دسترسی یکساله به بیش از ۵۰۰ ژورنال روز جهان موجود در سامانه
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Physical Fitness as a Prognostic Marker for Infectious Events in Kidney Transplant Recipients
Ortolan S.a · Neunhaeuserer D.a · Battista F.a · Patti A.a · Gobbo S.a · Di Bella C.b · Quinto G.a · Vecchiato M.a · Frigo A.C.c · Bergamin M.a · Furian L.b · Ermolao A.a
doi : 10.1159/000520758
Am J Nephrol 2022;53:1–9
Introduction: Infectious events are one of the leading causes of death in kidney transplant recipients (KTRs). KTRs have reduced cardiorespiratory fitness (CRF), a predictor for infections in other populations. The aim of this study was to investigate whether CRF and muscle strength are prognostic markers for infectious events in KTRs. Methods: In this retrospective cohort study, 155 KTRs underwent an incremental, maximal cardiopulmonary exercise test (CPET) 3 months after transplantation. CRF was analyzed with peak oxygen consumption (VO2 peak) while muscle strength with isometric handgrip (HG) test. Laboratory blood samples and drug therapy were collected. The median follow-up period was 54 (interquartile range 38–62) months. Cox regression analyses were performed to evaluate predictors of infectious events adjusting for potential confounders. Results: During this study, severe infectious events occurred in 41 subjects (26.5%). 15.5% (n = 24) of patients had a severely reduced CRF, defined as a VO2 peak below the 5th percentile of the reference values reported for a matched healthy population. The hazard ratio for infectious events in this subgroup was 2.389 (95% CI = 1.188–4.801, p = 0.014), independently of gender, age, BMI, time on dialysis, hemoglobin concentration, eGFR, diabetes, and immunosuppressive regimen. On the contrary, no significant association of HG strength and infections was found. Conclusion: Therefore, low CRF may be considered as a modifiable predictor of severe infectious events in KTRs. A CPET should thus be recommended for cardiovascular screening, evaluation of CRF, and tailored exercise prescription to reduce the risk of infections and potentially improve long-term outcomes of transplantation.
Development of Urinary Diagnostic Biomarker for IgA Nephropathy by Lectin Microarray
Onishi Y.a · Mise K.a,b · Kawakita C.a · Uchida H.A.a,c · Sugiyama H.a,d · Sugawara R.a · Yamaguchi S.a · Yoshida M.e · Mitsuhashi T.e · Yamada M.f · Hirabayashi J.g · Wada J.a
doi : 10.1159/000520998
Am J Nephrol 2022;53:10–20
Introduction: The pathogenic roles of aberrantly glycosylated IgA1 have been reported. However, it is unexplored whether the profiling of urinary glycans contributes to the diagnosis of IgAN. Methods: We conducted a retrospective study enrolling 493 patients who underwent renal biopsy at Okayama University Hospital between December 2010 and September 2017. We performed lectin microarray in urine samples and investigated whether c-statistics of the reference standard diagnosis model employing hematuria, proteinuria, and serum IgA were improved by adding the urinary glycan intensity. Results: Among 45 lectins, 3 lectins showed a significant improvement of the models: Amaranthus caudatus lectin (ACA) with the difference of c-statistics 0.038 (95% CI: 0.019–0.058, p < 0.001), Agaricus bisporus lectin (ABA) 0.035 (95% CI: 0.015–0.055, p < 0.001), and Maackia amurensis lectin (MAH) 0.035 (95% CI: 0.015–0.054, p < 0.001). In 3 lectins, each signal plus reference standard showed good reclassification (category-free NRI and relative IDI) and good model fitting associated with the improvement of AIC and BIC. Stratified by eGFR, the discriminatory ability of ACA plus reference standard was maintained, suggesting the robust renal function-independent diagnostic performance of ACA. By decision curve analysis, there was a 3.45% net benefit by adding urinary glycan intensity of ACA to the reference standard at the predefined threshold probability of 40%. Conclusions: The reduction of Gal(β1-3)GalNAc (T-antigen), Sia(α2-3)Gal(β1-3)GalNAc (Sialyl T), and Sia(α2-3)Gal(β1-3)Sia(α2-6)GalNAc (disialyl-T) was suggested by binding specificities of 3 lectins. C1GALT1 and COSMC were responsible for the biosynthesis of these glycans, and they were known to be downregulated in IgAN. The urinary glycan analysis by ACA is a useful and robust noninvasive strategy for the diagnosis of IgAN.
