140 mmHg or diastolic blood pressure higher than or equal to 90 mmHg. Hypertension is one of the main risk factors for chronic kidney disease. This research aims to know the impact of hypertension on chronic kidney disease patients in UKI General Hospital from 2019 – to 2020. The design of this research was retrospective. The sample used was 58 patients following inclusion criteria. The instruments used are medical records of hypertension patients in UKI General Hospital from 2019 – to 2020. The results showed that 23 (39.7%) patients with hypertension were male, 35 (60.3%) patients with hypertension were female, and 15 (25.9%) patients with hypertension aged 46 – 55 years and 56 – 65 years. The chi-square correlation test results between hypertension and chronic kidney disease obtained p &gt; 0.05. It was concluded that in UKI General Hospital during 2019 – 2020, hypertension has no significant impact on chronic kidney disease.&#x0D; Keywords: Cardiovascular Syndrome, Chronic Kidney Disease, Hypertension

Chronic constant light exposure aggravates high fat diet-induced renal injury in rats.

Obesity-related kidney disease is now recognized as a global health issue, with a substantial number of patients developing progressive renal failure and end-stage renal disease. Interestingly, recent studies indicate light pollution is a novel environmental risk factor for chronic kidney disease. However, the impact of light pollution on obesity-related kidney disease remains largely unknown, with its underlying mechanism insufficiently explained. Renal hypoxia induced factor 1α (HIF1α) is critical in the development of glomerulosclerosis and renal fibrosis. The present study explored effects of constant light exposure on high fat diet (HFD) -induced renal injury and its association with HIF1α signal pathway. Thirty-two male Sprague Dawley rats were divided into four groups according to diet (HFD or normal chow diet) and light cycles (light/dark or constant light). After 16 weeks treatment, rats were sacrificed and pathophysiological assessments were performed. In normal chow fed rats, constant light exposure led to glucose abnormalities and dyslipidemia. In HFD fed rats, constant light exposure exacerbated obesity, glucose abnormalities, insulin resistance, dyslipidemia, renal functional decline, proteinuria, glomerulomegaly, renal inflammation and fibrosis. And, constant light exposure caused an increase in HIF1α and a decrease in prolyl hydroxylase domain 1 (PHD1) and PHD2 expression in kidneys of HFD-fed rats. Then, we demonstrated that BMAL1 bound directly to the promoters of PHD1 in mouse podocyte clone 5 cell line (MPC5) by ChIP assays. In conclusion, chronic constant light exposure aggravates HFD-induced renal injuries in rats, and it is associated with activation of HIF1α signal pathway.

The association between a body shape index and elevated urinary albumin-creatinine ratio in Chinese community adults.

BackgroundObesity, especially visceral obesity, seems to be one of the most decisive risk factors for chronic kidney disease. A Body Shape Index (ABSI) is an emerging body size measurement marker of visceral obesity. This study aimed to explore whether ABSI is associated with albuminuria in Chinese community adults.MethodsThis cross-sectional study enrolled 40,726 participants aged 40 or older from seven provinces across China through a cluster random sampling method. ABSI was calculated by body mass index, waist circumference, and height. Increased albuminuria was defined as urinary albumin–creatinine ratio (UACR) ≥ 30 mg/g, indicating kidney injury. For ABSI, we divided it by quartile cutoff points and tried to determine the association between ABSI levels and UACR by multiple regression analysis. DAG (Directed Acyclic Graph) was plotted using literature and expert consensus to identify potential confounding factors.ResultsThe average age of subjects with elevated UACR was 61.43 ± 10.07, and 26% were men. The average age of subjects with normal UACR was 57.70 ± 9.02, and 30.5% were men. Multiple logistic regression analysis was conducted and demonstrated that the ABSI quartiles were related to elevated UACR positively (OR [95% CI] Q2 vs. Q1: 1.094 [1.004, 1.197]; OR [95% CI] Q3 vs. Q1: 1.126 [1.030, 1.231]; OR [95% CI] Q4 vs. Q1: 1.183 [1.080, 1.295], p for trend < 0.001) after adjustments for confounding factors. The stratified analysis further showed that with the mounting for ABSI levels, elevated UACR more easily occurred in the people characterized by the elderly, men, and hypertension.ConclusionsIn Chinese community adults, people with higher ABSI levels can be deemed as high-risk individuals with UACR elevation, and it will be beneficial for them to lose weight and significantly reduce visceral fat.

