Previous Chronic Kidney Disease Research Articles

#1689 Urosepsis and hypovolemia—the main causes of AKI in nursing home residents

Abstract Background and Aims Nursing home residents are at high risk for acute kidney injury (AKI) due to increased prevalence of comorbidities, prolonged immobilization in bed and altered cognitive function. As our nephrology department is confronted with high addressability of institutionalized adults with kidney impairment, we considered describing the epidemiology of AKI and risk factors for AKI-related mortality in this population. Method All adult patients admitted with AKI (KDIGO creatinine-based diagnostic criteria) in our nephrology department during a 6 months period (1st January-30th June 2023) were included in this study. Patients’ data (age, gender, comorbidities) and AKI-related data (causes, need for dialysis recovery of renal function, death) were compared between institutionalized and non-institutionalized patients. Factors associated with increased risk of death in AKI in nursing home residents were also analyzed. All the data was analyzed using IBM SPSS Statistics 25 (IBM, Corp.); the results were considered significant at P < 0.05. Results During the mentioned period a total of 297 patients with AKI were hospitalized: 57 nursing home residents (19.19%) and 240 patients with community-acquired AKI. The nursing-home residents were significantly older, female gender prevailed and history of stroke was significantly higher than in patients with community-acquired AKI (Table 1); no significant differences were found regarding prevalence of diabetes, chronic heart failure or previous chronic kidney disease. Chronic immobilization in bed was present in all institutionalized patients and in 21 patients with community acquired-AKI (8.75%). Multifactorial AKI, dehydration with hypovolemia and urosepsis were significantly more frequent in nursing-home residents, but there were no differences regarding other causes of AKI (Table 1). Increased prevalence of urosepsis in institutionalized patients was not associated with higher frequency of obstruction of urinary tract. Compared with community-acquired AKI, ICU admission and evolution with multiple organ failure were significantly more frequent in institutionalized patients with AKI, but there were no significant differences regarding the need for hemodialysis/hemodiafiltration, nor regarding the recovery of renal function in survivors. Analyzing factors associated with death in nursing home residents, we found that prolonged hospital stay, ICU admission, sepsis and multiorgan failure were associated with increased risk of in-hospital death (Table 2). Conclusion AKI in chronic institutionalized patients is mainly caused by dehydration and/or non-obstructive urosepsis, is often multifactorial and it is associated with increased risk of multiorgan failure, ICU admission and death. An early recognition and a better awareness of these risk factors in nursing homes can improve the epidemiology and the outcome of this severe disease.

#327 Impact of outpatient medication on community-acquired acute kidney injury

Abstract Background and Aims Medications are a relatively common cause of acute kidney injury (AKI) in hospitalized patients and those in the intensive care unit (ICU). However, we know less about the influence of outpatient medication in patients admitted from the emergency room who already have a community-acquired AKI (CA-AKI) The purpose of this study is to analyze the impact of outpatient medication in a cohort of patients with CA-AKI admitted to the nephrology service of a tertiary level hospital. Method This is a single-center, observational, longitudinal, and retrospective study based on a cohort of patients with CA-AKI admitted to the Nephology Service of a third level hospital from January 2010 to December 2018. We analyzed the characteristics of outpatient medication in these patients and their clinical consequences during admission and follow-up after hospital discharge. Results A total of 639 patients were included in the final analyses. The mean age was 72.93 ± 13.38 years. 61.7% were men. Charlson comorbidity index (CCI) was 5.87 ± 2.4 points. The length of stay was 11.63 ± 10.14 days. In view of the Etiology of AKI, 72.1% had prerenal AKI and 27.9% non-prerenal. 436 patients had a history of previous chronic kidney disease (CKD) (68.23%). AKI KDIGO stages were: stage I, 105 cases (16.4%); stage II, 67 cases (10.5%); stage III 467 cases (63.1%). Hemodialysis (HD) was required in 114 patients (17.8%). 62 patients (9.7%) died during hospital stay. The average number of drugs ingested prior to admission was 8.45 ± 4.11 with no differences by sex. Percentage of patients taking drug groups: diuretics 62.8%; Angiotensin-converting enzyme inhibitors (ACEI) or Angiotensin receptor Blockers (ARB) 68.4%; combination of diuretics with ACEI/ARB 50.9%; Proton-pump inhibitors (PPI) 64.1%; Statins 43.5%; Beta blockers 30.7%; allopurinol 25.8%; Anticoagulants 20.2%; Metformin 13.8%; Spironolactone 13.5%. There was a significant positive correlation between age (r=0.189; p<0.001), baseline creatinine (r=0.258; p<0.001), and CCI (r=0.43; p<0.001), with the number of drugs. There was a significant inverse correlation between peak creatinine during admission (r=−0.170; p<0.001), length of stay (r=−0.109; p 0 0.006), and number of drugs. Patients with prerenal etiology consumed significantly more drugs than those with parenchymal or obstructive etiology (9.09 ± 3.9 vs 6.77 ± 4.1 and 6.92 ± 4.3 respectively) The number of drugs did not influence the AKI stage, mortality during admission, nor the need for dialysis or ICU admission. Patients taking non-potassium sparing diuretics had significantly lower sodium (137.1 ± 5.73 vs 135.75 ± 5.9 mmol/L; p=0.005) and chloride levels (99.94 ± 9 vs 98.42 ± 8.1 mmol/L; p=0.029) compared to those who did not take them. Patients taking potassium-sparing diuretics (6.49 ± 1.55 vs 5.14 ± 1.32 mmol/L; p<0.001), ACEI/ARBs (5.42 ± 1.44 vs 5.12 ± 1.4 mmol/L; p=0.014) or beta-blockers (5.51 ± 1.38 vs 5.24 ± 1.44 mmol/L; p=0.030) presented significantly hyperkalemia compared to those who did not take them. After performing a multivariate linear regression analysis, the only drugs that was associated with hyperkalemia were potassium-sparing diuretics (B 1.35; 95% CI 1.05-1.66; p<0.001). In the follow-up after discharge, patients taking 6 or fewer drugs had better survival than those taking 7 to 12, and the latter better than those taking more than 12 drugs (log rank test: Chi square 24.47; p<0.0001) In the univariate cox regression, the number of drugs significantly influenced survival (Exp(B) 1.069; 95% CI 1.043-1.096; p<0.0001). Conclusion The patients in our series with CA-AKI were polymedicated, mainly those of prerenal etiology, with a clear correlation with age, baseline creatinine and previous comorbidity and with a prominence of ACEIs/ARBs, diuretics, and PPIs. Certain drugs had a significant impact on ionic alterations, adding morbidity to the condition. The number of drugs ingested is a marker of survival after hospital discharge. It is necessary to optimize outpatient drug management to prevent the development of CA-AKI and their consequences.

