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Showing papers in "BMC Nephrology in 2021"


Journal ArticleDOI
TL;DR: In this paper, the authors describe clinical, laboratory, and radiologic characteristics and determinants of mortality in a large group of maintenance hemodialysis patients hospitalized for COVID-19.
Abstract: Maintenance hemodialysis (MHD) patients are at increased risk for coronavirus disease 2019 (COVID-19). The aim of this study was to describe clinical, laboratory, and radiologic characteristics and determinants of mortality in a large group of MHD patients hospitalized for COVID-19. This multicenter, retrospective, observational study collected data from 47 nephrology clinics in Turkey. Baseline clinical, laboratory and radiological characteristics, and COVID-19 treatments during hospitalization, need for intensive care and mechanical ventilation were recorded. The main study outcome was in-hospital mortality and the determinants were analyzed by Cox regression survival analysis. Of 567 MHD patients, 93 (16.3%) patients died, 134 (23.6%) patients admitted to intensive care unit (ICU) and 91 of the ones in ICU (67.9%) needed mechanical ventilation. Patients who died were older (median age, 66 [57–74] vs. 63 [52–71] years, p = 0.019), had more congestive heart failure (34.9% versus 20.7%, p = 0.004) and chronic obstructive pulmonary disease (23.6% versus 12.7%, p = 0.008) compared to the discharged patients. Most patients (89.6%) had radiological manifestations compatible with COVID-19 pulmonary involvement. Median platelet (166 × 103 per mm3 versus 192 × 103 per mm3, p = 0.011) and lymphocyte (800 per mm3 versus 1000 per mm3, p < 0.001) counts and albumin levels (median, 3.2 g/dl versus 3.5 g/dl, p = 0.001) on admission were lower in patients who died. Age (HR: 1.022 [95% CI, 1.003–1.041], p = 0.025), severe-critical disease clinical presentation at the time of diagnosis (HR: 6.223 [95% CI, 2.168–17.863], p < 0.001), presence of congestive heart failure (HR: 2.247 [95% CI, 1.228–4.111], p = 0.009), ferritin levels on admission (HR; 1.057 [95% CI, 1.006–1.111], p = 0.028), elevation of aspartate aminotransferase (AST) (HR; 3.909 [95% CI, 2.143–7.132], p < 0.001) and low platelet count (< 150 × 103 per mm3) during hospitalization (HR; 1.864 [95% CI, 1.025–3.390], p = 0.041) were risk factors for mortality. Hospitalized MHD patients with COVID-19 had a high mortality rate. Older age, presence of heart failure, clinical severity of the disease at presentation, ferritin level on admission, decrease in platelet count and increase in AST level during hospitalization may be used to predict the mortality risk of these patients.

38 citations


Journal ArticleDOI
TL;DR: The Random Forest and J48 algorithms are used to obtain a sustainable and practicable model to detect various stages of CKD with comprehensive medical accuracy and it was revealed that J48 predicted CKD in all stages better than random forest with a 85.5% accuracy.
Abstract: Chronic Kidney Disease (CKD), i.e., gradual decrease in the renal function spanning over a duration of several months to years without any major symptoms, is a life-threatening disease. It progresses in six stages according to the severity level. It is categorized into various stages based on the Glomerular Filtration Rate (GFR), which in turn utilizes several attributes, like age, sex, race and Serum Creatinine. Among multiple available models for estimating GFR value, Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI), which is a linear model, has been found to be quite efficient because it allows detecting all CKD stages. Early detection and cure of CKD is extremely desirable as it can lead to the prevention of unwanted consequences. Machine learning methods are being extensively advocated for early detection of symptoms and diagnosis of several diseases recently. With the same motivation, the aim of this study is to predict the various stages of CKD using machine learning classification algorithms on the dataset obtained from the medical records of affected people. Specifically, we have used the Random Forest and J48 algorithms to obtain a sustainable and practicable model to detect various stages of CKD with comprehensive medical accuracy. Comparative analysis of the results revealed that J48 predicted CKD in all stages better than random forest with an accuracy of 85.5%. The study also showed that J48 shows improved performance over Random Forest. The study concluded that it may be used to build an automated system for the detection of severity of CKD.

36 citations


Journal ArticleDOI
TL;DR: In this paper, the authors conducted a systematic review to evaluate the incidence of acute kidney injury (AKI) in hospitalized patients with coronavirus disease-19 (COVID-19) and has also been associated with in-hospital mortality.
Abstract: Acute kidney injury (AKI) occurs among patients with coronavirus disease-19 (COVID-19) and has also been indicated to be associated with in-hospital mortality. Remdesivir has been authorized for the treatment of COVID-19. We conducted a systematic review to evaluate the incidence of AKI in hospitalized COVID-19 patients. The incidence of AKI in different subgroups was also investigated. A thorough search was performed to find relevant studies in PubMed, Web of Science, medRxiv and EMBASE from 1 Jan 2020 until 1 June 2020. The systematic review was performed using the meta package in R (4.0.1). A total of 16,199 COVID-19 patients were included in our systematic review. The pooled estimated incidence of AKI in all hospitalized COVID-19 patients was 10.0% (95% CI: 7.0–12.0%). The pooled estimated proportion of COVID-19 patients who needed continuous renal replacement therapy (CRRT) was 4% (95% CI: 3–6%). According to our subgroup analysis, the incidence of AKI could be associated with age, disease severity and ethnicity. The incidence of AKI in hospitalized COVID-19 patients being treated with remdesivir was 7% (95% CI: 3–13%) in a total of 5 studies. We found that AKI was not rare in hospitalized COVID-19 patients. The incidence of AKI could be associated with age, disease severity and ethnicity. Remdesivir probably did not induce AKI in COVID-19 patients. Our systematic review provides evidence that AKI might be closely associated with SARS-CoV-2 infection, which should be investigated in future studies.

31 citations


Journal ArticleDOI
TL;DR: In this paper, the demographic characteristics, clinical findings, laboratory parameters (hemogram, CRP, AST, ALT, LDH, and ferritin) at admission and follow-up, and treatment strategies were reviewed.
Abstract: We aimed to present the demographic characteristics, clinical presentation, and outcomes of our multicenter cohort of adult KTx recipients with COVID-19. We conducted a multicenter, retrospective study using data of patients hospitalized for COVID-19 collected from 34 centers in Turkey. Demographic characteristics, clinical findings, laboratory parameters (hemogram, CRP, AST, ALT, LDH, and ferritin) at admission and follow-up, and treatment strategies were reviewed. Predictors of poor clinical outcomes were analyzed. The primary outcomes were in-hospital mortality and the need for ICU admission. The secondary outcome was composite in-hospital mortality and/or ICU admission. One hundred nine patients (male/female: 63/46, mean age: 48.4 ± 12.4 years) were included in the study. Acute kidney injury (AKI) developed in 46 (42.2%) patients, and 4 (3.7%) of the patients required renal replacement therapy (RRT). A total of 22 (20.2%) patients were admitted in the ICU, and 19 (17.4%) patients required invasive mechanical ventilation. 14 (12.8%) of the patients died. Patients who were admitted in the ICU were significantly older (age over 60 years) (38.1% vs 14.9%, p = 0.016). 23 (21.1%) patients reached to composite outcome and these patients were significantly older (age over 60 years) (39.1% vs. 13.9%; p = 0.004), and had lower serum albumin (3.4 g/dl [2.9–3.8] vs. 3.8 g/dl [3.5–4.1], p = 0.002), higher serum ferritin (679 μg/L [184–2260] vs. 331 μg/L [128–839], p = 0.048), and lower lymphocyte counts (700/μl [460–950] vs. 860 /μl [545–1385], p = 0.018). Multivariable analysis identified presence of ischemic heart disease and initial serum creatinine levels as independent risk factors for mortality, whereas age over 60 years and initial serum creatinine levels were independently associated with ICU admission. On analysis for predicting secondary outcome, age above 60 and initial lymphocyte count were found to be independent variables in multivariable analysis. Over the age of 60, ischemic heart disease, lymphopenia, poor graft function were independent risk factors for severe COVID-19 in this patient group. Whereas presence of ischemic heart disease and poor graft function were independently associated with mortality.

