bluuebunny/crossref_metadata_2025 huggingface dataset:
MO329: Acute Kidney Injury (AKI) is Associated With Increased in-Hospital Mortality and With Impairment of Renal, Lung, Motor and Immune Function 1 Year After Discharge For COVID-19
Authors: Morosini Umberto , Marengo Marita , Prenna Stefania , Colombatto Andrea , Fornara Laura , Quaglia Marco , Merlotti Guido , Paolo Sainaghi Pier , Bellan Mattia , Cantaluppi Vincenzo
Published: May 2022

BACKGROUND AND AIMS

AKI is the most frequent complication after respiratory failure in COVID-19. AKI increases mortality risk, length of hospital stay and healthcare costs, with possible progression towards CKD. Study aims: (1) evaluation of AKI incidence in 1020 COVID-19 hospitalized patients; (2) comparison of AKI incidence in COVID-19 versus pre-pandemic period; (3) establishment of out-patient follow-up for monitoring kidney, lung, motor and immune function; (4) creation of a biobank for biomarker discovery studies.

METHOD

AKI incidence was calculated matching laboratory and administrative data of 26 214 hospitalized patients in 2018–2019 and in 1020 COVID-19 patients in 2020–2021: KDIGO algorithms were applied for AKI grading. After 12 months from discharge, 232 COVID AKI patients and relative controls matched for age and gender were evaluated for kidney (eGFR, biomarkers of tubular damage NGAL, CCl-14, DKK-3), lung (DLCO, CT scan) and neuro-motor (SPPB, 2-min walking test, post-traumatic stress test-IES) function.

RESULTS

Before the pandemic, in-hospital AKI incidence was 18% (10% KDIGO 1, 5% KDIGO 2, 3% KDIGO 3): median age of AKI patients was 69. In-hospital mortality was 3.5% in non-AKI group versus 15% in AKI group in accordance with KDIGO stages. In COVID patients, AKI incidence increased to 37% (20% KDIGO 1.11% KDIGO 2, 6% KDIGO 3): median age of patients was 54. In-hospital mortality was 31% in the AKI group; AKI is an independent risk factor for death. After 12 months from hospital discharge, COVID AKI patients showed a persistent reduction of respiratory function (severe DLCO impairment < 60%) related to the extent of CT scan abnormalities. AKI patients also presented the motor function impairment and a worse post-traumatic stress response. GFR reduction was 1.8 mL/min in non-AKI patients versus 9.7 mL/min in AKI COVID patients not related to age. Urinary DKK-3 and CCL-14 were also higher in the AKI group. Last, IgG response after SARS-CoV-2 vaccination was significantly lower in the AKI group.

CONCLUSION

AKI incidence was significantly increased during COVID-19 in respect to the pre-pandemic period, with an association with higher mortality in class 2–3 KDIGO. In the post-COVID follow-up, AKI was associated with lung and neuro-motor function impairment, a defective antibody response and a sudden GFR decline concomitant to the persistence of tubular injury biomarkers. These results suggest the importance of nephrological and multidisciplinary follow-up of frail patients who developed AKI during hospitalization for COVID-19.
MO331: Acute Kidney Failure as a Risk Factor for Longer Hospital Stay, Renal Replacement Therapy and Mortality: A Public Health System Analysis
Authors: Portoles Jose' M , Lopez Paula , De Valdenebro Recio Maria , Sanchez Briales Paula , Luisa Serrano Salazar Maria , Ramos-Vegue Arturo , Gil-Casares Casanova Beatriz , Marques Vidas Maria
Published: May 2022

BACKGROUND AND AIMS

Acute kidney failure (AKI) is a well-known risk factor in coronary care unit (CCU) and postoperative patients. We aim to analyse their role in a multicentre database (DB) from a public regional health system (6 million inhabitants).

METHOD

Observational, retrospective study, including all hospital admissions between January 2013 and December 2014 in all referral hospitals in Madrid. We grouped into three categories, admissions due to AKI (ON-AKI), AKI during stay (HOSP-AKI) secondary to other disease and admissions without AKI (no-AKI); ICD-9 code was 584. Admission from patients aged under 16, women to give birth or previous renal replacement therapy (RRT) were excluded. Study was approved by the ethics committee.

RESULTS

Of the 419 851 admissions registered in 2 years, 6.7% had an associated AKI (0.6% on arrival AKI and 6.1% during admission AKI). Patients admitted for AKI are older (ON-AKI: 74.8 years versus HOSP-AKI: 77.9 versus no-AKI: 63.6), with greater comorbidity (Charlson index 2.9 versus 3.1 versus 1.7); patients had more previous CV events (28.5% versus 46.8 versus 21.0), diabetes mellitus (34.1% versus 30.4 versus 17.1) and a higher prevalence of previous chronic kidney disease-CKD (41.3 versus 31.5 versus 4.9%). AKI kidney failure lengthens hospital stay by 3.2 days 95% confidence interval (95% CI) (2.8–3.5) after adjust by age, gender, Charlson index, surgery and major diagnostic categories.

Admissions with AKI are usually unscheduled and have a longer hospital stay (9.6 ON-AKI versus 12.6 HOSP-AKI versus 7.1 days in no-AKI admission). More patient died during hospital stay in AKI group (14.4% ON-AKI; 22.9 HOSP-AKI versus 3.5% No-AKI) and although 4.3% of admission needed dialysis, only 0.5% started a chronic RRT during admission.

Principal risk factor for developing secondary AKI (R2 = 16%) is previous CKD [OR 3.6; (3.48–3.74)], after corrected by age, male, the Charlson index and non-surgical admission.

Mortality risk for patients with an admission for AKI (R2 = 17%), corrected for age, sex, comorbidity, previous CKD, and type of admission is OR: 1.8 95% CI (1.57–2.08); secondary AKI is OR 3.73 (3.59–3.88) than no-AKI admission.

