Etiology Of Chronic Kidney Disease Research Articles

Association of anemia and hypoalbuminemia with mortality among patients undergoing routine hemodialysis

Background: The progressivity of chronic kidney disease (CKD) is associated with several clinical conditions which contribute to high morbidity and mortality, including anemia and hypoalbuminemia. This study aimed to assess the association of anemia and hypoalbuminemia with the mortality of CKD patients undergoing routine hemodialysis (HD) in Siloam Hospital Kupang.Methods: We conducted a retrospective cohort study based on Indonesia renal registry data system and hospital medical records. We studied the following variables: gender, age, etiology of CKD, vascular access of HD, and prevalence of anemia and hypoalbuminemia. All analysis was performed using SPSS software version 22.Results: There were 128 patients enrolled in this study. Of the total patients who died, most of them died within the first 3 months since the initiation of HD (62.1%). The majority of patients had anemia (67.2%) and hypoalbuminemia (69.5%). The bivariate analysis showed that anemia (p value=0.192), and hypoalbuminemia (p value=0.336) were not statistically significant associated with mortality among patients undergoing routine HD.Conclusions: Anemia and hypoalbuminemia are not statistically associated with mortality outcome of CKD patients in Siloam Hospital Kupang. However, these conditions may still have prognostic importance for CKD patients undergoing routine HD. Further studies with larger size of cohort and longer period of time are warranted.

Prevalence and risk factors for functional iron deficiency in children with chronic kidney disease.

Anemia in chronic kidney disease (CKD) is multifactorial. The presence of functional iron deficiency (FID), whereby, there is a block in the transport of iron from macrophage to erythroid marrow is one possible etiology. In this study, we aim to assess the prevalence and risk factors of FID in pediatric CKD. A cross-sectional study was performed from March to December 2018, after obtaining Institute Ethical Clearance. Children aged ≤ 12years with CKD, with or without iron supplementation who consented were enrolled. Patients on erythropoietin or on maintenance dialysis were excluded. Details of patients and diseases characteristics were recorded. Various laboratory parameters including complete blood count, red blood cell indices, hypochromic RBC, reticulocyte hemoglobin content, and serum ferritin were measured. Appropriate statistical tests were applied. Out of 174 children, 127 (73%) had structural kidney disease as an etiology of CKD, and 110 (63%) had anemia. Prevalence of anemia was 44%, 43%, 74%, 64% and 92% in CKD stage 1, 2, 3, 4 and 5, respectively. Absolute iron deficiency was found in 66 (38%) even when some children were already on iron supplementation. FID was seen in 44 (25%) and on multivariate analysis, lower estimated glomerular filtration rate and mineral bone disease are associated risk factors. FID is present in one-fourth of our CKD cohort. It should be considered when the response to adequate measures of improving hemoglobin level fails. More studies are required to know its impact on short-term and long-term patient-related outcomes such as quality of life and mortality.

Urine Uromodulin Is Not Associated With Blood Pressure in the Chronic Kidney Disease in Children Cohort.

Uromodulin regulates activity of the sodium-potassium-two-chloride transporter in the loop of Henle. In adults, higher urine uromodulin levels are associated with greater rise in blood pressure (BP) in response to salt intake. We hypothesized that higher urine uromodulin levels would be associated with higher BP in children with chronic kidney disease, and that there would be an interaction of dietary sodium on this association. In the chronic kidney disease in children Cohort, we utilized univariable and multivariable linear regression models to evaluate the relationship between baseline spot urine uromodulin levels indexed to urine creatinine (Umod/Cr mg/g) and 24-hour mean systolic and diastolic BP, as well as baseline clinic BP. We also tested whether sodium intake (g/day) modified these relationships. Among 436 participants, the median age was 12.4 years (8.9-15.2), median estimated glomerular filtration rate was 50 mL/min per 1.73 m2 (36-62), and median 24-hour mean systolic BP was 112 mm Hg (104-119). The etiology of chronic kidney disease was glomerular disease in 27%. In univariable models, each 2-fold higher Umod/Cr ratio was associated with a 1.66 mm Hg (95% CI, -2.31 to -1.00) lower 24-hour mean systolic and a 1.71 mm Hg (-2.45 to -0.97) lower clinic systolic BP. However, there was no statistically significant association between Umod/Cr and either 24-hour or clinic BP in multivariable models. We did not find a significant interaction between uromodulin and sodium intake in their effect on BP (P>0.05 in all models). Urine uromodulin levels are not associated with BP in the chronic kidney disease in children cohort. Further studies are needed to confirm this finding in healthy pediatric cohorts.

Etiology, Comorbidities, and Rate of Progression of Pediatric Chronic Kidney Disease: A Cohort Study.