Clinical Utility of KidneyIntelX in Early Stages of Diabetic Kidney Disease in the CANVAS Trial
Lam D.a · Nadkarni G.N.b · Mosoyan G.b · Neal B.c · Mahaffey K.W.d · Rosenthal N.e · Hansen M.K.e · Heerspink H.J.L.f · Fleming F.g · Coca S.G.b
doi : 10.1159/000519920
Am J Nephrol 2022;53:21–31
Introduction: KidneyIntelX is a composite risk score, incorporating biomarkers and clinical variables for predicting progression of diabetic kidney disease (DKD). The utility of this score in the context of sodium glucose co-transporter 2 inhibitors and how changes in the risk score associate with future kidney outcomes are unknown. Methods: We measured soluble tumor necrosis factor receptor (TNFR)-1, soluble TNFR-2, and kidney injury molecule 1 on banked samples from CANagliflozin cardioVascular Assessment Study (CANVAS) trial participants with baseline DKD (estimated glomerular filtration rate [eGFR] 30–59 mL/min/1.73 m2 or urine albumin-to-creatinine ratio [UACR] ≥30 mg/g) and generated KidneyIntelX risk scores at baseline and years 1, 3, and 6. We assessed the association of baseline and changes in KidneyIntelX with subsequent DKD progression (composite outcome of an eGFR decline of ≥5 mL/min/year [using the 6-week eGFR as the baseline in the canagliflozin group], ≥40% sustained decline in the eGFR, or kidney failure). Results: We included 1,325 CANVAS participants with concurrent DKD and available baseline plasma samples (mean eGFR 65 mL/min/1.73 m2 and median UACR 56 mg/g). During a mean follow-up of 5.6 years, 131 participants (9.9%) experienced the composite kidney outcome. Using risk cutoffs from prior validation studies, KidneyIntelX stratified patients to low- (42%), intermediate- (44%), and high-risk (15%) strata with cumulative incidence for the outcome of 3%, 11%, and 26% (risk ratio 8.4; 95% confidence interval [CI]: 5.0, 14.2) for the high-risk versus low-risk groups. The differences in eGFR slopes for canagliflozin versus placebo were 0.66, 1.52, and 2.16 mL/min/1.73 m2 in low, intermediate, and high KidneyIntelX risk strata, respectively. KidneyIntelX risk scores declined by 5.4% (95% CI: −6.9, −3.9) in the canagliflozin arm at year 1 versus an increase of 6.3% (95% CI: 3.8, 8.7) in the placebo arm (p < 0.001). Changes in the KidneyIntelX score at year 1 were associated with future risk of the composite outcome (odds ratio per 10 unit decrease 0.80; 95% CI: 0.77, 0.83; p < 0.001) after accounting for the treatment arm, without evidence of effect modification by the baseline KidneyIntelX risk stratum or by the treatment arm. Conclusions: KidneyIntelX successfully risk-stratified a large multinational external cohort for progression of DKD, and greater numerical differences in the eGFR slope for canagliflozin versus placebo were observed in those with higher baseline KidneyIntelX scores. Canagliflozin treatment reduced KidneyIntelX risk scores over time and changes in the KidneyIntelX score from baseline to 1 year associated with future risk of DKD progression, independent of the baseline risk score and treatment arm.