27 citations


Journal ArticleDOI
TL;DR: In this paper, the authors investigated the epidemiology, risk factors and outcomes of acute kidney injury in patients with COVID-19 in a large UK tertiary centre and found that AKI was a strong predictor of 30-day mortality with an increasing risk across AKI stages.
Abstract: Acute kidney injury (AKI) is common among patients hospitalised with COVID-19 and associated with worse prognosis. The aim of this study was to investigate the epidemiology, risk factors and outcomes of AKI in patients with COVID-19 in a large UK tertiary centre. We analysed data of consecutive adults admitted with a laboratory-confirmed diagnosis of COVID-19 across two sites of a hospital in London, UK, from 1st January to 13th May 2020. Of the 1248 inpatients included, 487 (39%) experienced AKI (51% stage 1, 13% stage 2, and 36% stage 3). The weekly AKI incidence rate gradually increased to peak at week 5 (3.12 cases/100 patient-days), before reducing to its nadir (0.83 cases/100 patient-days) at the end the study period (week 10). Among AKI survivors, 84.0% had recovered renal function to pre-admission levels before discharge and none required on-going renal replacement therapy (RRT). Pre-existing renal impairment [odds ratio (OR) 3.05, 95%CI 2.24–4,18; p < 0.0001], and inpatient diuretic use (OR 1.79, 95%CI 1.27–2.53; p < 0.005) were independently associated with a higher risk for AKI. AKI was a strong predictor of 30-day mortality with an increasing risk across AKI stages [adjusted hazard ratio (HR) 1.59 (95%CI 1.19–2.13) for stage 1; p < 0.005, 2.71(95%CI 1.82–4.05); p < 0.001for stage 2 and 2.99 (95%CI 2.17–4.11); p < 0.001for stage 3]. One third of AKI3 survivors (30.7%), had newly established renal impairment at 3 to 6 months. This large UK cohort demonstrated a high AKI incidence and was associated with increased mortality even at stage 1. Inpatient diuretic use was linked to a higher AKI risk. One third of survivors with AKI3 exhibited newly established renal impairment already at 3–6 months.

23 citations


Journal ArticleDOI
TL;DR: The levels of fecal SCFAs in the IgAN patients were reduced, and correlated with clinical parameters and gut microbiota, which may be involved in the pathogenesis of IgAN, and this finding may provide a new therapeutic approach.
Abstract: IgA nephropathy(IgAN)) is the common pathological type of glomerular diseases. The role of gut microbiota in mediating “gut-IgA nephropathy” has not received sufficient attention in the previous studies. The purpose of this study was to investigate the changes of fecal short-chain fatty acids(SCFAs), a metabolite of the intestinal microbiota, in patients with IgAN and its correlation with intestinal flora and clinical indicators, and to further investigate the role of the gut-renal axis in IgAN. There were 29 patients with IgAN and 29 normal control subjects recruited from January 2018 to May 2018. The fresh feces were collected. The fecal SCFAs were measured by gas chromatography/mass spectrometry and gut microbiota was analysed by16S rDNA sequences, followed by estimation of α- and β-diversity. Correlation analysis was performed using the spearman’s correlation test between SCFAs and gut microbiota. The levels of acetic acid, propionic acid, butyric acid, isobutyric acid and caproic acid in the IgAN patients were significantly reduced compared with control group(P < 0.05). Butyric acid(r=-0.336, P = 0.010) and isobutyric acid(r=-0.298, P = 0.022) were negatively correlated with urea acid; butyric acid(r=-0.316, P = 0.016) was negatively correlated with urea nitrogen; caproic acid(r=-0.415,P = 0.025) showed negative correlation with 24-h urine protein level.Exemplified by the results of α-diversity and β-diversity, the intestinal flora of IgAN patients was significantly different from that of the control group. Acetic acid was positively associated with c_Clostridia(r = 0.357, P = 0.008), o_Clostridiales(r = 0.357, P = 0.008) and g_Eubacterium_coprostanoligenes_group(r = 0.283, P = 0.036). Butyric acid was positively associated with g_Alistipes (r = 0.278, P = 0.040). The relative abundance of those were significantly decreased in IgAN group compared to control group. The levels of fecal SCFAs in the IgAN patients were reduced, and correlated with clinical parameters and gut microbiota, which may be involved in the pathogenesis of IgAN, and this finding may provide a new therapeutic approach.

23 citations


Journal ArticleDOI
TL;DR: In this paper, the authors measured the relationship between markers of glycocalyx damage, endothelial dysfunction, and uraemic toxins in patients with chronic kidney disease (CKD) and kidney transplant recipients.
Abstract: Damage to the endothelial glycocalyx is an early indicator of vascular damage and a potential marker of endothelial dysfunction. This study aimed to assess the relationship between markers of glycocalyx damage, endothelial dysfunction, and uraemic toxins in patients with chronic kidney disease. Healthy controls, CKD patients, dialysis patients, and kidney transplant recipients had biochemical markers of glycocalyx damage (syndecan-1 and hyaluronan), endothelial dysfunction (von Willebrand factor; vWF and vascular cell adhesion molecule; VCAM-1), and uraemic toxins (indoxyl sulphate and p-cresyl sulphate) measured. In addition, Sidestream Darkfield imaging was performed using the novel GlycoCheck™ device to measure glycocalyx width by the perfused boundary region (PBR) in the sublingual microcirculation. Serum markers of glycocalyx damage were highest in the dialysis group (n = 33), followed by CKD patients (n = 32) and kidney transplant recipients (n = 30) compared to controls (n = 30): hyaluronan: 137 (16-1414), 79 (11–257), 57 (14–218) and 23 (8-116) ng/mL, respectively, p < 0.0001; syndecan-1: 81 (40–529), 46 (21–134), 39 (23–72), and 30 (12–138) ng/mL, respectively, p < 0.0001. Markers of endothelial dysfunction followed a similar pattern. No difference in the width of the PBR was detected between these groups (2.01 ± 0.35, 2.07 ± 0.27, 2.06 ± 0.28, and 2.05 ± 0.3 µm, respectively, p = 0.89). Glycocalyx damage correlated with markers of endothelial dysfunction (log-hyaluronan and log-VCAM-1: r = 0.64, p < 0.001) and levels of uraemic toxins (log-hyaluronan and log-indoxyl sulphate: r = 0.48, p < 0.001). Levels of biochemical markers of glycocalyx and endothelial cell damage are highest in patients receiving dialysis. Glycocalyx and endothelial damage markers correlated with each other, and with uraemic toxins. Although we could not demonstrate a change in PBR, the biochemical markers suggest that glycocalyx damage is most marked in patients with higher levels of uraemic toxins.