CONCLUSION

AKI is a huge burden for health system and patients, and associates significant longer stay, cost and a higher mortality. Main factor to develop secondary AKI is age and previous CKD.
MO343: Deep Analysis of The AKI—CKD in Allogeneic Stem Cell Transplantation—A Big Data Approach
Authors: Brüder Nicole , Kielstein Jan T , Heinze Luca-Marie , Lück Catherina , Panagiota Victoria , Dammann Elke , Köhler Sophia , Talbot Steven , Stadler Michael , Heuser Michael , Ganser Arnold , Eder Matthias , Beutel Gernot
Published: May 2022

BACKGROUND AND AIMS

Acute kidney injury (AKI) is a common complication in allogeneic stem cell transplantation (SCT). Although short-lived, i.e. < 90 days, in the majority of patients renal injury can persist for more than 3 months fulfilling the criteria of chronic kidney disease (CKD). So far, only a few publications have shown robust data based on larger patient populations. The aim of this project is to analyse the incidence and severity of AKI in the context of an allogeneic SCT and the transition into CKD.

METHOD

Over a 17-year period, 1394 allogeneic stem cell transplants were performed at our tertiary center. Of those, 42 were second transplants. For 1387, a detailed history of creatinine (n = 142 563) and eGFR (n = 96 689) could be extracted from the Enterprise Clinical Research Data Warehouse. The classification of the respective AKI stages was based on the current KDIGO classification relying solely on the changes in serum creatinine. For AKI, an increase in serum creatinine of ≥ 0.3 mg/dL (26.5 µmol/L) within 48 h or an increase in serum creatinine to ≥ 1.5× baseline within 7 days was used. Persistence of impaired renal function beyond day 90 was defined as CKD. For the analysis of big data and classification of the AKI/CKD an algorithm was programmed. Validation of the results was performed using a colour-coded visualization of renal function (Fig. 1).

RESULTS

Between 1 January 2003 and 31 December 2020, 239 252 values for creatinine and eGFR were enriched for 1387 transplantations for a period between day –28 before today + 118 after allogeneic stem cell transplantation. The overall incidence of AKI was 86% (n = 1199). A total of 993 patients (83%) have shown an AKIN 1, 173 (14%) an AKIN 2 and 33 (3%) an AKIN 3. Of those, 122 (13%) patients died before day + 90 after allogeneic stem cell transplantation and were therefore excluded from CKD analysis. For 271 of 833 patients (33%), the transition to chronic kidney disease has been observed. Further information on patient characteristics, underlying disease, transplant coordinates and related complications and relapse mortality are shown in Table 1.

CONCLUSION

AKI after SCT is the rule and not the exception. As the vast majority of patients show AKIN 1, it might be often clinically overlooked. However, early intervention might mitigate the development of long-term renal impairment. Automated detection (AKI alert systems) as well as identification and subsequent avoidance of factors contributing or aggravating injury (e.g. conditioning, immunosuppression, perfusion, tissue edema, inappropriate dosing of drugs) might minimize long-term renal complications in allogeneic SCT.
MO380: Bio-Conductivity Measurement for Electrical Impedance Tomography (EIT) in Chronic Kidney Disease—A Non-Invasive and Portable Monitoring Approach
Authors: Yap Desmond , Ka Ying MA Elsa , Yi Oon Wei , Zouari Fedi , Chan Russell W , Wong Eddie C
Published: May 2022

BACKGROUND AND AIMS

Chronic kidney disease (CKD) is an escalating global health concern, and non-invasive means for early CKD detection is eagerly awaited. Kidneys are water- and electrolytes-rich organs with good bio-conductivity. Kidney fibrosis and tubular atrophy are characteristic pathological changes in CKD [1], and is associated with restricted blood perfusion, fluid diffusion [2,3] and hence reduced bio-conductivity. Electrical impedance tomography (EIT) emerges as a non-invasive, ionizing radiation-free imaging technique measuring dielectric properties of the body parts [4]. This study investigated the relationship of EIT indices and renal function in patients with various stages of CKD.

METHOD

We prospectively recruited 98 patients with different stages of CKD (Stage 1, n = 16; Stage 2, n = 15; Stage 3, n = 20, Stage 4, n = 36 and Stage 5, n = 11). EIT measurements were performed at two frequencies (33.6 and 100 kHz) using a portable EIT device with an electrode belt consisting of 16 gel electrodes. EIT data was pre-processed and reconstructed as mean conductivity maps. Frequency differencing was then performed between conductivity maps at two frequencies. Kidney-related dielectric parameters were extracted around the kidney region located at lower one-third of the frequency differencing conductivity map. Conductivity changes between frequencies were then computed and further regressed with individual biometrics. Predicted eGFR values was then computed and compared with the standard eGFR scores to evaluate its effectiveness on classifying CDK stages.

RESULTS

The detected mean bio-conductivity changes were −3.9, −67.5, −133.5, −212.6 and −294.7 (a.u.) in patients with CKD Stage 1, 2, 3, 4 and 5, respectively (Fig. 1A). Patients with more advanced stages of CKD tend to show more reduction in bio-conductivity, and eGFR correlated positively with reduction in bio-conductivity (R2 = 0.37, P < 0.001) (Fig. 1B). EIT-predicted eGFR (eGFREIT) was further computed by the captured conductivity changes and individual biometrics (Fig. 2). eGFREIT showed significant correlation with eGFR measured by blood tests (R2 = 0.54, P < 0.001).

CONCLUSION

EIT showed good correlation with renal function changes in CKD patients, and thus holds promise to be developed into a non-invasive and portable device for early CKD detection in both clinical and community settings.
MO388: A Critical Evaluation of Anthropological, Biological and Geo-Environmental Factors on Chronic Kidney Disease of unknown Aetiology in Affected Area Against Unaffected Area
Authors: Hewapathiranage Santhushya , Nayanamali Ayesha , Nanayakkara Nishantha
Published: May 2022

BACKGROUND AND AIMS

Chronic kidney disease of unknown etiology (CKDu) has been a critical health issue among the farming communities of Sri Lanka for decades [1]. However, the distribution of CKDu in Sri Lanka is geographically significant by representing endemicity on its own [2]. This study was conducted to identify the anthropological and geo-environmental characteristics of CKDu, in relation to the biochemical profile between known CKDu endemic and non-endemic communities.

