Risk Of Chronic Kidney Disease Research Articles

The Prevalence of Chronic Kidney Disease Risk Factors and their Population Attributable Risks in Yazd City, Iran: A Letter-to-Editor

The Prevalence of Chronic Kidney Disease Risk Factors and their Population Attributable Risks in Yazd City, Iran: A Letter-to-Editor

Acute kidney injury after CAR-T cell therapy: exploring clinical patterns, management, and outcomes.

Acute kidney injury (AKI) has been reported after CAR-T cells, but available data are limited. We sought to describe the incidence of AKI in a cohort of patients hospitalized in the intensive care unit (ICU) following CAR-T cell reinjection, identify the primary factors linked to the onset of AKI, and ascertain the key determinants associated with kidney outcomes and mortality. We retrospectively analyzed 119 patients hospitalized in ICU after CAR-T cell therapy between 2017 and 2023. Factors associated with AKI, mortality, and kidney sequelae were identified using multivariate analyses. Of the 119 patients, 41 patients fulfilled diagnostic criteria of AKI (34%). By multivariate analysis, grade ≥3 cytokine release syndrome (CRS) [OR=1.20 CI95% (1.01-1.43)] and elevated lactate dehydrogenase (LDH) levels at admission [OR=1.44 CI95% (1.04-1.99)] were significantly associated with the occurrence of AKI during ICU stay. AKI KDIGO ≥2 was an independent risk factor for hospital mortality [OR=1.50 (1.22-1.85), P<0.001]. Nine out of 12 (75%) and 6/9 (67%) patients who had experienced AKI and survived had chronic kidney disease (CKD) at 6 months and 1 year, respectively. We did not identify any specific factor associated with kidney recovery. AKI may occur in ICU patients receiving CAR-T cell therapy, especially those who experience CRS and exhibit elevated LDH levels. Early recognition of AKI is of utmost importance as it substantially compromises survival in these patients. Future studies should aim to elucidate the underlying pathophysiological mechanisms of AKI in this context and pinpoint predictive factors for long-term risks of CKD.

Arterial stiffness and incident chronic kidney disease: a large population-based cohort study.

Evidence from large population-based cohorts as to the association of arterial stiffness and incident chronic kidney disease (CKD) is mixed. This large population-based study aimed to investigate whether arterial stiffness, assessed oscillometrically, was associated with incident CKD. The study population comprised 4838 participants from the Vitamin D Assessment (ViDA) Study without known CKD (mean ± SD age = 66 ± 8). Arterial stiffness was assessed from 5 April, 2011 to 6 November, 2012 by way of aortic pulse wave velocity, estimated carotid-femoral pulse wave velocity, and aortic pulse pressure. Incident CKD was determined by linkage to national hospital discharge registers. Cox proportional hazards regression was used to assess the risk of CKD in relation to chosen arterial stiffness measures over the continuum and quartiles of values. During a mean ± SD follow-up of 10.5 ± 0.4years, 376 participants developed incident CKD. Following adjustment for potential confounders, aortic pulse wave velocity (hazard ratio (HR) per SD increase 1.69, 95% CI 1.45-1.97), estimated carotid-femoral pulse wave velocity (HR per SD increase 1.84, 95% CI 1.54-2.19), and aortic pulse pressure (HR per SD increase 1.37, 95% CI 1.22-1.53) were associated with the incidence of CKD. The risk of incident CKD was, compared to the first quartile, higher in the fourth quartile of aortic pulse wave velocity (HR 4.72, 95% CI 2.69-8.27; Ptrend < 0.001), estimated carotid-femoral pulse wave velocity (HR 4.28, 95% CI 2.45-7.50; Ptrend < 0.001) and aortic pulse pressure (HR 2.71, 95% CI 1.88-3.91; Ptrend < 0.001). Arterial stiffness, as measured by aortic pulse wave velocity, estimated carotid-femoral pulse wave velocity, and aortic pulse pressure may be utilised in clinical practice to help identify people at risk of future CKD. www.anzctr.org.au identifier:ACTRN12611000402943.

Machine learning algorithms for predicting the risk of chronic kidney disease in type 1 diabetes patients: a retrospective longitudinal study

Machine learning algorithms for predicting the risk of chronic kidney disease in type 1 diabetes patients: a retrospective longitudinal study

