Risk Factor For Development Of Chronic Kidney Disease Research Articles

Effects of long-term lithium therapy on kidney functioning in mood disorders: A population-based historical cohort study.

Lithium is Food and Drug Administration-approved for bipolar disorder (BD) and is also used in depressive disorders but is underutilized due to concerns about chronic kidney disease (CKD). We explored clinical and demographic profiles of patients on long-term lithium therapy (LTLT) and assessed kidney function. Our aims were to identify the predictors for CKD stage ≥3 and the impact of lithium discontinuation post-CKD diagnosis. We conducted a population-based historical cohort study of adult patients with mood disorders on LTLT at the Marshfield Clinical Health System from 1990 to 2019. Data on lithium therapy and kidney-related information (estimated glomerular filtration rate and CKD) were extracted from electronic medical records. Among 1603 patients with mood disorders (mean age 42.1 years, 60% females), 15.3% (n = 246) developed CKD stage ≥3. Patients without CKD were on lithium for 4.5 years, compared to 6.6 years for those with CKD. Hypertension, age, and BD were significant CKD risk factors. Kidney function declined linearly with lithium duration, returning to pre-treatment trajectory in patients without CKD but showed no improvement in those with CKD after lithium discontinuation. The findings suggest that CKD occurs in 15% of patients with mood disorder receiving LTLT, with its progression potentially influenced by existing comorbidities rather than lithium alone. These results underscore the importance of monitoring kidney function in patients on LTLT and considering individual risk factors for CKD development. In patients who developed CKD, Li discontinuation did not impact change in kidney function.

Chronic kidney disease following nephrectomy for renal tumours: retrospective analysis risk factors

ObjectiveWe aimed to determine factors responsible for chronic kidney disease (CKD) following nephrectomy for renal tumours.MethodsA retrospective study was undertaken in patients underwent partial or radical nephrectomy due to kidney tumour between January 2015 and June 2020. Patients with eGFR above 60 ml/min/1.73m2 were included in the study. Demographic information, surgical features, eGFR values and some comorbidities of patients were recorded. The patients were evaluated for the development of CKD according to the CKD-EPI equation postoperatively.ResultsOne hundred and sixty-six patients who underwent radical (n = 125) or partial (n = 41) nephrectomy were included to study. According to the logistic regression analysis, radical nephrectomy (adjusted OR 0.139 (95% CI 0.038–0.507), p = 0.003), age (adjusted OR 1.037 (95% CI 1.001–1.074), p = 0.045), preoperative proteinuria (adjusted OR 0.251 (95% CI 0.084–0.750) p = 0.013) and preoperative lower eGFR (adjusted OR 0.943 (95% CI 0.917–0.969) p < 0.001) were determined as independent predictor for development of CKD.ConclusionsCKD is an important disease that causes morbidity and mortality. Age, type of surgery and preoperative eGFR and preoperative proteinuria are an independent risk factor for CKD development. Patients should be informed about this problem before surgery.

The prevalence of chronic kidney disease among type 2 diabetes mellitus patients in central South Africa.

Type 2 diabetes mellitus (T2DM) is a leading cause of chronic kidney disease (CKD). The prevalence of CKD among T2DM patients in Africa is 22.0%. The cut-off age for dialysing diabetic patients in the resource-limited state sector in South Africa is 50 years. Type 2 diabetes mellitus patients who develop CKD are likely to be excluded from chronic dialysis and rely on control of risk factors, including blood pressure and blood glucose levels, to prevent CKD progression. We aimed to determine the prevalence of CKD among T2DM patients attending the diabetes clinic at Pelonomi Academic Hospital, Bloemfontein. In this retrospective cross-sectional study, medical records of patients (January 2016 and December 2018) were reviewed to collect demographic and clinical information. In total, 244 records were reviewed. Sixty-one (25.0%, 95% confidence interval [CI]: 20% - 30.8%) T2DM patients had CKD. The rate of CKD was slightly higher in males (n= 24/81; 29.6%) compared with females (n= 37/163; 22.7%). Most patients with CKD (n= 58; 95.1%) were 50 years of age. Only 17.8% of patients achieved a glycosylated haemoglobin (HbA1c) of 7.0%. Blood pressure was controlled in 14.3% of hypertensive patients. Renin-angiotensin-aldosterone system inhibitors were used by 78.6% of patients. A high prevalence of clinically significant CKD among T2DM patients with poor prospects of chronic dialysis in a resource-limited setting was observed. The risk factors for CKD development and progression should be adequately managed in T2DM patients.Contribution:This study emphasises the need for further research and innovation to improve outcomes of T2DM patients with CKD in resource-constrained settings.