To evaluate the etiology of pediatric chronic kidney disease (CKD), assess comorbidities, and identify rate of progression of CKD and its risk factors. Children aged 2-18 y with the Kidney Disease Improving Global Outcome (KDIGO) CKD stages 2-4 were enrolled. The etiology of CKD and its comorbidities were recorded. Kaplan-Meier survival curves were used to analyze the time to progression of CKD. Of the 131 patients enrolled, CKD stages 2, 3a, 3b, and 4 constituted 62 (47.3%), 17 (13%), 26 (19.8%), and 26 (19.8%), respectively. At the last follow-up [at median (IQR) 24 (12, 30) mo], the number of children in CKD stages 2, 3a, 3b, 4 and 5 were 48 (36.6%), 16 (12.2%), 23 (17.6%), 28 (21.4%), and 16 (12.2%), respectively. Etiologies of CKD included obstructive uropathy [48 (36.6%)], chronic glomerular disease [19 (14.5%)], reflux nephropathy [14 (10.7%)] and cystic renal disease [11 (8.3%)]. Comorbidities during follow-up included CKD-MBD [87 (66.4%)], metabolic acidosis [95 (72.5%)], hypertension [88 (67.1%)], growth retardation [69 (52.6%)], and anemia [63 (48.1%)]. The number of patients with metabolic acidosis, hypertension, MBD and anemia in CKD stage 2 were 27 (56%), 26 (54.2%), 24 (50%), 15 (30%), respectively. The median (IQR) rate of decline in eGFR was 3.3 (2, 4.6) mL/min/1.73 m2/y. On multivariable analysis, proteinuria [hazard ratio 3.5 (95% CI 1.4, 8.8) p = 0.01] and hyperphosphatemia [hazard ratio 2.2 (95% CI 1.1, 4.3) p = 0.03] were significant predictors for progression of CKD. Even the earlier stages of CKD had significant comorbidities. The median decline in eGFR was 3.3 mL/min/1.73 m2/y. Proteinuria and hyperphosphatemia were the risk factors for progression of CKD.

Chronic Kidney Disease (CKD) and Exposure to Fine Particulate Matter and Ozone: A Cross-Sectional Study Utilizing North Carolina Electronic Healthcare Records

Background and aims: Chronic kidney disease (CKD) affects more than 38 million people in the United States, predominantly those over 65 years of age. While CKD etiology is complex, recent research suggests associations with certain environmental exposures. Additional studies are needed to understand the strength of associations. We examine estimated glomerular filtration rate (eGFR) using a random sample of North Carolina electronic healthcare records (EHRs) and potential relationships with PM₂.₅ and O₃. Methods: Patient data came from a random sample of 7,065 EHRs within the EPA CARES resource, with recorded serum creatinine concentrations. Patients were seen at a University of North Carolina Healthcare System affiliated hospital or clinic from 2004-2017. We estimated eGFR using CKD-EPI equations. PM₂.₅ data comes from a hybrid model using 1x1 km grids and O₃ data from CMAQ 12x12 km grids. Exposures were annual average PM₂.₅ and O₃ based on the creatinine lab test date. We used multiple linear regression to estimate eGFR per IQR increase of PM₂.₅ & O₃. We adjusted for patient sex, race, age, comorbidities, and 2010 census block group measures of sociodemographic and economic factors. Results: Patients averaged 55.3 (SD: 16.2) years of age, with 58.3% female. There were 1,001 patients (14.2%) diagnosed with CKD, identified by ICD-9 & 10 codes. Mean concentrations for the study period of PM₂.₅ and O₃ were 9.92 (IQR: 1.61) µg/m³ and 40.20 (IQR: 2.53) ppb respectively. eGFR decreased 8.45 mL/min/1.73m² (95% CI: 7.92, 8.98) per IQR increase of PM₂.₅ and a more modest decrease of 0.66 mL/min/1.73m² (95% CI: -.08, 1.40) per IQR of O₃. Conclusions: Annual average PM₂.₅, and to a lesser extent O₃, were associated with lower (poorer) eGFR. Future work will examine the relationship between air pollution and onset of CKD and impaired renal function. This abstract does not reflect EPA policy.

Association between depressive symptoms and bone density in elderly patients with non-dialysis dependent chronic kidney disease

BackgroundDepression is a disease that is commonly accompanied by elderly chronic kidney disease (CKD) patients, but when the two diseases are accompanied, etiology or combination are not well known. We aimed to evaluate the etiology of CKD and comorbid depression by investigating bone disorders that are observed in persons affected by both CKD and depression. MethodsWe conducted a cross-sectional study with a total of 646 patients with CKD. We compared the sociodemographic factors, kidney function, markers for CKD-Mineral and Bone Disorder (CKD-MBD) and bone mineral density according to the depressive symptoms. We conducted a univariate and multivariate logistic regression analysis to calculate odd ratios (95 % confidence interval) between depressive symptoms and low bone mineral density. ResultsIndividuals with CKD and depressive symptoms were associated with lower level of education attained, living alone, exercising less, low 24-hour urine phosphorus, and low bone density. Depressive symptoms were significantly associated with low bone density in lowest parts (1.55 [1.06–2.29]) and in total hip (1.72 [1.17–2.53]) even after adjusting for diabetes mellitus, hypertension, kidney function, proteinuria, age, sex, smoking, and body mass index. LimitationsA cross-sectional design was used in this study and the bone biopsy for diagnosis of CKD-MBD was not done because of invasiveness and practical difficulties. ConclusionLow bone density was associated with depressive symptoms in elderly patients with non-dialysis chronic kidney disease.

Prevalence and Associates of Frailty Status in Different Stages of Chronic Kidney Disease: A Cross-Sectional Study.