Blood metabolites and chronic kidney disease: a Mendelian randomization study

BackgroundHuman blood metabolites have demonstrated close associations with chronic kidney disease (CKD) in observational studies. Nonetheless, the causal relationship between metabolites and CKD is still unclear. This study aimed to assess the associations between metabolites and CKD risk.MethodsWe applied a two-sample Mendelian randomization (MR) analysis to evaluate relationships between 1400 blood metabolites and eight phenotypes (outcomes) (CKD, estimated glomerular filtration rate(eGFR), urine albumin to creatinine ratio, rapid progress to CKD, rapid decline of eGFR, membranous nephropathy, immunoglobulin A nephropathy, and diabetic nephropathy). The inverse variance weighted (IVW), MR-Egger, and weighted median were used to investigate the causal relationship. Sensitivity analyses were performed with Cochran’s Q, MR-Egger intercept, MR-PRESSO Global test, and leave-one-out analysis. Bonferroni correction was used to test the strength of the causal relationship.ResultsThrough the MR analysis of 1400 metabolites and eight clinical phenotypes, a total of 48 metabolites were found to be associated with various outcomes. Among them, N-acetylleucine (OR = 0.923, 95%CI: 0.89–0.957, PIVW = 1.450 × 10–5) has a strong causal relationship with lower risk of CKD after the Bonferroni-corrected test, whereas Glycine to alanine ratio has a strong causal relationship with higher risk of CKD (OR = 1.106, 95%CI: 1.063–1.151, PIVW = 5.850 × 10–7). No horizontal pleiotropy and heterogeneity were detected.ConclusionOur study offers groundbreaking insights into the integration of metabolomics and genomics to reveal the pathogenesis of and therapeutic strategies for CKD. It underscores 48 metabolites as potential causal candidates, meriting further investigation.

Urinary cytokeratin 20 as a predictor for chronic kidney disease following acute kidney injury.

BACKGROUNDIdentifying patients with acute kidney injury (AKI) at high risk of chronic kidney disease (CKD) progression remains a challenge.METHODSKidney transcriptome sequencing was applied to identify the top upregulated genes in mice with AKI. The product of the top-ranking gene was identified in tubular cells and urine in mouse and human AKI. Two cohorts of patients with prehospitalization estimated glomerular filtration rate (eGFR) ≥ 45 mL/min/1.73 m2 who survived over 90 days after AKI were used to derive and validate the predictive models. AKI-CKD progression was defined as eGFR < 60 mL/min/1.73 m2 and with minimum 25% reduction from baseline 90 days after AKI in patients with prehospitalization eGFR ≥ 60 mL/min/1.73 m2. AKI-advanced CKD was defined as eGFR < 30 mL/min/1.73 m2 90 days after AKI in those with prehospitalization eGFR 45-59 mL/min/1.73 m2.RESULTSKidney cytokeratin 20 (CK20) was upregulated in injured proximal tubular cells and detectable in urine within 7 days after AKI. High concentrations of urinary CK20 (uCK20) were independently associated with the severity of histological AKI and the risk of AKI-CKD progression. In the Test set, the AUC of uCK20 for predicting AKI-CKD was 0.80, outperforming reported biomarkers for predicting AKI. Adding uCK20 to clinical variables improved the ability to predict AKI-CKD progression, with an AUC of 0.90, and improved the risk reclassification.CONCLUSIONThese findings highlight uCK20 as a useful predictor for AKI-CKD progression and may provide a tool to identify patients at high risk of CKD following AKI.FUNDINGNational Natural Science Foundation of China, National Key R&D Program of China, 111 Plan, Guangdong Key R&D Program.

Machine learning model for cardiovascular disease prediction in patients with chronic kidney disease.

Cardiovascular disease (CVD) is the leading cause of death in patients with chronic kidney disease (CKD). This study aimed to develop CVD risk prediction models using machine learning to support clinical decision making and improve patient prognosis. Electronic medical records from patients with CKD at a single center from 2015 to 2020 were used to develop machine learning models for the prediction of CVD. Least absolute shrinkage and selection operator (LASSO) regression was used to select important features predicting the risk of developing CVD. Seven machine learning classification algorithms were used to build models, which were evaluated by receiver operating characteristic curves, accuracy, sensitivity, specificity, and F1-score, and Shapley Additive explanations was used to interpret the model results. CVD was defined as composite cardiovascular events including coronary heart disease (coronary artery disease, myocardial infarction, angina pectoris, and coronary artery revascularization), cerebrovascular disease (hemorrhagic stroke and ischemic stroke), deaths from all causes (cardiovascular deaths, non-cardiovascular deaths, unknown cause of death), congestive heart failure, and peripheral artery disease (aortic aneurysm, aortic or other peripheral arterial revascularization). A cardiovascular event was a composite outcome of multiple cardiovascular events, as determined by reviewing medical records. This study included 8,894 patients with CKD, with a composite CVD event incidence of 25.9%; a total of 2,304 patients reached this outcome. LASSO regression identified eight important features for predicting the risk of CKD developing into CVD: age, history of hypertension, sex, antiplatelet drugs, high-density lipoprotein, sodium ions, 24-h urinary protein, and estimated glomerular filtration rate. The model developed using Extreme Gradient Boosting in the test set had an area under the curve of 0.89, outperforming the other models, indicating that it had the best CVD predictive performance. This study established a CVD risk prediction model for patients with CKD, based on routine clinical diagnostic and treatment data, with good predictive accuracy. This model is expected to provide a scientific basis for the management and treatment of patients with CKD.

Acute Kidney Disease following Acute Kidney Injury in Children-A Retrospective Observational Cohort Study on Risk Factors and Outcomes.