Obesity-related kidney disease: Beyond hypertension and insulin-resistance.

Chronic kidney disease (CKD) causes considerable morbidity, mortality, and health expenditures worldwide. Obesity is a significant risk factor for CKD development, partially explained by the high prevalence of diabetes mellitus and hypertension in obese patients. However, adipocytes also possess potent endocrine functions, secreting a myriad of cytokines and adipokines that contribute to insulin resistance and induce a chronic low-grade inflammatory state thereby damaging the kidney. CKD development itself is associated with various metabolic alterations that exacerbate adipose tissue dysfunction and insulin resistance. This adipose-renal axis is a major focus of current research, given the rising incidence of CKD and obesity. Cellular senescence is a biologic hallmark of aging, and age is another significant risk factor for obesity and CKD. An elevated senescent cell burden in adipose tissue predicts renal dysfunction in animal models, and senotherapies may alleviate these phenotypes. In this review, we discuss the direct mechanisms by which adipose tissue contributes to CKD development, emphasizing the potential clinical importance of such pathways in augmenting the care of CKD.

Strategies to Improve Long-Term Outcomes for Patients with Chronic Kidney Disease in China.

Chronic kidney disease (CKD) is an incurable disease requiring lifelong management. China has a high prevalence of CKD, which disproportionately affects older adults and those with chronic risk factors for CKD development. The rising prevalence of CKD in China places a substantial burden on the general population and the healthcare system. In China, there are currently many unmet needs for patients with CKD and high-risk individuals, resulting from a lack of education and support to reduce risk factors, delayed diagnoses, limited knowledge of CKD among primary-care physicians, and poor access to treatments among some patient populations. An integrated, nationwide approach is required to improve the current situation of CKD management in China. There are currently several national healthcare frameworks in place that focus on new major health policies to prevent disease and encourage people to adopt healthier lifestyles, and while they do not directly target CKD, they may have a positive indirect impact. We explore the unmet needs for patients with CKD in China and discuss the potential strategies that may be required to overcome them. Such strategies include improving physician and patient education, establishing a targeted screening programme, supporting patients to improve self-management behaviours, accelerating the creation of medical consortia and medical satellite centres, and migrating from hospital- to community-based management. In addition to policy-driven strategies, development of novel therapies will be key to providing new solutions for the long-term management of CKD. An integrated, nationwide approach is required, incorporating policy-driven changes to the clinical management of CKD, as well as the development of novel CKD treatments.

Risk Factors of Chronic Kidney Disease after Partial Nephrectomy

Background: In comparison with radical nephrectomy, partial nephrectomy (PN) is considered a better option for small renal mass surgery, because of optimal kidney tissue removal and parenchyma preservation. But there are patients with worsening postoperative renal function (RF) and chronic kidney disease (CKD) after PN. Therefore, the study aimed to evaluate and detect risk factors for CKD after PN.Materials and Methods. A prospective observational study was conducted, which consisted of 91 individuals who received PN with warm ischemia and an estimated preoperative glomerular filtration rate (eGFR) ≥ 60 ml/min/1.72m2 without pathologic albuminuria. Preoperative and intraoperative factors like intraoperative hypotension (IOH), blood loss, and resected part volume were analyzed.Results. At 6-month follow-up, 14 (15.4 %) patients experienced postoperative CKD. After 12 months of follow-up, 15 (16.5 %) patients had CKD. Patients with CKD had a lower preoperative eGFR than non-CKD group (69.0 vs 91.0 ml/min/1.72m2, p &lt; 0.001), longer ischemia (20.0 vs 14.0, p = 0.002) and IOH time (40.0 (40.0; 47.5) vs 0.0 (0.0; 26.2) min, p &lt; 0.001). Also, higher volumes of resected kidney part tumor and removed parenchyma with higher glomerulosclerosis amounts (73.3 % vs 14.5 %, p = 0.009) were found in CKD group. Estimated blood loss &gt; 500 ml during PN was discovered to be the major risk factor for CKD development (OR 11.13, 95 % CI 1.88–65.92, p = 0.008). Furthermore, kidney resected part volume (OR 1.05, 95% CI 1.05-1.10, p = 0.033) and IOH time (OR 1.11, 95% CI 1.03-1.19, p = 0.005) were identified as risk factors for postoperative CKD. Conclusions. Patients after PN are at an increased risk of CKD development. Most commonly, postoperative CKD occurs in the first 6 months after PN and appears stable after 12 months of follow-up. Blood loss &gt; 500 ml during PN, IOH and resected kidney volume can have an impact on postoperative RF and increase the risk of CKD.