METHOD

A total of 214 male individuals from Wilgamuwa (endemic) and 102 male individuals from Mathurata (non-endemic) of 30–60 years were recruited. For each participant, blood pressure (BP), random blood sugar (RBS), serum creatinine (μmol/L) and serum cholesterol (mg/dL) were tested using standard methods. Anthropological data including population structure, farming behaviour and poverty statistics were obtained from the respective government officials. Geo climatic data including elevation, monthly average (Avg.) temperature (°C), monthly Avg. rainfall (mm), monthly Avg. humidity (%) and monthly Avg. UV intensity, monthly Avg. Sun hours (hrs.) were obtained for the two study areas.

RESULTS

Most striking difference between two communities is significantly high serum creatinine (t = 3.5175, P = 0.0005) in male individuals between the age category of 40 to 65 years in CKDu endemic area (M = 109.00, SD = 66.41) in comparison to non-endemic participants in the same age category from non-endemic area for CKDu (M = 85.41, SD = 18.78). The non-endemic area for CKDu, Maturata was colonized since the 16th century due to natural population migrations while the colonization of Wilgamuwa was implemented in a more drastic manner, parallel to the green revolution after the 1960s. Mathurata is located at a high elevation level of 976 m, whereas Wilgamuwa is located at an elevation level of 528 m. In comparison with meteorological variables for the year of 2019, monthly Avg. rainfall (mm) (P = 0.005), monthly Avg. temperature (°C) (P = 0.001), monthly Avg. cloud cover (%) (P = 0.004), monthly Avg. Humidity (%) (P = 0.007), monthly Avg. Sun hours (hrs) (P = 0.001) were highly significant between the two geographical areas.

CONCLUSION

We report comparably adverse weather conditions, higher exposure to natural and artificial toxic exposure in genetically and behaviourally vulnerable group in the CKDu endemic area in comparison with non-endemic area for CKDu.
MO391: Association Between Skeletal Muscle and Level of Physical Activity in Patients With Chronic Kidney Disease: A Cross-Sectional Analysis of the Peaking Cohort
Authors: Xiao Cuixia , Zeng Jiahao , Yang Changyuan , Ling Xitao , Qin Xindong , Wu Yifan , Lu Fuhua , Liu Xusheng , Guobin Su and
Published: May 2022

BACKGROUND AND AIMS

Favorable skeletal muscles have been associated with higher physical activity (PA) in the general population. However, little is known regarding this relationship in a population of Chinese chronic kidney disease (CKD) patients. The aim of this study is to investigate the relationship between PA and skeletal muscle in Chinese non-dialysis CKD patients.

METHOD

This was a cross-sectional analysis of the PEAKING cohort—an open cohort aimed to explore the effect of PA on health-related outcomes in the Chinese non-dialysis CKD population from 2017. The PA of patients was assessed by wearing an accelerometer (ActiGraph) for 9 consecutive days. The levels of PA were classified into four categories (no PA, low, moderate and high level of PA) according to the 2008 U.S. Physical Activity Guidelines. The information of skeletal muscles was evaluated by Biospace Inbody 770 within 180 days after the enrollment. Multivariate linear analysis was conducted to investigate the association between PA and skeletal muscle, adjusted for age, sex, CKD stages, smoking and drinking status, drug use and complications.

RESULTS

A total of 104 non-dialysis CKD patients (median age 49.6 years, 48% female, 49% with CKD stage 3 or above) were enrolled in this study. None of the included CKD patients had no or low-level PA while 42 (40%) patients had moderate and 62 (60%) had high-level PA. Multivariate linear regression showed that there was no significant association between skeletal muscle and level of PA (B = 0.07, 95% CI −0.58, 2.01; P = 0.279).

CONCLUSION

Higher-level PA was not significantly associated with more skeletal muscle mass. Further work examining the relationship between skeletal muscle and level of PA needs to be done in a larger sample of non-dialysis CKD patients.
MO398: Salvianolic Acid C Attenuated Fibrosis Through Enhancer of Zeste Homolog 2 in Fibrotic Kidneys
Authors: Ye Chaoyang , Lin Junyan , Chen Dongping , Wu Ming
Published: May 2022

BACKGROUND AND AIMS

Salvianolic acid C (SAC) is a component of Danshen, a widely used herbal medicine for the treatment of renal cardiovascular diseases. Renal interstitial fibrosis is a common pathway of all kinds of chronic kidney diseases progressing to the end-stage of renal diseases. We aimed to study the effect of SAC on renal fibrosis and explore its underlining mechanisms.

METHOD

Mouse renal fibrosis model was induced by unilateral ureteral obstruction (UUO) or peritoneally injection of aristolochic acid I (AAI). Moreover, normal rat kidney interstitial fibroblast (NRK-49F) cells were treated with various concentrations of SAC (10 mM–100 mM). Protein samples from in vivo and in vitro experiments were collected to assess renal fibrosis.

RESULTS

Masson staining and Western blotting analysis showed that 2 weeks treatment with SAC attenuated renal fibrosis in UUO or AAI induced fibrotic kidneys. The expression of fibronectin, collagen-I and α smooth muscle actin (αSMA) were increased in UUO or AAI induced fibrotic kidneys, which were down-regulated in SAC treated UUO or AAI induced fibrotic kidneys. In parallel, treatment with SAC reduced the expression of fibronectin and αSMA in NRK-49F cells. Mechanistically, we found that enhancer of zeste homolog 2 (EZH2) is up-regulated in UUO or AAI induced fibrotic kidneys and Tan-I reduced the expression of EZH2 in fibrotic kidneys. Moreover, inhibition of EZH2 reduced the expression of pro-fibrotic markers and abolished the ani-fibrotic effect of SAC in rat renal fibroblasts.

CONCLUSION

We conclude that SAC attenuates fibrosis in fibrotic kidneys through inhibition of EZH2.
MO400: Treatment of Renal Artery Stenosis: Nephrology, the Best Surgery
Authors: Pérez Fernández Álvaro , García Pablos Nuria , Salcedo Herrero David , Delgadillo Valentin , Inmaculada Poveda García María , Javier Gonzalez Martinez Francisco
Published: May 2022

BACKGROUND AND AIMS

Renal artery stenosis causes hypertension in 10–40% of severe cases or refractory to treatment. As a gold standard test for its diagnosis, we have arteriography, which allows the interventional therapeutic option, through angioplasty and/or stenting. There is no consensus on which patient profile would be the optimal candidate for each treatment. We tried to reach an answer by studying a cohort of 25 patients from our centre with a diagnosis of renal artery stenosis in the last 5 years. The objective was to assess the efficacy of isolated or interventional medical treatment with respect to renal function and the number of antihypertensive drugs.