Background: Acute kidney disease (AKD) is a known risk factor for increased mortality and evolution towards chronic kidney disease (CKD) in adults. The data regarding AKD in children are scarce. The purpose of our study was to explore the risk factors for developing AKD based on exposures and susceptibilities in children with AKI doubled by the biological parameters from the first day of identified AKI. In addition, we followed the trajectory of AKD following an acute kidney injury (AKI) episode in children during hospital admission and after discharge with special considerations towards mortality and progression to new-onset CKD. Methods: We retrospectively evaluated 736 children, ages between 2 and 18 years old, with identified AKI during hospital admission in a tertiary care hospital from west Romania over a 9-year period. Results: AKD incidence following an AKI episode was 17%. Patients who developed AKD were older, with higher baseline serum creatinine, urea, C reactive protein and lower proteins, haemoglobin and sodium levels. In the adjusted model, no biological parameters influenced AKD development. Regarding certain exposures and personal susceptibilities in children with AKI, only anaemia independently increased the risk of AKD development by 2.47 times. However, out of the AKI causes, only the intrinsic causes of AKI independently increased the risk of progressing to AKD (glomerulonephritis by 4.94 and acute tubule-interstitial nephritis by 2.76 times). AKD increased the overall mortality by 2.6 times. The factors that independently increased the risk of CKD were AKD, acute tubular necrosis and higher baseline serum creatinine values. Conclusions: Only anaemia, glomerulonephritis and acute tubule-interstitial nephritis increased the risk of AKD development in children with AKI. AKD was an independent risk factor for mortality and new-onset CKD in children.

#2333 Risk of NDI and CKD in individuals treated with lithium

Abstract Background and Aims Nephrogenic diabetes insipidus (NDI) is a known side effect of lithium treatment. Lithium has also been associated with the development of chronic kidney disease (CKD). The aims of this study were to examine the risk factors for NDI among persons on lithium treatment and the association of NDI and other risk factors with the development of chronic kidney disease (CKD). Method This was a retrospective cohort study of all persons in Iceland using lithium in the years 2003-2018. Lithium exposure was defined as at least one lithium prescription or at least one serum lithium measurement with a detectable lithium level. Patients with affective disorders (ICD-10 codes F30-F39) attending the outpatient clinics of Landspitali–The National University Hospital Mental Health Services in 2014-2016, without lithium exposure, served as controls. NDI was defined as concomitant serum sodium (SNa) &amp;gt;144 mmol/L and urine specific gravity (SG) &amp;lt;1.005; individuals with no SNa measurement after 2003 were excluded from the analysis. CKD stages 3-5 were defined according to the KDIGO guidelines for CKD as estimated glomerular filtration rate (eGFR) less than 60 mL/min/1.73 m2. The eGFR was calculated from serum creatinine (SCr) using the CKD-EPI equation. The analysis of incident CKD was limited to the period when standardized SCr measurements had become available, in 2008-2018. Individuals with &amp;lt;2 SCr measurements after 2008 and those with CKD stages 3-5 before 2008 were excluded. In addition, this analysis specifically examined the relationship between the mean serum lithium concentration and the development of CKD, comparing those not exposed to lithium to 3 groups of lithium users with a mean serum lithium concentration of 0.3-0.59, 0.6-0.79 and 0.8-0.99 mmol/L. Acute kidney injury (AKI) was defined according to the SCr component of the KDIGO criteria for AKI, and other comorbid conditions were defined based on ICD-9 and ICD-10 diagnosis codes. Multivariable Cox regression with time-dependent covariables was used for risk assessment. Results In the analysis of the development of NDI, the group exposed to lithium consisted of 2252 individuals, of whom 58 (2.6%) met the criteria for NDI compared with 13 (1.0%) of the 1272 controls. When compared with those without lithium exposure. the risk of NDI was lithium concentration dependent, with a hazard ratio (HR) of 1.22 (95% CI, 0.50–2.98), 5.52 (95% CI, 2.81–10.85) and 10.03 (95% CI, 4.51–22.27) for groups with a mean lithium concentration of 0.3–0.59, 0.6–0.79 and 0.8–0.99 mmol/L, respectively. A previous diagnosis of CKD was also a significant risk factor (HR 3.00 [95% CI, 1.50–6.12]). In the CKD analysis, the group of lithium users comprised 1401 individuals. Of those, 192 (13.7%) developed CKD, compared with 39 (2.8%) of the 1406 controls. Analysis adjusted for initial eGFR showed that NDI was a significant risk factor for CKD (HR 1.90 [95% CI, 1.03-3.54]). Other significant risk factors were mean lithium concentration with HR of 1.25 (95% CI, 0.82–1.91), 2.84 (95% CI, 1.94–4.15) and 5.11 (95% CI, 3.22–8.07) for the groups with a mean lithium concentration of 0.6–0.79 and 0.8–0.99 mmol/L, respectively. Other significant risk factors were age per year (HR 1.03 [95% CI, 1.02–1.05]), diabetes (HR 1.62 (95% CI, 1.08–2.46]) and history of AKI (HR 1.92 [95% CI, 1.33–2.77]). Conclusion Lithium use is associated with NDI in a concentration-dependent manner. Long-term lithium treatment is associated with a risk of CKD, which also is concentration dependent, in patients with bipolar and unipolar mood disorders. NDI may be an important risk factor for CKD.