Frailty is a state of homeostenosis associated with adverse outcomes. Chronic kidney disease (CKD) increases considerably by aging and shares the common risk factors with frailty. We aimed to examine the prevalence and independent associates of frailty status in CKD patients. In this single-centre, cross-sectional study, we used the five-item Fatigue, Resistance, Ambulation, Illnesses and Loss of Weight (FRAIL) scale to evaluate frailty. A binary logistic regression analysis model including the parameters found to have relationship with frailty in univariate analyses was used to detect independent associates of frailty status. Odds ratio (OR) and 95% confidence interval (CI) were given. Study included 148 patients aged 18-80. Sixty (60) patients were end stage renal disease (ESRD) patients on maintenance hemodialysis (HD) (at least for 3 months) and 88 were stage 3-4 CKD patients. Thirty-seven (37) patients (42%) were eGFR G3a, 31 patients (35.3%) were eGFR G3b and 20 patients (22.7%) were eGFR G4 in stage 3-4 CKD patients. Demographics, etiology of CKD, comorbidities, regular drugs, dialysis-related and laboratory data were recorded. FRAIL scale was scored as follows; 0=robust, 1-2=prefrail, and ≥3= frail. The frailty status was compared between frail+prefrail group vs robust (non-frail) group. The prevalences of prefrailty and frailty were 68.3% and 3.3% in HD group and 53.4% and zero in stage 3-4 CKD group, respectively (p = 0.025). In the multivariate logistic regression analysis, being in HD group (OR=3.87, 95% CI= 1.06-14.19, p=0.04), older age (OR=1.09, 95% CI= 1.04-1.13) and female sex (OR=9.13, 95%CI= 2.82-29.46) were independent risk factors for frailty (p<0.001, for both). Prefrailty and frailty are quite common among HD and CKD stage 3-4 patients. Being an HD patient is an independent risk factor for non-robust (frail or prefrail) status. Our findings point out a remarkably high prevalence of frailty severity (prefrailty/frailty) phenotype among patients with advanced CKD stages.

Prevalence of ABO Blood Grouping among Hemodialysis Patients in Dubai

Background: Beyond their vital role in blood transfusion, ABO antigens were speculated to be involved in developing various human illnesses, including infectious, neoplastic, cardiovascular, and many others. Many researchers attempted to highlight the relationship between kidney disease and ABO phenotypes. The majority of these reports showed a predominance of blood group O antigen among patients with chronic kidney disease, while few had opposed these findings. We aimed in this study to elaborate on blood group typing among our hemodialysis patients and whether it has a prognostic effect on the overall mortality. Methods: This is an observational, cross-sectional, retrospective study among chronic adult hemodialysis patients being dialyzed at Dubai Hospital over the past six months, from Jan 2021 till June 2021. The patient's demographic characteristics (age, sex, etiology of chronic kidney disease, medical comorbidities, and blood groups) were retrieved using an electronic hospital medical record system. Results: Our study population constituted 224 hemodialysis patients; their mean age was 55.4 years (16-94 years), 83.6% were UAE nationals, and 59.8% were males. Diabetic nephropathy was the etiology of end-stage kidney disease in 46%. ABO blood group distribution among our study population was as follows; group O was the commonest (45%), followed by group B positive (23%) and A Positive (20.9%). Among the UAE national patients group, O+ constitutes 46.9%, followed by B+ in 24%, and A+ in 21%. Nevertheless, group O+ was still the commonest among the nonnational hemodialysis patients in 37.7%, A+ in 28.8%, and B+ in 24.4%. Additionally, group O-positive was the predominant group among all diabetic dialysis patients (47%). Nine patients died during the study period of different causes; out of them, 4 patients (44.4%) had group O positive. Conclusion: Blood group O was the commonest blood group among our hemodialysis patients. Additionally, it was the commonest group in all diabetic dialysis patients. More studies from Arab countries are needed to comprehend the relationship between ABO blood phenotypes and kidney disease and whether certain blood groups have any role in a patient's progression to ESKD.

316.16: Which Patients Over 60 Years Old Are Candidates for a Kidney Transplant? Usefulness of a Mortality Predictive Score

