Risk Of Developing Chronic Kidney Disease Research Articles

#2025 Associations of obesity, sarcopenia, and sarcopenic obesity with chronic kidney disease development in the elderly population

Abstract Background and Aims Previous studies indicate that sarcopenia and obesity increase the risk of chronic kidney disease (CKD) in middle-aged populations. Despite noting reverse epidemiology for cardiovascular disease in the elderly, the relationship between sarcopenic obesity and CKD incidence in older populations is insufficiently explored. This study aims to assess whether obesity modifies the association between sarcopenia and CKD development in elderly adults with preserved kidney function. Method Elderly individuals aged over 65 with preserved kidney function among UK Biobank participants were examined. Participants with an estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m² or albuminuria were excluded. The individuals were categorized based on the presence of sarcopenia and obesity, with sarcopenia defined as hand grip strength <27 kg in males and <16 kg in females. Obesity was defined as having a BMI of 30 kg/m² or higher, and sarcopenic obesity was identified in those with concomitant obesity and sarcopenia. The development of CKD was determined using ICD-10 codes in claim and death register records. Results A total of 62,735 individuals were assessed, with a mean age of 66.9 ± 1.5 years and 44.3% being male. Sarcopenia was identified in 8,648 individuals (13.8%), while obesity was present in 13,075 individuals (20.8%), resulting in a 3.29% prevalence of sarcopenic obesity. Over a median follow-up of 13.3 years (770,179 person-years), 5,567 participants (8.9%) developed CKD. A significant interaction between sarcopenia and obesity was observed for CKD development (P < 0.001). Incident CKD rates were 7.8% in non-obese without sarcopenia, 9.5% in obese without sarcopenia, 11.7% in non-obese with sarcopenia, and 14.7% in obese with sarcopenia. Compared to the non-obese without sarcopenia group, hazard ratios (HRs) and 95% confidence intervals (CIs) were 1.26 (1.16-1.37) in the obese without sarcopenia group, 1.55 (1.45-1.65) in the non-obese with sarcopenia group, and 2.02 (1.80-2.27) in the obese with sarcopenia group. After adjusting for confounding factors, the risk of CKD development in the obese without sarcopenia group was comparable to the non-obese without sarcopenia group (HR, 1.07, 95% CI, 0.99-1.15). However, elevated risk persisted in participants with sarcopenia and was most accentuated in those with sarcopenic obesity (non-obese with sarcopenia; HR, 95% CI, 1.22 [1.11-1.34]; obese with sarcopenia, 1.32 [1.15-1.50]). Conclusion Sarcopenia, not obesity, was significantly associated with an increased risk of chronic kidney disease (CKD) development in elderly individuals, with sarcopenic obesity showing the highest risk elevation for incident CKD in this group.

Association between familial aggregation of chronic kidney disease and its incidence and progression

This study aimed to examine the association between familial aggregation of chronic kidney disease (CKD) and risk of CKD development and its progression. This nationwide family study comprised 881,453 cases with newly diagnosed CKD between 2004 and 2017 and 881,453 controls without CKD matched by age and sex, using data from the Korean National Health Insurance Service with linkage to the family tree database. The risks of CKD development and disease progression, defined as an incident end-stage renal disease (ESRD), were evaluated. The presence of any affected family member with CKD was associated with a significantly higher risk of CKD with adjusted ORs (95% CI) of 1.42 (1.38–1.45), 1.50 (1.46–1.55), 1.70 (1.64–1.77), and 1.30 (1.27–1.33) for individuals with affected parents, offspring, siblings, and spouses, respectively. In Cox models conducted on patients with predialysis CKD, risk of incident ESRD was significantly higher in those with affected family members with ESRD. The corresponding HRs (95% CI) were 1.10 (1.05–1.15), 1.38 (1.32–1.46), 1.57 (1.49–1.65), and 1.14 (1.08–1.19) for individuals listed above, respectively. Familial aggregation of CKD was strongly associated with a higher risk of CKD development and disease progression to ESRD.