#1054 Dietary manganese intake and risk of chronic kidney disease: insights from the UK Biobank Study

Abstract Background and Aims Manganese, an essential trace element crucial for various physiological processes, has been linked to metabolic syndrome and cardiovascular health. Despite these associations, the relationship between dietary manganese intake and incident chronic kidney disease (CKD) remains unclear. In this study, the connection between dietary manganese consumption and the development of CKD in individuals with normal kidney function was investigated. Method A total of 135,577 participants enrolled in the UK Biobank were assessed. Dietary manganese intake was determined through a 24-hour dietary recall questionnaire and categorized into quartiles. Individuals with prevalent CKD or an estimated glomerular filtration rate (eGFR) &amp;lt;60 mL/min/1.73 m2 at baseline were excluded. The primary outcome was incident CKD diagnosed using ICD-10 and OPCS-4 codes. Incident CKD, defined as eGFR &amp;lt;60 mL/min/1.73 m2 or a urine albumin-to-creatinine ratio (UACR) ≥30 mg/g, was also evaluated in a sub-cohort that included eGFR and UACR follow-up data. Results During a follow-up period of 1,492,228 person-years (median, 11.2 years), incident CKD occurred in 4,900 (3.6%) participants. The incidence of CKD exhibited a progressive increase among individuals with low manganese intake (2.3, 3.0, 3.6, and 4.2 events per 1000 person-years in Q4–Q1, respectively). In a multivariate Cox proportional hazard model, the adjusted hazard ratios (95% confidence intervals) for the lowest, second, and third quartiles were 1.39 (1.26–1.54), 1.22 (1.11–1.34), and 1.12 (1.02–1.23), respectively, compared to the highest quartile. Similar findings were observed in relation to eGFR or UACR-defined CKD outcomes. Conclusion Lower dietary manganese consumption was found to be associated with an elevated risk of incident CKD in adults with normal kidney function. This implies that a deficiency in dietary manganese intake may contribute to an increased risk of CKD development.

#939 Association between alcohol consumption and the risk of incident chronic kidney disease in community-dwelling older adults

Abstract Background and Aims The relationship between alcohol consumption and kidney function decline is not well established, especially in older adults. This study aimed to investigate the effects of alcohol consumption on the risk of incident chronic kidney disease (CKD) in community-dwelling older adults. Method Adults aged ≥ 65 years with an estimated glomerular filtration rate (eGFR) ≥60 mL/min/1.73 m2 and without proteinuria between 2009 and 2010 were recruited and followed through December 2018 from a Korean national population-based cohort. Alcohol consumption was categorised into non-, mild, moderate, and heavy drinking groups based on self-administered questionnaires. New-onset CKD was defined as an eGFR &amp;lt;60 mL/min/1.73 m2. Results Of the total 122,319 subjects, the non-, mild, moderate, and heavy drinking groups were 99,091 (81.0%), 14,842 (12.1%), 4,257 (3.5%), and 4,139 (3.4%), respectively. During follow-up, 19,796 (20.0%), 4,636 (31.2%), 1,696 (39.8%), and 1,695 (41.0%) developed CKD in the non-, mild, moderate, and heavy drinking groups. Univariate Cox regression analyses showed a significantly increased risk of incident CKD in older adults in all drinking groups compared to non-drinkers (all P &amp;lt; 0.001). However, hazard ratios (HR) for developing CKD were 0.90 (95% confidence interval [CI] 0.87–0.94, P &amp;lt; 0.001) for mild, 0.89 (95% CI 0.84–0.95, P &amp;lt; 0.001) for moderate, and 0.93 (95% CI 0.88–0.99, P = 0.027) for heavy drinkers after fully adjusting for confounding variables. This inverse relationship between alcohol consumption and CKD risk was observed in males in all drinking groups, whereas in females it was found only in mild drinkers. Conclusion In the subgroup analysis, the beneficial effect of alcohol consumption on incident CKD was prominent among moderate drinkers aged 65–75 years, male mild drinkers aged ≥ 75 years, and female mild drinkers aged &amp;lt; 85 years. This study shows that alcohol consumption is inversely associated with the risk of incident CKD in older adults. Further studies are required to elucidate the effects of alcohol on kidney damage in older adults.

#804 The nonlinear association between body mass index and chronic kidney disease: a prospective cohort study and Mendelian randomization analysis

Abstract Background and Aims Previous studies mainly focused on linear association between body mass index (BMI) and the risk of chronic kidney disease (CKD). In the current research, we conducted a prospective cohort observational study and Mendelian Randomization analysis to explore whether non-linear relationship exists between BMI and CKD. Method In the prospective cohort study, 495,465 participants from the UK biobank were included. The Cox proportional hazards model with fractional polynomial transformation was used to estimate the hazard ratio of BMI for incident CKD. In addition, nonlinear Mendelian Randomization analysis was performed using the fractional polynomial method to verify the causality of the association. Results In the observational analysis, a J-shaped association was observed between BMI and the risk of CKD. The risk of CKD was lowest when the BMI was around 18-20 kg/m2, and the hazard of developing CKD increased in participants with lower or higher BMI (Fig. 1). When assessing the causal relationship, in Mendelian Randomization analysis, despite that a nonlinear relationship still held true (P-value for non-linearity = 0.008), the odds ratio for CKD monotonically rised with increasing BMI (Fig. 2). Conclusion The J-shape association between BMI and CKD revealed by the observational cohort study was not supported by the Mendelian Randomization, which indicated a monotonically causal relationship that the risk of CKD rised with increasing BMI.