Association of Variants of the NFE2L2 Gene with Metabolic and Kidney Function Parameters in Patients with Diabetes and/or Hypertension.

Background: Type 2 diabetes mellitus (T2DM) and high blood pressure (HBP) are the main risk factors for chronic kidney disease (CKD). Relationships between variants within the NFE2L2 gene and the presence of environmental risk factors for CKD, such as HBP and hyperglycemia have been suggested; however, their interactions remains unclear. Aim: To analyze the association of NFE2L2 variants with metabolic and kidney parameters. Materials and Methods: Six-hundred and fifty-one patients grouped according to the diagnosis of T2DM (n =166), T2DM+HBP (n =348) and HBP (n =137) were included. Metabolic characteristics were evaluated to identify risk factors and presence of CKD. Genotyping was performed by polymerase chain reaction (PCR) using two pairs primers for rs35652124 and rs6721961 and by real-time PCR for rs2364723. Logistic regression analyses, adjusted for confounding factors and correction for multiple tests were performed. Results: Significant associations between decreased risk for presenting with CKD and the rs35652124 (A allele) and the rs2364723 (G allele) variants were detected. Other variables consistently associated with these alleles were HBP, BMI, waist circumference, uric acid and triglycerides. Haplotypes AAC and GCG (loci order: rs35652124-rs6721961-rs2364723) showed similar trends. After adjustment for age and sex and correction for multiple tests, only rs35652124 (Odds Ratio [OR] = 0.5; Confidence Interval at 95% (CI95%), 0.3-0.9; p = 0.04) and rs2364723 (OR = 0.3; CI95%, 0.1-0.8; p = 0.009) variants remained associated with deceased risk for CKD in T2DM patients. Conclusion: This study showed for the first time that NFE2L2 variants are associated with decreased risk for CKD in the presence of environmental/metabolic risk factors related to kidney damage, including HBP, hyperuricemia and albuminuria in Mexican patients with diabetes.

Non-Renal Risk Factors for Chronic Kidney Disease in Liver Recipients with Functionally Intact Kidneys at 1 Month.

Chronic kidney disease (CKD) is a critical complication of liver transplants, of which non-renal risk factors are not fully understood yet. This study aimed to reveal pre- and post-transplant risk factors for CKD (<60 mL/min/1.73 m2), examining liver recipients with functionally intact kidneys one month after grafting using nationwide cohort data. Baseline risk factors were analyzed with multivariable Cox regression analyses and post-transplant risk factors were investigated with the time-dependent Cox model and matched analyses of time-conditional propensity scores. Of the 2274 recipients with a one-month eGFR ≥ 60 mL/min/1.73 m2, 494 (22.3%) developed CKD during a mean follow-up of 36.6 ± 14.4 months. Age, female sex, lower body mass index, pre-transplant diabetes mellitus, and lower performance status emerged as baseline risk factors for CKD. Time-dependent Cox analyses revealed that recurrent hepatocellular carcinoma (HR = 1.93, 95% CI 1.06–3.53) and infection (HR = 1.44, 95% CI 1.12–1.60) were significant post-transplant risk factors for CKD. Patients who experienced one of those factors showed a significantly higher risk of subsequent CKD compared with the matched controls who lacked these features (p = 0.013 for recurrent hepatocellular carcinoma, and p = 0.003 for infection, respectively). This study clarifies pre- and post-transplant non-renal risk factors, which lead to renal impairment after LT independently from patients’ renal functional reserve.