23 citations


Journal ArticleDOI
TL;DR: In this paper, the authors conducted a cohort study to investigate the risk factors for acute kidney injury in patients admitted to and intensive care unit with COVID-19, its incidence and associated outcomes.
Abstract: Acute kidney injury (AKI) is a common manifestation among patients critically ill with SARS-CoV-2 infection (Coronavirus 2019) and is associated with significant morbidity and mortality. The pathophysiology of renal failure in this context is not fully understood, but likely to be multifactorial. The intensive care unit outcomes of patients following COVID-19 acute critical illness with associated AKI have not been fully explored. We conducted a cohort study to investigate the risk factors for acute kidney injury in patients admitted to and intensive care unit with COVID-19, its incidence and associated outcomes. We reviewed the medical records of all patients admitted to our adult intensive care unit suffering from SARS-CoV-2 infection from 14th March 2020 until 12th May 2020. Acute kidney injury was defined using the Kidney Disease Improving Global Outcome (KDIGO) criteria. The outcome analysis was assessed up to date as 3rd of September 2020. A total of 81 patients admitted during this period. All patients had acute hypoxic respiratory failure and needed either noninvasive or invasive mechanical ventilatory support. Thirty-six patients (44%) had evidence of AKI (Stage I-33%, Stage II-22%, Renal Replacement Therapy (RRT)-44%). All patients with AKI stage III had RRT. Age, diabetes mellitus, immunosuppression, lymphopenia, high D-Dimer levels, increased APACHE II and SOFA scores, invasive mechanical ventilation and use of inotropic or vasopressor support were significantly associated with AKI. The peak AKI was at day 4 and mean duration of RRT was 12.5 days. The mortality was 25% for the AKI group compared to 6.7% in those without AKI. Among those received RRT and survived their illness, the renal function recovery is complete and back to baseline in all patients. Acute kidney injury and renal replacement therapy is common in critically ill patients presenting with COVID-19. It is associated with increased severity of illness on admission to ICU, increased mortality and prolonged ICU and hospital length of stay. Recovery of renal function was complete in all survived patients.

23 citations


Journal ArticleDOI
TL;DR: In this paper, the authors evaluated the incidence of acute kidney injury (AKI) and its association with mortality and morbidity in children infected with severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) who required hospital admission.
Abstract: Acute kidney injury (AKI) is a complication of coronavirus disease 2019 (COVID-19). The reported incidence of AKI, however, varies among studies. We aimed to evaluate the incidence of AKI and its association with mortality and morbidity in children infected with severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) who required hospital admission. This was a multicenter retrospective cohort study from three tertiary centers, which included children with confirmed COVID-19. All children were evaluated for AKI using the Kidney Disease Improving Global Outcomes (KDIGO) definition and staging. Of 89 children included, 19 (21 %) developed AKI (52.6 % stage I). A high renal angina index score was correlated with severity of AKI. Also, multisystem inflammatory syndrome in children (MIS-C) was increased in children with AKI compared to those with normal kidney function (15 % vs. 1.5 %). Patients with AKI had significantly more pediatric intensive care admissions (PICU) (32 % vs. 2.8 %, p < 0.001) and mortality (42 % vs. 0 %, p < 0.001). However, AKI was not associated with prolonged hospitalization (58 % vs. 40 %, p = 0.163) or development of MIS-C (10.5 % vs. 1.4 %, p = 0.051). No patient in the AKI group required renal replacement therapy. Residual renal impairment at discharge occurred in 9 % of patients. This was significantly influenced by the presence of comorbidities, hypotension, hypoxia, heart failure, acute respiratory distress, hypernatremia, abnormal liver profile, high C-reactive protein, and positive blood culture. AKI occurred in one-fifth of children with SARS-CoV-2 infection requiring hospital admission, with one-third of those requiring PICU. AKI was associated with increased morbidity and mortality, and residual renal impairment at time of discharge.

22 citations


Journal ArticleDOI
TL;DR: In this paper, a systematic review of the evidence on the association of physical activity with mortality and hospitalization in end-stage kidney disease patients was conducted, showing that higher physical activity was associated with reduced mortality.
Abstract: End-stage Kidney Disease patients have a high mortality and hospitalization risk. The association of these outcomes with physical activity is described in the general population and in other chronic diseases. However, few studies examining this association have been completed in end-stage Kidney Disease patients, raising the need to systematically review the evidence on the association of physical activity with mortality and hospitalization in this population. Electronic databases (EBSCO, Scopus and Web of Science) and hand search were performed until March 2020 for observational studies reporting the association of physical activity with mortality or hospitalization in adult end-stage Kidney Disease patients on renal replacement therapy (hemodialysis, peritoneal dialysis and kidney transplant). Methodological quality of the included studies was assessed using the Quality in Prognosis Studies tool. The review protocol was registered in PROSPERO (CRD42020155591). Eleven studies were included: six in hemodialysis, three in kidney transplant, and two in hemodialysis and peritoneal dialysis patients. Physical activity was self-reported, except in one study that used accelerometers. All-cause mortality was addressed in all studies and cardiovascular mortality in three studies. Nine studies reported a significant reduction in all-cause mortality with increased levels of physical activity. Evidence of a dose-response relationship was found. For cardiovascular mortality, a significant reduction was observed in two of the three studies. Only one study investigated the association of physical activity with hospitalization. Higher physical activity was associated with reduced mortality in end-stage Kidney Disease patients. Future studies using objective physical activity measures could strengthen these findings. The association of physical activity with hospitalization should be explored in future investigations.

20 citations


Journal ArticleDOI
TL;DR: In this paper, the efficacy of eculizumab, a monoclonal antibody targeting the terminal complement pathway, in patients with gemcitabine-induced TMA (G-TMA) was evaluated.
Abstract: Gemcitabine is a broadly prescribed chemotherapy, the use of which can be limited by renal adverse events, including thrombotic microangiopathy (TMA). This study evaluated the efficacy of eculizumab, a monoclonal antibody targeting the terminal complement pathway, in patients with gemcitabine-induced TMA (G-TMA). We conducted an observational, retrospective, multicenter study in 5 French centres, between 2011 and 2016. Twelve patients with a G-TMA treated by eculizumab were included. The main characteristics were acute renal failure (100%), including stage 3 acute kidney injury (AKI, 58%) and renal replacement therapy (17%), hypertension (92%) and diffuse oedema (83%). Eculizumab was started after a median of 15 days (range 4–44) following TMA diagnosis. A median of 4 injections of eculizumab was performed (range 2–22). Complete hematological remission was achieved in 10 patients (83%) and blood transfusion significantly decreased after only one injection of eculizumab (median of 3 packed red blood cells (range 0–10) before treatment vs 0 (range 0–1) after one injection, P < 0.001). Two patients recovered completely renal function (17%), and 8 achieved a partial remission (67%). Compared to a control group of G-TMA without use of eculizumab, renal outcome was more favourable. At the end of the follow up, median eGFR was 45 vs 33 ml/min/1.73m2 respectively in the eculizumab group and in the control group. These results suggest that eculizumab is efficient on haemolysis and reduces transfusion requirement in G-TMA. Moreover, eculizumab may improve renal function recovery.