#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) &amp;lt;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 &amp;lt;27 kg in males and &amp;lt;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 &amp;lt; 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.

#2088 Renal outcome, cardio-vascular events and infections in patients with lupus nephritis: MassiLUP cohort 2001-2022

Abstract Background and Aims Most epidemiological studies in lupus nephritis (LN) report the risk of end-stage kidney disease (ESKD) (10-20% of patients at 10-15 years in developed countries), but less data is available on the long-term risk of chronic kidney disease (CKD), even though CKD is a major risk factor for morbidity and mortality. While immunosuppressive therapy for LN aims to reach and maintain remission in order to prevent CKD, it also exposes patients to cardiovascular, infectious and neoplastic adverse events. We conducted a retrospective cohort study to evaluate survival without CKD and adverse events in patients with LN. Method The MassiLUP cohort comprises all patients who underwent a kidney biopsy for a first flare of LN between 2001 and 2022 in the University Hospital of Marseille, France. We assessed patient survival, renal survival and survival without CKD (defined by an estimated glomerular filtration rate &amp;lt; 60 mL/min/1.73 m2), without cardiovascular event, without severe infection (requiring hospitalization, or zoster), and without cancer. Results A total of 168 patients (82.7% female; mean age 33 years; mean serum creatinine 102 µmol/L at the time of the first kidney biopsy) were included, with a mean follow-up of 9.6 ± 5.7 years. One (0.6%) patient had class I LN (ISN/RPS 2003 classification), 17 (10.1%) class II LN, 45 (26.8%) had class III (± V) LN, 73 (43.5%) had class IV (± V) LN, 29 (17.3%) patients had pure class V LN; 3 biopsies could not be classified. Four patients died during the follow-up (3 of severe infections and 1 of stroke); 41 (24.4%) patients developed CKD, among whom 19 (11.3%) patients reached ESKD; 34 (20.2%) patients presented a cardiovascular event, 59 (35.1%) a severe infection, and 12 (7.1%) a cancer. Survival rates without CKD were 82.9%, 74.6% and 67.3% at 5, 10 and 15 years, respectively. Survival rates without ESKD were 94.4%, 88.6% and 79.9% at 5, 10 and 15 years, respectively. Survival rates without cardiovascular event were 85.7%, 77.3% and 75.5% at 5, 10 and 15 years, respectively. Survival rates without severe infection were 76.3%, 63.8% and 51.8% at 5, 10 and 15 years, respectively. Survival rates without cancer were 96.3%, 92.9% and 85.6% at 5, 10 and 15 years, respectively. Conclusion Despite free access to treatment and care in France, the long-term prognosis of patients with lupus nephritis remains burdened by both a risk of CKD and ESKD, and a significant risk of cardiovascular and infectious events. This calls for continued efforts to improve therapeutic strategies, both in terms of efficacy and toxicity, and to strengthen the therapeutic alliance in the care of patients with LN.

#2332 Systemic immune-inflammation index is associated with chronic kidney disease: evidence from NHANES 2009-2018

Abstract Background and Aims The systemic immune-inflammation index (SII), a novel inflammation index, reflects systemic inflammatory and immunologic conditions throughout the human body. However, the relationship between SII and chronic kidney disease (CKD) remains unknown. The purpose of this study was to investigate the possible relationship between SII and CKD. Method The cross-sectional study included participants with complete information on SII (platelet × neutrophil/lymphocyte count), serum creatinine (Scr), or urinary albumin-to-creatinine ratio (UACR) from the 2009-2018 National Health and Nutrition Examination Survey (NHANES). CKD was defined as the presence of either low estimated glomerular filtration rate (eGFR) or albuminuria. Univariate and multivariate logistic regression and restricted cubic spline regression were used to assess the linear and nonlinear association between SII and renal function. Subgroup and interactive analyses were performed to explore potential interactive effects of covariates. Missing values were imputed using random forest. Results A total of 23 236 participants were enrolled in the study, of whom 4518 (17.9%) were diagnosed with CKD. After adjustment for covariates, the odds ratios (ORs) for prevalent CKD were 1.01 (95% CI = 0.91-1.11, p &amp;gt;0.05) for the Q2 group, 1.18 (95% CI = 1.08-1.30, p &amp;lt; 0. 001) for the Q3 group, and 1.64 (95% CI = 1.50-1.80, p &amp;lt; 0.001) for the Q4 group. In the association between SII and CKD, there was a significant interaction in age (p for interaction &amp;lt; 0.05). And non-linear association between SII levels and CKD in the whole population (p for non-linear = 0.001). All sensitivity analyses supported the positive association between SII and CKD. Conclusion SII was positively correlated with increased risk of CKD. The SII may serve as a practical and cost-effective tool for identifying and intervening the individuals at risk for CKD.

