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Given its progressive deterioration in the clinical course, noninvasive assessment and risk stratification for the severity of renal fibrosis in chronic kidney disease (CKD) are required. We aimed to develop and validate an end-to-end multilayer perceptron (MLP) model for assessing renal fibrosis in CKD patients based on real-time two-dimensional shear wave elastography (2D-SWE) and clinical variables. From April 2019 to December 2021, a total of 162 patients with CKD who underwent a kidney biopsy and 2D-SWE examination were included in this single-center, cross-sectional, and prospective clinical study. 2D-SWE was performed to measure the right renal cortex stiffness, and the corresponding elastic values were recorded. Patients were categorized into two groups according to their histopathological results: mild and moderate-severe renal fibrosis. The patients were randomly divided into a training cohort (n = 114) or a test cohort (n = 48). The MLP classifier using a machine learning algorithm was used to construct a diagnostic model incorporating elastic values with clinical features. Discrimination, calibration, and clinical utility were used to appraise the performance of the established MLP model in the training and test sets, respectively. The developed MLP model demonstrated good calibration and discrimination in both the training [area under the receiver operating characteristic curve (AUC) = 0.93; 95% confidence interval (CI) = 0.88 to 0.98] and test cohorts [AUC = 0.86; 95% CI = 0.75 to 0.97]. A decision curve analysis and a clinical impact curve also showed that the MLP model had a positive clinical impact and relatively few negative effects. The proposed MLP model exhibited the satisfactory performance in identifying the individualized risk of moderate-severe renal fibrosis in patients with CKD, which is potentially helpful for clinical management and treatment decision-making.

Background Chronic kidney disease (CKD) is a catabolic condition associated with muscle wasting and dysfunction, which associates with morbidity and mortality. There is a need for simple techniques capable of monitoring changes in muscle size with disease progression and in response to interventions aiming to increase muscle mass and function. Ultrasound is one such technique; however, it is unknown how well changes in muscle cross‐sectional area (CSA) measured using ultrasound relate to changes in whole muscle volume measured using magnetic resonance imaging. We tested whether rectus femoris CSA (RF‐CSA) could be used as a valid indication of changes in quadriceps muscle volume as a single measure of muscle size and following a 12 week exercise intervention that resulted in muscle hypertrophy. Methods Secondary analysis of data was collected from the ExTra CKD study (ISRCTN 36489137). Quadriceps muscle size was assessed from 36 patients with non‐dialysis CKD before and after 12 weeks of supervised exercise that resulted in muscle hypertrophy. Results Strong positive correlations were observed between RF‐CSA and quadriceps volume at baseline (r2 = 0.815, CI 0.661 to 0.903; P < 0.001) and following 12 week exercise (r2 = 0.845, CI 0.700 to 0.923; P < 0.001). A moderate positive association was also observed between changes in RF‐CSA and quadriceps following exercise training (rho = 0.441, CI 0.085 to 0.697; P = 0.015). Bland–Altman analysis revealed a small bias (bias 0.6% ± 12.5) between the mean percentage changes in RF‐CSA and quadriceps volume but wide limits of agreement from −24 to 25. Conclusions Rectus femoris CSA appears to be a reliable index of total quadriceps volume as a simple measure of muscle size, both as a single observation and in response to exercise training in non‐dialysis CKD patients.

Purpose Ultrasonography (US) is an inexpensive, noninvasive and easy imaging procedure to comment on the kidney disease. Data are limited about the relation between estimated glomerular filtration rate (e-GFR) and all 3 renal US parameters, including kidney length, parenchymal thickness and parenchymal echogenicity, in chronic kidney disease (CKD). In this study, we aimed to investigate the association between e-GFR and ultrasonographic CKD score calculated via these ultrasonographic parameters. Methods One hundred and twenty patients with stage 1–5 CKD were enrolled in this study. The glomerular filtration rate was estimated by the Chronic Kidney Disease Epidemiology Collaboration equation. US was performed by the same radiologist who was blinded to patients’ histories and laboratory results. US parameters including kidney length, parenchymal thickness and parenchymal echogenicity were obtained from both kidneys. All 3 parameters were scored for each kidney, separately. The sum of the average scores of these parameters was used to calculate ultrasonographic CKD score. Results The mean age of patients was 63.34 ± 14.19 years. Mean kidney length, parenchymal thickness, ultrasonographic CKD score and median parenchymal echogenicity were found as 96.2 ± 12.3, 10.97 ± 2.59 mm, 6.28 ± 2.52 and 1.0 (0–3.5), respectively. e-GFR was positively correlated with kidney length ( r  = 0.343, p  < 0.001), parenchymal thickness ( r  = 0.37, p  < 0.001) and negatively correlated with CKD score ( r  = −0.587, p  < 0.001) and parenchymal echogenicity ( r  = −0.683, p  < 0.001). Receiver operating characteristic curve analysis for distinction of e-GFR lower than 60 mL/min showed that the ultrasonographic CKD score higher than 4.75 was the best parameter with the sensitivity of 81% and positive predictivity of 92% (AUC, 0.829; 95% CI, 0.74–0.92; p  < 0.001). Conclusion We found correlation between e-GFR and ultrasonographic CKD score via using all ultrasonographic parameters. Also, our study showed that ultrasonographic CKD score can be useful for distinction of CKD stage 3–5 from stage 1 and 2. We suggested that the ultrasonographic CKD score provided more objective data in the assessment of CKD.