Journal ArticleDOI
TL;DR: In this article, a cross-sectional and descriptive correlational design using Qualtrics software was performed to determine the prevalence of fatigue, anxiety, depression and sleep quality among patients receiving haemodialysis during the coronavirus disease 2019 (COVID-19) pandemic, and to explore the contributing predictors.
Abstract: Patients undergoing haemodialysis may experience troubling symptoms such as fatigue, anxiety, depression and sleep quality, which may affect their quality of life. The main objective of this study is to determine the prevalence of fatigue, anxiety, depression and sleep quality among patients receiving haemodialysis during the coronavirus disease 2019 (COVID-19) pandemic, and to explore the contributing predictors. A cross-sectional and descriptive correlational design using Qualtrics software was performed. Data were collected using the Functional Assessment of Cancer Therapy-Fatigue (FACT-F), the Hospital Anxiety and Depression Scale (HADS) and the Pittsburgh Sleep Quality Index (PSQI). Logistic regression analyses were used to explore the predictors that were associated with fatigue, anxiety, depression and sleep quality. Of the 123 patients undergoing haemodialysis who participated, 53.7% (n = 66) reported fatigue, 43.9% (n = 54) reported anxiety, 33.3% (n = 41) reported depression and 56.9% (n = 70) reported poor sleep. Fatigue, anxiety and sleep quality (P < .05) were significantly associated with being female, and whether family members or relatives were suspected or confirmed with COVID-19. Logistic regression showed that being within the age group 31–40, having a secondary education level, anxiety, depression and sleep quality were the main predictors affecting the fatigue group. Fatigue, anxiety, depression and sleep quality are significant problems for patients receiving haemodialysis during the COVID-19 pandemic. Appropriate interventions to monitor and reduce fatigue, psychological problems and sleep quality amongst these patients are needed. This can help to strengthen preparations for responding to possible future outbreaks or pandemics of infectious diseases for patients receiving haemodialysis.

Journal ArticleDOI
TL;DR: In this paper, the first case of minimal change disease (MCD) after receiving the Moderna COVID-19 vaccine was reported, which is the first reported case of MCD after receiving a Moderna vaccine.
Abstract: Background There have been cases of minimal change disease (MCD) reported following previous vaccines. During the COVID-19 era, only 3 cases of new-onset MCD and a case of MCD relapse were reported following the Pfizer-BioNTech COVID-19 vaccine. We herein report the first case of MCD after receiving the Moderna COVID-19 vaccine. Case presentation A 43-year-old man presented to hospital 3 weeks after receiving the first dose of the Moderna vaccine, with both bilateral lower extremities and scrotal edema. He initially developed a sudden-onset bilateral lower extremities swelling on day 7 post-vaccine. He, then, developed dyspnea and scrotal swelling over a time span of 2 weeks. On physical examination, his blood pressure was 150/92 mmHg. There was a decreased air entry at lung bases, bilateral lower extremities and scrotal edema. Labs revealed hypoalbuminemia, hyperlipidemia and 15 g of proteinuria. His immunologic and serologic work up was negative. Renal biopsy showed concomitant MCD and IgA nephropathy. Patient was treated with oral steroids and had a good response; his edema resolved, serum albumin improved, and proteinuria decreased to 1 g within 2 weeks of treatment. Conclusions To the best of our knowledge, MCD has not been previously reported after receiving the Moderna COVID-19 vaccine. It remains unclear whether the COVID-19 mRNA vaccines are associated with the development of MCD, or it coincided with the mass vaccination. Further studies are needed to determine the incidence of MCD post COVID-19 vaccines and the underlying pathophysiology of glomerular injury post vaccination.

Journal ArticleDOI
TL;DR: In this article, a kidney biopsy was performed and revealed granulomatous tubulo-interstitial nephritis with some acute tubular injury, which led to a change in therapy, which was associated with subsequent patient improvement.
Abstract: Acute kidney injury (AKI) associated with severe coronavirus disease 19 (COVID-19) is common and is a significant predictor of morbidity and mortality, especially when dialysis is required. Case reports and autopsy series have revealed that most patients with COVID-19 – associated acute kidney injury have evidence of acute tubular injury and necrosis - not unexpected in critically ill patients. Others have been found to have collapsing glomerulopathy, thrombotic microangiopathy and diverse underlying kidney diseases. A primary kidney pathology related to COVID-19 has not yet emerged. Thus far direct infection of the kidney, or its impact on clinical disease remains controversial. The management of AKI is currently supportive. The patient presented here was positive for SARS-CoV-2, had severe acute respiratory distress syndrome and multi-organ failure. Within days of admission to the intensive care unit he developed oliguric acute kidney failure requiring dialysis. Acute kidney injury developed in the setting of hemodynamic instability, sepsis and a maculopapular rash. Over the ensuing days the patient also developed transfusion-requiring severe hemolysis which was Coombs negative. Schistocytes were present on the peripheral smear. Given the broad differential diagnoses for acute kidney injury, a kidney biopsy was performed and revealed granulomatous tubulo-interstitial nephritis with some acute tubular injury. Based on the biopsy findings, a decision was taken to adjust medications and initiate corticosteroids for presumed medication-induced interstitial nephritis, hemolysis and maculo-papular rash. The kidney function and hemolysis improved over the subsequent days and the patient was discharged to a rehabilitation facility, no-longer required dialysis. Acute kidney injury in patients with severe COVID-19 may have multiple causes. We present the first case of granulomatous interstitial nephritis in a patient with COVID-19. Drug-reactions may be more frequent than currently recognized in COVID-19 and are potentially reversible. The kidney biopsy findings in this case led to a change in therapy, which was associated with subsequent patient improvement. Kidney biopsy may therefore have significant value in pulling together a clinical diagnosis, and may impact outcome if a treatable cause is identified.