Hypertriglyceridemia and Other Risk Factors of Chronic Kidney Disease in Type 2 Diabetes: A Hospital-Based Clinic Population in Greece.

Aims/Introduction: Several reports indicate an increasing prevalence of chronic kidney disease (CKD) in type 2 diabetes mellitus (T2DM). Hyperglycemia and hypertension are the main risk factors for CKD development and progression. However, despite the achievement of recommended targets for blood glucose and blood pressure (BP), the residual risk of diabetic chronic kidney disease (DCKD) remains relatively high. The aim of this study is to examine dyslipidemia and other major risk factors to provide support for the prevention and treatment of DCKD. Materials and Methods: Participants are from the Redit-2-Diag study that examines 1759 subjects within a period of 6 months. DCKD severity is staged according to KDIGO criteria. Results: An increase in hemoglobin A1c (1 unit) and systolic blood pressure (1 mm Hg) increases the probability of being classified into a higher CKD stage by 14% and 26%, respectively. Moreover, an increase of triglycerides by 88.5 mg/dL increases the risk of classification to a worse CKD stage by 24%. Conclusions: Elevated triglycerides, systolic blood pressure, and poor glycemic control increase the risk of CKD in T2DM and should be addressed in the treatment strategies.

Exosomes Derived from BM-MSCs Mitigate the Development of Chronic Kidney Damage Post-Menopause via Interfering with Fibrosis and Apoptosis.

The rate of chronic kidney disease (CKD) is increasing globally, and it is caused by continuous damage to kidney tissue. With time the renal damage becomes irreversible, leading to CKD development. In females, post-menopause lack of estrogen supply has been described as a risk factor for CKD development, and studies targeting post-menopause CKD are scarce. In the present study, we used exosomes isolated from bone marrow mesenchymal stem/stromal cells (BM-MSCs) to test their therapeutic potential against the development of CKD. At first, the menopause model was achieved by surgical bilateral ovariectomy in female albino rats. After that, 100 µg of exosomes was given to ovariectomized rats, and the study continued for 2 months. Changes in urine volume, urine protein content, kidney function biochemical parameters (creatinine and BUN), kidney antioxidant parameters (SOD, GPx and CAT), histological changes, immunohistochemical levels of caspase 3, and the gene expression of NGAL (related to kidney damage), TGFβ1 and αSMA (related to fibrosis and EMT), and caspase 3 (related to apoptosis) were studied. After the ovariectomy, the occurrence of CKD was confirmed in the rats by the drastic reduction of serum estrogen and progesterone levels, reduced urine output, increased urinary protein excretion, elevated serum creatinine and BUN, reduced GPx SOD, and CAT in kidney tissue, degenerative and fibrotic lesions in the histopathological examination, higher immunohistochemical expression of caspase 3 and increased expression of all studied genes. After exosomes administration, the entire chronic inflammatory picture in the kidney was corrected, and a near-normal kidney structure and function were attained. This study shows for the first time that BM-MSCs exosomes are potent for reducing apoptosis and fibrosis levels and, thus, can reduce the chronic damage of the kidneys in females that are in their menopause period. Therefore, MSCs-derived exosomes should be considered a valuable therapy for preserving postmenopausal kidney structure and function and, subsequently, could improve the quality of females’ life during menopause.

Is Renoprotection Real for Patients with Hyperuricemia?