MO301: The Incremental Chronic Kidney Disease Risk Among Post-Hospitalized Leptospirosis Patients With Acute Kidney Injury: Systematic Review And Meta-Analysis

Abstract BACKGROUND AND AIMS Leptospirosis is a global zoonotic bacterial disease that may cause life-threatening complications, such as acute kidney injury (AKI). Patients with AKI may recover fully, but some can progress to chronic kidney disease (CKD) or even become dialysis-dependent. This study aims to evaluate the CKD and dialysis-dependent incidences and risks among post-hospitalized leptospirosis patients with AKI. METHOD Comprehensive searching was performed through the online databases of Pubmed, EMBASE, ScienceDirect and The Cochrane Library to include all relevant literature from 2000 to 2021. This study followed the PRISMA guidelines. The inclusion criteria are all observational studies that assess the incidence and risk for CKD development and dialysis dependence among post-hospitalized leptospirosis-associated AKI patients. The quality of included studies was accessed by using the Newcastle–Ottawa Scale. Analysis was conducted to obtain the pooled odds ratio (OR) with a 95% confidence interval (CI) with a fixed-effect heterogeneity test. RESULTS Five observational studies met the inclusion criteria. About 7%–14% of post-hospitalized leptospirosis patients with AKI deteriorate significantly to become CKD risk (pooled OR = 1.78, 95% confidence interval 1.41–2.23; P < .0001, I2 = 0%). A population cohort study suggested that Leptospira-seropositive population is correlated with the eGFR decline, even in the non-diabetic subgroup. Multivariate analysis from a cohort study showed that the elderly patients were predictors of dialysis-dependency and mortality. The funnel plot is symmetrical suggesting no publication bias. CONCLUSION Post-hospitalized leptospirosis with AKI patients has an incremental CKD risk. However, further studies are warranted to confirm the association and causality.

Epidemiological and Metabolic Aspects and Risk Factors of Chronic Kidney Disease in Comorbid Pathology of Type 2 Diabetes Mellitus and Primary Hypothyroidism

INTRODUCTION: The increasing number of patients with diabetes mellitus (DM) and chronic kidney disease (CKD) is one of the most pressing problems of modern medicine. In comorbid pathology a combination of type 2 DM and thyroid hypofunction the negative effect of hypothyroidism on carbohydrate metabolism, lipid metabolism, endothelial function, and glomerular filtration rate (GFR) is a risk factor for the formation and progression of diabetic nephropathy and CKD and requires further study.
 AIM: To identify risk factors and epidemiological peculiarities of CKD in type 2 DM in combination with thyroid hypofunction and to determine the possibility of using cystatin C levels for the evaluation of the kidney function in this pathology.
 MATERIALS AND METHODS: The prospective study involved 203 patients with type 2 DM undergoing inpatient treatment in the endocrinology department of the Ryazan Regional Clinical Hospital: group 1 (n = 76), type 2 DM combined with the primary hypothyroidism, and group 2 (n = 127), type 2 DM without thyroid pathology. Carbohydrate, lipid metabolism, albuminuria (AU), thyroid hormone spectrum, adipokines (leptin, plasminogen activator inhibitor-1, interleukin-6, and tumor necrosis factor-) were analyzed. The GFR was calculated using the CKD-EPI formula based on the levels of creatinine and cystatin C. Arterial pressure daily monitoring (APDM) was conducted, and intra-abdominal fat thickness was evaluated by ultrasonography.
 RESULTS: The incidence of kidney pathology in patients with type 2 DM was 52.22%. In group 1, there was a significant increase in the prevalence of CKD (64.47%, p = 0.006) and of normoalbuminuric CKD (NAU-CKD, 32.89%; p = 0.010). The risk of CKD development in patients with concomitant PH was more than twice that in patients without thyroid pathology with an odds ratio of 2.229 (95% confidence interval (CI) 1.2414.003) and that for NAU-CKD was 2.474 (95% CI 1.2674.833). Significant impairment of several metabolic parameters and individual APDM parameters was revealed in group 1 in comparison with group 2. The dependence of AU and GFR on the body mass index and of AU on the intra-abdominal fat thickness was noted. A negative relationship between GFR and leptin was revealed; in group 1, a correlation of interleukin-6 and thyrotropic hormone was found (r = 0.809, p = 0.001). With concomitant PH, cystatin C values were lower, and the GFR (CKD-EPI-cys) was reliably higher.
 CONCLUSION: Hypothyroidism is a risk factor for CKD development including NAU-CKD in type 2 DM. Obesity and hormonal activities of the intra-abdominal fatty tissue facilitate AU progression and GFR reduction. The use of cystatin C as a marker of the filtration function of the kidney in patients with hypothyroidism may lead to the underestimation of kidney function; thus, further investigation is required.