Asociación del polimorfismo rs5186 del gen AGTR1 con disminución de la TFGe en pacientes con diabetes tipo 2 de la Ciudad de México

BackgroundEarly biomarkers search for Diabetic Kidney Disease (DKD) in patients with Type 2 Diabetes Mellitus (T2DM), as genetic markers to identify vulnerable carriers of the disease even before Glomerular Filtration Rate (GFR) decline or microalbuminuria development, has been relevant during the last few years.The rs5186 (A116C) polymorphism of the Angiotensin II Receptor Type I gene (AGTR1), has been associated to multiple effects of renal injury risk, commonly detected in patients with Diabetes Mellitus (DM). It has been described that rs5186 could have an effect in stability proteins that assemble Angiotensin II Receptor Type I (AT1), modifying its action, which is why it should be considered as a risk factor for Chronic Kidney Disease (CKD), characterized by a GFR progressive reduction. Even though, the association between rs5186 AGTR1 gene polymorphism and DKD in patients with T2DM has been controversial, inconclusive, and even absent. This disputable issue might be as a result of association studies in which many and varied clinical phenotypes included are contemplated as CKD inductors and enhancers. Although, the sample sizes studied in patients with T2DM are undersized and did not have a strict inclusion criteria, lacking of biochemical markers or KDOQI classification, which have hindered its examination. ObjectiveThe aim of our study was to establish an association between rs5186 AGTR1 gene polymorphism and GFR depletion, assessed as a risk factor to DKD development in patients with T2DM. MethodsWe analyzed 297 not related patients with T2DM, divided into 221 controls (KDOQI 1) and 76 cases (KDOQI 2). Arterial pressure, anthropometric and biochemical parameters were measured. rs5186 of AGTR1 genotyping was performed by TaqMan assay real-time PCR method. Allele and genotype frequencies, and Hardy-Weinberg equilibrium were measured. Normality test for data distribution was analyzed by Shapiro-Wilk test, variable comparison by Student's t-test for continuous variables, and Chi-squared test for categorical variables; ANOVA test was used for mean comparison of more than two groups. Effect of rs5186 to DKD was estimated by multiple heritability adjustment models for risk variables of DKD. Statistical significance was indicated by p<0.05. Data was analyzed using Statistical Package STATA v11 software. ResultsDominant and Over-dominant models showed a likelihood ratio to GFR depletion of 1.89 (1.05-3.39, p = 0.031) and 2.01 (1.08-3.73, p = 0.023) in patients with T2DM. Risk factor increased to 2.54 (1.10-5.89) in women in Over-dominant model. ConclusiónIn clinical practice, most of nephropathies progress at a slow pace into a total breakdown of renal function, even asymptomatic. This is the first study, reporting that rs5186 polymorphism of AGTR1 gene contribution to GFR depletion, and this could be evaluated as a predisposing factor for DKD in patients with T2DM.

Urate Transporter ABCG2 Function and Asymptomatic Hyperuricemia: A Retrospective Cohort Study of CKD Progression