METHOD

A retrospective observational cohort study was conducted. The study population was the patients who underwent renal arteriography in the last 5 years in our center (n = 25).

We define significant stenosis as greater than 60%, bilateral involvement or of other main arteries. We compared the evolution of glomerular filtration in stages (KDIGO), proteinuria (albumin/creatinine ratio in urine) and number of antihypertensive drugs before and 6 months after the therapy used.

RESULTS

Renal arteriography was diagnostic in 18 patients: 13 of them presented significant stenosis, performing angioplasty in 4, stenting in 6 and angioplasty + stenting in 3.

One antihypertensive drug was reduced in 17% of the patients, two in 22%, and one drug was increased in one of them.

In 83% of the patients, the KDIGO stage of renal function did not change after treatment. An improvement was observed in three patients, who only received medical treatment. No differences were found in the evolution of proteinuria.

CONCLUSION

There were no statistically significant differences in renal function and the number of antihypertensive drugs between isolated medical versus medical and interventional treatment.

It is necessary to expand the patient database, or start multicenter studies, to improve the significance.
MO403: The Association Between Urinary 11-Dehydrothromboxane B2 and Laboratory Parameters in Aspirin-Treated Patients With Cardiorenal Syndrome
Authors: Lukianets Kseniia , Vasilkova Volha , Pchelin Ivan , Shishkin Alexander
Published: May 2022

BACKGROUND AND AIMS

Evaluation of urinary levels of the 11-dehydrothromboxane B2 is one of the methods for assessing platelet reactivity while taking aspirin. High levels of 11-dehydrothromboxane B2 in urine indicate continued thromboxane generation which is associated with an increased risk of atherothrombotic cardiovascular events. The present study aimed to evaluate the association between 11-dehydrothromboxane B2 in urine and laboratory parameters in aspirin-treated patients with the cardiorenal syndrome in subgroups from quartile with the highest and the lowest levels of thromboxane metabolite.

METHOD

A total of 82 patients with stable coronary artery disease (CAD) and CKD (stages 2–4) were included in the study. Urinary levels of 11-dehydrothromboxane B2 (a stable metabolite of thromboxane A2) were assessed using ELISA kit by Enzo Life Sciences (Switzerland). Statistical analysis was performed using the chi-squared test and Spearman's rank correlation coefficient.

RESULTS

In the subgroup of patients from the quartile with the highest levels of urinary 11-dehydrothromboxane B2, a history of ischemic stroke (P = 0.032) and a history of myocardial infarction (P = 0.048) were more common. There were significant correlations between urinary 11-dehydrothromboxane B2 and platelet count (rs = 0.457, P = 0.043), platelet crit (rs = 0.481, P = 0.037), pulmonary artery systolic pressure (rs = 0.847, P = 0.016) and left ventricular ejection fraction (rs = −0.719, P = 0.045) in the same subgroup of patients. In the subgroup of patients from the quartile with the lowest levels of 11-dehydrothromboxane B2 in urine statistically significant correlations between thromboxane metabolite and fasting plasma glucose (rs = 0.581, P = 0.007) and hematocrit (rs = 0.441, P = 0.003) were found.

CONCLUSION

Our study identified the relationships between the urinary concentration of 11-dehydrothromboxane B2 and laboratory and echocardiography parameters in aspirin-treated patients with cardiorenal syndrome. Accordingly, the received results represent the varying response to aspirin in patients with stable CAD and CKD. Additional research is needed to clarify the impact of platelet indices and the association between platelet reactivity while taking aspirin and pulmonary hypertension on behalf of the possibility of personalization of antiplatelet therapy.
MO405: Leucine-Rich Alpha-2-Glycoprotein as a Potential Marker of Mesangial Cell Proliferation in Immunoglobulin a Nephropathy
Authors: Popova Anna , Rācenis Kārlis , Kuzema Viktorija , Jana Saulīte Anna , Saulīte Mikus , Broks Renārs , Oļeiņika Kristīne , Šlisere Baiba , Petersons Aivars , Laurinavicius Arvydas , Cernevskis Harijs , Lejnieks Aivars , Kroiča Juta
Published: May 2022

BACKGROUND AND AIMS

Leucine-rich alpha-2-glycoprotein (LRG1) is a novel proangiogenic factor involved in the abnormal angiogenesis and renal fibrosis in diabetic nephropathy by potentiating endothelial transforming growth factor-beta/activin receptor-like kinase 1 (TGF-β/ALK1) signalling [1]. TGF-β mediates mesangial matrix accumulation culminating in the development of glomerulosclerosis [2], which also occurs in immunoglobulin A nephropathy (IgAN) patients. Our study aims to evaluate LRG1 as a marker of mesangial cell proliferation in IgAN patients.

METHODS: Adults with a morphologically confirmed IgAN by the presence of IgA deposits by immunofluorescence microscopy were included in the study. Diabetes mellitus, oncology, acute inflammation processes were exclusion criteria. Serum LRG1 was detected using ELISA.

RESULTS

A total of 73 patients with IgAN were included [mean age 41 years, interquartile range (IQR) 35–47; range, 21–65; 65.8% men]. The median estimated glomerular filtration rate (eGFR) was 44 (IQR 24–83, range 4–133) mL/min/1.73m2. Kidney biopsies were analyzed according to the Oxford classification: M0 in 10 (13,7%), M1 in 56 (76.7%) patients. The median serum LRG1 was 49 µg/mL (IQR 40.7–57.7, range 29–133.3). Bivariate analyses showed that plasma LRG1 was negatively associated with eGFR (rho = −0.342, P = 0.003). A linear model showed that GFR decline for 1 mL/min was associated with an increase of LRG1 for 0.194 µg/mL. In IgAN patients with an M1-score LRG1 was higher (P = 0027, Mann–Whitney U test), the area under the ROC curve value for serum LRG1 was 0.739.