Journal ArticleDOI
TL;DR: In this article, the authors evaluated the renal toxicity induced by AgNPs after repeated oral exposure and to determine the relevant molecular mechanisms, which showed that AgNs played a critical role in in vivo renal toxicity.
Abstract: BACKGROUND Silver nanoparticles (AgNPs) can accumulate in various organs after oral exposure. The main objective of the current study is to evaluate the renal toxicity induced by AgNPs after repeated oral exposure and to determine the relevant molecular mechanisms. METHODS In this study, 40 male Wistar rats were treated with solutions containing 30, 125, 300, and 700 mg/kg of AgNPs. After 28 days of exposure, histopathological changes were assessed using hematoxylin-eosin (H&E), Masson's trichrome, and periodic acid-Schiff (PAS) staining. Apoptosis was quantified by TUNEL and immunohistochemistry of caspase-3, and the level of expression of the mRNAs of growth factors was determined using RT-PCR. RESULTS Histopathologic examination revealed degenerative changes in the glomeruli, loss of tubular architecture, loss of brush border, and interrupted tubular basal laminae. These changes were more noticeable in groups treated with 30 and 125 mg/kg. The collagen intensity increased in the group treated with 30 mg/kg in both the cortex and the medulla. Apoptosis was much more evident in middle-dose groups (i.e., 125 and 300 mg/kg). The results of RT-PCR indicated that Bcl-2 and Bax mRNAs upregulated in the treated groups (p < 0.05). Moreover, the data related to EGF, TNF-α, and TGF-β1 revealed that AgNPs induced significant changes in gene expression in the groups treated with 30 and 700 mg/kg compared to the control group. CONCLUSION Our observations showed that AgNPs played a critical role in in vivo renal toxicity.

Journal ArticleDOI
TL;DR: In general, patients with CKD5 live for a shorter time on CKM than on dialysis, and in elderly individuals with comorbidities, the survival benefits of dialysis seem to be lost.
Abstract: Background Patients with stage 5 chronic kidney disease (CKD5) collaborate with their clinicians when choosing their future treatment modality. Most elderly patients with CKD5 may only have two treatment options: dialysis or conservative kidney management (CKM). The objective of this systematic review was to investigate whether CKM offers a quantity or quality of life benefit compared to dialysis for some patients with CKD5. Methods The databases MEDLINE, EMBASE, the Cochrane Library, and CINAHL were systematically searched for studies comparing patients with CKD5 who had chosen or were treated with either CKM or dialysis. The primary outcomes were mortality and quality of life (QoL). Hospitalization, symptom burden, and place of death were secondary outcomes. For studies reporting hazard ratios, pooled values were calculated, and forest plots conducted. Results Twenty-five primary studies, all observational, were identified. All studies reported an increased mortality in patients treated with CKM (pooled hazard ratio 0.47, 95 % confidence interval 0.34-0.65). For patients aged ≥ 80 years and for elderly individuals with comorbidities, results were ambiguous. In most studies, CKM seemed advantageous for QoL and secondary outcomes. Findings were limited by the heterogeneity of studies and biased outcomes favouring dialysis. Conclusions In general, patients with CKD5 who have chosen or are on CKM live for a shorter time than patients who have chosen or are on dialysis. In patients aged ≥ 80 years old, and in elderly individuals with comorbidities, the survival benefits of dialysis seem to be lost. Regarding QoL, symptom burden, hospitalization, and place of death, CKM may have advantages. Higher quality studies are needed to guide patients and clinicians in the decision-making process.

Journal ArticleDOI
TL;DR: In this article, the authors used weighted gene co-expression network analysis (WGCNA) algorithm for better understanding of diabetic nephropathy (DN) pathogenesis and exploring key genes in the disease progression.
Abstract: Background Diabetic nephropathy (DN) is the major complication of diabetes mellitus, and leading cause of end-stage renal disease. The underlying molecular mechanism of DN is not yet completely clear. The aim of this study was to analyze a DN microarray dataset using weighted gene co-expression network analysis (WGCNA) algorithm for better understanding of DN pathogenesis and exploring key genes in the disease progression. Methods The identified differentially expressed genes (DEGs) in DN dataset GSE47183 were introduced to WGCNA algorithm to construct co-expression modules. STRING database was used for construction of Protein-protein interaction (PPI) networks of the genes in all modules and the hub genes were identified considering both the degree centrality in the PPI networks and the ranked lists of weighted networks. Gene ontology and Reactome pathway enrichment analyses were performed on each module to understand their involvement in the biological processes and pathways. Following validation of the hub genes in another DN dataset (GSE96804), their up-stream regulators, including microRNAs and transcription factors were predicted and a regulatory network comprising of all these molecules was constructed. Results After normalization and analysis of the dataset, 2475 significant DEGs were identified and clustered into six different co-expression modules by WGCNA algorithm. Then, DEGs of each module were subjected to functional enrichment analyses and PPI network constructions. Metabolic processes, cell cycle control, and apoptosis were among the top enriched terms. In the next step, 23 hub genes were identified among the modules in genes and five of them, including FN1, SLC2A2, FABP1, EHHADH and PIPOX were validated in another DN dataset. In the regulatory network, FN1 was the most affected hub gene and mir-27a and REAL were recognized as two main upstream-regulators of the hub genes. Conclusions The identified hub genes from the hearts of co-expression modules could widen our understanding of the DN development and might be of targets of future investigations, exploring their therapeutic potentials for treatment of this complicated disease.

Journal ArticleDOI
TL;DR: In this article, a cross-sectional study was performed on 300 dialysis patients (218 HD and 82 PD) referred to two Dialysis Centers, where data were collected using demographic information and a 9-item Shared Decision Making Questionnaire (SDM-Q-9).
Abstract: Shared decision making (SDM) is recognized as the gold standard for patient-centered care. This study aimed to assess and compare the SDM among patients undergoing hemodialysis and peritoneal dialysis for choosing a dialysis modality. This is a cross-sectional study that was performed on 300 dialysis patients (218 HD and 82 PD) referred to two Dialysis Centers. Data were collected using demographic information and a 9-item Shared Decision Making Questionnaire (SDM-Q-9). The data were analyzed using ANOVA and independent t-test by SPSS software. The mean SDM-Q-9 score in all samples (PD and HD) was 21.94 ± 15.08 (in a possible range of 0 to 45). Results of the independent t-test showed that the mean SDM-Q-9 score in PD patients (33.11 ± 10.08) was higher than HD patients (17.14 ± 74.24) (p < 0.001). The results showed a statistically significant difference in mean SDM-Q-9 score based on patients’ age, educational level, and income (p < 0.05). Implementing shared decision making and providing information on RRT should be started in the early stage of CKD. The health care providers should involve patients with CKD and their families in dialysis-related decisions and it should be started in the early stage of CKD.

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TL;DR: In this paper, the authors used univariable and multivariable Cox regression models to assess the association of underlying condition ESRD with the COVID-19 in-hospital mortality.
Abstract: The extent to which patients with End-stage renal disease (ESRD) are at a higher risk of COVID-19-related death is still unclear. Therefore, the aim of this study was to identify the ESRD patients at increased risk of COVID-19 -related death and its associated factors. This retrospective cohort study was conducted on 74 patients with ESRD and 446 patients without ESRD hospitalized for COVID-19 in Alborz province, Iran, from Feb 20 2020 to Apr 26 2020. Data on demographic factors, medical history, Covid-19- related symptoms, and blood tests were obtained from the medical records of patients with confirmed COVID-19. We fitted univariable and multivariable Cox regression models to assess the association of underlying condition ESRD with the COVID-19 in-hospital mortality. Results were presented as crude and adjusted Hazard Ratios (HRs) and 95% confidence intervals (CIs). In the ESRD subgroup, demographic factors, medical history, symptoms, and blood parameters on the admission of survivors were compared with non-survivors to identify factors that might predict a high risk of mortality. COVID-19 patients with ESRD had in-hospital mortality of 37.8% compared to 11.9% for those without ESRD (P value < 0.001). After adjusting for confounding factors, age, sex, and comorbidities, ESRD patients were more likely to experience in-hospital mortality compared to non-ESRD patients (Adjusted HR (95% CI): 2.59 (1.55–4.32)). The Log-rank test revealed that there was a significant difference between the ESRD and non-ESRD groups in terms of the survival distribution (χ2 (1) = 21.18, P-value < 0.001). In the ESRD subgroup, compared to survivors, non-survivors were older, and more likely to present with lack of consciousness or O2 saturation less than 93%; they also had lower lymphocyte but higher neutrophil counts and AST concentration at the presentation (all p –values < 0.05). Our findings suggested that the presence of ESRD would be regarded as an important risk factor for mortality in COVID-19 patients, especially in those who are older than age 65 years and presented with a lack of consciousness or O2 saturation less than 93%.