#1786 Correlation of electrolyte disturbances in community-acquired acute kidney injury

Abstract Background and Aims Acute renal injury can cause electrolyte disorders that increase patient morbidity and mortality. There are few data in the literature describing these alterations and the possible correlation between them in patients with community-acquired AKI (CA-AKI). The purpose of this study is to analyze the correlation between electrolyte disorders in a cohort of patients with CA-AKI admitted to the nephrology service of a tertiary level hospital. Method This is a single-center, observational, longitudinal, and retrospective study based on a cohort of patients with CA-AKI admitted to the Nephology Service of a third level hospital from January 2010 to December 2018. We analyzed the incidence of changes in sodium, potassium, chloride, bicarbonate, calcium, and phosphorus in these patients and their correlations. Results A total of 639 patients were included in the final analyses. The mean age was 72.93 ± 13.38 years. 61.7% were men. Charlson comorbidity index was 5.87 ± 2.4 points. The length of stay was 11.63 ± 10.14 days. In view of the Etiology of AKI, 72.1% had prerenal AKI and 27.9% non-prerenal. 436 patients had a history of previous chronic kidney disease (CKD) (68.23%). AKI KDIGO stages were: stage I, 105 cases (16.4%); stage II, 67 cases (10.5%); stage III 467 cases (63.1%). Hemodialysis (HD) was required in 114 patients (17.8%). 62 patients (9.7%) died during hospital stay. The most frequent ionic alterations at a global level were low bicarbonate (78.3%), hyperkalemia (53.05%), hypocalcemia (49.6%) and hyponatremia (41.5%). When analyzing whether electrolyte alterations occurred simultaneously: 2.2% of cases did not present any, 6.3% only one, 18.2% two, 26.4% three, 26.1% four, 14.9% five and 5.9% six simultaneous alterations. There were no statistically significant differences between groups on mortality during admission. Higher mortality at discharge has been found in patients with a greater number of ionic alterations (p = 0.046). In our sample, positive correlations were found between sodium-bicarbonate (r = 0.184; p < 0.001), peak creatinine-potassium (r = 0.182; p < 0.001), potassium-chloride (r = 0.167 p < 0.001), sodium-chloride (r = 0.614; p < 0.001), phosphorus-peak creatinine (r = 0.394; p < 0.001), pH-bicarbonate (r = 0.747, p < 0.001) and phosphorus–PTH (r = 0.330; p < 0.001). Negative correlations were found between sodium–potassium (r = −0,123; p = 0.002), bicarbonate-potassium (r = −0.354; p < 0.001), potassium-pH (r = −0.390; p < 0.001), peak creatinine–chlorine (r = −0.013; p = 0.004), bicarbonate–chlorine (r = −0.236; p < 0.001), calcium–phosphorus (r = −0.174; p < 0.001), calcium–peak creatinine (r = −0.138; p = 0.001) and bicarbonate–peak creatinine (r = −0.274; p < 0.001). Conclusion In our series of patients with CA-AKI, many statistically significant correlations were found between altered electrolytes in acute renal failure. Most of these associations can be explained by the pathophysiology of acute kidney injury. However, it should be noted that not all cases have such a clear explanation. It is important to consider that all patients in our study had already developed acute renal failure upon admission. Therefore, these results should be interpreted with caution and confirmed through further evaluations. We suggest that additional research in this area is necessary to improve the management and prognosis of this condition.

#2271 Cardiovascular event prediction in kidney transplant recipients: a new risk score derivation and internal validation

Abstract Background and Aims Kidney transplant recipients (KTRs) have a cardiovascular (CV) risk 3 to 5-fold higher than that of the general population.CV disease represents the main cause of death in KTRs, both due to the presence of traditional risk factors and factors strictly related to transplant. The main CV risk calculators proved to be poorly predictive in the KTR population. We, therefore, aimed to compare the performance of CV risk scores already in use and to develop and validate a CV risk score in our KTRs population. Method Our analysis included 371 adult KTRs in follow-up at the outpatient clinic from 1 January 2015 to 31 December 2016. The composite outcome was the occurrence of MACE. We compared the performance of three main CV risk calculators (Framingham Risk Score-FRS-, INDANA score and PORT score). Thereafter, we built a predictive model selecting study variables by backward stepwise Cox regression. The risk score for each variable was weighted according to the HR of the final multivariable model. Internal and external validation of the prediction score and its discriminative capacity was assessed via area under the curve (AUC) curve, and the calibration via the Hosmer–Lemeshow test. Results After a mean follow-up of 68 months, CV events occurred in 71 (19%) KTRs. FRS, INDANA and PORT were demonstrated to have low predictive power in our population (Fig. 1). The accuracy did not improve after adjustment for immunological and transplant-related variables. Therefore, we derived a model including significative variables at multivariate analysis: age, dialysis vintage, systolic blood pressure, eGFR and 24-hour proteinuria (Akaike information criteria 713). The model discrimination was good (Harrel's c: 0.73). According to the hazard ratio, 3 points have been attributed to age higher than 60 years and 24 h proteinuria higher than 1 g/d, 2 points to dialysis vintage longer than 5 years, systolic blood pressure higher than 140 mmHg and eGFR less than 30 ml/min/1.73 m2. The new score demonstrated good discrimination (AUC 0.70, Fig. 2) and calibration (Hosmer-Lemeshow test 11.34, P = 0.12). The new score was internally validated by 10-fold cross-validation (mean AUC 0.70, 95% CI 0.60-0.77). For each point of the new score, the risk of the event increased by 40% and a score higher than three was associated with a 4-fold increased risk of composite endpoint. Conclusion We confirmed the poor predictive power of the known CV risk assessment tools in our real-world KTRs population. Moreover, their discriminatory power was not improved by adjustment for the occurrence of biopsy-proven rejection, HLA compatibility and donor-specific antibody. A new score for CV event prediction including traditional risk factors, such as age and systolic blood pressure, and variables related to renal function and the effects of previous chronic kidney disease, was developed and internally validated.

Role of Vascular Function in the Prognosis of Heart Failure Patients.