#1966 Participation rate and yield of screening for albuminuria in the primary care setting for early identification of chronic kidney disease (SALINE)

Abstract Background and Aims Although guidelines recommend opportunistic screening for chronic kidney disease (CKD) in individuals with established risk factors, such as diabetes, hypertension, or cardiovascular disease, screening for CKD in these individuals remains suboptimal. This study aimed to evaluate the effectiveness of an additional systematic home-based albuminuria screening program in patients at risk for CKD in a primary care setting. Method A cross-sectional screening study was performed in 10 general practices and 5 pharmacies in the Netherlands between Nov 2021-Nov 2023. A random selection of patients aged 45-80 years with risk factors for CKD progression was invited for home-based albuminuria screening. These patients were registered at their general practitioner (GP) or at the pharmacy. Patients in the GP-group were identified based on the following risk factors: diabetes, cardiovascular disease, hypertension, hypercholesterolemia, or obesity. Patients were excluded in case of a normal albuminuria status (ACR (albumin-creatinine ratio) &amp;lt;3.0 mg/mmol) within 18 months prior to the screening. Patients in the pharmacy-group were identified based on drug prescriptions for the aforementioned risk factors in the last 6 months. Home-based albuminuria screening was performed using a urine collection device that was sent by post to a central laboratory for ACR measurement. If the test result was positive upon confirmation (i.e. ≥two tests ACR ≥3 mg/mmol), patients were invited for an elaborate visit in the general practice or pharmacy, to assess presence of CKD and cardiovascular risk factors. Main outcomes were participation rate and yield of the home-based albuminuria screening in the total study population and in both screening groups separately. Secondary outcomes were the yield of persistent albuminuria despite treatment with RAS-inhibition in both screening groups and the yield of previously undiagnosed albuminuria in the GP-group. Results We invited 6 380 patients (2 578 via pharmacy registries and 3 802 via GP registries), of whom 2 147 completed the home-based screening, corresponding to a participation rate of 33.7%. The participation rate among GP patients was 41.4% (1 575/3 802), compared to 22.2% (572/2 578) among pharmacy patients (P &amp;lt; .001). Albuminuria was confirmed in 8.5% (134/3 802) and 5.6% (32/2 578) of the participants in the GP- and pharmacy-group, respectively. Among participants in the GP-group, 59.7% (80/134) had a positive albuminuria test within one year prior to the screening; the remaining 40.3% either had no albuminuria test (or a normal albuminuria test within one year prior to the screening. Of those with increased albuminuria in the GP- and pharmacy-group, 85.8% (115/134) and 81.3% (26/32) attended the elaborate screening visit, respectively. In the GP-group, 72.2% (83/115) had an eGFR &amp;gt;60 and only 19.1% (22/115) an adequate blood pressure (&amp;lt;130/80 mmHg), compared to 69.2% (18/26) and 19.2% (5/26) in the pharmacy-group. Of the albuminuric participants in the GP- and pharmacy-group, respectively, 44.3% (51/115) and 23.1% (6/26) were not treated with RAS inhibition, and 94.8% (109/115) and 96.2% (25/26), respectively, were not treated with an SGLT2 inhibitor. Many patients were not aware of having albuminuria before participating in the systematic home-based screening program 42.6% (109/115) in the GP-group vs. 61.5% (16/26) in the pharmacy-group). Conclusion In conclusion, systematic albuminuria screening in the primary care setting when added to regular opportunistic screening has an acceptable participation rate and yield when performed via GPs, but is less effective when performed via pharmacies. It identifies patients with yet unknown albuminuria and most of the identified patients may benefit of initiation or optimization of albuminuria-lowering treatment. The introduction of such systematic albuminuria screening programs via GPs merits further study.

#986 Sarcopenia and chronic kidney disease among adults over 45 years old: findings from CHARLS

Abstract Background and Aims Little is known about the association between sarcopenia and chronic kidney disease (CKD) among Chinese adults older than 45. The present study sought to investigate the relationship between sarcopenia and CKD based on a large, nationally representative survey. Method The China Health and Retirement Longitudinal Study (CHARLS) provided data for the study in four waves in 2011, 2013, 2015, and 2018. Based on the Asia Working Group for Sarcopenia 2019 (AWGS 2019) criteria, sarcopenia and possible sarcopenia were defined. CKD was defined as eGFR less than 60 mL/min/1.73 m2, calculated according to the CKD Epidemiology Collaboration (CKD-EPI) equation, or self-reported CKD. Logistic regression models were conducted to analyze the cross-sectional relationship between sarcopenia and CKD. Cox proportional hazards regression models were used to examine the effect of sarcopenia on CKD. Stratified analyses were used to assess the association between sarcopenia status and CKD in various subgroups. Results Totally, 12323 participants over 45 years old (48.2% males; mean age 59.3 ± 9.5 years) were enrolled in a cross-sectional study in 2011, and further 10445 individuals were followed up in 2013, 2015 and 2018. The prevalence of CKD was 8.4% (1040/12323) in general populations, 7.2% (556/7703) in individuals without sarcopenia, 10.1% (380/3760) in adults with possible sarcopenia, and 12.1% (104/860) in individuals with sarcopenia, respectively. In cross-sectional study, possible sarcopenia [OR (95% CI): 1.236 (1.069-1.430)] was significantly associated with CKD (P &amp;lt; 0.01). While sarcopenia was not significantly associated with CKD. 783 cases (7.5%) with incident CKD events were identified during the 7 years of follow-up. In subgroup analyses, the incidence of CKD was 1.855 (95% CI 1.176-2.928) in the sarcopenia group compared with non-sarcopenia group among the female participants. The sarcopenia group (HR: 1.639, 95% CI 1.099-2.443) was independently associated with a higher incidence of CKD among non-smokers. Low muscle mass alone was not significantly associated with an increased risk of incident CKD (P &amp;gt; 0.05). Conclusion In our cross-sectional analysis, possible sarcopenia determined by AWGS2019 criteria was associated with a higher prevalence of CKD. In our longitudinal study, sarcopenia assessed using AWGS2019 criteria was associated with a higher risk of CKD in Chinese women over 45 years old or non-smokers.