Introduction: The decision to indicate a kidney transplant (KT) to an elderly patient with end-stage chronic kidney disease is not simple due to the high morbidity and mortality associated. The Dusseux et al. score was originally developed in France to predict 3-year post kidney transplant mortality in subjects older than 70 years. The objective of this study was to evaluate the usefulness of this score to predict 1-year post KT mortality in patients older than 60 years and to identify the best cut-off point. Methods: A retrospective cohort study was performed. All patients over 60 years old who received a KT at Hospital Privado Universitario de Córdoba between January 2009 and December 2015 were consecutively included. A one-year post-KT follow-up was carried out and variables associated with mortality were analyzed. The Dusseux et al. score considers as predictive variables: sex, age, etiology of chronic kidney disease, comorbidities, mobility status, body mass index and the presence of a temporary catheter at the time of dialysis initiation. The t test or Mann-Whitney test were used to evaluate differences between continuous variables t, and chi2 or Fisher’s test for categorical variables, as appropriate. To evaluate the predictive capacity, the area under the curve (AUC) was used and the Youdex Index J was applied to identify the best cut-off point, with its sensitivity and specificity. Kaplan Meier survival curves were made and then compared with the logRank test. A value of p<0.05 was considered statistically significant. Results: We included 111 patients aged 66.2 ± 5.2 years, 54.9% were men. As relevant comorbidities, 30.7% were diabetic and 13.5% had ischemic heart disease. 82% received a cadaveric KT. As induction, 100% were given steroids, 60.3% basiliximab, 22.5% thymoglobulin and 9.9% gamma globulin. As maintenance, 93.7% were treated with steroids, tacrolimus and mycophenolate. Mortality during follow-up was 9.9% (n:11; 8 due to infectious etiology and 3 from cardiovascular disease). The patients who died were older (70.3 ± 6.6 vs 65.8 ± 4.9; p=0.05), had a greater history of ischemic heart disease (36.7% vs 11%; p=0.04), and had a higher mortality predictive score (9.4 ± 3 vs 6.8 ± 2.5, p=0.02). There were no differences in the rest of the variables. This score obtained a high AUC to predict mortality (AUC=0.75; p<0.01; figure 1) and the best cut-off point was 8, with a sensitivity of 72.7% and a specificity of 78%. Subjects with a score >8 had higher mortality than those with a score ≤8 (26.7% vs 3.7% respectively; p<0.01). There were significant differences between the survival curves of these groups (p<0.01; figure 2). Conclusion: This clinical score is a good predictor of mortality 1-year after KT in patients over 60 years old. The best cut-off point of the score was 8 points. This could be a useful and simple tool to help in the decision to indicate a KT in this type of patients. Fundación Nefrológica de Córdoba.

Potential Mechanisms Involved in Chronic Kidney Disease of Unclear Etiology.

The etiology of chronic kidney disease of unclear etiology, also known as Mesoamerican nephropathy, remains unclear. We investigated potential etiologies for Mesoamerican nephropathy in an immigrant dialysis population. Migrants with Mesoamerican nephropathy kidney failure (n=52) were identified by exclusion of known causes of kidney disease and compared using a cross-sectional survey with demographically similar patients with kidney failure from other causes (n=63) and age/sex/place of origin-matched healthy participants (n=16). Survey results were extended to the bench; C57BL/6 mice (n=73) received 10-15 weekly intraperitoneal injections of paraquat (a reactive oxygen species-generating herbicide) or vehicle. Kidney function, histology, and expression of organic cation transporter-2 (proximal tubule entry for paraquat) and multidrug and toxin extrusion 1 (extrusion pathway) were examined. Kidney biopsies from Nicaraguan patients with acute Mesoamerican nephropathy were stained for the above transporters and compared with patients with tubulointerstitial nephritis and without Mesoamerican nephropathy. Patients with Mesoamerican nephropathy and kidney failure were young agricultural workers, almost exclusively men; the majority were from Mexico and El Salvador; and they had prior exposures to agrochemicals, including paraquat (27%). After adjustment for age/sex, exposure to any agrochemical or paraquat was associated with Mesoamerican nephropathy kidney failure (odds ratio, 4.86; 95% confidence interval, 1.82 to 12.96; P=0.002 and odds ratio, 12.25; 95% confidence interval, 1.51 to 99.36; P=0.02, respectively). Adjusted for age/sex and other covariates, 1 year of agrochemical exposure was associated with Mesoamerican nephropathy kidney failure (odds ratio, 1.23; 95% confidence interval, 1.04 to 1.44; P=0.02). Compared with 16 matched healthy controls, Mesoamerican nephropathy kidney failure was significantly associated with exposure to paraquat and agrochemicals. Paraquat-treated male mice developed kidney failure and tubulointerstitial nephritis consistent with Mesoamerican nephropathy. Organic cation transporter-2 expression was higher in male kidneys versus female kidneys. Paraquat treatment increased organic cation transporter-2 expression and decreased multidrug and toxin extrusion 1 expression in male kidneys; similar results were observed in the kidneys of Nicaraguan patients with Mesoamerican nephropathy. Exposure to agrochemicals is associated with Mesoamerican nephropathy, and chronic exposure of mice to paraquat, a prototypical oxidant, induced kidney failure similar to Mesoamerican nephropathy.

Effects of a nutrition education program on self-care behavior and kidney functions in pre-dialysis chronic kidney disease patients

The kidneys play a vital role in eliminating wastes and maintaining electrolyte and acid balance in the human body. Chronic kidney disease (CKD) is a condition in which the kidney functions irreversibly decline and eventually requires hemodialysis or renal transplantation. This present study aimed to investigate the effects of an 8-week nutrition education program on self-care behavior and kidney functions in pre-dialysis CKD patients. Twenty-one patients diagnosed with pre-dialysis CKD in the CKD Clinic were appointed to the 8-week nutrition education program on basic kidney functions, CKD etiology, CKD delaying strategies, and dietary counseling. Primary outcomes were the knowledge, attitude, and behavior scores on pre-dialysis self-care. Secondary outcomes were the estimated glomerular filtration rate (eGFR), blood urea nitrogen (BUN), serum creatinine (sCr), sodium, potassium, and phosphorus. Baseline and post-intervention scores of all outcomes were measured. Results show that most of the participants were female and aged ≥ 60. The nutrition education program significantly improved post-intervention knowledge, attitude, and behavior scores. Moreover, laboratory results of BUN, sCr, eGFR, and serum sodium levels were stable. Even though the mean potassium and phosphorus levels increased, there were improvements in the post-intervention measurements.