Treatment of asymptomatic hyperuricemia is not commonly implemented. However, it is unclear whether urate deposition that begins during asymptomatic hyperuricemia can induce nephropathy. Dysfunction of ATP-binding cassette subfamily G member 2 (ABCG2), a urate efflux transporter, leads to elevated serum uric acid concentration (SUA). We investigated the association between asymptomatic hyperuricemia and decreased estimated glomerular filtration rate (eGFR), and the impact of ABCG2 on this relationship. Retrospective cohort study. 1,885 Japanese adults undergoing routine health care follow-up between 2007 and 2017 who had eGFR≥60 mL/min/1.73 m2, of which 311 had asymptomatic hyperuricemia (SUA >7.0 mg/dL). Study participants were classified into 3 categories of estimated ABCG2 function (full, 75%, and≤50% function). Baseline SUA and estimated ABCG2 function. Change in eGFR over time. Linear mixed-effect models were used to analyze the relationship between asymptomatic hyperuricemia, ABCG2 function, and eGFR decline. Asymptomatic hyperuricemia was negligibly associated with eGFR decline overall. However, among those with eGFR 60-89 mL/min/1.73 m2 and≤50% ABCG2 function, eGFR decline was associated with asymptomatic hyperuricemia (P= 0.03). ABCG2 was not associated with eGFR reductions when the SUA was<6.0 mg/dL. Among participants with SUA≥6.0 mg/dL and eGFR 60-89 mL/min/1.73 m2,≤50% ABCG2 function was associated with approximately 1.2-fold faster eGFR decline compared with fully functional ABCG2 (P= 0.02). Among the participants with SUA≥6.0 mg/dL and eGFR 60-89 mL/min/1.73 m2, the adjusted eGFR slopes (given as mean ± standard error of the mean, in mL/min/1.73 m2 per year) were-0.946 ± 0.049,-1.040 ± 0.046, and-1.148 ± 0.069 for full, 75%, and≤50% ABCG2 function, respectively. Lack of measurement of urinary urate and uremic toxins that are known to be transported by ABCG2, and no independent validation cohort. Asymptomatic hyperuricemia was not associated with eGFR decline, except when in the presence of≤50% ABCG2 function. The urate transporter ABCG2 is a protein that regulates serum urate concentrations; when dysfunctional, it can lead to elevated serum concentrations of this compound (ie, hyperuricemia). Although persistent hyperuricemia induces gout and kidney injury, the effects on organs during the asymptomatic phase have yet to be established. Therefore, to clarify the relationship between ABCG2, asymptomatic hyperuricemia, and kidney function, we conducted a retrospective cohort study of 1,885 healthy participants, including 311 participants with asymptomatic hyperuricemia. We found that the coexistence of asymptomatic hyperuricemia and severe ABCG2 dysfunction was associated with the age-dependent decline in kidney function. We concluded that asymptomatic hyperuricemia represents a risk factor for chronic kidney disease, at least in individuals with highly dysfunctional ABCG2. This new finding highlights the potential importance of ABCG2 in the pathogenesis of hyperuricemia-induced kidney injury.

Super-Resolution Ultrasound Imaging Provides Quantification of the Renal Cortical and Medullary Vasculature in Obese Zucker Rats: A Pilot Study.

Obesity is a risk factor of chronic kidney disease (CKD), leading to alterations in the renal vascular structure. This study tested if renal vascular density and tortuosity was quantifiable in vivo in obese rats using microbubble-based super-resolution ultrasound imaging. The kidneys of two 11-week-old and two 20-week-old male obese Zucker rats were compared with age-matched male lean Zucker rats. The super-resolution ultrasound images were manually divided into inner medulla, outer medulla, and cortex, and each area was subdivided into arteries and veins. We quantified vascular density and tortuosity, number of detected microbubbles, and generated tracks. For comparison, we assessed glomerular filtration rate, albumin/creatinine ratio, and renal histology to evaluate CKD. The number of detected microbubbles and generated tracks varied between animals and significantly affected quantification of vessel density. In areas with a comparable number of tracks, density increased in the obese animals, concomitant with a decrease in glomerular filtration rate and an increase in albumin/creatinine ratio, but without any pathology in the histological staining. The results indicate that super-resolution ultrasound imaging can be used to quantify structural alterations in the renal vasculature. Techniques to generate more comparable number of microbubble tracks and confirmation of the findings in larger-scale studies are needed.

The Dutch Childhood Cancer Survivor Study (DCCSS)-LATER 2 kidney analysis examined long-term glomerular dysfunction in childhood cancer survivors