Background: Blood vessels have the Windkessel effect and are involved in blood circulation. The breakdown of this mechanism is also involved in the pathogenesis of heart failure (HF); however, the relationship between vascular dysfunction and HF prognosis is not fully understood. Methods: We evaluated 214 patients hospitalized for HF at our institution who underwent a cardio-ankle vascular index (CAVI), which evaluates vascular function, between January 2012 and July 2018. To investigate factors (including CAVI) associated with major adverse cardiac events (MACE) during 1 year after patients with HF were discharged, we evaluated clinical profiles, blood tests, chest X-P, 12-lead electrocardiography, and transthoracic echocardiographic findings. MACE was defined as cardiovascular death or readmission for HF. Results: The severity of HF between the MACE and non-MACE was not significantly different. Previous HF and chronic kidney disease were significantly more common in the MACE group. CAVI and % mean atrial pressure in the MACE group were statistically higher than those in the non-MACE group. The cardiac shadow as shown by chest X-P and left ventricular size in the MACE group were significantly bigger, and HF preserved ejection fraction (EF) (EF > 50%) was significantly more common in the MACE group. In multivariate analysis, CAVI was an independent predictive factor for the occurrence of MACE (model 1; hazard ratio (HR): 1.33, 95% confidence interval (CI): 1.05-1.68, p = 0.018; model 2; HR: 1.31, 95% CI: 1.07-1.60, p = 0.009). Conclusions: Because high CAVI is associated with poor prognosis of HF, these patients require more careful treatment.

Longitudinal plasma metabolome patterns and relation to kidney function and proteinuria in pediatric chronic kidney disease.

Understanding plasma metabolome patterns in relation to changing kidney function in pediatric chronic kidney disease (CKD) is important for continued research for identifying novel biomarkers, characterizing biochemical pathophysiology, and developing targeted interventions. There is a limited number of studies of longitudinal metabolomics, and virtually none in pediatric CKD. The Chronic Kidney Disease in Children (CKiD) study is a multi-institutional, prospective cohort that enrolled children aged six-months to 16-years with estimated glomerular filtration rate (eGFR) 30-90ml/min/1.73m2. Untargeted metabolomics profiling was performed on plasma samples from the baseline, two-, and four-year study visits. There were technologic updates in the metabolomic profiling platform used between the baseline and follow-up assays. Statistical approaches were adopted to avoid direct comparison of baseline and follow-up measurements.To identify metabolite associations with eGFR or urine protein:creatinine (UPCR) among all three timepoints, we applied linear mixed effects (LME) models. To identify metabolites associated with time, we applied LME models to the two- and four-year follow-up data. We applied linear regression analysis to examine associations between change in metabolite level over time (∆level) and change in eGFR (∆eGFR) and UPCR (∆UPCR). We reported significance based on both the False Discovery Rate (FDR) <0.05 and p<0.05. There were 1156 person-visits (N: baseline=626, 2-year=254, 4-year=276) included. There were 622 metabolites with standardized measurements at all three timepoints. In LME modeling, 406 and 343 metabolites associated with eGFR and UPCR at FDR<0.05 respectively. Among 530 follow-up person-visits, 158 metabolites showed differences over time at FDR<0.05. For participants with complete data at both follow-up visits (N=123), we report 35 metabolites with ∆level∼∆eGFR associations significant at FDR<0.05. There were no metabolites with significant ∆level∼∆UPCR associations at FDR<0.05. We report 16 metabolites with ∆level∼∆UPCR associations at p<0.05 and associations with UPCR in LME modeling at FDR<0.05. We characterized longitudinal plasma metabolomic patterns associated with eGFR and UPCR in a large pediatric CKD population. Many of these metabolite signals have been associated with CKD progression, etiology, and proteinuria in previous CKD Biomarkers Consortium studies. There were also novel metabolite associations with eGFR and proteinuria detected.

Impact of dexamethasone in severe COVID-19-induced acute kidney injury: a multicenter cohort study

BackgroundAcute kidney injury (AKI) in intensive care unit (ICU) patients with severe COVID-19 is common (> 50%). A specific inflammatory process has been suggested in the pathogenesis of AKI, which could be improved by dexamethasone (DXM). In a small monocenter study (n = 100 patients), we reported a potential protective effect of DXM on the risk of AKI. This study aimed to investigate the preventive impact of DXM on AKI in a multicenter study of patients with severe COVID-19.MethodsWe conducted a multicenter study in three French ICUs from March 2020 to August 2021. All patients admitted to ICU for severe COVID-19 were included. Individuals with preexistent AKI or DXM administration before admission to ICU were excluded. While never used during the first wave, DXM was used subsequently at ICU entry, providing two treatment groups. Multivariate Cause-specific Cox models taking into account changes in ICU practices over time, were utilized to determine the association between DXM and occurrence of AKI.ResultsSeven hundred and ninety-eight patients were included. Mean age was 62.6 ± 12.1 years, 402/798 (50%) patients had hypertension, and 46/798 (6%) had previous chronic kidney disease. Median SOFA was 4 [3–6] and 420/798 (53%) required invasive mechanical ventilation. ICU mortality was 208/798 (26%). AKI was present in 598/798 (75%) patients: 266/598 (38%), 163/598 (27%), and 210/598 (35%) had, respectively, AKI KDIGO 1, 2, 3, and 61/598 (10%) patients required renal replacement therapy. Patients receiving DXM had a significantly decreased hazard of AKI occurrence compared to patients without DXM (HR 0.67; 95CI 0.55–0.81). These results were consistent in analyses that (1) excluded patients with DXM administration to AKI onset delay of less than 12 h, (2) incorporating the different ‘waves’ of the COVID-19 pandemic.ConclusionsDXM was associated with a decrease in the risk of AKI in severe COVID-19 patients admitted to ICU. This supports the hypothesis that the inflammatory injury of AKI may be preventable.