CONCLUSION

Serum LRG1 increases with GFR decline in patients with IgAN and at the same time correlates with mesangial hypercellularity according to Oxford classification. Therefore, LRG1 might be a potential marker of advanced disease in IgAN.
MO407: Clinical Features & Outcome of 352 Covid-19 Positive Maintenance Haemodialysis Patients in Second Covid Wave in Tertiary Care Centre in South India
Authors: Chege Prafull , Yadla Manjusha
Published: May 2022

BACKGROUND

Coronavirus disease (COVID-19) infection by severe acute respiratory syndrome coronavirus 2 (SARS CoV-2) virus is an ongoing pandemic with high morbidity and mortality rates. The second COVID-19 wave was observed between April–July 2021. Patients with underlying CKD, ˃ 65 years, immunocompromised, post-transplants are at high risk for COVID-19 infection.

AIMS AND OBJECTIVES

Clinical features and outcome of 352 COVID-19 positive maintenance hemodialysis (MHD) patients in a tertiary care centre in South India.

METHOD

Patients admitted with respiratory symptoms with nasal RTPCR positive and on MHD referred to us from April to July 2021, were included. The study design was an observational study. The analysis included clinical profile, epidemiological data, vascular access, lab parameters and outcomes. Data analysed using SPSS version 17 (P-value < 0.05-significant)

STUDY DESIGN: This is an Observational Retrospective study

RESULTS

Clinical profile constituted fever (82.6%), SOB (61.2%), cough (29.8%). Baseline characteristics were: Oxygen was required in 244 patients (69.31%), CPAP in 71 patients (20.17%) and mechanical ventilation in 21 patients (5.96%). Mortality seen in 132 patients (37.5%). Factors affecting mortality were age (P = 0.001), thrombocytopenia (P = 0.004), q SOFA >1 (P = 0.001), CPAP (P = 0.002) and mechanical ventilation (P = 0.0001).

CONCLUSION

The mortality rate was 37.5%. The factors associated with mortality were age, thrombocytopenia, q SOFA score > 1, hypoxemia, patients on oxygen support, CPAP, mechanical ventilation.
MO408: Hepatic Steatosis in Patients With Type 2 Diabetes and Chronic Kidney Disease
Authors: Adrian Therese , Hornum Mads , K. Knop Filip , Peter Almdal Thomas , Rossing Peter , Lida Lisa , Søndergaard Heinrich Niels , Boer Vincent , Marsman Anouk , Petersen Esben , Siebner Hartwig , Feldt-Rasmussen Bo
Published: May 2022

BACKGROUND AND AIMS

Non-alcoholic fatty liver disease (NAFLD) is suggested as being a risk factor for chronic kidney disease (CKD). The incidence of NAFLD is rising globally parallel to the increasing incidences of obesity and type 2 diabetes. As diabetes remains the leading cause of CKD the co-existence of NAFLD, CKD and type 2 diabetes needs to be explored. Here, we evaluated the prevalence of hepatic steatosis in patients with type 2 diabetes and CKD and patients with type 2 diabetes without CKD.

METHOD

This cross-sectional study included 50 patients with type 2 diabetes and CKD stages 3–5 and 50 patients with type 2 diabetes without CKD. Liver fat content was estimated by proton magnetic resonance spectroscopy (1H-MRS) and magnetic resonance imaging proton density fat fraction (MRI-PDFF) by the multi-echo Dixon-technique in a 3 Tesla full-body MRI scanner. Hepatic steatosis was defined as ≥ 5.56% liver fat. Further, continuous glucose monitoring (CGM) was performed for 4 days.

RESULTS

Mean age 72.0 ± 4.9 years and body mass index (BMI) 28.6 ± 3.5 kg/m2 in patients with CKD, and mean age 65.9 ± 7.8 years and BMI 27.0 ± 4.0 kg/m2 in patients without CKD with a predominance of men in both groups. Hepatic steatosis was identified in 22 (44%) patients with CKD and 19 (38%) patients without CKD (P = 0.68). Median (IQR) values of percentage liver fat were 4.7% (3.0–8.5) and 4.1% (2.9–7.7) in patients with and without CKD, respectively, corresponding to 5.3% higher levels of hepatic fat percentage in patients with CKD [95% confidence interval (CI) −23; 45, P = 0.75]. Mean sensor glucose from CGM was 9.0 ± 1.6 mmol/L and 8.7 ± 1.8 mmol/L in patients with and without CKD, respectively (P = 0.47). There was no statistically significant difference between the two groups regarding the percentage of time spent in different CGM ranges: time-below-range, <3.9 mmol/L (P = 0.83), time-in-target-range, 3.9–10.0 mmol/L (P = 0.20) and time-above-range, >10.0 mmol/L (P = 0.20). Pooled data from both groups showed no significant association between the mean sensor glucose from CGM and hepatic fat percentages (P = 0.38).

CONCLUSION

These findings do not support any association between hepatic steatosis and CKD stages 3–5 in patients with type 2 diabetes.
MO410: Early Endothelial Glycocalyx Injury Damage Associated With Further Kidney Dysfunction in Hiv Patients: Five Years Follow-Up
Authors: Gadelha Cavalcante Malena , Cavalcante Meneses Gdayllon , Bezerra Geraldo , Maria Costa Martins Alice , Gondim Lima Oliveira Manuela , Gabriel Monteiro Santos Sérgio , Alaíde Andrade Do Vale Vanessa , De Francesco Daher Elizabeth
Published: May 2022

BACKGROUND AND AIMS

HIV patients have an increased risk of chronic kidney disease (CKD) development. Endothelial dysfunction was previously associated with kidney dysfunction markers. This study aims to investigate the association between renal markers and renal dysfunction biomarkers among outpatient HIV patients.