This investigation aimed to evaluate glomerular dysfunction among childhood cancer survivors in comparison with matched controls from the general population. In the Dutch Childhood Cancer Survivor Study (DCCSS)-LATER 2 kidney analysis, a nationwide cross-sectional cohort study, 1024 survivors five or more years after diagnosis, aged 18 or more years at study, treated between 1963-2001 with nephrectomy, abdominal radiotherapy, total body irradiation, cisplatin, carboplatin, ifosfamide, high-dose cyclophosphamide or hematopoietic stem cell transplantation participated. In addition, 500 age- and sex-matched controls from Lifelines, a prospective population-based cohort study in the Netherlands, participated. At a median age of 32.0 years (interquartile range 26.6-37.4), the glomerular filtration rate was under 60 ml/min/1.73m2 in 3.7% of survivors and in none of the controls. Ten survivors had kidney failure. Chronic kidney disease according to age-thresholds (glomerular filtration rate respectively under 75 for age under 40, under 60 for ages 40-65, and under 40 for age over 65) was 6.6% in survivors vs. 0.2% in controls. Albuminuria (albumin-to-creatinine ratio over3 mg/mmol) was found in 16.2% of survivors and 1.2% of controls. Risk factors for chronic kidney disease, based on multivariable analyses, were nephrectomy (odds ratio 3.7 (95% Confidence interval 2.1-6.4)), abdominal radiotherapy (1.8 (1.1-2.9)), ifosfamide (2.9 (1.9-4.4)) and cisplatin over 500 mg/m2 (7.2 (3.4-15.2)). For albuminuria, risk factors were total body irradiation (2.3 (1.2-4.4)), abdominal radiotherapy over 30 Gy (2.6 (1.4- 5.0)) and ifosfamide (1.6 (1.0-2.4)). Hypertension and follow-up 30 or more years increased the risk for glomerular dysfunction. Thus, lifetime monitoring of glomerular function in survivors exposed to these identified high risk factors is warranted.

Activation of PAR2 promotes high-fat diet-induced renal injury by inducing oxidative stress and inflammation

A high-fat diet (HFD) is a major risk factor for chronic kidney disease. Although HFD promotes renal injury, characterized by increased inflammation and oxidative stress leading to fibrosis, the underlying mechanism remains elusive. Here, we investigated the role and mechanism of protease-activating receptor 2 (PAR2) activation during HFD-induced renal injury in C57/BL6 mice. HFD for 16 weeks resulted in kidney injury, manifested by increased blood levels of blood urea nitrogen, increased levels of oxidative stress with inflammation, and structural changes in the kidney tubules. HFD-fed kidneys showed elevated PAR2 expression level in the tubular epithelial region. To elucidate the role of PAR2, PAR2 knockout mice and their littermates were administered HFD. PAR2 deficient kidneys showed reduced extent of renal injury. PAR2 deficient kidneys showed significantly decreased levels of inflammatory gene expression and macrophage infiltration, followed by reduced accumulation of extracellular matrix proteins. Using NRK52E kidney epithelial cells, we further elucidated the mechanism and role of PAR2 activation during renal injury. Palmitate treatment increased PAR2 expression level in NRK52E cells and scavenging of oxidative stress blocked PAR2 expression. Under palmitate-treated conditions, PAR2 agonist-induced NF-κB activation level was higher with increased chemokine expression level in the cells. These changes were attenuated by the depletion of oxidative stress. Taken together, our results suggest that HFD-induced PAR2 activation is associated with increased levels of renal oxidative stress, inflammatory response, and fibrosis.

Metabolic Syndrome-Related Kidney Injury: A Review and Update.

Metabolic syndrome (MetS) includes visceral obesity, hyperglycemia, dyslipidemia, and hypertension. The prevalence of MetS is 20-25%, which is an important risk factor for chronic kidney disease (CKD). MetS causes effects on renal pathophysiology, including glomerular hyperfiltration, RAAS, microalbuminuria, profibrotic factors and podocyte injury. This review compares several criteria of MetS and analyzes their differences. MetS and the pathogenesis of CKD includes insulin resistance, obesity, dyslipidemia, inflammation, oxidative stress, and endothelial dysfunction. The intervention of MetS-related renal damage is the focus of this article and includes controlling body weight, hypertension, hyperglycemia, and hyperlipidemia, requiring all components to meet the criteria. In addition, interventions such as endoplasmic reticulum stress, oxidative stress, gut microbiota, body metabolism, appetite inhibition, podocyte apoptosis, and mesenchymal stem cells are reviewed.