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TL;DR: In this paper, the authors proposed a 1:1 randomised, double-blind, placebo-controlled trial in which participants will receive either SZC or placebo and up-titrate participants' RAASi therapy while monitoring their serum potassium levels.
Abstract: CKD is common in heart failure (HF) and associated with morbidity and mortality, yet life-prolonging medications such as renin-angiotensin-aldosterone inhibitors (RAASi) are underused due to risk of hyperkalaemia. Sodium zirconium cyclosilicate (SZC) is a potassium-binding medication that has been shown to reduce incidence of hyperkalaemia in CKD, non-CKD, and HF populations, which we propose will support maximisation of RAASi therapy. We propose a 1:1 randomised, double-blind, placebo-controlled trial in which participants will receive either SZC or placebo. We will up-titrate participants’ RAASi therapy while monitoring their serum potassium levels and adjusting their SZC dose if necessary. Participants with CKD and HF will be recruited from CKD and HF clinics at St George’s Hospital. The total study period will be 18 months; 130 participants will be enrolled for approximately two months each following screening. Our primary outcome will be the proportion of participants who achieve maximum RAASi dose while maintaining normokalaemia. Secondary outcomes include participants reaching maximum RAASi dose without severe hyperkalaemia; time from randomisation to hyperkalaemia; time from randomisation to severe hyperkalaemia; number of RAASi dose escalations per participant; final doses of RAASi therapy; changes in quality of life score, eGFR, ACR, serum sodium, troponin T; number and duration of hospital admissions; and within-participant change in serum potassium compared to baseline. This trial will be the first to examine the use of SZC for the maximisation of RAASi dosing in patients with advanced CKD and HF. We will assess the impact of achieving target RAASi dosing on hospital admission rates and duration of stay, with the hope that optimum RAASi treatment will translate into reduced morbidity and improved QoL. If clinical benefit is demonstrated, we hope that the joint multidisciplinary CKD-HF approach will be expanded. EudraCT number 2020–002946-18. Registered on 08 June 2020. Online record pending.

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TL;DR: A literature search of Pubmed, EMBASE and Cochrane Databases was performed to identify studies investigating risk factors of acute kidney injury (AKI) after liver transplantation.
Abstract: Acute kidney injury (AKI) is a common and critical complication of liver transplantation (LT), which is associated with increased morbidity, mortality and health care cost. We aimed to identify modifiable risk factors of AKI after LT. A literature search of Pubmed, EMBASE and Cochrane Databases was performed to identify studies investigating risk factors of AKI after LT. The Newcastle-Ottawa Scale was used to rate study quality. Effect size and 95% confidence interval were pooled using a random-effect model with inverse-variance method. Sixty-seven articles with 28,844 patients were included in the meta-analysis. Seventeen modifiable risk factors were found, including overweight, preoperative use of diuretic, preoperative anemia, donation after cardiac death organ, donor BMI ≥ 30 kg/m2, ABO-incompatible LT, low graft to recipient body weight ratio, intraoperative hypotension, major bleeding, intraoperative use of vasopressor, large RBC transfusion, postreperfusion syndrome, postoperative use of vasopressors, overexposure to calcineurin inhibitor, calcineurin inhibitor without mycophenolate mofetil, graft dysfunction and infection. A total of 38 articles were included in the systematic review, in which 8 modifiable risk factors and 1 protective factor were additionally associated in single studies with the incidence of AKI after LT. Effective interventions based on identified modifiable risk factors in the perioperative management and graft allocation and preservation may be promising to reduce the incidence of AKI after LT. The protocol for this systematic review is registered with PROSPERO (No. CRD42020166918 ).

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Abstract: Haemodialysis (HD) patients tend to have higher levels of oxidative stress (OS), associated with increased morbidity and premature mortality, compared to the general population Levels of malondialdehyde (MDA), a biomarker of OS, are reduced by the antioxidant properties of vitamin E (VE) but outcomes from randomised control trials of VE supplementation on MDA in HD patients have been inconsistent We undertook a systematic review and meta-analysis of adult HD patients from VE supplementation studies with measures of MDA The following search criteria of MEDLINE and EMBASE were considered from inception to January 2020: ‘dialysis’ AND ‘Vitamin E OR tocopherol’ AND ‘malondialdehyde OR MDA’ Two reviewers independently extracted study data and assessed risk of bias Mean MDA levels and standard deviation were determined before and after VE supplementation Standardised mean difference (SMD) and standard error were calculated as the within person difference and units of measure were not consistently recorded across all studies The SMD were pooled using random effects meta-analysis The SMD of MDA levels from 18 comparisons was significantly lower in HD patients following VE supplementation (− 155; confidence interval: − 217 to − 094, P < 000001) There were significant levels of heterogeneity between studies (I2 value = 91%; P < 000001) with evidence of potential publication bias toward smaller studies Our findings support the use of VE to reduce the effects of OS in HD patients although high levels of heterogeneity and variation in the methodological approaches used by some studies highlight the need for further investigation

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TL;DR: In this article, the expression and function of programmed cell death protein (PD)-1 molecules on immune and kidney parenchymal cells were reviewed in the healthy kidney, PD-1 immunotherapy-induced nephrotoxicity, glomerulopathies and RCC.
Abstract: Programmed cell death protein (PD)-1 receptors and ligands on immune cells and kidney parenchymal cells help maintain immunological homeostasis in the kidney. Dysregulated PD-1:PD-L1 binding interactions occur during the pathogenesis of glomerulopathies and renal cell carcinoma (RCC). The regulation of these molecules in the kidney is important to PD-1/PD-L1 immunotherapies that treat RCC and may induce glomerulopathies as an adverse event. The expression and function of PD-1 molecules on immune and kidney parenchymal cells were reviewed in the healthy kidney, PD-1 immunotherapy-induced nephrotoxicity, glomerulopathies and RCC. PD-1 and/or its ligands are expressed on kidney macrophages, dendritic cells, lymphocytes, and renal proximal tubule epithelial cells. Vitamin D3, glutathione and AMP-activated protein kinase (AMPK) regulate hypoxic cell signals involved in the expression and function of PD-1 molecules. These pathways are altered in kidney disease and are linked to the production of vascular endothelial growth factor, erythropoietin, adiponectin, interleukin (IL)-18, IL-23, and chemokines that bind CXCR3, CXCR4, and/or CXCR7. These factors are differentially produced in glomerulonephritis and RCC and may be important biomarkers in patients that receive PD-1 therapies and/or develop glomerulonephritis as an adverse event By comparing the functions of the PD-1 axis in glomerulopathies and RCC, we identified similar chemokines involved in the recruitment of immune cells and distinct mediators in T cell differentiation. The expression and function of PD-1 and PD-1 ligands in diseased tissue and particularly on double-negative T cells and parenchymal kidney cells needs continued exploration. The possible regulation of the PD-1 axis by vitamin D3, glutathione and/or AMPK cell signals may be important to kidney disease and the PD-1 immunotherapeutic response.