METHOD

Cohort study carried out with HIV patients in chronic use of Antiretroviral therapy followed up at a public outpatient service located in northeastern Brazil. Clinical and laboratory parameters of HIV patients were evaluated annually between 5 years: 2015 and 2019. Kidney dysfunction markers were blood creatinine and estimated glomerular filtration rate (GFR). Urinary kidney biomarkers NGAL, MCP-1, KIM-1 and serum endothelial biomarkers Syndecan-1 (glycocalyx), ICAM-1 and E-selectin were quantified in first-year using ELISA assays.

RESULTS

In total 66 patients completed the follow-up. Most patients were male (77.3%), of mixed race/color (57.6%), aged 39.33 ± 9.04 years. No patient had CKD development. However, Syndecan-1 showed a significant correlation with maximum creatinine (P < 0.001) and minimum GFR (P 0.003) over the years. Moreover, both creatinine and GFR in the last year had a significant association with syndecan-1 levels quantified 4 years ago. Multivariate linear regression with confounders showed a significant and independent association of syndecan-1 levels, current age and CD4 + count with minimum GFR.

CONCLUSION

HIV patients in chronic use of Antiretroviral therapy and glycocalyx injury may have an increased risk for long-term impacts on renal tissue. These data reinforce that endothelial impacts evaluation using biomarkers is a way to optimize the diagnosis and prognosis of kidney diseases, promoting the prevention of complications.
MO414: Sucroferric Oxyhydroxide (Velphoro®) Treatment Mitigates the Signs of Ageing-Related Sarcopaenia in Old Mice
Authors: Alcalde-Estévez Elena , Asenjo-Bueno Ana , Sosa Patricia , Plaza Patricia , Rodríguez-Puyol Diego , Olmos Gemma , López-Ongil Susana , Piedad Ruiz-Torres Maria
Published: May 2022

BACKGROUND AND AIMS

Sarcopaenia, defined as the loss of muscle mass and function, is an ageing-related pathology associated with some important diseases such as chronic kidney disease (CKD). Hyperphosphatemia has been associated with both, ageing and CKD. Old mice show an increase in serum phosphate concentration and a reduction in muscle mass, forelimb strength, gait speed and transition time in the static bar, with respect to young mice. Previous results of our group showed the beneficial effects of a low phosphate diet on ageing-related sarcopaenia. Given that the implementation of dietary phosphate restriction entails difficulties in the elderly, the aim of this work was to analyse the beneficial effects of a diet supplemented with a phosphate binder on the signs of sarcopaenia.

METHOD

C57BL6 male mice were used for in vivo studies: 5-month-old (young) and 24-month-old (old), which were fed with a powder standard diet (containing 0.6% of phosphate). Some old mice were fed with a hypophosphatemic diet (containing 0.2% of phosphate) or with a diet supplemented with 5% sucroferric oxyhydroxide (Velphoro®) for the last 3 months before sacrifice. Serum phosphate levels were analysed with a commercial kit. Muscle mass was estimated by measuring the gastrocnemius muscle mass divided by total body mass, muscle force was measured by a grip test and physical performance was evaluated by a gait test and the static bar test.

RESULTS

Velphoro® treated old mice showed a significant and more effective reduction in phosphate serum levels than old mice fed with the hypophosphatemic diet. No differences were observed in the relative gastrocnemius muscle mass between the three old mice experimental groups. By contrast, old mice fed with the standard diet supplemented with Velphoro® displayed an increased muscular strength and physical performance, improving the gait speed and reducing the transition time in the static bar, compared with old mice fed with the standard diet. Results obtained with Velphoro® treatment were similar to those observed in old mice fed with the hyphophosphatemic diet, but Velphoro® treatment achieve better results in motor coordination in the static bar test.

CONCLUSION

Dietary restriction of phosphate is a useful approach to mitigate the signs of ageing-related sarcopaenia (muscle strength and physical performance) in old mice. The use of Velphoro®, as a phosphate binder, exhibits similar or even better results than the hypophosphatemic diet. Therefore, the administration of Velphoro® could attenuate the signs of sarcopaenia in the elderly or in ageing-related diseases in which sarcopaenia is common, like CKD.
MO415: Kidney Expression of Canonical WNT Inhibitors and Β-Catenin in Experimental Models of Arterial Hypertension and Nephrectomy Induced CKD
Authors: Bogdanova Evdokia , Beresneva Olga
Published: May 2022

BACKGROUND AND AIMS

The canonical Wnt (cWnt) is known to be involved in tubular recovery after kidney injury and fibrosis, while arterial hypertension (AH) promotes cWnt activity. The aim of the study was to investigate the kidney expression of β-catenin and cWnt inhibitors in AH and chronic kidney disease (CKD) models.

METHOD

AH-CKD was performed by 3/4 nephrectomy (NE) in spontaneously hypertensive rats (SHR) with 2 or 6 months of experimental exposure (Table). Sham-operated (SO) SHRs and Wistar Kyoto rats (WKY) served as controls, and 6 mo exposure SO-SHRs were used as AH-induced CKD. Serum creatinine (Cr), renal sclerostin (Sost) and dickkopf-1 (Dkk1) gene expression were measured. The following parameters of kidney morphology were analyzed and calculated quantitatively: the areas of tubular dystrophy (TD) (PAS), renal fibrosis (RF) (Masson's trichrome), β-catenin (BC), sclerostin (SOST) and dickkopf-1 (DKK1) IHC-staining.

RESULTS

The experimental models were corresponded to early (SO6, NE2) and mild (NE6) CKD (Table). In all groups, BC membrane IHC staining in epithelial cells and nuclear expression in podocytes were determined, SOST and DKK1 cytoplasmic IHC staining in tubular epithelium were detected (Figure). The tubular and interstitial lesions in NE (Table) were accompanied by cytoplasmic BC localization in epithelial and interstitial cells (Figure) with a decrease in dickkopf-1 gene (Table) and protein (Figure) expression, increase in Sost gene expression and SOST IHC staining of tubular intracellular vesicles (Figure). Long-term exposure to hypertension (SO6) resulted in the renal function decline and RF comparable to NE2 (Table), while TD and levels of Wnt inhibitors and BC IHC staining area did not differ significantly vs SO2, WKY (Table). In the pooled analysis, the RF directly correlated with the BC renal expression (r = 0.76, P = 0.005) and negatively with Dkk1 expression (r = −0.45, P = 0.028); the TD negatively correlated with Sost expression (r = −0.80, P = 0.002).