Number of patients with progressive chronic kidney disease (CKD) is increasing all over the world. One of the risk factors for CKD development and progression is increased serum uric acid (sUA) level. Possibly, control of hyperurcemia with urate lowering therapy drugs can slow the decline in kidney function. The objective: to determine efficacy and safety of allopurinol and febuxostat in treatment of patients with CKD and hyperurcemia to reduce the sUA level and analyze its influence on glomerular filtration rate (GFR). Materials and methods. The study included 45 CKD patients (stages 3b-5) without other severe/decompensated diseases and contraindications to the allopurinol/febuxostat. All patients underwent a comprehensive clinical and laboratory examination, and were divided into the study groups: Group I (28 patients, 61.3±3.2 y.o., CKD3b-12, CKD4-10, on hemodialysis-6 patients) received febuxostat, Group II (24 patients, 60.7Ѓ}4.1 y.o., CKD3b-9, CKD4-10, on hemodialysis – 5 patients) took allopurinol. Results. Achievement of the target level of sUA was significantly often registered in Group I: after 1 month – in 45.5% (in group II – in 15.9%, p&lt;0.001); after 3 months – in 67.5% (in group II – 21.2% p&lt;0.01); after 6 months, these figures were 90% and 37.1%, respectively (p&lt;0.01). sUA level &lt;300 μmol/l was accompanied by significant positive GFR changes in group I patients; in group II there was a gradual progression of GFR deterioration in 31.8% of patients. Conclusions. In patients with pre-dialysis stages of CKD febuxostat demonstrates renoprotective abilities. Use of febuxostat in patients with CKD stage 3b-4 and in patients on hemodialysis is safe and more effective for target sUA level achievement than the use of allopurinol.

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.&#x0D; 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.&#x0D; 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.&#x0D; 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.&#x0D; 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.

The Role of Hyperuricemia in the Pathogenesis and Progressivity of Chronic Kidney Disease

In humans, the end product of purine metabolism is uric acid. Over 70% of uric acid is excreted through the kidneys. When renal function is impaired, uric acid secretion is also impaired. This directly correlates the prevalence of hyperuricemia with the severity of chronic kidney disease (CKD). It has been reported that the prevalence of hyperuricemia in patients with Stage I-III CKD is 40–60% and up to 70% in patients with Stage IV-V CKD. Some studies found a link between serum uric acid levels and decreased glomerular filtration rate (GFR), an independent risk factor for CKD development. Because CKD and serum uric acid levels are related, the relationship between the two frequently generates controversy. As such, this review of the literature discusses the role of uric acid in the pathogenesis and progression of CKD.

Degree of Portal and Systemic Hemodynamic Alterations Predict Recurrent AKI and Chronic Kidney Disease in Patients With Cirrhosis.

The relevance of hemodynamic derangements on the incidence of recurrent acute kidney injury (AKI) and chronic kidney disease (CKD) in patients with cirrhosis is largely unknown. Consecutive patients with cirrhosis with a complete record of baseline hemodynamics were followed for identifying risk factors for the development of recurrent AKI and CKD by using negative binomial regression and competing risk analysis, respectively. Consecutive patients with cirrhosis (n = 2013, age 50.1 ± 11.8 years, 80% male, Child A:B:C percentage 13.7:52.9:33.4, and mean Child‐Turcotte‐Pugh score 8.6 ± 1.8) were enrolled, 893 (44.3%) of whom received beta‐blockers, with 44.2% responders. Prior AKI was noted in 12.4% at enrollment. At a median follow‐up of 379 (interquartile range: 68‐869) days, AKI developed at a rate of 0.37 episodes per person‐year, and 26% patients developed CKD. A lower mean number of AKI episodes (0.05 ± 0.25 vs. 0.42 ± 0.868; P < 0.001), CKD (subdistribution hazard ratio 0.74 [0.54‐1.02]), and mortality (hazard ratio 0.21 [0.06‐0.73]) were observed in beta‐blocker responders. Albuminuria was an independent risk factor for recurrent AKI, CKD, and mortality (P < 0.05). Lower systemic vascular resistance index predicted hemodynamic response (odds ratio 2.04 [1.29‐3.22]), cumulative AKI episodes (ratio of means 0.10 [0.08‐0.14]), and development of CKD (subdistribution hazard ratio 0.70 [0.58‐0.83]). Higher hepatic venous pressure gradient (≥17 mm Hg) predicted AKI episodes (ratio of means 1.76 [1.32‐2.35]) but not CKD. Conclusion: High portal pressure and severe vasodilatation predispose patients with cirrhosis to repeated AKI episodes and development of CKD. Response to beta‐blockers and therapies targeting the vasodilatory state could prevent frequent AKI and the risk of CKD development. Albuminuria could serve as an early marker of renal dysfunction in patients with cirrhosis.