Purpose Patients with chronic kidney disease (CKD) have an increased risk of adverse cardio-cerebrovascular events. We examined whether stress myocardial perfusion single photon emission computed tomography (SPECT) provides reliable prognostic markers for these patients. Methods In this multicenter, prospective cohort trial from the Gunma-CKD SPECT study protocol, patients with CKD [estimated glomerular filtration rate (eGFR) < 60 min/ml per 1.73 m 2 ] undergoing stress 99m Tc-tetrofosmin SPECT for suspected or possible ischemic heart disease were initially followed for 1 year, with the following study endpoints: primary, the occurrence of cardiac deaths (CDs), and secondary, major adverse cardiac, cerebrovascular, and renal events (MACCREs). The summed stress score (SSS), summed rest score, and summed difference score (SDS) were estimated with the standard 17-segment, 5-point scoring model. Left ventricular end-diastolic volume, end-systolic volume (ESV), and ejection fraction were measured using electrocardiogram-gated SPECT. Results During the first year of follow-up, 69 of 299 patients experienced MACCREs (CD, n  = 7; non-fatal myocardial infarction, n  = 3; hospitalization for heart failure, n  = 13; cerebrovascular accident, n  = 1; need for revascularization, n  = 38; and renal failure, i.e., hemodialysis initiation, n  = 7). ESV and SSS were associated with CDs ( p  < 0.05), and eGFR and SDS were associated with MACCREs ( p  < 0.05), in multivariate logistic analysis. Patients with high ESV and high SSS had a significantly higher CD rate during the first year than the other CKD patient subgroups ( p  < 0.05). Patients with low eGFR and high SDS had a significantly higher MACCRE rate than the other subgroups ( p  < 0.05). Conclusion Myocardial perfusion SPECT can provide reliable prognostic markers for patients with CKD.

Regadenoson is predominantly renally metabolized. Patients with severe chronic kidney disease (CKD) experience more frequent gastrointestinal adverse effects (AE) from regadenoson. Aminophylline use following regadenoson reduces the incidence of regadenoson-related AE. We investigated whether patients with severe CKD receive incremental benefit from aminophylline administration in reducing regadenoson AE. We performed post hoc analysis of the pooled database of the ASSUAGE and ASSUAGE-CKD trials. These were randomized placebo-controlled clinical trials which tested the benefit of intravenous aminophylline vs placebo after regadenoson injection in patients undergoing a clinically indicated stress MPI. Patients were categorized into two treatment arms: aminophylline vs placebo; and two groups: Severe CKD (GFR < 30 mL·min−1/1.73 m2 or dialysis) and Control (GFR ≥ 30 mL·min−1/1.73 m2). The study endpoints were gastrointestinal AE, non-gastrointestinal AE and composite of any regadenoson AE. The pooled database of the two trials yielded 548 patients, of whom 274 patients received aminophylline and 274 received placebo. Aminophylline was associated with greater absolute risk reduction (ARR) in gastrointestinal AE among patients with severe CKD vs controls (25% vs 4%, p < .001). A significant interaction was identified between severe CKD and aminophylline in reducing gastrointestinal AE (p = .007), indicating greater reduction in gastrointestinal AE with aminophylline use among patients with severe CKD. Aminophylline use was associated with a trend toward greater ARR in any regadenoson-related AE (32% vs 21%, p = .08). Aminophylline is associated with incremental benefit in reducing gastrointestinal AE in patients with severe CKD undergoing regadenoson stress MPI. Potentially, this population could be targeted for prophylactic administration of aminophylline in order to improve their overall experience with the test.

The role of brain natriuretic peptide (BNP) in the prevention of contrast-induced nephropathy (CIN) is unknown. This study aimed to investigate BNP’s effect on CIN in chronic kidney disease (CKD) patients undergoing elective percutaneous coronary intervention (PCI) or coronary angiography (CAG). The patients were randomized to BNP (0.005 μg/kg/min before contrast media (CM) exposure and saline hydration, n=106) or saline hydration alone (n=103). Cystatin C, serum creatinine (SCr) levels, and estimated glomerular filtration rates (eGFR) were assessed at several time points. The primary endpoint was CIN incidence; secondary endpoint included changes in cystatin C, SCr, and eGFR. CIN incidence was significantly lower in the BNP group compared to controls (6.6% versus 16.5%, P=0.025). In addition, a more significant deterioration of eGFR, cystatin C, and SCr from 48 h to 1 week (P<0.05) was observed in controls compared to the BNP group. Although eGFR gradually deteriorated in both groups, a faster recovery was achieved in the BNP group. Multivariate logistic regression revealed that using >100 mL of CM (odds ratio: 4.36, P=0.004) and BNP administration (odds ratio: 0.21, P=0.006) were independently associated with CIN. Combined with hydration, exogenous BNP administration before CM effectively decreases CIN incidence in CKD patients.