Effect of Intravitreal Anti-Endothelial Growth Factor Agents on Renal Function in Patients With Diabetes Mellitus

BackgroundIntravitreal administration of vascular endothelial growth factor inhibitors (anti-VEGF) is the treatment of choice in retinal pathology associated with type 2 diabetes mellitus (DM2). We aimed to analyze the effect on renal function in patients with DM2 after intravitreal anti-VEGF administration. MethodsSingle-center retrospective and observational study of patients with DM2 with and without chronic kidney disease (CKD). We analyzed the evolution of renal function after anti-VEGF onset, compared with a control group. ResultsWe included 45 patients (55.6% male) who received anti-VEGF therapy. Mean age was 74.4±11.5 (50-91) years. These were compared with 45 patients with similar characteristics. After 12-months, 76.3% had CKD with a mean reduction in estimate glomerular filtration rate (eGFR) of 19.4%. Nine patients (20%) had a >25% reduction in eGFR, and three patients (6.7%) had a >50% reduction in GFR. At 24-months, 80% of patients had CKD with a mean eGFR drop of 28%. The mean eGRF slope of patients who had received anti-VEGF treatment was 10 ml/min/year compared to 1,5 ml/min/year in the control group (p<0.05). After the first administration, five patients (17.2%) in the CKD group required renal replacement therapy during follow-up (mean time 22±12 months). Main risk factors for need of dialysis were age, presence of previous CKD, and baseline proteinuria. ConclusionIntravitreal anti-VEGF administration is a risk factor for CKD and rapid progression to end-stage kidney disease in patients with previous CKD. Knowing these drugs' implications is crucial to avoid CKD progression and opportunely limit their use in certain patients.

Post-discharge all-cause mortality in COVID-19 recovered patients hospitalized in 2020: the impact of chronic kidney disease.

In Brazil, the COVID-19 burden was substantial, and risk factors associated with higher in-hospital mortality rates have been extensively studied. However, information on short-term all-cause mortality and the factors associated with death in patients who survived the hospitalization period of acute SARS-CoV-2 infection is limited. We analyzed the six-month post-hospitalization mortality rate and possible risk factors of COVID-19 patients in a single center in Brazil. This is a retrospective cohort study focused on a six-month follow-up. The exclusion criteria were death during hospitalization, transference to another hospital, and age under 18. We collected data from the charts of all hospitalized patients from March 2020 to December 2020 with a positive RT-PCR test for SARS-CoV-2, resulting in a sample size of 106 patients. The main outcome was death after hospitalization, whereas comorbidities and demographics were evaluated as risk factors. The crude post-hospitalization death rate was 16%. The first 30 days of follow-up had the highest mortality rate. In a Cox regression model for post-hospitalization mortality, previous chronic kidney disease (HR, 4.06, 95%CI 1.46 - 11.30) and longer hospital stay (HR 1.01, 95%CI 1.00 - 1.02) were the only factors statistically associated with death. In conclusion, a high six-month all-cause mortality was observed. Within the six-month follow-up, a higher risk of death was observed for patients who had prior CKD and longer hospital stay. These findings highlight the importance of more intensive medical surveillance during this period.

Impact of Access Site on Periprocedural Bleeding and Cerebral and Coronary Events in High-Bleeding-Risk Percutaneous Coronary Intervention: Findings from the RIVA-PCI Trial.

The preference for using transradial access (TRA) over transfemoral access (TFA) in patients requiring percutaneous coronary intervention (PCI) is based on evidence suggesting that TRA is associated with less bleeding and fewer vascular complications, shorter hospital stays, improved quality of life, and a potential beneficial effect on mortality. We have limited study data comparing the two access routes in a patient population with atrial fibrillation (AF) undergoing PCI, who have a particular increased risk of bleeding, while AF itself is associated with an increased risk of thromboembolism. Using data from the RIVA-PCI registry, which includes patients with AF undergoing PCI, we analyzed a high-bleeding-risk (HBR) cohort. These patients were predominantly on oral anticoagulants (OAC) for AF, and the PCI was performed via radial or femoral access. Endpoints examined were in-hospital bleeding (BARC 2-5), cerebral events (TIA, hemorrhagic or ischemic stroke) and coronary events (stent thrombosis and myocardial infarction). Out of 1636 patients, 854 (52.2%) underwent TFA, while 782 (47.8%) underwent the procedure via TRA, including nine patients with brachial artery puncture. The mean age was 75.5years. Groups were similar in terms of age, sex distribution, AF type, cardiovascular history, risk factors, and comorbidities, except for a higher incidence of previous bypass surgeries, heart failure, hyperlipidemia, and chronic kidney disease (CKD) with a glomerular filtration rate (GFR) < 60ml/min in the TFA group. No clinically relevant differences in antithrombotic therapy and combinations were present at the time of PCI. However, upon discharge, transradial PCI patients had a higher rate of triple therapy, while dual therapy was preferred after transfemoral procedures. Radial access was more frequently chosen for non-ST-segment elevation myocardial infarction (NSTEMI) and unstable angina pectoris (UAP) cases (NSTEMI 26.6% vs. 17.0%, p < 0.0001; UAP 21.5% vs. 14.5%, p < 0.001), while femoral access was more common for elective PCI (60.3% vs. 44.1%, p < 0.0001). No differences were observed for ST-segment elevation myocardial infarction (STEMI). Both groups had similar rates of cerebral events (TFA 0.2% vs. TRA 0.3%, p = 0.93), but the TFA group had a higher incidence of bleeding (BARC 2-5) (4.2% vs. 1.5%, p < 0.01), mainly driven by BARC 3 bleeding (1.5% vs. 0.4%, p < 0.05). No significant differences were found for stent thrombosis and myocardial infarction (TFA 0.2% vs. TRA 0.3%, p = 0.93; TFA 0.4% vs. TRA 0.1%, p = 0.36). In HBR patients with AF undergoing PCI for acute or chronic coronary syndrome, the use of TRA might be associated with a decrease in in-hospital bleeding, while not increasing the risk of embolic or ischemic events compared to femoral access. Further studies are required to confirm these preliminary findings.

Decreased circulating transforming growth factor-beta (TGF-β) and kidney TGF-β immunoreactivity predict renal disease in cats with naturally occurring chronic kidney disease.

The aim of the present study was to compare the circulating transforming growth factor-beta (TGF-β) of clinically normal age-matched and naturally occurring chronic kidney disease (CKD) cats and to determine the correlation between the TGF-β expression and histopathological changes in cats with CKD. A total of 11 clinically normal age-matched and 27 cats with naturally occurring CKD were included in this study. Circulating TGF-β was quantified by immunoassays. Kaplan-Meier analysis was used to calculate the association between survival time and the concentration of circulating TGF-β. A general linear model was used to compare the circulating TGF-β between groups. Immunohistochemical analyses revealed TGF-β expression in renal tissues from cats with CKD that died during the study (n = 7) and in available archived renal tissue specimens taken at necropsy from cats that had previous CKD with renal lesions (n = 10). Correlations of the TGF-β expression and clinical parameters (n = 7) and histopathological changes (n = 17) were analysed using Spearman's rank correlation. The median survival time of cats with a lower concentration of circulating TGF-β was shorter than that of cats with a higher concentration. The area under the curve of circulating TGF-β for predicting CKD was 0.781, indicating good differentiation. The study indicated a significant difference in circulating TGF-β concentrations between clinically normal cats and those with CKD and demonstrated that TGF-β expression is correlated with tubular atrophy. The study findings suggest that decreased serum TGF-β and tubular atrophy with TGF-β immunoreactivity may be significant in cats with CKD.

