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Soft set theory has evolved to provide a set of valuable tools for dealing with ambiguity and uncertainty in a variety of data structures related to real-world challenges. A soft set is characterized via a multivalued function of a set of parameters with certain conditions. In this study, we relax some conditions on the set of parameters and generalize some basic concepts in soft set theory. Specifically, we introduce generalized finite relaxed soft equality and generalized finite relaxed soft unions and intersections. The new operations offer a great improvement in the theory of soft sets in the sense of proper generalization and applicability.

In the last decades, improvements in the average life expectancy in the world population have been associated with a significant increase in the proportion of elderly people, in parallel with a higher prevalence of non-communicable diseases, such as hypertension and diabetes. As the kidney is a common target organ of a variety of diseases, an adequate evaluation of renal function in the approach of this population is of special relevance. It is also known that the kidneys undergo aging-related changes expressed by a decline in the glomerular filtration rate (GFR), reflecting the loss of kidney function, either by a natural senescence process associated with healthy aging or by the length of exposure to diseases with potential kidney damage. Accurate assessment of renal function in the older population is of particular importance to evaluate the degree of kidney function loss, enabling tailored therapeutic interventions. The present review addresses a relevant topic, which is the effects of aging on renal function. In order to do that, we analyze and discuss age-related structural and functional changes. The text also examines the different options for evaluating GFR, from the use of direct methods to the implementation of several estimating equations. Finally, this manuscript supports clinicians in the interpretation of GFR changes associated with age and the management of the older patients with decreased kidney function.

Flavonoid synthesis is predominantly regulated at the transcriptional level through the MYB–basic helix-loop-helix (bHLH)–WD40 (MBW) (MYB: transcription factor of the myeloblastosis protein family,WD40: tanscription factor with a short structural motif of 40 amino acids which terminates in an aspartic acid–tryptophan dipeptide) complex, and responds to both environmental and developmental stimuli. Although the developmental regulation of flavonoid accumulation in Arabidopsis thaliana has been examined in great detail, the response of the flavonoid synthesis pathway to abiotic stress (particularly low temperature) remains unclear. A screen of a Dissociation element (Ds) transposon-induced mutation collection identified two lines which exhibited an altered profile of phenylpropanoid accumulation following exposure to low-temperature stress. One of the mutated genes (BRASSINOSTEROID ENHANCED EXPRESSION1 (BEE1)) encoded a brassinosteroid enhanced expression transcription factor, while the other (G2-LIKE FLAVONOID REGULATOR (GFR)) encoded a G2-like flavonoid regulator. Phenylpropanoid-targeted analysis was performed using high-performance LC-MS, and gene expression analysis using quantitative reverse transcription–PCR. In both mutants, the accumulation of quercetins and scopolin was reduced under lowtemperature growing conditions, whereas that of anthocyanin was increased. BEE1 and GFR were both shown to negatively regulate anthocyanin accumulation by inhibiting anthocyanin synthesis genes via the suppression of the bHLH (TRANSPARENT TESTA8 (TT8) and GLABROUS3 (GL3)) and/or the MYB (PRODUCTION OF ANTHOCYANIN PIGMENTS2 (PAP2)) components of the MBW complex. Our results provide new insight into the regulatory control of phenylpropanoid metabolism at low temperatures, and reveal that BEE1 and GFR act as important components of the signal transduction chain.

Previous studies have indicated that creatinine (Cr)-based glomerular filtration rate (GFR) estimating equations - including the new Chronic Kidney Disease Epidemiology creatinine (CKD-EPI ) equation without race and the estimated glomerular filtration rate (eGFR) equation developed for the Chinese population - displayed suboptimal performance in patients with neurogenic lower urinary tract dysfunction (NLUTD), which limited their clinical application for detecting changes in GFR levels in all cohorts. To develop a neural network model based on multilayer perceptron (MLP) for evaluating GFR in Chinese NLUTD patients, and compare the diagnostic performance with Cr-based multiple linear regression equations for Chinese and the CKD-EPI equation without race. Single-center, cross-sectional study of GFR estimation from serum Cr, demographic data, and clinical characteristics in Chinese patients with NLUTD. A total of 204 NLUTD patients, from 27 different geographic regions of China, were selected. A random sample of 141 of these subjects was included in the training sample set, and the remaining 63 patients were included in the testing sample set. The reference GFR (rGFR) was assessed by the technetium-99m-labeled diethylenetriaminepentaacetic acid ( Tc-DTPA) double plasma sample method. A neural network model based on MLP was developed to evaluate GFR in the training sample set, which was then validated in the testing sample set and compared with Cr-based GFR equations. The MLP-based model showed significant performance improvement in evaluating the difference, absolute difference, precision, and accuracy of GFR estimation compared with the Cr-based GFR equations. Additionally, compared with the rGFR, we found that the MLP-based model provided an acceptable level of accuracy (greater than 85%, which was within a 30% deviation from the rGFR). The MLP-based model offered significant advantages in estimating GFR in Chinese NLUTD patients, and its application could be suggested in clinical practice.