Renal Outcomes of Dialysis-Dependent Acute Kidney Injury in Noncritically Ill Patients: A Retrospective Study

Introduction: Acute kidney injury (AKI) is a common complication among hospitalized patients, potentially affecting short- and long-term clinical outcomes. In this retrospective study, we evaluated renal outcomes in noncritically ill patients who required acute hemodialysis (HD) because of an AKI episode occurring during hospitalization. Methods: Sixty-three hemodynamically stable patients with AKI undergoing acute intermittent HD were included. Kidney function was evaluated at baseline control (pre-AKI), at AKI diagnosis and during the follow-up. According to serum creatinine and the estimated glomerular filtration rate (eGFR), we defined three clinical conditions: renal recovery, different stages of acute kidney disease (AKD), and chronic kidney disease (CKD). Results: Among the 63 patients evaluated, 34 patients (54%) had a history of CKD. Six patients (10%) presented early full renal recovery. HD treatment was stopped in 38 patients (60%), while 25 patients (40%) required maintenance HD. Dialysis-independent patients presented lower comorbidity and higher baseline eGFR and delta creatinine, compared to dialysis-dependent patients. Baseline CKD, previous AKI episodes, and parenchymal causes of AKI were associated with a significant risk of dialysis dependence. At 1-month control, 15 patients (39%) presented AKD stage 0, 6 patients (16%) AKD stage 1, and 17 patients (44%) AKD stage 2–3. At 3-month control, 29 out of 38 patients recovering from AKI (76%) presented CKD. AKD stage was significantly correlated with the risk of CKD development, which, resulted higher in patients with lower baseline eGFR. Conclusions: AKI might represent a risk factor for the development of chronic kidney damage, even in noncritically ill patients.

Review on Inflammation Markers in Chronic Kidney Disease.

Chronic kidney disease (CKD) is one of the major health problems of the modern age. It represents an important public health challenge with an ever-lasting rising prevalence, which reached almost 700 million by the year 2017. Therefore, it is very important to identify patients at risk for CKD development and discover risk factors that cause the progression of the disease. Several studies have tackled this conundrum in recent years, novel markers have been identified, and new insights into the pathogenesis of CKD have been gained. This review summarizes the evidence on markers of inflammation and their role in the development and progression of CKD. It will focus primarily on cytokines, chemokines, and cell adhesion molecules. Nevertheless, further large, multicenter studies are needed to establish the role of these markers and confirm possible treatment options in everyday clinical practice.

Inhibition of microbiota-dependent TMAO production attenuates chronic kidney disease in mice

Patients with chronic kidney disease (CKD) have elevated circulating levels of trimethylamine N-oxide (TMAO), a metabolite derived from gut microbes and associated with cardiovascular diseases. High circulating levels of TMAO and its dietary precursor, choline, predict increased risk for development of CKD in apparently healthy subjects, and studies in mice fed TMAO or choline suggest that TMAO can contribute to kidney impairment and renal fibrosis. Here we examined the interactions between TMAO, kidney disease, and cardiovascular disease in mouse models. We observed that while female hyperlipidemic apoE KO mice fed a 0.2% adenine diet for 14 weeks developed CKD with elevated plasma levels of TMAO, provision of a non-lethal inhibitor of gut microbial trimethylamine (TMA) production, iodomethylcholine (IMC), significantly reduced multiple markers of renal injury (plasma creatinine, cystatin C, FGF23, and TMAO), reduced histopathologic evidence of fibrosis, and markedly attenuated development of microalbuminuria. In addition, while the adenine-induced CKD model significantly increased heart weight, a surrogate marker for myocardial hypertrophy, this was largely prevented by IMC supplementation. Surprisingly, adenine feeding did not increase atherosclerosis and significantly decreased the expression of inflammatory genes in the aorta compared to the control groups, effects unrelated to TMAO levels. Our data demonstrate that inhibition of TMAO production attenuated CKD development and cardiac hypertrophy in mice, suggesting that TMAO reduction may be a novel strategy in treating CKD and its cardiovascular disease complications.

Značaj polimorfizama regulatornih i katalitičkih antioksidativnih proteina u hroničnoj bubrežnoj slabosti