Complement Factor H and Related Proteins as Markers of Cardiovascular Risk in Pediatric Chronic Kidney Disease.

Cardiovascular disease (CVD) is the main cause of mortality among chronic kidney disease (CKD) patients, both in adults and in children. Hypertension is one of the risk factors of CVD. For early detection of subclinical CVD in pediatric CKD, 24 h ambulatory blood pressure monitoring (ABPM), cardiosonography, and arterial stiffness assessment were evaluated. CAKUT (congenital anomalies of the kidney and urinary tract) are the main etiologies of pediatric CKD. Previously, by a proteomic approach, we identified complement factor H (CFH) and related proteins differentially expressed between children with CAKUT and non-CAKUT CKD. In this study, we aimed to evaluate whether CFH, CFH-related protein-2 (CFHR2), and CFH-related protein-3 (CFHR3) were related to CVD risk in children with CKD. This study included 102 subjects aged 6 to 18 years old. The non-CAKUT group had higher plasma CFHR3 levels than the CAKUT group (p = 0.046). CFHR3 was negatively correlated with LV mass (p = 0.009). CFHR2 was higher in children with CKD with 24 h hypertension in the ABPM profile (p < 0.05). In addition, children with non-CAKUT CKD with day-time hypertension (p = 0.036) and increased BP load (p = 0.018) displayed a lower plasma CFHR3 level. Our results highlight that CFH and related proteins play a role for CVD in children with CKD. Early assessment of CFH, CFHR2, and CFHR3 may have clinical utility in discriminating CV risk in children with CKD with different etiologies.

Plasma Galectin-9 Is a Useful Biomarker for Predicting Renal Function in Patients Undergoing Native Kidney Biopsy.

Galectin-9 reduces tissue damage in certain immune-mediated glomerular diseases. However, its role in structural and functional renal changes in patients with varying types of chronic kidney disease (CKD) is less clear. To investigate the association between plasma galectin-9 levels, proteinuria, tubulointerstitial lesions, and renal function in different CKD stages. We measured plasma galectin-9 levels in 243 patients undergoing renal biopsy for determining the CKD etiology. mRNA and protein expression levels of intrarenal galectin-9 were assessed by quantitative real-time polymerase chain reaction and immunostaining. Relationships between plasma galectin-9, clinical characteristics, and tubulointerstitial damage were analyzed with logistic regression. We investigated galectin-9 expression patterns in vitro in murine J774 macrophages treated with differing stimuli. To analyze the relationship between galectin-9 and clinical features, we divided the patients into 2 groups according to median plasma galectin-9 levels. The high galectin-9 group tended to be older and to have decreased renal function, higher proteinuria, and greater interstitial fibrosis. After multivariable adjustment, elevated plasma galectin-9 levels were independently associated with stage 3b or higher CKD. An analysis of gene expression in the tubulointerstitial compartment in the biopsy samples showed a significant positive correlation between intrarenal galectin-9 mRNA expression and plasma galectin-9 levels. Immunohistochemistry confirmed increased galectin-9 expression in the renal interstitium of patients with advanced CKD, and most galectin-9-positive cells were macrophages, as determined by double-immunofluorescence staining. In vitro experiments showed that galectin-9 expression in macrophages was significantly increased after interferon-γ stimulation. Our findings suggest that plasma galectin-9 is a good biomarker for diagnosing advanced CKD.

NMR-Based Metabolomics in Differential Diagnosis of Chronic Kidney Disease (CKD) Subtypes.

Chronic Kidney Disease (CKD) is considered as a major public health problem as it can lead to end-stage kidney failure, which requires replacement therapy. A prompt and accurate diagnosis, along with the appropriate treatment, can delay CKD’s progression, significantly. Herein, we sought to determine whether CKD etiology can be reflected in urine metabolomics during its early stage. This is achieved through the analysis of the urine metabolic fingerprint from 108 CKD patients by means of Nuclear Magnetic Resonance (NMR) spectroscopy metabolomic analysis. We report the first NMR—metabolomics data regarding the three most common etiologies of CKD: Chronic Glomerulonephritis (IgA and Membranous Nephropathy), Diabetic Nephropathy (DN) and Hypertensive Nephrosclerosis (HN). Analysis aided a moderate glomerulonephritis clustering, providing characterization of the metabolic fluctuations between the CKD subtypes and control disease. The urine metabolome of IgA Nephropathy reveals a specific metabolism, reflecting its different etiology or origin and is useful for determining the origin of the disease. In contrast, urine metabolomes from DN and HN patients did not reveal any indicative metabolic pattern, which is consistent with their fused clinical phenotype. These findings may contribute to improving diagnostics and prognostic approaches for CKD, as well as improving our understanding of its pathology.

Hemostasis and oxidative stress in chronic kidney disease in children and adolescents.