Abstract Background Establishment and improvement of glomerular filtration rate estimating equations requires accurate and precise laboratory measurement procedures (MPs) for filtration markers. The Advanced Research and Diagnostic Laboratory (ARDL) at the University of Minnesota, which has served as the central laboratory for the Chronic Kidney Disease Epidemiology Collaboration since 2009, has implemented several quality assurance measures to monitor the accuracy and stability of filtration marker assays over time. Methods To assess longitudinal stability for filtration marker assays, a 40-sample calibration panel was created using pooled serum, divided into multiple frozen aliquots stored at −80 °C. ARDL monitored 4 markers—creatinine, cystatin C, beta-2-microglobulin (B2M) and beta-trace protein—measuring 15 calibration panel aliquots from 2009 to 2019. Initial target values were established using the mean of the first 3 measurements performed in 2009–10, and differences from target were monitored over time. New MPs for cystatin C and B2M were added in 2012, with target values established using the first measurement. Results The mean percentage difference from mean target values across time was <2% for all original MPs (−0.59% for creatinine; −0.94% for cystatin C; −0.82% for B2M; 1.24% for beta-trace protein). Conclusions Close monitoring of filtration marker trends with a calibration panel at ARDL demonstrates remarkable long-term stability of the MPs. Routine use of a calibration panel for both research studies and clinical care is recommended for filtration markers where longitudinal monitoring is important to detect analytical biases, which can mask or confound true clinical trends in patients.

Abstract Aims To evaluate diagnostic performance of glomerular filtration rate (GFR) estimated by modification of diet in renal disease (MDRD), chronic kidney disease epidemiology collaboration (CKD-EPI), full age spectrum (FAS), and revised Lund–Malmö (r-LM) equations in adults with diabetes. Methods Individuals were included in this cross-sectional study if they had at least 1 measurement of technetium-99m diethylenetriamine-pentaacetic acid (99mTc-DTPA) GFR (mGFR) and serum creatinine (1487 patients with 2703 measures). GFR calculated by estimation equations was compared with mGFR. Diagnostic performance was assessed using concordance correlation coefficient (CCC), bias, precision, accuracy, reduced major axis regression (RMAR), and Bland–Altman plot. Analysis was repeated in subgroups based on sex, diabetes type, Hemoglobin A1C, and GFR level. Results Of all patients, 1189 (86%) had type 2 diabetes. Mean mGFR, MDRD, CKD-EPI, FAS, and revised Lund-Malmö eGFR were 66, 72, 74, 71, and 67 mL/min/1.73m2, respectively. Overall, the r-LM had the highest CCC (0.83), lowest bias (–1.4 mL/min/1.73 m2), highest precision (16.2 mL/min/1.73 m2), and highest accuracy (P10 = 39%). The RMAR (slope, intercept) in r-LM, FAS, MDRD, and CKD-EPI was 1.18, –13.35; 0.97, –2.9; 1, -6.4, and 1.04, –11.3, respectively. The Bland–Altman plot showed that r-LM had the lowest mean difference and the narrowest 95% limit of agreement (–1.0, 54.1 mL/min/1.73 m2), while mean difference was more than 5-fold higher in FAS, MDRD, and CKD-EPI (–5.2, –6.3, and –8.2, respectively). Conclusions In adults with diabetes the revised Lund-Malmö performs better than MDRD, CKD-EPI, and FAS in calculating point estimates of GFR.

Accurately assessing the glomerular filtration rate (GFR) is critical in patients with cancer for acute kidney injury diagnosis, chemotherapy selection, drug dosing, and clinical trial eligibility. Yet, traditional equations such as Cockcroft–Gault and MDRD fail due to multiple physiological changes specific to this vulnerable population. Cancer-related sarcopenia, creatinine secretion blockade, and total body volume fluctuations may lead to inaccurate GFR estimations. This ultimately leads to undertreatment of underlying malignancy, overdosing of nephrotoxic therapies with adverse effects, and excluding patients from clinical trials unnecessarily. The 2024 KDIGO guidelines as well as the American Society of Onconephrology position statement recommend the use of combined GFR equation such as CKD-EPI 2021 that utilizes both cystatin C and creatinine to improve GFR estimation accuracy. Direct GFR measurement via exogenous filtration markers should be pursued in high-risk patients when precise values are warranted. This review highlights current challenges associated with GFR evaluation in patients with cancer and outlines clinical implications as well as recent recommendations for optimal clinical practice.