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TL;DR: In this paper, the authors found that acute kidney injury (AKI) is a recognised complication of coronavirus disease 2019 (COVID-19), yet the reported incidence varies widely and the associated risk factors are poorly understood.
Abstract: Acute kidney injury (AKI) is a recognised complication of coronavirus disease 2019 (COVID-19), yet the reported incidence varies widely and the associated risk factors are poorly understood. Data was collected on all adult patients who returned a positive COVID-19 swab while hospitalised at a large UK teaching hospital between 1st March 2020 and 3rd June 2020. Patients were stratified into community- and hospital-acquired AKI based on the timing of AKI onset. Out of the 448 eligible patients with COVID-19, 118 (26.3 %) recorded an AKI during their admission. Significant independent risk factors for community-acquired AKI were chronic kidney disease (CKD), diabetes, clinical frailty score and admission C-reactive protein (CRP), systolic blood pressure and respiratory rate. Similar risk factors were significant for hospital-acquired AKI including CKD and trough systolic blood pressure, peak heart rate, peak CRP and trough lymphocytes during admission. In addition, invasive mechanical ventilation was the most significant risk factor for hospital-acquired AKI (adjusted odds ratio 9.1, p < 0.0001) while atrial fibrillation conferred a protective effect (adjusted odds ratio 0.29, p < 0.0209). Mortality was significantly higher for patients who had an AKI compared to those who didn’t have an AKI (54.3 % vs. 29.4 % respectively, p < 0.0001). On Cox regression, hospital-acquired AKI was significantly associated with mortality (adjusted hazard ratio 4.64, p < 0.0001) while community-acquired AKI was not. AKI occurred in over a quarter of our hospitalised COVID-19 patients. Community- and hospital-acquired AKI have many shared risk factors which appear to converge on a pre-renal mechanism of injury. Hospital- but not community acquired AKI was a significant risk factor for death.

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TL;DR: The Iron and the Heart Study as discussed by the authors investigated whether 1000mg of IV iron (ferric derisomaltose (FDI)) could improve exercise capacity in comparison to placebo measured at 1 and 3 months post infusion.
Abstract: Iron deficiency (ID) is common in patients with chronic kidney disease (CKD). Intravenous (IV) iron in heart failure leads to improvement in exercise capacity and improvement in quality-of-life measurements; however, data in patients with CKD are lacking. The Iron and the Heart Study was a prospective double blinded randomised study in non-anaemic CKD stages 3b-5 patients with ID which investigated whether 1000 mg of IV iron (ferric derisomaltose (FDI)) could improve exercise capacity in comparison to placebo measured at 1 and 3 months post infusion. Secondary objectives included effects on haematinic profiles and haemoglobin, safety analysis and quality of life questionnaires (QoL). We randomly assigned 54 patients mean (SD) age for FDI (n = 26) 61.6 (10.1) years vs placebo (n = 28; 57.8 (12.9) years) and mean eGFR (33.2 (9.3) vs. 29.1 (9.6) ml/min/1.73m2) at baseline, respectively. Adjusting for baseline measurements, six-minute walk test (6MWT) showed no statistically significant difference between arms at 1 month (p = 0.736), or 3 months (p = 0.741). There were non-significant increases in 6MWT from baseline to 1 and 3 months in the FDI arm. Haemoglobin (Hb) at 1 and 3 months remained stable. There were statistically significant increases in ferritin (SF) and transferrin saturation (TSAT) at 1 and 3 months (p < 0.001). There was a modest numerical improvement in QoL parameters. There were no adverse events attributable to IV iron. This study demonstrated a short-term beneficial effect of FDI on exercise capacity, but it was not significant despite improvements in parameters of iron status, maintenance of Hb concentration, and numerical increases in functional capacity and quality of life scores. A larger study will be required to confirm if intravenous iron is beneficial in iron deficient non-anaemic non-dialysis CKD patients without heart failure to improve the 6MWT. European Clinical Trials Database (EudraCT) No: 2014-004133-16 REC no: 14/YH/1209 Date First Registered: 2015-02-17 and date of end of trail 2015-05-23 Sponsor ref R1766 and Protocol No: IHI 141

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TL;DR: In this article, the authors analyzed prescription patterns and barriers to initiating SGLT2i in patients with Type 2 diabetes and chronic kidney disease in real practice, and found that the older patient group and clinical inertia are the main barriers to initiate SG2i for eligible patients.
Abstract: Sodium-glucose cotransporter 2 inhibitor (SGLT2i) should be considered for patients with type 2 diabetes (T2D) and chronic kidney disease (CKD) having estimated glomerular filtration rate (eGFR) ≥ 30 mL/min/1.73 m2 and urine albumin-to-creatinine ratio (UACR) > 30 mg/g. However, SGLT2i is currently underprescribed among eligible, at-risk patients for CKD progression. We analyzed prescription patterns and barriers to initiating SGLT2i in patients with T2D and CKD in real practice. A total of 3,703 consecutive outpatients with T2D from four teaching hospitals during six months (2019 ~ 2020) were reviewed. Five eGFR categories (G1, ≥ 90; G2, 60–89; G3ab, 30–59; G4-5, 300 mg/g) were used to define CKD status. Overall, 25.8 % patients received SGLT2i in the following eGFR and albuminuria categories: G1 (A1, 31 %; A2, 48 %; A3, 45 %); G2 (A1, 18 %; A2, 24 %; A3, 30%); and G3 (A1, 9 %; A2, 7 %; A3, 13 %). Total prevalence estimate of CKD was 33.8 % (n = 1,253), of whom 25.6 % patients received SGLT2i. We defined eGFR ≥ 45 mL/min/1.73 m2 and UACR ≥ 30 mg/g as high-risk CKD group eligible for SGLT2i (n = 905), of whom 32.9 % patients were treated with an SGLT2i. In this high-risk group, SGLT2i initiation showed negative correlations with age ≥ 65 years and recent hospitalization. Conversely, HbA1c level, body mass index (BMI), presence of diabetic retinopathy, and previous heart failure events were positively correlated with SGLT2i initiation. Only 32.9 % of T2D with CKD eligible for SGLT2i is currently treated with SGLT2i in real-world clinical practice. The older patient group and clinical inertia are the main barriers to initiate SGLT2i for eligible patients. Clinicians should change the glucocentric approach and focus on reducing renal events in T2D.