CONCLUSION

Tubular and interstitial damage in NE and AH-induced CKD is associated with BC up-regulation. The decrease in dickkopf1 and BC cytoplasmic accumulation may be required for renal fibrosis. The sclerostin expression is likely to be essential for the pathogenesis of TD.
MO421: Chronic Kidney Disease is Associated With Cardiac Downregulation of Vascular Endothelial Growth Factor a (VEGFA) and Development of Diastolic Dysfunction: Epigenetics and Micrornas
Authors: Chade Alejandro , Eirin Alfonso
Published: May 2022

BACKGROUND AND AIMS

Patients with chronic kidney disease (CKD) have a higher risk to develop heart failure with preserved ejection fraction (HFpEF). We showed in a swine model of CKD with diastolic dysfunction and cardiac remodelling that these cardiac features are associated with blunted cardiac mRNA and protein expression of vascular endothelial growth factor (VEGF), a pro-angiogenic cytokine that plays important roles in cardiac vascular development, morphogenesis and contractility. Hence, we aim to identify potential underlying mechanisms of cardiac VEGF downregulation in CKD.

METHOD

CKD and normal pigs (n = 3 each) were studied for 14 weeks. Cardiac morphology and function (echocardiography) were quantified in vivo and microvascular density (3D micro-CT) ex vivo. Then, cardiac micro-RNA (miRNA) and 5-hydroxymethylcytosine (5-hmC) profiles of VEGFA gene were examined by hydroxymethylated DNA immunoprecipitation and miRNA sequencing (hMeDIP-seq and miRNA-seq, respectively) and validated by qPCR and Western blotting.

RESULTS

Blunted renal function in CKD pigs associated with left ventricular (LV) hypertrophy, and abnormal LV strain and diastolic dysfunction with pEF (Figure 1A) and reduced subendocardial microvascular density (Figure 1B) compared to normal. miRNA-seq showed that mir-183 was the only miRNA capable of targeting VEGFA and upregulated in CKD hearts (Figure 1C), accompanied by downregulation of VEGFA gene and VEGF protein (Figure 1D), whereas hMeDIP-seq revealed reduced VEGFA 5hmC levels in the hearts of CKD versus normal pigs (Figure 1E).

CONCLUSION

Our study suggests that miRNA-modulation and cardiac epigenetic changes in VEGF might contribute to cardiac damage and the development of HF in CKD. These observations may assist in developing novel therapies, like miRNA antagonists or epigenetic modulators, to preserve VEGF signalling and protect the heart in patients with CKD.
MO427: Protein Arginine Methyltransferase 1 Increases The Expression of P63 and Promotes Renal Interstitial Fibrosis
Authors: Ye Chaoyang , Lin Junyan , Wu Ming , Chen Dongping
Published: May 2022

BACKGROUND AND AIMS

Mammalian Protein Arginine Methyltransferase 1 (PRMT1) catalyzes the monomethylation and dimethylation of the Arginine residues of proteins. It has been shown that PRMT1 inhibitor attenuates renal fibrosis, however, the role of PRMT1 in renal interstitial fibrosis is not fully understood. Using kidney-specific PRMT1 knockout mice, we aimed to study the role of PRMT1 in renal fibrosis and explored its underlining mechanisms.

METHOD

Sham or unilateral ureteral obstruction (UUO) operation was performed in PRMT1 Ksp-cre knockout mice, which were sacrificed on day 14. The effect of PRMT 1 on renal interstitial fibrosis was further studied using PRMT1 specific inhibitor AMI-1 in WT UUO mice. RNA-seq analysis was performed to analyze differential expressed genes in WT versus PRMT 1 knockout UUO kidneys. Moreover, TGF-β stimulated HK2 renal epithelial cells were treated with various concentrations of AMI-1(2μM to 10μM). Protein samples from in vivo and in vitro experiments were collected to assess renal fibrosis.

RESULTS

Strong interstitial fibrosis was observed in Ksp-Cre- (WT) UUO mice as shown by Masson staining, and kidney-specific deletion of PRMT 1 gene attenuated interstitial fibrosis in mouse kidneys. The expression of collagen-I in mouse kidneys was analyzed by Western blotting. UUO operation increased the expression of collagen-I in WT mouse kidneys, which were reduced by kidney-specific deletion of PRMT 1 gene. Inhibition of AMI-1 on renal interstitial fibrosis in UUO kidneys was confirmed by Masson staining and Western blotting analysis of pro-fibrotic markers. Mechanistically, using RNA-seq analysis, we found P63 was down-regulated in PRMT 1 knockout UUO kidneys. We further confirmed the down-regulation of P63 by qPCR and Western blotting analysis in PRMT1 knockout UUO kidneys and AMI-1 treated UUO kidneys. Moreover, we showed that AMI-1 dose-dependently inhibited the expression of P63 in TGF-β stimulated HK2 renal epithelial cells, which was correlated with down-regulation of pro-fibrotic markers.

CONCLUSION

PRMT1 promotes renal interstitial fibrosis probably through increasing the expression of P63.
MO435: The Prognostic Implication of 24-h Urine Urea Excretion With Renal Progression: Analysis of KNOW-CKD Study
Authors: Cheol Jeong Jong , Oh Kook-Hwan , Chae Dong-Wan
Published: May 2022

BACKGROUND AND AIMS

Urea excretion is the basic function of the nephron. However, its prognostic implication has been not extensively studied in a specific subpopulation of chronic kidney diseases (CKD).

METHOD

Total of 2232 patients in KNOW-CKD cohort were analyzed. Baseline characteristics were used as a prognosticator in the Cox regression model. For categorical comparison, tertiles of 24-h urea excretion were used as high, low and moderate excretion of urea. Linear modelling and nonlinear modelling based on restricted cubic splines were used to study the impact of 24-h urea excretion on renal survival.