Both excessive production of reactive oxygen species (ROS) and impaired antioxidant function are found in patients with chronic kidney disease (CKD). Therefore, individual susceptibility towards CKD can be induced by functional variations of genes encoding antioxidant regulatory (nuclear factor erythroid 2 - related factor 2 (Nrf2)) and catalytic (superoxide dismutase (SOD2) and glutathione peroxidase (GPX1)) proteins. Several types of single nucleotide polymorphisms (SNPs) have been found within the genes encoding these proteins, with Nrf2 (-617C/A), SOD2 (Ala16Val) and GPX1 (Pro198Leu) conferring impaired catalytic activity. The most unexplored gene polymorphism in CKD susceptibility, progression and survival, with only two original studies published, is the Nrf2 (-617C/A) polymorphism. The results of these studies showed that there was no individual impact of this polymorphism on the susceptibility towards end stage renal disease (ESRD) development, oxidative phenotype and mortality. However, Nrf2 had a significant role in ESRD risk and survival, when combined with other antioxidant genes. The results regarding the impact of SOD2 (Ala16Val) and GPX1 (Pro198Leu) polymorphisms on either CKD or ESRD are still inconclusive. Namely, some studies showed that patients having variant SOD2 (Val) or GPX1 (Leu) allele were at increased risk of CKD development and progression, while other studies reported only weak or no association between these polymorphisms and CKD. Surprisingly, the only study that reported an association of GPX1 polymorphism with overall/cardiovascular survival in ESRD patients showed a significant impact of low activity GPX1 (Leu/Leu) genotype on better survival. In this review, we comprehensively and critically appraise the literature on these polymorphisms related to oxidative stress in CKD patients, in order to identify gaps and provide recommendations for further clinical research and translation. New developments in the field of antioxidant polymorphisms in CKD patients could lead to better stratification of CKD patients, based on a prognostic antioxidant gene panel, and provide a more personalised medicine approach for the need of antioxidant therapy in these patients.

Association of Reproductive Lifespan Duration and Chronic Kidney Disease in Postmenopausal Women

ObjectiveTo investigate the relationship between endogenous estrogen exposure and renal function, the association of female reproductive life span duration (RLD) and chronic kidney disease (CKD) was analyzed in postmenopausal women. Patients and MethodsData were retrieved from the Korean Genome and Epidemiology Study, which was constructed from May 1, 2001, through December 25, 2017. A total of 50,338 and 3155 postmenopausal women were each included in the cross-sectional and longitudinal analyses. The RLD was determined by subtracting the age at menarche from the age at menopause. Participants were grouped into RLD quartiles. Participants with estimated glomerular filtration rates less than 60 mL/min/1.73 m2 were regarded to have CKD. ResultsIn the cross-sectional analysis, mean ± SD age and estimated glomerular filtration rate were 56.3±4.9 years and 93.1±13.6 mL/min/1.73 m2, respectively. Mean ± SD RLD was 34.2±4.0 years. A total of 765 of 50,338 (1.52%) women were found to have CKD. Logistic regression analysis revealed that the odds ratio for CKD was lower in groups with longer RLDs as compared with the shortest RLD group. In longitudinal analysis, postmenopausal women with normal kidney function were followed up for 9.7 years and incident CKD occurred in 221 of 3155 (7.00%) participants. Cox analysis revealed that the risk for CKD development was significantly lower in longer RLD groups. This finding was significant even after adjustments for confounding factors. ConclusionThe risk for CKD was lower in women with longer RLDs. The amount of endogenous estrogen exposure could be a determining factor for renal function in postmenopausal women.

Physical performance and chronic kidney disease development in elderly adults: results from a nationwide cohort study.

Sarcopenia, which is characterized by muscle mass and physical performance, is closely associated with morbidities and mortality, especially among the elderly. However, the effect of physical performance on chronic kidney disease (CKD) development is not yet fully elucidated. A total of 30,871 adults aged 66 years with preserved renal function who underwent health screening examinations were evaluated. Physical performance was assessed using a 3-m timed up and go (TUG) test and the one-leg stand (OLS) test. The primary outcome was the development of CKD, defined as at least two consecutive measurements of estimated glomerular filtration rate < 60 mL/min/1.73 m2. The rates of mortality and incident CKD development were significantly elevated with increases in TUG test scores but not in OLS scores. In the Cox hazards model, the highest TUG test score tertile was associated with an increased risk for CKD development (hazard ratio, 1.23; 95% confidence interval, 1.10-1.38) compared with the lowest tertile. No significant relationship was observed between OLS score and incident CKD risk. Poor physical performance, assessed using the TUG test, was related to an increased risk of CKD development.