Causes of Death in End-Stage Kidney Disease: Comparison between the United States Renal Data System and a Large Integrated Health Care System
Bhandari S.K.a,b · Zhou H.c,d · Shaw S.F.c · Shi J.c · Tilluckdharry N.S.e · Rhee C.M.f · Jacobsen S.J.c · Sim J.J.b,e
doi : 10.1159/000520466
Am J Nephrol 2022;53:32–40
Introduction: Using a large diverse population of incident end-stage kidney disease (ESKD) patients from an integrated health system, we sought to evaluate the concordance of causes of death (CODs) between the underlying COD from the United States Renal Data System (USRDS) registry and CODs obtained from Kaiser Permanente Southern California (KPSC). Methods: A retrospective cohort study was performed among incident ESKD patients who had mortality records and CODs reported in both KPSC and USRDS databases between January 1, 2007, and December 31, 2016. Underlying CODs reported by the KPSC were compared to the CODs reported by USRDS. Overall and subcategory-specific COD agreements were assessed using Cohen’s weighted kappa statistic (95% CI). Proportions of positive and negative agreement were also determined. Results: Among 4,188 ESKD patient deaths, 4,118 patients had CODs recorded in both KPSC and USRDS. The most common KPSC CODs were circulatory system diseases (35.7%), endocrine/nutritional/metabolic diseases (24.2%), genitourinary diseases (12.9%), and neoplasms (9.6%). Most common USRDS CODs were cardiac disease (46.9%), withdrawal from dialysis (12.6%), and infection (10.1%). Of 2,593 records with causes listed NOT as “Other,� 453 (17.4%) had no agreement in CODs between the USRDS and the underlying, secondary, tertiary, or quaternary causes recorded by KPSC. In comparing CODs recorded within KPSC to the USRDS, Cohen’s weighted kappa (95% CI) was 0.20 (0.18–0.22) with overall agreement of 36.4%. Conclusion: Among an incident ESKD population with mortality records, we found that there was only fair or slight agreement between CODs reported between the USRDS registry and KPSC, a large integrated health care system.
Direct Determination rather than Oscillometric Estimation of Systolic Blood Pressure in Patients with Severe Chronic Kidney Disease
Benmira A.M.a,b · Moranne O.b,c · Prelipcean C.c · Pambrun E.c · Dauzat M.a,d · Demattei C.e · Pérez-Martin A.a,b
doi : 10.1159/000520996
Am J Nephrol 2022;53:41–49
Introduction: Although arterial hypertension is a major concern in patients with chronic kidney disease (CKD), obtaining accurate systolic blood pressure (SBP) measurement is challenging in this population for whom automatic oscillometric devices may yield erroneous results. Methods: This cross-sectional study was conducted in 89 patients with stages 4, 5, and 5D CKD, for whom we compared SBP values obtained by the recently described systolic foot-to-apex time interval (SFATI) technique which provides direct SBP determination, the standard technique (Korotkoff sounds), and oscillometry. We investigated the effects of age, sex, diabetes, CKD stage, and pulse pressure to explain measurement errors defined as biases or misclassification relative to the SBP thresholds of 110–130-mm Hg. Results: All 3 techniques showed satisfactory reproducibility for SBP measurement (CCC > 0.84 and >0.91, respectively, in dialyzed and nondialyzed patients). The mean ± SD from SBP as determined via Korotkoff sounds was 1.7 ± 4.6 mm Hg for SFATI (CCC = 0.98) and 5.9 ± 9.3 mm Hg for oscillometry (CCC = 0.88). Referring to the 110–130-mm Hg SBP range outside which treatment prescription or adaptation is recommended for CKD patients, SFATI underestimated SBP in 3 patients and overestimated it in 1, whereas oscillometry underestimated SBP in 12 patients and overestimated it in 3. Higher pulse pressure was the main explanatory factor for measurement and classification errors. Discussion/Conclusion: SFATI provides accurate SBP measurements in patients with severe CKD and paves the way for the standardization of automated noninvasive blood pressure measurement devices. Before prescribing or adjusting antihypertensive therapy, physicians should be aware of the risk of misclassification when using oscillometry.