Chronic kidney disease is an independent risk factor of postoperative seizures after burr hole surgery for chronic subdural hematomas

Background: Postoperative seizures are serious neurological complications of chronic subdural hematomas (CSDH). The identification of risk factors of seizures after CSDH is needed to determine which patients require antiepileptic prophylaxis. Methods: We retrospectively collected data on patients diagnosed with CSDH from 2015 to 2018. Postoperative seizures are defined as those occurring within 30 days after surgery. Non-hemorrhagic subdural effusion and acute subdural hemorrhage after craniotomy were precluded in the study. We collected data from 221 patients who had burr hole surgery. We retrospectively recorded patient characteristics, hematoma characteristics, symptoms at admission, comorbid conditions, and other related parameters to evaluate the impact of these parameters on postoperative seizures. Results: Postoperative seizures occurred in 16 patients (7.24%). The univariate analysis showed that previous chronic kidney disease (31.25% vs. 5.37%, p= 0.001), age (60.44 vs. 66.54 y, p = 0.029), low Glasgow Coma Score (GCS) at admission (13.69 vs. 14.46, p = 0.015), and preoperative midline shift (9.79 vs. 8.57 mm, p = 0.021) were significantly correlated with postoperative seizures. The multivariate analysis revealed that previous chronic kidney disease (odds ratio [OR] = 27.103; 95% confidence interval [CI] = 4.887-150.296; p &lt; 0.001), younger age (OR = 0.921; 95% CI = 0.866-0.979; p = 0.009) and preoperative midline shift (OR = 1.782; 95% CI = 1.175-2.702; p = 0.007) were independent risk factors of seizures. However, there was no significant difference in GCS at admission. Conclusions: The independent predictors of postoperative seizures in patients with CSDH were preoperative midline shift, chronic kidney disease, and younger age. For younger patients with chronic kidney disease and preoperative midline displacement, we recommend antiepileptic preventive measures during the perioperative period.

Inflammatory Bowel Disease With Chronic Kidney Disease and Acute Kidney Injury

It remains unclear whether inflammatory bowel disease is associated with long-term risk of chronic kidney disease (CKD) and acute kidney injury (AKI) in the general population. A total of 417,302 participants, including 2,940 patients with ulcerative colitis and 1,261 patients with Crohn's disease, without previous CKD and AKI at baseline (2006-2010) from the UK Biobank were included. The study outcomes included incident CKD and AKI, ascertained by self-report data and data linkage with primary care, hospital admissions, and death registry records. Analysis was conducted in 2022. During a median follow-up of 12.5 years, 13,564 and 14,331 participants developed CKD and AKI, respectively. Compared with the hazard ratio for non-inflammatory bowel diseases, the hazard ratios for CKD and AKI related to inflammatory bowel diseases were 1.57 (95% CI=1.37, 1.79) and 1.96 (95% CI=1.74, 2.20) after adjustments for age, sex, and race and were 1.32 (95% CI=1.15, 1.51) and 1.70 (95% CI=1.51, 1.91) after further adjustments for biological, behavioral, and socioeconomic factors in addition to mental health and self-rated health. Similar results were found for patients with Crohn's disease (adjusted hazard ratio=1.38 (95% CI=1.09, 1.75) for CKD and 1.62 [95% CI=1.30, 2.02] for AKI) and those with ulcerative colitis (adjusted hazard ratio=1.29 (95% CI=1.09, 1.51) for CKD and 1.71 [95% CI=1.49, 1.97] for AKI) in the fully adjusted models. Genetic risks of kidney diseases did not significantly affect the association of inflammatory bowel disease with incident CKD and AKI (both p-interactions>0.05). The association between inflammatory bowel disease and the risk of incident CKD (p-interaction=0.010) and AKI (p-interaction<0.001) were stronger in younger participants than in older participants. Inflammatory bowel disease was associated with higher risks for CKD and AKI, independent of genetic risks of kidney diseases.

Outcomes of Transcatheter Aortic Valve Implant Among Patients With A Previous Coronary Artery Bypass Graft: A Nationwide Analysis

There is a paucity of data regarding the temporal trends and outcomes of transcatheter aortic valve implant (TAVI) among patients with a previous coronary artery bypass graft (CABG) surgery. We queried the Nationwide Readmissions Database (2016 to 2019) for hospitalized patients who underwent TAVI using the appropriate International Classification of Diseases, Tenth Revision procedural codes. A multivariable regression analysis was used to adjust for the patients' and hospitals' characteristics in comparing the study groups. The primary outcome was in-hospital mortality. The final analysis included 237,829 patients who underwent TAVI, of whom 42,671 (17.9%) had a previous CABG. During the study period, there was a decrease in the proportion of patients with previous CABG who underwent TAVI (21.0% in 2016 vs 15.5% in 2019, ptrend=0.01), although there was no change in their in-hospital mortality rate (1.08% in 2016 vs 1.25% in 2019, ptrend=0.43). Patients with a previous CABG were younger and less likely to be women than those without a previous CABG. TAVI among those with a previous CABG was associated with lower in-hospital mortality (adjusted odds ratio [aOR] 0.79, 95% confidence interval [CI] 0.69 to 0.91), similar rate of ischemic stroke (aOR 0.81, 95% CI 0.71 to 0.93) and permanent pacemaker implant (aOR 1.00, 95% CI 0.93 to 1.05). Patients with a previous CABG had a lower all-cause 90-day readmission (odds ratio 0.95, 95% CI 0.94 to 1.06) but higher readmission for transient ischemic attack. Among those with a previous CABG, female gender and chronic kidney disease stage ≥3 were independently associated with a higher in-hospital mortality, whereas obesity was associated with a lower in-hospital mortality. In conclusion, there was a decrease in the proportion of patients with a previous CABG among those who underwent TAVI. TAVI among those with a previous CABG was not associated with increased in-hospital adverse events or 90-day all-cause readmissions.