AKI: an increasingly recognized risk factor for CKD development and progression.

Acute kidney injury (AKI) is an increasing health burden with high morbidity and mortality rates worldwide. AKI is a risk factor for chronic kidney disease (CKD) development and progression to end stage renal disease (ESRD). Rapid action is required to find treatment options for AKI, plus to anticipate the development of CKD and other complications. Therefore, it is essential to understand the pathophysiology of AKI to CKD transition. Over the last several years, research has revealed maladaptive repair to be an interplay of cell death, endothelial dysfunction, tubular epithelial cell senescence, inflammatory processes and more-terminating in fibrosis. Various pathological mechanisms have been discovered and reveal targets for potential interventions. Furthermore, there have been clinical efforts measures for AKI prevention and progression including the development of novel biomarkers and prediction models. In this review, we provide an overview of pathophysiological mechanisms involved in kidney fibrosis. Furthermore, we discuss research gaps and promising therapeutic approaches for AKI to CKD progression.

P0688GREATER MUSCLE STRENGTH IS ASSOCIATED WITH LOWER RISK OF CHRONIC KIDNEY DISEASE

Abstract Background and Aims Frailty is a known risk factor for chronic disease and mortality. However, the association between frailty assessed by hand grip strength (HGS) and chronic kidney disease (CKD) among adults has not been elucidated. This study evaluated the association between muscle strength and the risk of CKD. Method Data were retrieved from a nationwide cohort study (Korean National Health and Nutrition Examination Surveys VI-VII, 2014-2017) and participants aged 40 to 80 years were included in the study analysis (male=6,660, female=8,195). HGS was measured using digital hand dynamometer and normalized to body mass index (BMI). The association between the risk of CKD (estimated glomerular filtration rate [eGFR] &amp;lt;60 mL/min/1.73 m2 or the presence of proteinuria) and quartile of HGS per BMI was evaluated among male and female subjects. Results The mean age was 58.8 ± 11.6 years and mean eGFR level was 88.2 ± 18.7 mL/min/1.73 m2. The mean levels of HGS per BMI were 1.5 ± 0.3 and 0.9 ± 0.2 in male and female subjects, respectively. Those in higher quartile of HGS per BMI showed lower prevalences of advanced CKD stages than lowest quartile among both male and female subjects. When univariable logistic regression analysis for the risk of CKD was performed, higher quartile of HGS per BMI was significantly associated with lower risk of CKD in both male and female subjects. After adjustment for confounding factors including age, systolic blood pressure, smoking and alcohol intake, education and income levels, history of hypertension, diabetes, or arthritis, physical activity, baseline eGFR, total cholesterol, hemoglobin, and daily protein intake, the higher quartile of HGS per BMI were associated with lower risk of CKD in both male and female subjects (odds ratio [OR], 0.66; 95% confidence interval [CI], 0.49-0.88 in Q4; OR, 0.64; 95% CI 0.49-0.83 in Q3 in male; OR, 0.59; 95% CI, 0.43-0.81 in Q4; OR, 0.61; 95% CI, 0.47-0.80 in Q3; OR, 0.70;95% CI, 0.55-0.90 in Q2 in female, Q1 as reference group). These associations were consistent when the HGS per BMI was treated as continuous variable that 34% and 54% of risk was reduced as 1 m2 increase in male and female subjects. Conclusion Greater muscle strength normalized to BMI is associated with lower risk of CKD in adults. These findings suggest that frailty in adults is an important risk factor for CKD development.