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TL;DR: In this article, the authors reported on a patient with recurrence of anti-GBM disease after SARS-CoV-2 infection, which is a rare autoimmune disease causing rapidly progressive glomerulonephritis and pulmonary haemorrhage.
Abstract: Anti-glomerular basement membrane disease (GBM) disease is a rare autoimmune disease causing rapidly progressive glomerulonephritis and pulmonary haemorrhage. Recently, an association between COVID-19 and anti-glomerular basement membrane (anti-GBM) disease has been proposed. We report on a patient with recurrence of anti-GBM disease after SARS-CoV-2 infection. The 31-year-old woman had a past medical history of anti-GBM disease, first diagnosed 11 years ago, and a first relapse 5 years ago. She was admitted with severe dyspnoea, haemoptysis, pulmonary infiltrates and acute on chronic kidney injury. A SARS-CoV-2 PCR was positive with a high cycle threshold. Anti-GBM autoantibodies were undetectable. A kidney biopsy revealed necrotising crescentic glomerulonephritis with linear deposits of IgG, IgM and C3 along the glomerular basement membrane, confirming a recurrence of anti-GBM disease. She was treated with steroids, plasma exchange and two doses of rituximab. Pulmonary disease resolved, but the patient remained dialysis-dependent. We propose that pulmonary involvement of COVID-19 caused exposure of alveolar basement membranes leading to the production of high avidity autoantibodies by long-lived plasma cells, resulting in severe pulmonary renal syndrome. Our case supports the assumption of a possible association between COVID-19 and anti-GBM disease.

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TL;DR: In this article, a risk-predicted nomogram of acute kidney injury (AKI) associated sepsis associated-SA-AKI was developed and validated using decision curve analysis.
Abstract: Acute kidney injury (AKI) is a prevalent and severe complication of sepsis contributing to high morbidity and mortality among critically ill patients. In this retrospective study, we develop a novel risk-predicted nomogram of sepsis associated-AKI (SA-AKI). A total of 2,871 patients from the Medical Information Mart for Intensive Care III (MIMIC-III) critical care database were randomly assigned to primary (2,012 patients) and validation (859 patients) cohorts. A risk-predicted nomogram for SA-AKI was developed through multivariate logistic regression analysis in the primary cohort while the nomogram was evaluated in the validation cohort. Nomogram discrimination and calibration were assessed using C-index and calibration curves in the primary and external validation cohorts. The clinical utility of the final nomogram was evaluated using decision curve analysis. Risk predictors included in the prediction nomogram included length of stay in intensive care unit (LOS in ICU), baseline serum creatinine (SCr), glucose, anemia, and vasoactive drugs. Nomogram revealed moderate discrimination and calibration in estimating the risk of SA-AKI, with an unadjusted C-index of 0.752, 95 %Cl (0.730–0.774), and a bootstrap-corrected C index of 0.749. Application of the nomogram in the validation cohort provided moderate discrimination (C-index, 0.757 [95 % CI, 0.724–0.790]) and good calibration. Besides, the decision curve analysis (DCA) confirmed the clinical usefulness of the nomogram. This study developed and validated an AKI risk prediction nomogram applied to critically ill patients with sepsis, which may help identify reasonable risk judgments and treatment strategies to a certain extent. Nevertheless, further verification using external data is essential to enhance its applicability in clinical practice.

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TL;DR: A systematic review and meta-analysis as mentioned in this paper evaluated all the randomized clinical trials about the impact of omega-3 FAs supplementation on cardiometabolic outcomes and oxidative stress parameters in patients with chronic kidney disease.
Abstract: Omega-3 fatty acids (FAs) have been suggested as a beneficial supplement in chronic kidney disease (CKD) patients, but the results of randomized clinical trials (RCTs) are controversial. We conducted a systematic review and meta-analysis to evaluate all the RCTs about the impact of omega-3 FAs supplementation on cardiometabolic outcomes and oxidative stress parameters in patients with CKD. We performed a systematic database search in PubMed/MEDLINE, EMBASE, Scopus, Web of Science, and Cochrane Central, up to May 2020. We included all placebo-controlled randomized trials that assessed the effect of omega-3 FAs supplementation on any cardiometabolic outcomes: blood pressure, total cholesterol (TC), low-density lipoprotein (LDL) and high-density lipoprotein (HDL) or triglycerides (TG) and oxidative stress parameters. Data were pooled using DerSimonian–Laird’s random-effects model. Finally, thirteen articles met the inclusion criteria for this review omega-3 FAs supplementation significantly decrease TC (SMD: -0.26; 95% CI: − 0.51, − 0.02; I2 = 52.7%), TG (SMD: -0.22; 95% CI: − 0.43, − 0.02; I2 = 36.0%) and Malondialdehyde (MDA) levels (SMD: -0.91; 95% CI: − 1.29, − 0.54; I2 = 00.0%) and also significantly increase superoxide dismutase (SOD) (SMD: 0.58; 95% CI: 0.27, 0.90; I2 = 00.0%) and Glutathione peroxidase (GPx) (SMD: 0.50; 95% CI: 0.14, 0.86; I2 = 00.0%) activities. However our results show that omega-3 FAs supplementation have no significant effects on HDL, LDL and blood pressure. Conclusion This systematic review and meta-analysis supports current evidence for the clinical benefit of omega-3 FAs intake to improve cardiometabolic parameters in CKD patients. However, well-designed RCTs still needed to provide a conclusive picture in this field.

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TL;DR: Elevated cFGF23 concentrations at baseline are independently associated with an increased risk of overall graft loss and iF GF23 measurements were not independently associated With Overall graft loss.
Abstract: Increased fibroblast growth factor 23 (FGF23) is a risk factor for mortality, cardiovascular disease, and progression of chronic kidney disease. Limited data exist comparing the association of either c-terminal FGF23 (cFGF23) or intact FGF23 (iFGF23) in kidney transplant recipients (KTRs) with overall (all-cause) graft loss. We conducted a prospective observational cohort study in 562 stable kidney transplant recipients. Patients were followed for graft loss and all-cause mortality for a median follow-up of 48 months. During a median follow-up of 48 months, 94 patients had overall graft loss (primary graft loss or death with functioning graft). Both cFGF23 and iFGF23 concentrations were significantly higher in patients with overall graft loss than those without (24.59 [11.43–87.82] versus 10.67 [5.99–22.73] pg/ml; p < 0.0001 and 45.24 [18.63–159.00] versus 29.04 [15.23–60.65] pg/ml; p = 0.002 for cFGF23 and iFGF23, respectively). Time-dependent ROC analysis showed that cFGF23 concentrations had a better discriminatory ability than iFGF23 concentrations in predicting overall (all-cause) graft loss. Cox regression analyses adjusted for risk factors showed that cFGF23 (HR for one unit increase of log transformed cFGF23: 1.35; 95% CI, 1.01–1.79; p = 0.043) but not iFGF23 (HR for one unit increase of log transformed iFGF23: 0.97; 95% CI, 0.75–1.25; p = 0.794) was associated with the overall graft loss. Elevated cFGF23 concentrations at baseline are independently associated with an increased risk of overall graft loss. iFGF23 measurements were not independently associated with overall graft loss. The cFGF23 ELISA might detect bioactive FGF23 fragments that are not detected by the iFGF23 ELISA.