#5703 COVID-19, RENAL DAMAGE AND ITS EVOLUTION IN HOSPITALISED PATIENTS IN THE FIRST WAVE OF THE PANDEMIC: EXPERIENCE OF ONE CENTRE

Abstract Background and Aims The damage that SARS Cov2 virus exerts at the renal level has been the subject of analysis in many studies. We analysed the extent of Acute Kidney Injury (AKI), possible factors involved and mortality in patients hospitalised with Covid-19 during the first wave of the pandemic. We reassessed renal function, as well as inflammatory and nutritional status of patients 18 months after admission, together with the capacity for recovery of renal function. Method Observational and retrospective study of patients admitted to the ward or intensive care unit (ICU) for Covid-19 during the month of March 2020. We defined the stage of renal damage according to the KDIGO guidelines. Among the possible risk factors associated with AKI and mortality, we analysed haematological analytical parameters (lymphopenia and plateletopenia), inflammatory markers such as CRP and ferritin, and nutritional status, vitamin D and cholesterol, among others. We evaluated ICU mortality using the Odin scale and the life expectancy at 10 years using the Charlson scale. We used the Chi-square test and Fisher's test, considering significant values p&amp;lt;0.05. Results A total of 576 patients were admitted during the study period, of whom 10.6% were admitted to the ICU (n 61). A total of 45.9% (n 28) had some degree of AKI, the most frequent being grade 2 (22.9%), followed by grade 3 (18%) and grade 1 (4.9%). Of all patients requiring admission to the ICU, 78.6% of those with AKI died. The Odin scale was significantly associated with AKI and mortality, but the Charlson scale was not. The maximum dose of Cisatracurium was significantly associated with AKI. Among the patients admitted to inpatient areas (n 515), 9.9% (n 51) had AKI and 31.4% of these patients died. In most cases the degree of renal damage was mild (82.4% grade 1 vs. 13.7% grade 2 and 3.9% grade 3). When we studied the patients who presented with AKI (n 79), we observed that CK and LDH values were significantly higher, indicating a more inflammatory state. Of the 79 patients, 48.1% (n 38) died, with significant differences in serum CRP and D-dimer levels. Of the 41 patients who survived, we conducted an 18-month follow-up study that only 36.6% (n 15) completed, with a mean age of 69.7 years, 73.3% being male and 20% with previous chronic kidney disease (CKD). At the end of follow-up 86% of them recovered renal function, according to pre-admission figures, including those patients with baseline CKD. Only 13% of the patients who completed follow-up showed a slight worsening of renal function with respect to their baseline situation. We observed differences in the values of calcium, vitamin B12 and vitamin D in the group of patients who recovered renal function compared to those who showed deterioration with respect to their situation prior to admission (p&amp;lt;0.02). Conclusion The incidence of AKI in COVID patients requiring admission to the ICU was four times higher than in patients admitted to the ward. The severity of renal damage was greater in the ICU, predominantly AKI 2-3 vs AKI 1, with mortality 2.5 times higher than in the ward. The group of patients who develop AKI have an elevation of inflammatory markers, which increases in the group of deceased patients. In ICU, the Odin scale was significantly related to AKI and mortality. - The mortality rate in the group of patients with AKI was high. Most of the patients have recovered pre-admission renal function after 18 months of follow-up, with differences in nutritional parameters such as calcium, vitamin B12 and vitamin D.

#5781 DRUG-INDUCED ACUTE INTERSTITIAL NEPHRITIS (D-AIN): HOW TO IDENTIFY THE RESPONSIBLE DRUG?

Abstract Background and Aims The mainstay of D-AIN treatment is the removal of the responsible drug. However, it is not always easy to identify the culprit drug as this entity mainly affects elderly patients on multiple medications, they rarely associate systemic symptoms (rash, fever), and the timeline regarding the diagnosis and the associated drug is not always clear. Therefore, the diagnosis and treatment are delayed, making full renal function recovery less likely. The lymphocyte transformation test (LTT) has demonstrated to be useful in the identification of the involved drug in other hypersensitivity-mediated lymphocyte T diseases such as Stevens-Johnson Syndrome or Dress Syndrome. For this reason, we wonder if this test could be relevant in identifying the responsible drug in D-AIN. The aim of this study is to test LTT in patients with clinical and histological diagnosis of D-AIN. Method We have conducted a retrospective observational study in which we have collected data from 2019 to 2022 from our electronic databases. Results: We have registered 9 cases of D-AIN diagnosed with histological confirmation in whom the LTT had been performed. 22.2% of these patients were men. The mean age was 48.1 years (standard deviation of 15.8). None of them had previous chronic kidney disease (CKD). Mean peak creatinine at diagnosis was 4.66 mg/dl (standard deviation of 1.95). Regarding the typical symptoms of the D-AIN, three patients (33%) presented with fever and none of them suffered from rash. 6 patients had sterile pyuria (66%). All of them received steroid treatment. Concerning the LTT results, 7 cases were positive for one of the drugs the patient was taking, and 2 were negative. Among the positive cases, the identified drugs were 1 case of beta lactams (piperacillin), 1 case of PPIs (omeprazole), 1 case of metamizole, 1 case of paracetamol, 1 case of eslicarbazepine and 2 cases of NSAIDs (dexketoprofen), while the negative cases have not been suspected of taking any culprit drug. Conclusion LTT may be a useful test to identify the responsible drug for D-AIN, especially in patients taking multiple medications in which may be included some of great importance like immunotherapy (typical cause of D-AIN) in oncological treatments. In negative cases, it could be expected that the patient had taken medications difficult to be identified in the clinical history or, in some situations, the drug hapten responsible for kidney damage might be a drug metabolite and not the drug itself, which cannot be detected by the test.