Chronic kidney disease (CKD) is associated with the development of mineral bone disorder (MBD), osteoporosis, and fragility fractures. Among CKD patients, adynamic bone disease or low bone turnover is the most common type of renal osteodystrophy. The consequences of CKD-MBD include increased fracture risk, greater morbidity, and mortality. Thus, the goal is to prevent the occurrences of fractures by means of alleviating CKD-induced MBD and treating subsequent osteoporosis. Changes in mineral and humoral metabolism as well as bone structure develop early in the course of CKD. CKD-MBD includes abnormalities of calcium, phosphorus, PTH, and/or vitamin D; abnormalities in bone turnover, mineralization, volume, linear growth, or strength; and/or vascular or other soft tissue calcification. In patients with CKD-MBD, using either DXA or FRAX to screen fracture risk should be considered. Biomarkers such as bALP and iPTH may assist to assess bone turnover. Before initiating an antiresorptive or anabolic agent to treat osteoporosis in CKD patients, lifestyle modifications, such as exercise, calcium, and vitamin D supplementation, smoking cessation, and avoidance of excessive alcohol intake are important. Managing hyperphosphatemia and SHPT are also crucial. Understanding the complex pathogenesis of CKD-MBD is crucial in improving one’s short- and long-term outcomes. Treatment strategies for CKD-associated osteoporosis should be patient-centered to determine the type of renal osteodystrophy. This review focuses on the mechanism, evaluation and management of patients with CKD-MBD. However, further studies are needed to explore more details regarding the underlying pathophysiology and to assess the safety and efficacy of agents for treating CKD-MBD.

Elevated fibroblast growth factor 23 (FGF23) is associated with cardiovascular disease in patients with chronic kidney disease. As a potential mediating mechanism, FGF23 induces left ventricular hypertrophy; however, its role in arterial calcification is less clear. In order to study this, we quantified coronary artery and thoracic aorta calcium by computed tomography in 1501 patients from the Chronic Renal Insufficiency Cohort (CRIC) study within a median of 376 days (interquartile range 331–420 days) of baseline. Baseline plasma FGF23 was not associated with the prevalence or severity of coronary artery calcium after multivariable adjustment. In contrast, higher serum phosphate levels were associated with prevalence and severity of coronary artery calcium, even after adjustment for FGF23. Neither FGF23 nor serum phosphate were consistently associated with thoracic aorta calcium. We could not detect mRNA expression of FGF23 or its coreceptor, klotho, in human or mouse vascular smooth muscle cells, or normal or calcified mouse aorta. Whereas elevated phosphate concentrations induced calcification in vitro, FGF23 had no effect on phosphate uptake or phosphate-induced calcification regardless of phosphate concentration or even in the presence of soluble klotho. Thus, in contrast to serum phosphate, FGF23 is not associated with arterial calcification and does not promote calcification experimentally. Hence, phosphate and FGF23 promote cardiovascular disease through distinct mechanisms.

Objectives To investigate the diagnostic value of functional MRI to assess renal interstitial fibrosis in patients with chronic kidney disease (CKD). Methods We prospectively recruited 80 CKD patients who underwent renal biopsies and 16 healthy volunteers to undergo multiparametric functional MRI examinations. The Oxford MEST-C classification was used to score the interstitial fibrosis. The diagnostic performance of functional MRI to discriminate interstitial fibrosis was evaluated by calculating the area under the receiver operating characteristic (ROC) curves. Results IgA nephropathy (60%) accounted for the majority of pathologic type in the CKD patients. Apparent diffusion coefficient (ADC) from diffusion-weighted imaging (DWI) was correlated with interstitial fibrosis (rho = −0.73). Decreased renal blood flow (RBF) derived from arterial spin labeling (rho = −0.78) and decreased perfusion fraction (f) derived from DWI (rho = −0.70) were accompanied by increased interstitial fibrosis. The T1 value from T1 mapping correlated with interstitial fibrosis (rho = 0.67) (all p < 0.01). The areas under the ROC curve for the discrimination of ≤ 25% vs. > 25% and ≤ 50% vs. > 50% interstitial fibrosis were 0.87 (95% confidence interval, 0.78 to 0.94) and 0.93 (0.86 to 0.98) by ADC, 0.84 (0.74 to 0.91) and 0.94 (0.86 to 0.98) by f, 0.93 (0.85 to 0.98) and 0.90 (0.82 to 0.96) by RBF, and 0.91 (0.83 to 0.96) and 0.77 (0.66 to 0.85) by T1, respectively. Conclusions Functional MRI parameters were strongly correlated with the interstitial fibrosis of CKD. Therefore, it might a powerful tool to assess interstitial fibrosis of CKD noninvasively. Key Points • In CKD patients, the renal cortical ADC value decreased and T1 value increased significantly compared with healthy volunteers. • Functional MRI revealed significantly decreased renal perfusion in CKD patients compared with healthy volunteers. • The renal cortical ADC, f, RBF, and T1 values were strongly correlated with the interstitial fibrosis of CKD.