Autosomal polycystic kidney disease (ADPKD) is the most common genetic form of kidney failure, reflecting unmet needs in management. Prescription of the only approved treatment (tolvaptan) is limited to persons with rapidly progressing ADPKD. Rapid progression may be diagnosed by assessing glomerular filtration rate (GFR) decline, usually estimated (eGFR) from equations based on serum creatinine (eGFRcr) or cystatin-C (eGFRcys). We have assessed the concordance between eGFR decline and identification of rapid progression (rapid eGFR loss), and measured GFR (mGFR) declines (rapid mGFR loss) using iohexol clearance in 140 adults with ADPKD with ≥3 mGFR and eGFRcr assessments, of which 97 also had eGFRcys assessments. The agreement between mGFR and eGFR decline was poor: mean concordance correlation coefficients (CCCs) between the method declines were low (0.661, range 0.628 to 0.713), and Bland and Altman limits of agreement between eGFR and mGFR declines were wide. CCC was lower for eGFRcys. From a practical point of view, creatinine-based formulas failed to detect rapid mGFR loss (−3 mL/min/y or faster) in around 37% of the cases. Moreover, formulas falsely indicated around 40% of the cases with moderate or stable decline as rapid progressors. The reliability of formulas in detecting real mGFR decline was lower in the non-rapid-progressors group with respect to that in rapid-progressor patients. The performance of eGFRcys and eGFRcr-cys equations was even worse. In conclusion, eGFR decline may misrepresent mGFR decline in ADPKD in a significant percentage of patients, potentially misclassifying them as progressors or non-progressors and impacting decisions of initiation of tolvaptan therapy.

Abstract Context Burosumab has been approved for the treatment of children and adults with X-linked hypophosphatemia (XLH). Real-world data and evidence for its efficacy in adolescents are lacking. Objective To assess the effects of 12 months of burosumab treatment on mineral metabolism in children (aged <12 years) and adolescents (aged 12-18 years) with XLH. Design Prospective national registry. Setting Hospital clinics. Patients A total of 93 patients with XLH (65 children, 28 adolescents). Main Outcome Measures Z scores for serum phosphate, alkaline phosphatase (ALP), and renal tubular reabsorption of phosphate per glomerular filtration rate (TmP/GFR) at 12 months. Results At baseline, patients showed hypophosphatemia (−4.4 SD), reduced TmP/GFR (−6.5 SD), and elevated ALP (2.7 SD, each P < .001 vs healthy children) irrespective of age, suggesting active rickets despite prior therapy with oral phosphate and active vitamin D in 88% of patients. Burosumab treatment resulted in comparable increases in serum phosphate and TmP/GFR in children and adolescents with XLH and a steady decline in serum ALP (each P < .001 vs baseline). At 12 months, serum phosphate, TmP/GFR, and ALP levels were within the age-related normal range in approximately 42%, 27%, and 80% of patients in both groups, respectively, with a lower, weight-based final burosumab dose in adolescents compared with children (0.72 vs 1.06 mg/kg, P < .01). Conclusions In this real-world setting, 12 months of burosumab treatment was equally effective in normalizing serum ALP in adolescents and children, despite persistent mild hypophosphatemia in one-half of patients, suggesting that complete normalization of serum phosphate is not mandatory for substantial improvement of rickets in these patients. Adolescents appear to require lower weight-based burosumab dosage than children.

Background Estimating glomerular filtration rate (eGFR) in kidney transplant recipients (KTR) typically relies on plasma creatinine, which is influenced by muscle mass. Reduced muscle mass is suspected to reduce eGFR performance in this population but this effect has not been rigorously evaluated. This study quantified the impact of muscle mass on eGFR accuracy and its confounding effect on the association between kidney function and mortality in KTR. Methods We studied a prospective and consecutive cohort of 1829 KTR (mean age 52 ± 14 years; 38.9% female) who underwent GFR measurement using iohexol clearance (ioGFR). Muscle mass was assessed by creatinine excretion rate (CER) from timed urine collections. We evaluated the impact of muscle mass on the performance of five eGFR equations (MDRD, CKDEPI2009, CKDEPI2021, EKFC and RFKTS) using multiple regression and subgroup analysis. The association between eGFRs, ioGFR and mortality was examined using Cox proportional hazards models. Results All eGFR equations showed a significant negative correlation with CER. EKFC was the least sensitive to CER (β coefficient 95% confidence interval [CI]: −0.17 to −0.12). All eGFR equations demonstrated reduced accuracy in the lowest muscle mass tertile. In multivariable analyses, ioGFR was significantly associated with mortality (hazard ratio 95% CI: 0.972–0.995) but eGFRs were not. Including CER in the Cox models resulted in convergence of the mortality hazard ratios for ioGFR and eGFRs (hazard ratio 95% CI: ioGFR: 0.98–0.999; MDRD: 0.98–0.999; CKDEPI2021: 0.99–1; EKFC (0.98–1) RFKS: 0.98–0999). Conclusion The performance of all tested creatinine‐based eGFR equations is strongly impacted by muscle mass. Muscle mass is also a key confounder in the mortality risk assessment using eGFR. Incorporating muscle mass into KTR's evaluations may improve kidney function assessments in KTR.