#5535 CALCIUM EXCRETION FRACTION AS AN EMERGING PARAMETER FOR AN ACCURATE DIFFERENTIAL DIAGNOSIS OF ACUTE KIDNEY INJURY

Abstract Background and Aims Urinary parameter determination is an essential tool for differentiating acute kidney injury (AKI) etiology. The most used ion in clinical practice is sodium (and its excretion fraction, NaEF), followed by urea (UreaEF) (that is useful in certain circumstances such as diuretic treatment). However, tubular transport includes other anions and cations that have not been widely studied. In the present study, we aim to evaluate the relation between AKI etiology (i.e. functional vs acute tubular necrosis) and calcium excretion fraction (CaEF). Method This is a transversal study including consecutive patients with diagnosis of AKI. Patients with suspicion of non-functional or ATN etiology (such as those with proteinuria, hematuria) were excluded. At admission, we collected epidemiological data, comorbidities and active treatments. AKI etiology was determined based on urinary parameters (sodium, urea) and recovery pattern of kidney function after treatment instauration. We compared CaEF in patients with ATN and functional AKI in the whole sample and among patients with and without previous CKD and diuretic prescription. Results We included 94 AKI episodes (55% female, 76±15 years). Forty-five (48%) patients had chronic kidney disease (CKD) at baseline and 56 (60%) were receiving treatment with diuretics. Of the 94 AKI, 78 (83%) presented a functional etiology and 16 (17%) were catalogued as ATN. Median CaEF was 1.09 (0.63-2.58) %. CaEF was associated to the etiology of AKI. In patients with functional AKI, median of CaEF was 0.95 (0.60-1.84) % in contrast to ATN (2.33 [1.22-7.27] %)(p&amp;lt;0.001). CaEF presented a positive and significant correlation to NaEF (ρ 0.574, p&amp;lt;0.001) and UreaEF (ρ 0.409, p&amp;lt;0.001). An adjusted regression model including the presence of CKD at baseline and diuretic treatment showed that CaEF independently predicted ATN (OR per 1% increase 1.42, 95%CI [1.16-1.75), p&amp;lt;0.001]. In patients without CKD, CaEF predicted ATN (OR 1.61, 95%CI [1.13-2.28], p = 0.008), in contrast to the cohort with CKD where only a trend was demonstrated (OR 1.29, 95%CI [0.99-1.69], p = 0.057) (Figure 1). CaEF also predicted ATN irrespective of the diuretic prescription at baseline (OR 1.35, 95%CI [1.05-1.74], p = 0.018 for diuretic users and OR 1.57, 95%CI [1.06-2.32], p = 0.025 for non-diuretic users) (Figure 1). Receiving operator curves (ROC) demonstrated a 0,712 area under the curve (AUC) of CaEF &amp;gt;1.6% for ATN, that was the best value for diagnosis in terms of sensitivity and specificity. CaEF&amp;gt;1,6% predicted ATN (OR 8.09, 95%CI [2.32-28.2], p = 0.001) after adjusting for the presence of CKD at baseline and diuretic treatment. Conclusion CaEF could help in the identification of the AKI etiology as higher values (i.e. &amp;gt;1.6%) are independently associated with ATN.

#3235 ELECTROLYTE DISORDERS IN COMMUNITY-ACQUIRED ACUTE KIDNEY INJURY

Abstract Background and Aims The kidney plays a decisive role in regulating the homeostasis of the internal environment. Acute kidney injury (AKI) compromises the kidney's ability to maintain this regulation intact, and the appearance of various electrolyte disorders is to be expected in this situation. There are few data in the literature that describe these alterations in patients with community-acquired AKI (CA-AKI). The purpose of this study is to analyze the incidence of electrolyte disorders in a cohort of patients with CA-AKI admitted to the nephrology service of a tertiary level hospital. Method This is a single-center, observational, longitudinal, and retrospective study based on a cohort of patients with CA-AKI admitted to the Nephology Service of a third level hospital from January 2010 to December 2018. We analyzed the incidence of changes in sodium, potassium, chloride, bicarbonate, calcium, and phosphorus in these patients and their clinical consequences during admission and follow-up after hospital discharge. Results A total of 639 patients were included in the final analyses. The mean age was 72,93±13,38 years. 61,7% were men. Charlson comorbidity index was 5,87 ±2,4 points. The length of stay was 11,63±10,14 days. In view of the Etiology of AKI, 72,1% had prerenal AKI and 27,9% non-prerenal. 436 patients had a history of previous chronic kidney disease (CKD) (68.23%). AKI KDIGO stages were: stage I, 105 cases (16.4%); stage II, 67 cases (10.5%); stage III 467 cases (63.1%). Hemodialysis (HD) was required in 114 patients (17.8 %). 62 patients (9.7 %) died during hospital stay. The percentage of patients with alterations in the different ions was: chlorine 54%, potassium 60.1%, sodium 45.23%, bicarbonate 85.67%, calcium 52.68%, phosphorus 54.49%. The most frequent ionic alterations at a global level were low bicarbonate (78.3%), hyperkalemia (53.05%), hypocalcemia (49.6%) and hyponatremia (41.5%). No significant differences were observed in these percentages when comparing patients with previous CKD with respect to carriers of normal baseline renal function (glomerular filtration rate &amp;gt; 60 ml/min). When analyzing whether electrolyte alterations occurred simultaneously: 2.2% of cases did not present any, 6.3% only one, 18.2% two, 26.4% three, 26.1% four, 14.9% five and 5.9% six simultaneous alterations. In the univariate analysis, patients with hypernatremia (Chi square 22.7; p &amp;lt; 0.001), hyperkalemia (Chi square 9.7; p = 0.008) and hyperphosphatemia (Chi square 18.5; p &amp;lt; 0.001) had higher mortality during admission. In the multivariate analysis using logistic regression, the variables that were independently associated with mortality during hospitalization were phosphorus (OR 1.425; 95% CI 1.212 - 1.676) and chlorine (OR 1.045; 95% CI 1.002 - 1.089). In the follow-up after hospital discharge, the Kaplan-Meier curves in the univariate analysis showed higher mortality in patients who presented hyperkalemia (log rank test: Chi square 15.5; p &amp;lt; 0.0001), hypernatremia (log rank test: Chi square 47.7; p &amp;lt; 0.0001), hypocalcemia (log rank test: Chi square 6.73; p &amp;lt; 0.034) and hyperphosphatemia (log rank test: Chi square 10.24; p &amp;lt; 0.006). In the multivariate analysis using Cox regression, the variables that were independently associated with mortality after hospital discharge were sodium (Exp(B) 1.001; 95% CI 1.002 - 1.048; p = 0.048), potassium (Exp(B) 1.140; 95% CI 1.055 - 1.233; p = 0.001) and phosphorus (Exp(B) 1.087; 95% CI 1.023 - 1.048; p = 0.154). Conclusion In our series of patients with CA-AKI, we detected a high prevalence of electrolyte disorders, without a history of previous CKD having any influence on it. The most frequent was the finding of three or four simultaneous alterations. Phosphorus and chlorine independently influenced mortality during admission. In the follow-up after hospital discharge, sodium, potassium, and phosphorus were independent predictors of mortality. The clinician who treats cases of CA-AKI must expect the appearance of frequent electrolyte disorders and must be prepared for their correct management.