Dietary zinc intake and incident chronic kidney disease

Previous studies have shown that dietary zinc intake is closely related to cardiovascular complications and metabolic derangements. However, the effect of dietary zinc intake on renal function is not fully elucidated. Data from the Korean Genome and Epidemiology Study were used. Dietary zinc intake was assessed by a Food Frequency Questionnaire and dietary zinc density was calculated as absolute zinc intake amount per daily energy intake (mg/1000kcal day). The participants were categorized into quartiles according to dietary zinc density. The primary end point was incident chronic kidney disease (CKD), defined as estimated glomerular filtration rate (eGFR)<60ml/min/1.73m2. A total of 7735 participants with normal renal function was included in the final analysis. The mean age was 52.0±8.8 years, 47.5% were male, and mean eGFR was 92.1±16.1ml/min/1.73m2. The mean daily zinc intake and zinc intake density were 8.6±3.4mg and 4.4±0.9mg/1000kcal, respectively. During a median follow up of 11.5 (1.7-12.5) years and 70,617 person-years of observation, CKD developed in 1409 (18.2%) participants. Multivariable cox hazard analysis revealed that risk for CKD development was significantly higher in the quartile with a mean zinc intake density of 3.6±0.2mg/1000kcal compared with the quartile with a mean zinc intake density of 5.6±1.0mg/1000kcal (Hazard ratio; 1.36; 95% Confidence Interval 1.18-1.58; P<0.001). This relationship remained significant even after adjustments for confounding factors. Low dietary zinc intake may increase the risk of CKD development in individuals with normal renal function.

Lymphoma survivors have an increased long-term risk of chronic kidney disease

With improving lymphoma survival, late effects of therapy have emerged. Here, we describe pattern of long-term chronic kidney disease (CKD) in lymphoma survivors. Demographics, comorbidities, lymphoma histology, treatment, and outcome were recorded. Glomerular filtration rate (GFR) was recorded at diagnosis, 1, 2, 5, and 10 years. Rate of GFR decline with time and CKD-free survival were recorded. In 397 patients, median age was 55.3 (18–88), 54% were male, 60% were African Americans, 42% had hypertension (HTN), 15% had DM, 13% had hyperuricemia, 86% received chemotherapy, and 14% had baseline CKD. Total 125 (31%) patients developed CKD in 10 years after lymphoma diagnosis. Probability of CKD development increased significantly with time (23% at 1 year to 41% at 10 years). Rate of GFR decline was 4.6 mL/min/per year. Age, HTN, hyperuricemia, and DM (in young patients) predicted risk of CKD. Thus, lymphoma survivors are at substantial long-term risk of CKD development.

P0825ASSOCIATION OF BODY MASS INDEX CHANGES WITH CHRONIC KIDNEY DISEASE IN A JAPANESE GENERAL POPULATION

Abstract Background and Aims Obesity is a risk factor for chronic kidney disease (CKD), but the effect of reducing body mass index (BMI) on the prevention of CKD is controversial. One of reasons for this disagreement is that part of patients with a BMI decrease may have an unfavourable health status. In such cases, the BMI decrease could be a risk factor for the development of CKD. Therefore, by analysing the data of annual health check-ups, we examined an association between BMI change and CKD development to determine whether BMI reduction helps prevent CKD development. Method We analysed the data of 6,959 subjects who underwent annual health check-ups in both 2013 and 2018. By a multivariate logistic regression analysis, we investigated a relationship between BMI change and CKD development within the 5 years between 2013 and 2018. The percent change in the BMI (ΔBMI) was calculated using the following equation: {(BMI in 2018 − BMI in 2013)/BMI in 2013} ×100. For analyses, we classified the subjects into five groups based on their ΔBMI value: (i) severe BMI decrease (ΔBMI &amp;lt;−2.5%); (ii) moderate BMI decrease (ΔBMI ≥−2.5% but &amp;lt;0%); (iii) maintained BMI (ΔBMI ≥0% but &amp;lt;2.5%); (iv) moderate BMI increase (ΔBMI ≥2.5% but &amp;lt;5%); (v) severe BMI increase (ΔBMI ≥5%). For further analysis, we divided the subjects into non-obesity category (basal BMI &amp;lt;25 Kg/m2) and obesity category (basal BMI ≥25 Kg/m2). Subjects with an estimated glomerular filtration rate &amp;lt;60 mL/min./1.73 m2 were defined as having a CKD. Results After adjusting several covariates, compared with the maintained BMI group, the severe BMI decrease group showed a significantly low risk of CKD development (odds ratio (OR) 0.70, 95% confidence intervals (CI) 0.54-0.91, p &amp;lt;0.01) and the severe BMI increase group had a significantly high risk (OR 1.40, CI 1.08-1.81, p = 0.01). A farther analysis revealed that the OR of CKD development for the severe BMI increase group in the obesity category was higher than that in the non-obesity category (OR 1.75 vs. 1.29). Conclusion In subjects who underwent annual health check-ups, BMI reduction had a significant effect on the prevention of CKD development, whereas an increase in the BMI was a risk factor for CKD development. Moreover, by severe increase in the BMI, obesity subjects showed higher risk of CKD development than non-obesity subjects.