RESULTS

Mean daily urea excretion was 8.2 ± 3.6 g/day. Mean daily urea excretion was 12.1 ± 3.1 g/day versus 4.8 ± 1.3 g/day in the high urea excretion group (HUG) and low urea excretion group (LUG) (P < 0.001). Mean eGFR of LUG was 47.0 ± 30.9 mL/min/1.73m2 and mean eGFR of HUG was 60.6 ± 29.9 mL/min/1.73m2 (P < 0.001). Serum albumin level was higher in HUG with 4.3 ± 0.4 g/dL versus 4.1 ± 0.5 g/dL of LUG (P < 0.001). Compared with HUG, LUG showed a hazard ratio of end-stage renal disease (ESRD) with 1.407 [95% confidence interval (CI) 1.115–1.774, P = 0.004] in the linear multiple regression model, which was adjusted by eGFR, age, gender, body mass index, type of CKD, proteinuria amount, systolic blood pressure, hemoglobin, blood urea nitrogen, serum albumin, serum cholesterol, serum uric acid, hsCRP, statin usage, renin-angiotensin-aldosterone system blocker usage. In the non-linear modeling, daily urea excretion showed a two-step change in log hazard ratio to ESRD. Threshold points of log hazard ratio among the whole study population were observed at 5 g/day and 15 g/day, respectively. The reduction of log hazard ratio in the HUG was more clear in the eGFR 30–60 mL/min/1.73m2 subpopulation (Figure 1C). Similarly, a reduction in log hazard ratio in the HUG was observed in glomerulonephritis, polycystic kidney disease subpopulations, but not in the diabetes mellitus nephropathy subpopulation (Figure 1D–F).

CONCLUSION

Daily urea urine excretion showed prognostic implications in the CKD stage 3 subgroups, glomerulonephritis subgroups and polycystic kidney disease subgroups. In the following researches, studies focusing on interventional targets in the context of daily urea excretion in those subgroups should be warranted.
MO440: Intramyocardial Artery Fibrosis and Media Hypertrophy are Associated With Beta-Catenin and Calcineurin Expression in the Model of Arterial Hypertension and CKD
Authors: Bogdanova Evdokia , Beresneva Olga , Ivanova Galina , Dobronravov Vladimir
Published: May 2022

BACKGROUND AND AIMS

Intramyocardial arteries (IA) are one of the components of pathological cardiac remodeling. We have previously shown that cardiomyocytes hypertrophy and interstitial fibrosis are accompanied by calcineurin (CaN) and β-catenin (βCat) up-regulation in the model of arterial hypertension (AH) and chronic kidney disease (AH-CKD). In this pilot study, we investigated whether IA remodeling is associated with CaN and βCat expressions in medial (MC) and adventitial (AC) cells in AH-CKD.

METHOD

AH-CKD was induced by 5/6 nephrectomy (5/6NE) in spontaneously hypertensive rats (SHR-NE, n = 8). Sham-operated (SO) SHR (SHR-SO, n = 8) and Wistar Kyoto rats (WKY-SO, n = 8) were controls. Systolic blood pressure (SBP), myocardial mass index (MMI), serum creatinine (Cr), FGF23, renal Klotho (rKl), IA wall thickness (WT), perivascular fibrosis (PF), number of AC, βCat-positive AC (βCat + AC) to all AC ratio, CaN and βCat expression in MC were analyzed for 2 months after 5/6NE or SO.

RESULTS

The cardiac remodeling indexes—SBP, MMI, WT, AC, PF, as well as FGF23, were higher and rKl was lower in SHRs vs WKY-SO and in SHR-NE versus SHR-SO (Table). The increase in WT was accompanied by MC hypertrophy (Figure 1) with cytoplasmic CaN expression (data not shown) and PF with the increase in the number of AC in SHR-SO vs WKY-SO (Table). PF, medial hypertrophy and fibrosis of IA were accompanied by the apparent expression of CaN and βCat in the MC (Figure 1), an increase in the total number of AC and the βCat + AC accumulation in AH-CKD (Table, Figure 2).

CONCLUSION

IA remodeling in the setting of AH and CKD seems to be associated with СаN and βCat up-regulation in medial and adventitial cells subpopulations. Further study is needed to identify the origin of CaN/βCat expressing cells and the mechanisms of their involvement in the pathology of vascular wall alterations.
MO450: A New Hematuria Score, Semi-Quantitative Analysis of Hematuria Normalized for Urine Concentration Predicts the Progression of Chronic Kidney Disease: From the KNOW-CKD Study
Authors: Koh Jaehee , Min Jo Sang , Kim Sangeun , Hoon Jung Sung , Lee Kyu-Beck , Kim Hyang , Oh Kook-Hwan , Youl Hyun Young
Published: May 2022

BACKGROUND AND AIMS

It is unclear whether hematuria is a risk factor for chronic kidney disease (CKD) progression. In addition, quantitative evaluation considering urine concentration as in proteinuria has not been established in hematuria. The aim of this study is to verify the relationship between semi-quantitative analysis of hematuria normalized for urine concentration and the progression in CKD.

METHOD

We analyzed 1909 patients with pre-dialysis CKD from KNOW-CKD cohort who assessed baseline urine microscopy. Patients were scored according to the number of red blood cells (RBC) in high power field (1 point for < 1, 2 points for 1–4, 3 points for 5̵119 and 4 points for ≥ 20). To obtain the hematuria score, these points were divided by the random urine creatinine level and multiplied by 100. The study endpoint was CKD progression, defined as a composite of a ≥ 50% decrease in estimated glomerular filtration rate (eGFR) from baseline values or end-stage kidney disease.

RESULTS

The hematuria score ranged from 1.86 to 20.3 (2.2 ± 1.86). During a median follow-up of 4.6 years (9657 person-years), 729 patients reached study endpoint. There was a graded association between hematuria score and the risk of progression of CKD. The hazard ratios (95% confidence intervals) for second, third and fourth quartile of hematuria score were 1.32 (1.04–1.67), 1.43 (1.12–1.82) and 1.50 (1.17–1.91), respectively, compared to the first quartile. For each 1 point increase in hematuria score, the risk of progression increased by 5%.

CONCLUSION

This study showed that there was a graded relationship between a new hematuria score and the risk of the progression of CKD. Microscopic hematuria is a risk factor for CKD progression and might be used as a quantitative risk assessment tool.