#3153 HEMOPERFUSION WITH CYTOSORB AND RENAL REPLACEMENT THERAPY IN PATIENTS WITH ACUTE KIDNEY INJURY IN THE INTENSIVE CARE UNIT

Abstract Background and Aims Severe acute kidney injury (AKI) requiring renal replacement therapy (RRT) is a serious clinical disorder in the intensive care unit (ICU), occurring in a substantial proportion of critically ill patients. The aim of our single centre retrospective observational study was to analyse the outcomes of patients admitted to a non-surgical ICU and treated with RRT and with/without continuous hemoperfusion with Cytosorb. Method One hundred critically ill patients (mean age, 64.3 years; 69 men) admitted to the ICU and requiring RRT for AKI were analysed. Patient demographics, concomitant diseases, type of RRT, and survival were obtained from the medical record. APACHE II and Sofa Scores on admission were calculated. 30-day mortality was assessed using Kaplan-Meyer or Cox proportional hazards models. Results Reasons for ICU admission were acute respiratory failure (39%), cardiopulmonary resuscitation (14%), shock (13%), acute coronary syndrome (9%), sepsis (3%), acute pancreatitis (3%), and other (19%). Prior comorbidities were hypertension (70%), diabetes (43%), heart failure (32%), chronic kidney disease (CKD) (30%), coronary artery disease (CAD) (27%), chronic obstructive pulmonary disease (COPD) (15%), malignancies (12%). Eighty-six patients were treated with continuous RRT (CRRT) and 14 with intermittent hemodialysis (IHD). Twenty-four (24%) of patients treated with CRRT were also treated with hemoperfusion with Cytosorb. Using an independent-samples T test, we compared the two groups of patients with respect to the use of Cytosorb (Table 1). 30-day mortality was 82% in all patients and 87.5% in patients treated with CRRT and Cytosorb. Among concomitant diseases, only patients with previous heart failure had worse survival (p = 0.032), previous CKD, CAD, COPD, malignancy had no statistically significant impact. We found no statistically significant differences in 30-day mortality between patients treated with CRRT+Cytosorb and patients treated with CRRT or IHD alone. Multivariate Cox proportional hazard regression showed that of all the variables in the statistical model (age, sex, body mass index, previous diabetes, C-reactive protein, lactate, procalcitonin, serum creatinine, mean arterial pressure, APACHE II, ultrafiltration between CRRT), only lactate levels on admission (p = 0.002; 95%CI 1.08-1.38) were significant predictor of survival. Conclusion The use of hemoperfusion with Cytosorb in ICU patients with AKI did not reduce 30-day mortality. Patients with prior heart failure had a worse outcome. Serum lactate levels at ICU admission were an independent highly prognostic factor for death within 30 days of admission.

#5831 LIGHT CHAIN REMOVAL IN MULTIPLE MYELOMA PATIENTS WITH HFR-SUPRA HEMODIALYSIS: OUR EXPERIENCE

Abstract Background and Aims Kidney injury is a common complication in multiple myeloma (MM) and it has a negative prognostic implication. Most common cause of Acute Kidney Injury (AKI) in these patients is Light chain Cast Nephropathy, where free light chains precipitate in the tubules and bind with uromodulin, turning into intratubular casts that obstruct the tubules and also promote local giant cell reaction and interstitial inflammation and fibrosis. Free light chains (FLCs) can also damage the kidneys due to direct tubular toxicity when excessive amounts are reabsorbed by the proximal tubules. Targeted therapy to reduce FLC load can help recover renal function. Both total reduction and reduction speed are relevant for prognosis. FLC removal through extracorporeal techniques can be used as an adjuvant therapy, having an important part on the evolution of the disease. We gathered data from our experience treating MM patients with AKI with HFR-supra hemodialysis (HD) and analized the evolution and possible influence of this technique on renal recovery. Method This is an observational retrospective study. We included all patients with a diagnosis of multiple myeloma and acute kidney injury who received HFR-Supra hemodialysis in between years 2016-2022 in Hospital Virgen Macarena (Seville). We initially performed 6-10 daily HFR-Supra HD sessions and then modulated the frequency based on renal response (if renal replacement therapy had to be continued they underwent a usual hemodialysis regime 3 days a week). We continued these sessions until renal recovery was achieved or free light chain levels were reduced in agreement with the Hematology team. Measurement of pre and post dialysis FLCs was made always at first and last session and at least once in between, depending on the total number of sessions. Results 12 patients, with mean age at diagnosis 63.6 (43-86) years, presented with AKI stage KDIGO 3. 1 of them was oliguric. Median serum creatinine at diagnosis was 4.4 mg/dL [2,2-17], mean proteinuria was 4,1g/24 h [0,7-8,7] and 66,7% had positive Bence Jones proteinuria (mean 2,3g/24 h). 2 of the patients had previous chronic kidney disease stage 3a. All of them were diagnosed with Light Chain Multiple Myeloma (75% kappa, mean 10346 mg/L; 25% lambda, mean 5990 mg/L). Mean clonal bone marrow plasma cell was 20,7% [2-55]. According to the Revised International Staging System (R-ISS), 25% were stage 2 and 75% were stage 3. Renal biopsy was performed in 4 patients, all showed evidence of Cast Nephropathy. The indication for starting HFR-Supra HD was FLC removal in 9 patients, need of renal replacement therapy in 1 and both in 2 patients. We have experience in our center with using this therapy as an adyuvant treatment and often we start the technique in patients who present with AKI but would not necessarily have immediate need for renal replacement therapy. The goal is to remove FLCs and avoid further damage to the kidney tissue. Out of the 12 patients, 9 were able so stop dialysis (75%). They received a mean number of 12,4 [3-41] sessions in 3,7 [0,2-25] months). Free light chain removal per session was 24% on average [5-43%]. All of them were started on bortezomib-dexamethasone regime as initial chemotherapy for MM. As per renal recovery, at 3 months 33,3% achieved complete response, 11,1% partial response and 55,6% minimal response. At 1 year, 42,9% achieved complete response, 14,3% partial response and 42,9% minimal response. One-year survival rate was 91,7% (1 patient died from respiratory sepsis less than 1 month after diagnosis). Conclusion HFR-Supra hemodialyisis achieved a 24% free light chain removal per session on average. After presenting severe AKI (KDIGO 3), almost 43% of patients who received this adyuvant therapy obtained full renal recovery at 1 year and in 75% of patients withdrawal from hemodialysis was possible. 1 year survival was 91,7%.