P0602CLINICAL PATTERN, RENAL RECOVERY AND PATIENT OUTCOMES AFTER ACUTE KIDNEY INJURY IN ADULTS IN AN EMERGING COUNTRY

Abstract Background and Aims Acute Kidney Injury (AKI) is an important determinant of outcome in hospitalized patients. Further, there is a risk for development of Chronic Kidney Disease (CKD) in the future. Though the long-term impact of AKI has been studied in developed countries, there is a paucity of data in this area from the Indian subcontinent. This single-centre study aimed to assess the pattern, clinical spectrum, short-term and long-term outcomes of AKI. Method In this prospective observational cohort study, detailed demographic and clinical data at presentation, during hospital stay and follow-up at 1, 3, 6 and 12 months after discharge were obtained prospectively for a cohort of patients with AKI. Both community (CAAKI) and hospital acquired AKI (HAAKI) were included. Patient with pre-existing CKD were excluded. Outcome variables examined were in-hospital mortality, renal function at discharge and on follow-up after discharge from hospital. Results In our study cohort with 476 patients, majority of the cases were CAAKI (395, 83%). The mean age at presentation was 44.8 ± 18.7 years. Medical causes (84%) contributed to the majority of AKI while the remaining were due to surgical (10%) and obstetrical (6%) causes. Sepsis (176/476; 36.9%) was the most common cause of AKI. The most common source for sepsis was respiratory (41%) followed by urological source (18.7%). The in-hospital mortality rate for patients with AKI was 38%. Age &amp;gt;60 years (HR = 1.51; 95% CI, 1.11 – 2.07), oliguria (HR = 1.48; 95% CI, 1.05 – 2.10), need for ventilator (HR = 2.45; 95% CI, 1.36 – 4.41) and/or inotropes (HR = 14.4; 95% CI, 6.28 – 33.05) were predictors of mortality. At discharge, 146 (30.7%) patients had complete renal recovery, while 149 (31.3%) had partial renal recovery. Oliguria (p &amp;lt; 0.001), hypoalbuminemia (p = 0.001) and need for renal replacement therapy (RRT) (p = 0.01) were significantly associated with partial recovery. Of the 295 patients on follow-up at discharge, 211 (71.5%) patients had normal renal function, 4 (1.4%) died and 33 (11.2%) were lost to follow up; 47(15.9%) patients developed CKD of which 6 (2%) were dialysis dependent. Elderly patients, higher AKIN stage with oliguria and those requiring RRT were more likely to develop CKD. Among these, the need for in-hospital RRT was the single most important factor predicting the risk of CKD (OR 1.77, 95% CI, 1.12-2.78). Conclusion In conclusion, our data shows that AKI in hospitalized patients still has high mortality in emerging countries like India. Though a fairly good percentage of cases recovered, there is a definite risk of CKD development, especially in patients who required RRT during hospitalization.

SAT-258 PHYSICAL ACTIVITY IS ASSOCIATED WITH THE INCIDENT CKD IN SUBJECTS WITH NORMAL RENAL FUNCTION: COMMUNITY BASED PROSPECTIVE COHORT STUDY

Physical exercise has a beneficial effect on the prevention of cardiovascular disease and diabetes via improvement in the cardio-metabolic disturbances and is associated with better survival in patients with various chronic diseases as well as general population. However, the effects of physical activity on renal outcomes remains unclear. We aimed to investigate the association between daily physical activity and the development of chronic kidney disease (CKD) in relatively healthy population with normal renal function. Data were retrieved from the Korean Genome and Epidemiology Study, a prospective community-based cohort study. Daily physical activity was estimated by semi quantitative daily activity questionnaire. The eGFR calculated by the CKD-EPI equation from a total of 8,261 subjects were followed up biennially from 2001 to 2014. The primary endpoint was incident CKD, defined as a composite of eGFR <60 mL×min-1×1.73 m-2 and/or the development of proteinuria during the follow up period. The mean age of study subjects was 52.0 years and 3,953 (47.9%) participants were male. At baseline, the mean eGFR was 94.16 ± 14.16 mL×min-1×1.73 m-2. And the average daily physical activity was 1443.3 ± 896.5 MET·h. During a mean follow-up duration of 119.2 (79.1 – 159.3) months, CKD newly developed in 1,518 (18.4%) subjects. The incidence of proteinuria and eGFR decline lower than 60 mL×min-1×1.73 m-2 were 288 (3.5%) and 1,319 (15.9%) subjects, respectively. When divided into quartiles according to daily physical activity, Kaplan-Meier analysis revealed that the risk of CKD development in the highest quartile (Q4) was significantly lower than that of the lowest quartile (Q1) (P <0.001). This association was remained significant even after adjustments were made for confounding factors by multivariable Cox proportional hazards model. (HR [95% CI] = 0.75 [0.65–0.87], P < 0.01). High physical activity is independently associated with decreased risk of incident CKD in healthy population with normal renal function.