Hyperuricemia—a serious complication among patients with chronic kidney disease: a systematic review and meta-analysis

Aim: Hyperuricemia as a putative risk factor for chronic kidney disease (CKD) progression remains controversial and debatable. This systematic review aims to explore the prevalence of hyperuricemia among CKD patients worldwide. Methods: This study was conducted in accordance with the Meta-analysis Of Observational Studies in Epidemiology (MOOSE) guidelines by using the existing literature from online databases such as MEDLINE/PubMed, ScienceDirect, Google Scholar, Cochrane library and grey literature. The effect size with corresponding 95% confidence interval (CI) was calculated to assess the pooled prevalence of hyperuricemia in chronic kidney patients. The subgroup analysis based on gender and geography was also carried out by utilizing comprehensive meta-analysis, version 2.0. Results: Twenty-three studies containing 212,740 participants were eligible for quantitative synthesis. The pooled prevalence of 43.6% (35.2–52.4%) hyperuricemia was reported in patients with CKD globally. In India, 38.4% of prevalence was observed. The gender specific prevalence (9 studies) was reported as 67.4% (60.9–73.3%) in case of male patients and 32.6% (26.7–39.1%) in female patients with 95% CI. Conclusions: The prevalence of hyperuricemia was reported to be reasonably high among CKD patients worldwide. During the management of CKD, this high prevalence demands more prudent attention for this clinical complication which possibly can lead to positive renal outcomes.

Metabolisches Syndrom und Adipositas bei Nierentransplantation

BackgroundObesity and the metabolic syndrome (MS) are risk factors for chronic kidney disease (CKD) and are associated with challenges before, during and after kidney transplantation.ObjectiveThe significance of obesity and the MS in CKD and recommendations for the management at various stages of kidney transplantation.Material and methodsSearch of the literature and screening of selected guidelines on kidney transplantation.ResultsAlthough the negative impact of obesity and MS on the outcome of kidney transplantation is well known, there are few specific recommendations in the current guidelines. The lack of comparative studies and meta-analyses on the best risk stratification of obesity in the context of CKD as well as the inconsistent definition of the MS, complicate the ability to draw conclusions.ConclusionThe body mass index (BMI) serves as a measure of obesity in all guidelines, although its validity is controversial. The standardized collation of measures of central obesity, weight reduction through multidisciplinary programs and accurate screening of obesity-associated cardiovascular risk factors before transplantation appear to be meaningful. Consideration of bariatric interventions is recommended only on a case by case basis and with a careful risk-benefit analysis. The effects of immunosuppressive agents on absorption should particularly be considered.

In-center Nocturnal Hemodialysis Reduced the Circulating FGF23, Left Ventricular Hypertrophy, and All-Cause Mortality: A Retrospective Cohort Study.

Fibroblast growth factor 23(FGF23) is the most important biomarker and pathogenic factor in Chronic Kidney Disease–Mineral and Bone Disorder (CKD–MBD). In the moderate and severe stages of chronic renal failure, abnormally elevated circulating FGF23 can lead to some complications, including myocardial hypertrophy, which is positively correlated with all-cause mortality. However, the circulating FGF23 level of different hemodialysis modalities, the underlying essential regulatory factors, and potential clinical benefits remain to be elucidated. In this retrospective cohort study, 90 in-center nocturnal hemodialysis (INHD) and 90 matched conventional hemodialysis (CHD) patients were enrolled. The complete blood count, intact FGF23(iFGF23), calcium, phosphorus, PTH, and other biochemical and echocardiographic parameters of INHD and CHD patients were collected and analyzed at 1-year follow-up. The all-cause mortality was recorded during the 7-year follow-up. Furthermore, the regulatory factors of iFGF23 and its association with echocardiographic parameters and mortality were investigated by multivariate regression. The levels of iFGF23 and serum phosphate in patients undergoing INHD were significantly lower than those in patients undergoing CHD. The left ventricular volume index (LVMI) in patients with INHD was significantly attenuated and positively correlated with the drop of serum iFGF23. The INHD group had reduced all-cause mortality compared to the CHD group. Multivariate analysis showed that iFGF23 was positively correlated with serum calcium, serum phosphorus, and calcium-phosphate product. The calcium-phosphate product is an independent determining factor of serum iFGF23. Compared with the CHD group, the INHD group presented with a significantly reduced circulating iFGF23 level, which was closely associated with attenuation of left ventricular hypertrophy, but INHD reduced all-cause mortality in an FGF23 independent manner.