P0361THE PREDICTIVE VALUE OF SERUM URIC ACID IN PRIMARY GLOMERULONEPHRITIS PATIENTS: A 5-YEARS RENAL PROGNOSIS

Abstract Background and Aims Primary glomerulonephritis (PGN) is one of the leading causes of end-stage renal disease worldwide. Preservation of renal function is a crucial global goal in the management of patients with chronic kidney disease (CKD) in general and PGN in particular. In addition to classical risk factors, hyperuricemia is regarded to be an independent risk factor for CKD development and progression. However, only a few studies have investigated the impact of hyperuricemia on PGN progression. Therefore, this study aimed to analyze the association between serum uric acid (SUA) concentration and renal prognosis in PGN patients during a 5-year follow-up. Method A total of 344 patients with CKD 1-3 stages were included in this retrospective observational single-center study. Among them, there were 194 (56.4 %) patients with biopsy-proven PGN and 150 (43.6 %) patients with a clinical diagnosis of PGN. All patients were treated according to the KDIGO Practice Clinical Guidelines for Glomerulonephritis. eGFR (milliliters per minute per 1.73 m2) was calculated using the CKD-EPI formula and its baseline value was based on the first available eGFR in PGN diagnosed patients. The patients with eGFR&amp;lt; 30 mL//min/1.73 m2 were excluded from the study at the time of PGN diagnosis. None of the patients was on urate- or lipid-lowering therapy at the time of baseline data. Hyperuricemia was defined as SUA concentration ≥420 μmol/L (7 mg/dL) for males and ≥360 μmol/L (6 mg/dL) for females. The rate of eGFR fall per year was used to assess CKD progression. It was calculated as the difference between eGFR (mL/min/1.73m2) at baseline and the last values: (Last eGFR – Baseline eGFR) / Follow-up period per year). For the analysis, the patients were gender-stratified into 3 SUA quartiles according to average SUA levels at baseline: Q1- &amp;lt; 265 μmol/L for men and &amp;lt;220 μmol/L for women, Q2- 265-446 μmol/L for men and 220-369 μmol/L for women, Q3- ≥ 447 μmol/L for men and ≥ 370 for women. The analysis and all graphs were performed using MedCalc (Belgium). Results Hyperuricemia was found in 72/206 (35 %) men and 38/138 (27.5 %) women (p = 0.0003). During the average 5-years follow-up period (5.3 [3.8-6.2]), there were 114 (33.1%) patients who eventually progressed to eGFR&amp;lt;15 mL/min/1.73 m2 or started RRT. Among them there were: Q1- 10 (12%) patients, Q2 - 52 (31.5%) patients, Q3 - 52 (54.7%) patients (p&amp;lt; 0.0001). The highest renal progression level was observed in Q3 patients: -5.5 [-15.4; -1.8] mL/min/1.73 m2 versus -3.5 [-6.4; -1.7] and -4.6 [-10.6; -2.7] mL/min/1.73 m2 in Q2 and Q1 patients, respectively. In multivariate logistic regression analysis, SUA level in men (≥ 447 μmol/L) and women (≥ 370) was determined as an independent risk factor for rapid CKD progression (OR: 2.5, 95% CI: 1.47-4.23, P = 0.0007). Conclusion. Our study showed that a higher SUA level was associated with a significant rapid eGFR decline during a 5-year follow-up. The study findings suggest that hyperuricemia is a potentially modifiable factor for CKD progression.

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.

Incidence, Risk Factors, and Outcomes of Transition of Acute Kidney Injury to Chronic Kidney Disease in Cirrhosis: A Prospective Cohort Study.

Transition to chronic kidney disease (CKD) after an episode of acute kidney injury (AKI) is known in patients without cirrhosis. We studied the incidence and risk factors for development of CKD in patients with cirrhosis. Competing risk analysis was performed to identify risk factors for CKD development. Of 818 patients with cirrhosis (age, 50.4±11.8years; 84% males; Model for End-Stage Liver Disease [MELD], 19.9±9.9), 36% had AKI at enrollment, 27% had previous AKI, and 61% developed new episodes of AKI during the follow-up period. CKD developed in 269 (33%) patients. Serum cystatin C (CysC; subdistribution hazard ratio [SHR], 1.58; 1.07-2.33), episodes of previous AKI (SHR, 1.26; 1.02-1.56), and AKI stage at enrollment (no AKI [SHR, 1] vs. stage 1 [SHR, 3.28; 1.30-8.25] vs. stage 2 [SHR, 4.33; 1.76-10.66] vs. stage 3 [SHR, 4.5; 1.59-12.73]) were identified as baseline risk factors for CKD development. On time-varying competing risk analysis, MELD (SHR, 1.01; 1.00-1.03), number of AKI episodes (SHR, 1.25; 1.15-1.37), and CysC (SHR, 1.38; 1.01-1.89) predicted CKD development. Development of CKD was associated with higher risk of death. Reduction in glomerular filtration rate (GFR) not meeting CKD criteria was observed in 66% of patients with cirrhosis, more so in those with previous AKI episodes and a high CysC level and MELD score. Renal histology, available in 55 patients, showed tubulointerstitial injury in 86%, cholemic nephrosis in 29%, and glomerular changes in 38%. Conclusion: Almost two-thirds of patients with cirrhosis develop episodes of AKI and reduction in GFR; one-third progress to CKD, resulting in adverse outcomes. Higher MELD and CysC levels and number of AKI episodes predict development of CKD in patients with cirrhosis.