Visit-to-visit variability in blood pressure and the development of chronic kidney disease in treated general hypertensive patients.

Data on the association between visit-to-visit variability (VVV) in blood pressure (BP) and the risk of chronic kidney disease (CKD) in general treated hypertensive patients were limited. We aimed to evaluate the relation of VVV in BP with the development of CKD, and examine any possible effect modifiers in hypertensive patients without prior cardiovascular diseases (CVDs) or CKD. This is a post hoc analysis of the Renal Sub-study of the China Stroke Primary Prevention Trial (CSPPT). A total of 10051 hypertensives without CVD and CKD and with at least six visits of BP measurements from randomization to the 24-month visit were included. The main VVV in BP was expressed as standard deviation (SD). The primary outcome was the development of CKD, defined as a decrease in estimated glomerular filtration rate ≥30% and to a level of <60 mL/min/1.73 m2, or end-stage renal disease. The median treatment duration was 4.4 years. After multivariable adjustment, including baseline systolic blood pressure (SBP) and mean SBP during the first 2-year treatment period, there was a significantly positive relationship of SD of SBP with the risk of CKD development (per SD increment; odds ratio, 1.27; 95% confidence interval: 1.10-1.46). The results were similar for coefficient of variation (CV) of SBP. Results across various subgroups, including age, sex, SBP at baseline, treatment compliance, concomitant antihypertensive medications and mean SBP during the first 24-month treatment period, were consistent. SBP variability, irrespective of mean BP level, was significantly associated with the development of CKD in general treated hypertensive patients.

Association between prediabetes (defined by HbA1C, fasting plasma glucose, and impaired glucose tolerance) and the development of chronic kidney disease: a 9-year prospective cohort study

BackgroundThe aim of the present study was to investigate the clinical impact of prediabetes on the development of incident chronic kidney disease (CKD) in a Korean adult population, using data from the Korea Genome and Epidemiology Study.MethodsThis prospective cohort study included 7728 Korean adults without baseline CKD and type 2 diabetes. Prediabetes was defined by impaired fasting glucose (IFG), impaired glucose tolerance (IGT), and HbA1C level. CKD was defined as estimated glomerular filtration rate < 60 mL/min/1.73 m2. We assessed the predictive value of prediabetes for the incidence of CKD, and investigated the incidence of cardiovascular disease including coronary artery disease and stroke.ResultsOver a median follow-up period of 8.7 years, 871 of 7728 (11.3%) subjects developed incident CKD. Patients with prediabetes, as defined by IGT or HbA1C, developed incident CKD more frequently than the non-prediabetic group did. The risk of CKD development at follow-up was analyzed according to different prediabetes definitions. Compared with the non-prediabetic group, the IGT- (Hazard ratio [HR] = 1.135, 95% confidence interval [CI] = 1.182–1.310, P = 0.043) and HbA1C-defined prediabetic groups (HR = 1.391, 95% CI = 1.213–1.595, P < 0.001) were significantly associated with incident CKD after adjusting for traditional CKD risk factors; however, IFG was not associated with incident CKD.ConclusionIGT- or HbA1C-defined prediabetes is an independent predictor of incident CKD. The measurement of these parameters might enable early detection of CKD risk, allowing physicians to initiate preventive measures and improve patient outcomes.