Chronic kidney disease (CKD) can be defined as the progressive loss of renal function, characterized by a decreased glomerular filtration rate (GFR). The etiology of CKD in childhood is mainly associated with congenital anomalies of the kidneys and urinary tract (CAKUT) and with glomerular diseases. The goal of this study was to investigate the hemostasis and oxidative stress in pediatric CKD of different etiologies. Fifty-four CKD children and adolescents and 52 controls were enrolled in this study. The evaluation of hemostasis was carried out by determination of D-dimer (D-Di) and plasminogen activator inhibitor (PAI-1) plasma levels, while oxidative stress was evaluated by thiobarbituric acid reactive substance (TBARS) levels, protein carbonyl content, plasma antioxidant capacity (MTT), and ascorbate. The D-Di was increased in CAKUT stage 3 or 4 patients compared with those with glomerular disease. PAI-1 was increased in patients with glomerular disease compared with CAKUT. Carbonyl protein content was higher in the control group compared with glomerular disease stage 3 or 4 patients. Our findings showed that the reduction in GFR is associated with a state of hypercoagulability. The analysis of integrated networks showed an expansion of connections among hemostatic and oxidative stress markers in CKD children and adolescents compared with controls.

Prevalence and Determinants of Predialysis Dietitian Follow-Up: Results From the Brazilian Dialysis Registry

We aimed to evaluate the prevalence and sociodemographic determinants of predialysis dietitian follow-up in a large cohort of Brazilian dialysis patients. We retrospectively evaluated data from all incident adult dialysis patients included in the Brazilian Dialysis Registry from January 2011 to September 2021. Predialysis dietitian follow-up was classified as present when a period more than 6months of dietitian care was reported. Gender, age, skin color, education, body mass index, chronic kidney disease etiology, first chronic dialysis program, healthcare provider, and geographic regions were tested in logistic regression models. Ten thousand three hundred and eighty two patients met the inclusion criteria and 1,254 (12.1%) reported predialysis dietitian follow-up, most of them referred by a nephrologist (94.2%). The independent determinants of dietitian follow-up were older age, white skin color, higher education level, not having diabetes, living in North/Northeast and South (compared to Southeast), and having a nonpublic healthcare provider. When considered only patients under a predialysis care of a nephrologist, higher education, hemodialysis as the first dialysis modality, and living in the North/Northeast and South regions (compared with Southeast) were associated with dietitian follow-up. Predialysis dietitian follow-up for more than 6months in a country where the public health system is the main dialysis provider is still very low. The nephrologist is pivotal for referral to dietitians but socioeconomic factors also seem to play a role in this regard.

MO520: Prevalence of Anemia in Patients With Stage 3 or 4 Chronic Kidney Disease in Portugal–The Nefropor Study

Abstract BACKGROUND AND AIMS Anemia is a highly prevalent and modifiable comorbidity in patients with chronic kidney disease (CKD), which tends to aggravate as the disease progresses. The economic burden of anemia in CKD is high, and quality of life issues (e.g. fatigue, reduced productivity) is common in these patients. Data on the prevalence and treatment of anemia in CKD stages 3 and 4 (based on the estimated glomerular filtration rate according to KDIGO classification) in Portugal are lacking. The NEFROPOR study aimed to estimate the prevalence of anemia in patients with CKD stage 3 or 4 admitted to a Nephrology consultation between 1 January and 31 March 2017 and characterize anemia treatment in this patient population. METHODS NEFROPOR was a retrospective, multicentric study carried out in 10 Portuguese centers. All patients aged ≥18 years with stage 3 or 4 CKD admitted to a Nephrology consultation in one of those centers between 1 January and 31 March 2017 were invited to participate, and data for up to 24 months after admission were collected from patients’ clinical files. Retrieved data included age, body mass index (BMI), anemia status according to the World Health Organization (WHO) diagnostic criteria, and anemia treatment type and duration. Three assessments of the prevalence anemia were performed: at the time of the first Nephrology visit (presentation), at the first analytical results and the overall prevalence in the study cohort. Statistical analysis was performed in SPSS Statistics (v26) and a 0.05 significance level was adopted. RESULTS A total of 176 patients were included in this study, mostly (61.9%) male, with a median age of 76 years (range, 26–97) and a mean BMI indicative of pre-obesity (28.2; standard deviation, 4.2). CKD stage 3b was predominant (43.2%), followed by stage 4 (32.4%) and stage 3a (24.4%). The most frequent CKD etiologies in this cohort were diabetes (39.8%), followed by arterial hypertension (27.8%) and unknown cause (25.6%). Arterial hypertension was largely the most frequent comorbidity, present in 90.3% of patients, followed by diabetes (54.0%). Although less prevalent, coronary artery disease (18.2%) and congestive heart failure (14.8%) were also identified in this patient population. A total of 44.9% of patients [95% confidence interval (CI), 37.7%–52.3%] had anemia at presentation, which was significantly associated with CKD stage, diabetes, peripheral vascular disease and myocardial infarction comorbidities, and diabetes and unknown CKD etiology. The overall prevalence of anemia in the study cohort was 61.9% (95% CI 54.6%–68.9%), and it was significantly associated with diabetes and peripheral vascular disease comorbidities and with diabetes and primary glomerulonephritis as CKD etiologies. The prevalence of anemia at the first analytical results was 49.4% (95% CI 42.1%–56.8%), and it was significantly associated with CKD stage, diabetes, non-skin cancer, peripheral vascular disease and myocardial infarction comorbidities, and diabetes as CKD etiology. Figure 1 shows the evolution of anemia treatment in this cohort over 24 + months. CONCLUSION The three estimates of the prevalence of anemia in this study were consistent with each other, particularly those for the first visit and first analytical results. The latter were also consistent with evidence in the literature reporting a prevalence of anemia in the population of patients with CKD stages 3 and 4 between 40% and 60%. The overall prevalence of anemia in this study was 12%–15% higher than first visit and first analytical results estimates, in agreement with the fact that this refers to a cumulative prevalence. These data support the need for optimized and individualized treatment strategies for patients with CKD stages 3 and 4, maximizing the efficiency of health-care resource use.