Renal injury and recovery in pediatric patients after ventricular assist device implantation and cardiac transplant

The use of ventricular assist devices (VADs) in children with heart failure may be of particular benefit to those with accompanying renal failure, as improved renal function is seen in some, but not all recipients. We hypothesized that persistent renal dysfunction at 7days and/or 1month after VAD implantation would predict chronic kidney disease (CKD) 1year after heart transplantation (HT). Linkage analysis of all VAD patients enrolled in both the PEDIMACS and PHTS registries between 2012 and 2016. Persistent acute kidney injury (P-AKI), defined as a serum creatinine ≥1.5× baseline, was assessed at post-implant day 7. Estimated glomerular filtration rate (eGFR) was determined at implant, 30days thereafter, and 12months post-HT. Pre-implant eGFR, eGFR normalization (to ≥90mL/min/1.73m2 ), and P-AKI were used to predict post-HT CKD (eGFR <90mL/min/1.73m2 ). The mean implant eGFR was 85.4±46.5mL/min/1.73m2 . P-AKI was present in 19/188 (10%). Mean eGFR at 1month post-VAD implant was 131.1±62.1mL/min/1.73m2 , significantly increased above baseline (P<0.001). At 1year post-HT (n=133), 60 (45%) had CKD. Lower pre-implant eGFR was associated with post-HT CKD (OR 0.99, CI: 0.97-0.99, P=0.005); P-AKI was not (OR 0.96, CI: 0.3-3.0, P=0.9). Failure to normalize renal function 30days after implant was highly associated with CKD at 1year post-transplant (OR 12.5, CI 2.8-55, P=0.003). Renal function improves after VAD implantation. Lower pre-implant eGFR and failure to normalize renal function during the support period are risk factors for CKD development after HT.

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.

Effect of Uric Acid on the Development of Chronic Kidney Disease: The Korean Multi-Rural Communities Cohort Study.

ObjectivesSeveral studies have investigated the effects of serum uric acid (SUA) levels on chronic kidney disease (CKD), with discrepant results. The effect of SUA levels on CKD development was studied in the Korean rural population.MethodsA total of 9695 participants aged ≥40 years were recruited from 3 rural communities in Korea between 2005 and 2009. Of those participants, 5577 who participated in the follow-up and did not have cerebrovascular disease, myocardial infarction, cancer, or CKD at baseline were studied. The participants, of whom 2133 were men and 3444 were women, were grouped into 5 categories according to their quintile of SUA levels. An estimated glomerular filtration rate of <60 mL/min/1.73 m2 at the time of follow-up was considered to indicate newly developed CKD. The effects of SUA levels on CKD development after adjusting for potential confounders were assessed using Cox proportional hazard models.ResultsAmong the 5577 participants, 9.4 and 11.0% of men and women developed CKD. The hazard ratio (HR) of CKD was higher in the highest quintile of SUA levels than in the third quintile in men (adjusted HR, 1.60; 95% confidence interval [CI], 1.02 to 2.51) and women (adjusted HR, 1.56; 95% CI, 1.14 to 2.15). Furthermore, CKD development was also more common in the lowest quintile of SUA levels than in the third quintile in men (adjusted HR, 1.83; 95% CI, 1.15 to 2.90). The effect of SUA was consistent in younger, obese, and hypertensive men.ConclusionsBoth high and low SUA levels were risk factors for CKD development in rural Korean men, while only high levels were a risk factor in their women counterparts.