#2665 Acute kidney injury (AKI) and chronic kidney disease (CKD) in living kidney donors (LKD): time for a new “surgical” classification system?

Abstract Background and Aims Acute Kidney Injury (AKI) and Chronic Kidney Disease (CKD) represent two significant complications in patients who undergo radical (RN) nephrectomy in oncological patients. However, Living kidney donors (LKD) undergo a similar surgery, but kidney dysfunctions are rare. Our study aimed to investigate the incidence of AKI and CKD in a consecutive cohort of LKD. Method This multi-institutional study involved 256 kidney donors who performed RN between 2014 and 2021 in four tertiary care hospitals. Clinical and laboratory data were collected at baseline pre-surgery, six months after surgery, and then every 12 months for a five-year follow-up. eGFR was calculated with the CKD-EPI equation. Statistical analysis was performed using descriptive statistics and logistic regression. Results Descriptive analysis is reported in Table 1. Of note, the rate of AKI was high (85%), even though it was 100% of stage 1. At 12 months, LKD missed 27.9 ± 19.67 ml/min/1.73 m2, persisting stable at 60 months. 26% of patients developed CKD stage GIII, and 10% of patients lost about 30 ml/min/1.73 m2 from the baseline eGFR (Fig. 1 and Tables 1 and 2). The multivariate analysis (logistic regression) showed that age had a direct correlation with the risk of AKI (OR 1.057, p = 0.019), while the female sex was inversely correlated (OR 0.180, p = 0.006); on the other hand, age had a direct correlation with the risk of CKD (OR 1.15, p = 0.001), as well as eGFR before the surgery (OR 1,053, p = 0.027). Conclusion AKI and CKD affected a non-negligible percentage of LKD. However, it is remarkable that most LKD had a medium final eGFR &amp;gt;60 ml/min/1.73 m2 due to a healthy solitary kidney that worked properly, increasing its function by about 30% of its baseline capacity.

#2997 Characterising the natural history of renal recovery after AKI in a prospective cohort—does timing matter?

Abstract Background and Aims Acute kidney injury (AKI) is associated with an increased risk of chronic kidney disease (CKD). Failure of recovery of serum creatinine by 90 days after AKI strongly associates with subsequent long-term reductions in renal function, however there is no consensus agreement on the definition of renal recovery. Further, detailed prospective descriptions of the ‘renal recovery phase’ between AKI and 90 days are lacking. Here we describe outcomes at serial timepoints (days 30, 60 and 90) for a prospective cohort of hospitalised patients with AKI. Method Single centre, prospective cohort study of participants with all stages of AKI. Each participant was characterised in detail, including AKI aetiology, co-morbidities and frailty. Baseline blood and urine samples were obtained at the time of consent. Participants were then followed up at days 30, 60 and 90 with clinical measurements and blood and urine sample collection. Blood tests included serum creatinine and GFR measured by the CKD-EPI equation. The proportion of participants with renal recovery at different creatinine above baseline thresholds as well as major adverse kidney events (MAKE) a composite outcome of death, new dialysis, and persistent renal dysfunction, defined as a 25% or greater decline in GFR was determined at day 30, 60 and 90. Where data was missing, last creatinine / GFR was carried forward for day 60 and 90, or discharge creatinine for day 30. Results A total of 124 participants were recruited. 63% of patients had AKI on hospital admission. The median baseline creatinine was 88 (IQR 70–117) μmol/L and median GFR was 68 (46–87) mL/min/1.73 m2. Median peak creatinine of 306 (IQR 177–458) μmol/L. The majority of AKI was severe (stage 1 (24%) vs stages 2 &amp; 3 (76%)). The most common primary aetiology of AKI was dehydration (46%) followed by sepsis (22%). Table 1 demonstrates the number of participants with ‘recovered’ renal function as defined by a creatinine above baseline of 10%, 20% and 50% from baseline (the latter being reversal of KDIGO AKI stage 1) across the timepoints. Non-recovery of renal function was common across all time points, ranging from 22% to 59% at day 90 depending on which definition of recovery was applied. Table 2 summarises the rate of major adverse kidney events (MAKE) for day 30, 60 and 90, that was predominantly driven by persistent renal dysfunction. Conclusion This study is one of the few prospective descriptions of the AKI recovery from time of AKI to day 90. Whilst it is known that failure to recover creatinine by day 90 is predictive of future renal dysfunction, these data suggest that there is little dynamic change after day 30 and suggests that interventions to prevent the AKI to CKD transition should be targeted in the first 30 days after AKI in order to have the biggest impact. These data also highlight the need for a consensus definition of non-recovery of renal function. Future work on this cohort will therefore include relating different thresholds of renal recovery to outcomes.