MO722: Cardiac Biomarkers (NT-proBNP, Troponin I) and Heart Failure in Haemodialysis Patients

Abstract BACKGROUND AND AIMS Patients with chronic kidney disease (CKD) stage 5 on haemodialysis are at a high risk of cardiovascular disease according to 10-year estimation validated risk models (SCORE system) [1, 2]. Cardiac biomarkers, such as N-terminal pro-BNP (NT-proBNP) and troponin I (Tn-I), have been studied in this population enabling patient classification and prediction of cardiovascular morbimortality in chronic haemodialysis [3–5]. The primary objective of this study is to determine serum levels of the cardiac biomarkers NT-proBNP and TnI, and to evaluate the relationships between ecocardiographic signs of heart failure and its treatment, and to identify those patients in chronic haemodialysis at the highest cardiovascular risk. METHOD We performed an observational, descriptive study in patients on maintenance haemodialysis at our haemodialysis unit (n = 118). We collected different data: gender, age, dialysis vintage and etiology of CKD. We examined medical records and transthoracic echocardiography reports of the last year and classified patients according to heart failure diagnosis (yes/no). Levels of NT-proBNP were divided into three categories with different cut-off points: group 1 (&amp;lt;50-year-old, NT-proBNP &amp;lt; 450 pg/mL), group 2 (50–75-year-old, NT-proBNP &amp;lt; 900 pg/mL), group 3 (&amp;gt;75-year-old, NT-proBNP &amp;lt; 1800 pg/mL). TnI levels were considered positive above 20 pg/mL in all age groups. RESULTS Participants’ mean age was 64.65 ± 2.84 years, and 62.7% were identified as male. The mean age was 4.4 years older in women (67.43 years in women and 62.92 years in men). A total of 66.9% of patients had started renal replacement therapy in the last 5 years. The most common etiology of CKD (number of patients) was diabetes (31) followed in decreasing order by unknown (22), glomerular disease (18), hypertension (13), hereditary disease (8), systemic disease (4) and other kidney and urologic disorders (22). The diagnosis of heart failure stated by medical records and echocardiography was positive only in 26.27% (31 patients), thus the 73.73% (87 patients) did not present that diagnosis. Of those 31 patients with heart failure, 26 patients had raised NT-proBNP levels, in accordance with their predefined age-group (group 1, 2 or 3). On the other hand, 77 (or 65% of the total sample) of the 87 patients without clinically diagnosed heart failure had elevated cardiac biomarkers that could support a heart failure diagnosis, not previously stated in their medical history. Tn-I levels were positive in 35% (39 patients) without dyspnea, chest pain or other heart disease symptoms. CONCLUSION In conclusion, cardiac biomarkers allowed us to broaden the diagnostic process of heart failure and to identify those patients at a higher cardiovascular risk. Our results suggest the majority of patients of our haemodialysis unit would benefit of a closer monitoring, with echocardiography and assessment of serum cardiac biomarkers.

MO540: Are the Haematological Markers of Inflammation Predictors of Fibroblast Growth Factor-23 in Non-Dialysis Chronic Kidney Disease?