RISK FACTORS OF CHRONIC KIDNEY DISEASE AMONG PATIENTS ATTENDING IBN SINA TEACHING HOSPITAL IN MOSUL CITY

Background: Chronic kidney disease (CKD) is a long-term health condition that in many cases is preventable. Many people do not know they have kidney disease, because up to 90% of kidney function can be lost before symptoms are evident. Fortunately, simple tests performed by a general practitioner can identify most cases of CKD when the disease is in its early stages, enabling treatment to prevent or slow progress. Objective: To evaluate the risk factors for the development of CKD. Methods: A case-control study conducted to 300 persons (150 cases and 150 controls) selected from Medical Wards, Dialysis Kidney Unit and in Outpatient Clinic at Ibn Sina Teaching Hospital in Mosul City. Results: Diabetes mellitus (DM) had 12.9 folds risk for developing of CKD and both type 1 and type 2 D.M. had significant role for developing CKD. Diabetic patients for (&gt; 15 years) had 29.8 times risk for development of CKD. Hypertension (HT) had 3.5 folds risk for CKD and those having HT more than 15 years had 12.9 times risk for CKD. Cardiovascular disease (CVD) had 13.6 folds risk for CKD and having more than one type of CVD had 37 times risk for CKD than heart failure, ischemic heart disease. Family history of renal diseases had 7.1 times risk for CKD and there was statistically significant role of having family history of CKD that had more than 22 times risk for CKD. Statistically significant role of having proteinuria with 383 times risk for CKD. Conclusion: There are many risk factors significantly contributing to the development of CKD in Mosul especially DM, HT, CVD, family history of renal disease, family history of chronic diseases, and from this study it has been concluded that proteinuria plays a major role for the development and progress of CKD. Keywords: Chronic kidney disease, risk factors Citation: Khaleel FF, Hussain SS, Hmood AH. Risk factors of chronic kidney disease among patients attending Ibn Sina Teaching Hospital in Mosul City. Iraqi JMS. 2019; 17(1): 24-31. doi: 10.22578/IJMS.17.1.5

Association of Thyrotropin Concentration with Chronic Kidney Disease in a Japanese General Population Cohort

Background: Previous studies have indicated an association between hypothyroidism and kidney dysfunction; however, few studies have investigated whether thyroid dysfunction is a risk factor for chronic kidney disease (CKD) development. And their result is not consistent. Objectives: We evaluated the association of thyroid dysfunction with CKD prevalence and development by a multivariate logistic regression analysis. Method: In cross-sectional and longitudinal studies, 16,390 subjects and 7,609 subjects, respectively, who underwent annual health check-ups were analyzed. We categorized the subjects into the following 4 groups based on their serum thyrotropin (TSH) ­concentrations: below-normal (TSH < 0.54 mU/L), lower-normal ­(0.54–2.40 mU/L), higher-normal (2.41–4.26 mU/L) and above-normal (> 4.26 mU/L). Subjects with eGFR <60 mL/min/1.73 m² were determined to have CKD. Results: The cross-sectional study revealed a positive correlation between TSH concentration and CKD ­prevalence. Compared with the lower-normal TSH group, the ORs and 95% CIs of CKD prevalence were 0.61 (0.45–0.82, p = 0.001) for the below-normal group, 1.49 (1.33–1.67, p < 0.001) for the higher-normal group, and 1.90 (1.57–2.30, p < 0.001) for the above-normal group. The longitudinal study revealed that the risk of CKD development within 3 years was significantly higher in the above-normal TSH group than in the lower-normal TSH group (OR 1.58, 95% CI 1.02–2.45, p = 0.04). Conclusions: Our data indicate that higher TSH concentrations are positively correlated with CKD prevalence and that a high TSH concentration is a risk factor for CKD development.

Outcome of posterior urethral valve in 64 children: a single center's 22-year experience.

Posterior urethral valve (PUV) is the most serious form of congenital anomalies of kidney and urinary tract (CAKUT) in boys with significant risk of progression to chronic kidney disease (CKD). We present our long-term results in children with PUV. Retrospective chart review of 113 children with PUV followed within the years of 1996-2018 was performed. Clinical, laboratory and epidemiologic parameters were analyzed for their impact on renal outcome. The median age of diagnosis was 1.00 month (1.00-132.00) and the median follow-up period was 70 months (60.00-216.00). Antenatal diagnosis was present in 33 patients (51.5%) mainly with bilateral hydronephrosis and oligohydramnios. The most common postnatal presentation was recurrent urinary tract infection (UTI) in 14 cases (21.9%) and incontinence in three cases (4.7%). Vesicoureteral-reflux (VUR) was present in 31 cases (48.4%). All patients had surgery and urinary diversion was needed in 18 (28.2%). Varying stages of chronic kidney disease (CKD) developed in 23 cases (35.9%) and rise in serum creatinine was especially prominent after the 4th year of follow-up. Of 23 CKD patients, seven (10.9%) were in ESRD and on dialysis. Mortality occurred in one (1.5%) patient. Hypertension, proteinuria and high initial serum creatinine (>1.28 mg/dL) were statistically significant risk factors for CKD, as expected. Surprisingly VUR and UTI did not show such a significant impact on CKD development. Antenatal detection was with significantly less risk for CKD. Our results confirm that PUV has a considerable risk for CKD development. Antenatal diagnosis, management of proteinuria and hypertension may modify this progression. But already injured kidneys still have a potential risk. The need for further research to evaluate the impact of any intervention on long term renal outcome is obvious.