#1430 Acid excretion is disturbed in calcium oxalate and calcium phosphate stone formers in the Swiss kidney stone cohort

Abstract Background and Aims Kidney stone is a highly prevalent disease worldwide that causes high morbidity and may increase the risk for chronic kidney disease. Urine pH influences the crystallization of some types of kidney stones, such as calcium phosphate and uric acid. This study aimed to identify whether other acid-base parameters are associated with stone formation in the Swiss kidney stone cohort. Method Urinary, serum, clinical, and anthropomorphic baseline data were obtained from the Swiss Kidney Stone Cohort, a prospective, longitudinal, and multi-centric observational study. We included 200 non-stone formers (NSF, determined by CT scan), and 265 calcium oxalate (CaOx) and 113 calcium phosphate (CaP) stone formers with complete data for urine pH (collected under oil). Titratable acids were calculated based on urine phosphate and creatinine levels and urine bicarbonate based on urine pH. Net acid excretion (NAE) was calculated and NAE capacity (NAEC), the NAE for a given urine pH, which reveals the ability of kidneys to excrete acids, was calculated from the residuals of the relation between urine pH and NAE. Logistic regression analyses were used to estimate the potential contributions of various acid-base variables to the occurrence of CaOx or CaP kidney stones. Odds ratio (OR) are reported as “OR [95% confidence interval]” Results CaOx stone formers were slightly older than NSF individuals and CaP stone formers (NSF = 42.9 ± 13.6 y.o., CaOx = 47.3 ± 14.3 y.o., CaP = 43.3 ± 12.9 y.o.), slightly more overweight (NSF = 25.0 ± 4.15, CaOx = 27.1 ± 4.72, CaP = 25.9 ± 4.55), and had a higher prevalence of males (NSF = 56.0%, CaOx= 72.1%, CaP = 59.3%), but had similar baseline estimated glomerular filtration rate (NSF = 97.1 ± 16.5, CaOx = 96.3 ± 18.3, CaP = 99.5 ± 18.0 ml/min/1.73 m2). Hypertension, type 2 diabetes, pyelonephritis, and nephrocalcinosis were more prevalent among people with either type of kidney stones in comparison with NSFs, while inflammatory bowel disease was more common among CaOx stone formers in comparison with NSF individuals. CaOx and CaP stone formers showed disturbed capacity of excreting acids in relation to NSF (NAEC NSF = 1.81 ± 8.21 µmol/min; CaOx = −1.35 ± 8.45, P &amp;lt; .001; CaP = −0.89 ± 7.66, P = .016) and lower 24 h urine excretion of ammonium (NSF = 19.8 ± 8.70 µmol/min; CaOx = 17.4 ± 8.54, P = .012; CaP = 16.5 ± 8.23, P = .005), but also of citrate, oxalate, and potassium (Table 1). In addition, CaOx exhibited a lower urine volume. In contrast, both CaOx and CaP excreted more calcium (NSF = 3.12 ± 1.85 µmol/min; CaOx = 3.82 ± 1.91 p &amp;lt;0.001; CaP = 4.63 ± 2.27, p &amp;lt;0.001). Urine pH was more acidic in CaOx (p &amp;lt; 0.001) in comparison with NSFs and CaP (P = .004), NSF = 6.05 ± 0.51; CaOx = 5.86 ± 0.53; CaP = 6.16 ± 0.62. The correlations between urine pH and both urine calcium and ammonium were disturbed in CaOx stone formers and shifted in CaP stone formers (Fig. 1). Logistic models including urine ammonium, pH, citrate, phosphate, potassium, calcium, magnesium, oxalate, protein, and volume showed that ammonium is negatively associated with both CaOx and CaP stone formation (unadjusted model OR 0.41[0.26-0.57], p&amp;lt; 0.001 for CaOx and OR 0.42[0.26–0.67], P &amp;lt; .001 for CaP) and urine calcium is positively associated with kidney stones (OR 2.37 [1.72-3.43], P &amp;lt; .001 for CaOx and OR 5.82 [3.6–10.1], P &amp;lt; .001 for CaP). Similar results were obtained after adjustment for age, sex, and BMI. Removing urine ammonium, pH, and phosphate from our logistic model and adding NAEC rendered comparable goodness of fit and model complexity. Holding all other independent variables constant, the odds of CaOx associated with NAEC were 0.45 [0.33–0.61], P &amp;lt; .001 and with calcium of 2.6 [1.91–3.64], P &amp;lt; .001. For CaP, NAEC was still associated with it, but urine magnesium showed a lower odds ratio value (0.44 [0.27–0.72], P = .001 vs 0.54 [0.36–0.80], P = .003). Urine citrate was only associated with CaOx stones. Conclusion Baseline urine ammonium and net acid excretion capacity are strongly associated with the occurrence of CaOx and CaP kidney stones. Reduced NAEC indicates that poor control of ammonium excretion is a hallmark of both types of kidney stones, although more strongly apparent in CaOx.