Abstract BACKGROUND AND AIMS Recently, a growing body of evidence point to the relationships between inflammation and fibroblast growth factor 23 (FGF23) in adults with and without chronic kidney disease (CKD). On the other hand, some haematological indices derived from the complete blood count appear as simple and inexpensive biomarkers of systemic inflammation. Therefore, this study aimed to evaluate the association between the haematological markers of inflammation and FGF23 in non-dialysis CKD. METHOD This single centre, cross-sectional study prospectively enrolled 90 subjects with moderate to severe stable CKD [median estimated glomerular filtration rate (eGFR) 25 (95% confidence interval 95% CI 24.9–30.5) mL/min, 46% in stage G3, urinary albumin-to-creatinine ratio (ACR) 221 (95% CI 498–954) mg/g], mostly males (61%), aged 62 (95% CI 57–64) years. Patients on renal replacement therapy (RRT) and those with active malignancies, infectious and inflammatory diseases were excluded. Demographic, past medical history (CKD vintage and etiology, comorbidities, chronic medications) and laboratory data were collected. Haematological markers of systemic inflammation [red blood cell distribution width (RDW), platelet distribution width (PDW), neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR)] were obtained from the complete blood count. Other measured lab parameters were: c-terminal FGF23 (cFGF23), intact parathyroid hormone (iPTH), serum calcidiol (25OHD), total calcium (tCa), phosphate (PO4), alkaline phosphatase, C-reactive protein, albumin, transferrin, ferritin and transferrin saturation, as markers of mineral metabolism, inflammatory, nutritional and iron status, respectively. Associations among studied parameters were assessed by Spearman rank test, multivariate linear regression and logistic regression models. Non-parametric variables were log-transformed. RESULTS The median cFGF23 was 4.65 (95% CI 7.57–14.4) pg/mL. Subjects in the highest cFGF23 quartile [n = 22, cFGF23 20.8 (95% CI 20.8–40.8) pg/mL] had higher RDW (P = 0.02), iPTH (P &amp;lt; 0.001), PO4 (P = 0.005) and ACR (P = 0.004), but lower tCa (P = 0.04), haemoglobin (P = 0.01) and eGFR (P &amp;lt; 0.001) as compared to those in the lowest quartile [n = 23, cFGF23 0.84 (95% CI 0.71–1.10) pg/mL]. Moreover, they had higher proportions of arterial hypertension (P = 0.01) and previous treatment with intravenous iron (P = 0.03). A trend to higher PLR (P = 0.052), NLR (P = 0.064), and ferritin (P = 0.076) was also observed. However, beside the expected bivariate correlations with eGFR, ACR, iPTH, tCa and PO4, cFGF23 was further correlated solely with haemoglobin (rs = –0.33, P = 0.002). In a multivariate linear regression model which explained 34% of the log(cFGF23) variance, log(PLR) (B 1.59, 95% CI 0.14–3.03, P = 0.03) and log(eGFR) (B –1.65, 95% CI –2.51 to –0.80, P &amp;lt; 0.001) were independent predictors. After adjustment for history of arterial hypertension and previous intravenous iron treatment, in a model of logistic regression (Nagelkerke R2 0.57, Chi2 16.7, P = 0.03), log(eGFR) was found as independent predictor of the log(FGF23) [odds ratio (OR) 0.07, 95% CI 0.01–0.36, P = 0.002]. However, RDW was retained in the last step of this model with a borderline significance (OR 4.3, 95% CI 0.98–19.02, P = 0.052). CONCLUSION Taken together, our findings suggest that, in addition to the kidney function, RDW and PLR seem to predict cFGF23 in non-inflammed, stable, non-dialysis CKD adults. Thus, one might speculate in favour of the association between chronic inflammatory state and FGF23 metabolism and in support of the revelatory role of some haematological markers of inflammation, a hypothesis that needs further research.

MO485: Chronic Kidney Disease in Patients With Lung Transplant

Abstract BACKGROUND AND AIMS The incidence of chronic kidney disease (CKD) in patients with lung transplantation (LTx) has increased over the last decades. Progression factors recognized in the development of CKD are: older age and comorbidity of recipients, immunosuppressive (IS) toxicity and longer survival. There is a lack of specific information about other risk factors or specific preventive management of CKD. METHOD Retrospective, single-centre study including all patients with LTx on Nephrology outpatient clinic among 2007 and 2020. Demographic, comorbidity and intercurrent events, renal function impairment, proteinuria and IS treatment were analyzed. We defined composite renal event (MARE) as renal replacement therapy (RRT), death or doubling serum creatinine. RESULTS A total of 69 LTx receptors (79.4% double LTx) were followed in a dedicated outpatient nephrology clinic. A total of 52.2% male, mean age at LTx 48.3 years (SD 16.6). Etiology of lung disease: cystic fibrosis (30.4%), obstructive lung disease or emphysema (33.3%) and interstitial disease (30.4%). After LTx, as complications, infection was the most frequent event (89.7%) and 49.3% presented neoplasic illness. The mean time from LTx until first nephrologist evaluation was 6.6 years (2 months–19.9 years) and main comorbidities were: hypertension (81.2%), diabetes mellitus (52.2%), dyslipidemia (50.7%), 60.3% former smokers and 26.1% had suffer from a previous CV event. After 1 year of LTx, mean eGFR decreased to 49.8 mL/min, which means that only in the first year after LTx there is a loss of ∼50% of mean kidney function. Factor associated with impaired kidney function at the first year after LTxw was cystic fibrosis (higher percentage in the rapid progression group). At first evaluation by Nephrology, the mean eGFR was 30.9 mL/min (SD 15.3), with a CKD distribution: 39.4% CKD 3; 45.5% CKD 4 and 12.1% CKD 5 (&amp;lt;15). Clinical study and biopsy define CKD etiologies: CNI toxicity (68.1%) thrombotic microangiopathy (11.6%), tubular (10.1%), vascular (7.3%) and glomerulopathies (2.9%). A total of 88.4% patients reached MARE at the end of the study. A total of 24 patients required RRT (mean time since LTx 9.2 years) and thereafter, 10 received a kidney transplantation (KTx). In Dyalisis group, a higher mortality was observed versus no dialysis group (24 versus 2.2%), a higher percentage of vascular origin disease with a further deterioration of eGFR at the time of referral to Nephrology. At the end of follow-up, 15 patients died (14 were in RRT), 5 continued on HD and 5 with a functional KTx, and 44 patients were still without RRT. CONCLUSION