Sex-specific association between coffee consumption and incident chronic kidney disease: a population-based analysis of 359,906 participants from the UK Biobank.

Background:The risk for chronic kidney disease (CKD) is influenced by genetic predisposition, sex, and lifestyle. Previous research indicates that coffee is a potentially protective factor in CKD. The current study aims to investigate whether sex disparity exists in the coffee–CKD association, and whether genetic risk of CKD or genetic polymorphisms of caffeine metabolism affect this association.Methods:A total of 359,906 participants from the UK Biobank who were enrolled between 2006 and 2010 were included in this prospective cohort study, which aimed to estimate the hazard ratios for coffee intake and incident CKD using a Cox proportional hazard model. Allele scores of CKD and caffeine metabolism were additionally adjusted for in a subsample with qualified genetic data (n = 255,343). Analyses stratified by genetic predisposition, comorbidities, and sex hormones were performed. Tests based on Bayesian model averaging were conducted to ascertain the robustness of the results.Results:Coffee was inversely associated with CKD in a dose-dependent manner. The effects of coffee did not differ across different strata of genetic risk for CKD, but were more evident among slower genetically predicted caffeine metabolizers. Significant sex disparity was observed (P value for interaction = 0.013), in that coffee drinking was only associated with the risk reduction of CKD in females. Subgroup analysis revealed that testosterone and sex hormone-binding globulin (SHBG), but not estradiol, modified the coffee–CKD association.Conclusions:In addition to the overall inverse coffee–CKD association that was observed in the general population, we could also establish that a sex disparity existed, in that females were more likely to experience the benefit of the association. Testosterone and SHBG may partly account for the sex disparity.

The Effect of Mild Renal Dysfunction on the Assessment of Plasma Amino Acid Concentration and Insulin Resistance in Patients with Type 2 Diabetes Mellitus.

Background An increase in the levels of branched-chain amino acids (BCAAs) and certain aromatic amino acids, such as alanine, in plasma is correlated with insulin resistance (IR) in type 2 diabetes mellitus (T2DM). T2DM is a leading risk factor for chronic kidney disease. Meanwhile, renal dysfunction causes changes in plasma amino acid levels. To date, no study has examined how mild renal dysfunction and IR interact with plasma amino acid levels. This study examines the effects of IR and renal dysfunction on plasma amino acid concentrations in T2DM. Methods Data were collected from healthy male participants (controls) and male patients with T2DM between May 2018 and February 2022. Blood samples were collected after overnight fasting. IR and renal function were evaluated using the homeostasis model assessment of IR (HOMA-IR) and serum cystatin C (CysC), respectively. Results A total of 49 and 93 participants were included in the control and T2DM groups, respectively. In the T2DM group, eight amino acids (alanine, glutamic acid, glutamine, glycine, isoleucine, leucine, tyrosine, and valine) and total BCAA showed a significant correlation with HOMA-IR (p < 0.01), whereas six amino acids (γ-aminobutyric acid, citrulline, cysteine, glycine, methionine, and valine) and total BCAA showed a significant correlation with 1/CysC (p < 0.02). However, only alanine, glutamic acid, and each BCAA showed significant differences between the control group and the IR T2DM subgroup. Increases in the BCAA levels with T2DM were canceled by renal dysfunction (CysC ≥ 0.93) in patients with intermediate IR. Conclusion To use plasma BCAA concentration as a marker of IR, renal function must be considered, even in mild renal dysfunction. Increased alanine and glutamic acid levels indicate IR, regardless of mild renal dysfunction.