Novel Renal Autologous Cell Therapy for Type 2 Diabetes Mellitus Chronic Diabetic Kidney Disease: Clinical Trial Design
Stavas J.a · Gerber D.b · Coca S.G.c · Silva A.L.d · Johns A.a · Jain D.a · Bertram T.a · DÃaz-González de Ferris M.e · Bakris G.f
doi : 10.1159/000520231
Am J Nephrol 2022;53:50–58
Background: Cell therapies explore unmet clinical needs of patients with chronic kidney disease with the potential to alter the pathway toward end-stage kidney disease. We describe the design and baseline patient characteristics of a phase II multicenter clinical trial utilizing the novel renal autologous cell therapy (REACT), by direct kidney parenchymal injection via the percutaneous approach in adults with type 2 diabetic kidney disease (T2DKD), to delay or potentially avoid renal replacement therapy. Design: The study conducted a prospective, multicenter, randomized control, open-label, phase II clinical trial between an active treatment group (ATG) receiving REACT from the beginning of the trial and a contemporaneous deferred treatment group (DTG) receiving standard of care for 12 months before crossing over to receive REACT. Objectives: The objective of this study was to establish the safety and efficacy of 2 REACT injections with computed tomography guidance, into the renal cortex of patients with T2DKD administered 6 months apart, and to compare the longitudinal change in renal function between the ATG and the DTG. Setting: This was a multicenter study conducted in major US hospitals. Patients: We enrolled eighty-three adult patients with T2DKD, who have estimated glomerular filtration rates (eGFRs) between 20 and 50 mL/min/1.73 m2. Methods: All patients undergo an image-guided percutaneous kidney biopsy to obtain epithelial phenotype selective renal cells isolated from the kidney tissue that is then expanded ex vivo over 4–6 weeks, resulting in the REACT biologic product. Patients are randomized 1:1 into the ATG or the DTG. Primary efficacy endpoints for both study groups include eGFR measurements at baseline and at 3-month intervals, through 24 months after the last REACT injection. Safety analyses include biopsy-related complications, REACT injection, and cellular-related adverse events. The study utilizes Good Clinical and Manufacturing Practices and a Data and Safety Monitoring Board. The sample size confers a statistical power of 80% to detect an eGFR change in the ATG compared to the DTG at 24 months with an α = 0.05. Limitations: Blinding cannot occur due to the intent to treat procedure, biopsy in both groups, and open trial design. Conclusion: This multicenter phase II randomized clinical trial is designed to determine the efficacy and safety of REACT in improving or stabilizing renal function among patients with T2DKD stages 3a–4.
Early Renal Recovery after the First Flare of Pauci-Immune Glomerulonephritis
Zaworski J.a · Gnemmi V.b · Bataille P.c · Hachulla E.d · Glowacki F.e · Gibier J.-B.b · Daroux M.c · Ratsimbazafy A.f · Bitton L.b · Humez S.b · Guincestre T.g · Béhal H.h · Azar R.i · Hoffmann M.j · Cardon G.k · Bourdon F.l · Lemoine C.m · Auxenfant E.n · Copin M.-C.b · Vandenbussche C.a · Quéméneur T.a · pour la cohorte RENVAS
doi : 10.1159/000520285
Am J Nephrol 2022;53:59–68
Renal involvement is a severe manifestation of antineutrophil cytoplasmic antibody-associated vasculitis. Patients often progress to end-stage renal disease. The potential for renal recovery after the first flare has seldom been studied. Our objectives were to describe the evolution of the estimated glomerular filtration rate (eGFR) and identify factors associated with the change in the eGFR between diagnosis and the follow-up at 3 months (ΔeGFRM0–M3).
Serum Uric Acid Levels and Nephrosclerosis in a Population-Based Autopsy Study: The Hisayama Study
Maki K.a,b · Hata J.a,b,c · Sakata S.a,b,c · Oishi E.a,b · Furuta Y.a,b · Nakano T.b,c · Oda Y.d · Kitazono T.b,c · Ninomiya T.a,c
doi : 10.1159/000521426
Am J Nephrol 2022;53:69–77
Information regarding the influence of serum uric acid (SUA) levels on pathological changes in the kidney is limited. In this study, we examined the association between SUA levels and pathological findings of nephrosclerosis in population-based autopsy samples.
Prevalence and Outcomes Associated with Hyperuricemia in Hospitalized Patients with COVID-19
Chauhan K.a · Pattharanitima P.b · Piani F.c · Johnson R.J.c · Uribarri J.a · Chan L.a · Coca S.G.a
doi : 10.1159/000520355
Am J Nephrol 2022;53:78–86
Coronavirus 2019 (COVID-19) can increase catabolism and result in hyperuricemia. Uric acid (UA) potentially causes kidney damage by alteration of renal autoregulation, inhibition of endothelial cell proliferation, cell apoptosis, activation of the pro-inflammatory cascade, and crystal deposition. Hyperuricemia in patients with COVID-19 may contribute to acute kidney injury (AKI) and poor outcomes.
