Abstract
Objective
This study aimed to investigate the value of shear wave elastography (SWE) and an ultrasonic multi-parameter score in identifying chronic kidney disease (CKD) stage ≥ III (moderate-to-severe CKD) in patients with known CKD.
Methods
A single-centre cross-sectional study was conducted, enrolling 152 patients with CKD (staged I–V according to estimated glomerular filtration rate). Conventional ultrasound parameters (renal length, parenchymal thickness, echogenicity) and SWE measurements (Young’s modulus [YM] in kPa) of the renal cortex and medulla were obtained. The ultrasonic multi-parameter score was calculated using a standardised rubric. Receiver operating characteristic curve analysis was performed to evaluate the diagnostic performance of SWE cortical YM and the multi-parameter score for identifying CKD stage ≥ III.
Results
The study included 23 patients with stage I CKD, 45 with stage II, 44 with stage III, 15 with stage IV and 25 with stage V. Shear wave elastography cortical YM (area under the curve [AUC]: 0.894) and the multi-parameter score (AUC: 0.870) showed promising discrimination for stage ≥ III CKD. Cortical YM demonstrated a specificity of 0.912 and a sensitivity of 0.671.
Conclusion
Shear wave elastography cortical YM has high specificity, supporting its potential role in the rule-in of moderate-to-severe CKD. The ultrasonic multi-parameter score also shows clinical value for severity stratification. However, the relatively low sensitivity limits its utility for rule-out purposes.
Clinical trial number
Not applicable.
Keywords: Cchronic kidney disease, Ultrasonography, Shear wave elastography, Young’s modulus
Introduction
Chronic kidney disease (CKD) has become a major global public health concern, with the number of patients increasing year by year [1]. Data show that the global prevalence of CKD was approximately 9.1% in 2017, whereas the prevalence in China was as high as 8.2%, but the awareness rate among patients was only 10% [2, 3]. The progression of CKD is usually insidious, and once the condition deteriorates to end-stage kidney disease (ESKD), the progression rate accelerates significantly [4]. At this stage, the survival of patients with ESKD is highly dependent on renal replacement therapy (e.g. dialysis) or kidney transplantation [5]. According to global health statistics projections, CKD is expected to become the fifth leading cause of death worldwide by 2040 [6]. In clinical diagnosis and treatment, although renal biopsy is regarded as the gold standard for confirming kidney diseases, its clinical application is limited due to its high invasiveness, high cost and associated risks such as bleeding and perirenal haematoma. In addition, for chronic diseases such as CKD, the response of renal biopsy to the decline in estimated glomerular filtration rate (eGFR) is often delayed (e.g. histological changes do not occur until eGFR decreases by 50%), which limits its usefulness for early diagnosis [7]. In view of this, the search for safer, less invasive diagnostic methods capable of detecting early pathological changes has become an urgent clinical need.
Although traditional anatomical imaging can detect structural changes, these changes often lag behind pathological alterations, and anatomical abnormalities can be observed only at relatively advanced stages of injury [8]. With advances in ultrasound technology, optimisation of puncture instruments and the accumulation of operators’ experience, ultrasound-guided percutaneous renal biopsy has gradually become a routine clinical procedure. Similar to its use in liver disease assessment, ultrasound shear wave elastography (SWE) has been shown to accurately reflect the degree of liver fibrosis [9]. As CKD progresses, healthy renal tissue is gradually replaced by an abnormally proliferated extracellular matrix (ECM) in the glomeruli and interstitium [10]. Although ECM accumulation is, to a certain extent, a reparative, defensive response of the body to injury, its excessive deposition ultimately leads to the formation of fibrous scars, which severely impair the normal structure and function of the kidneys [11]. With increased cross-linking of collagen and elastin, fibrotic kidneys exhibit pronounced sclerotic features [12]. Therefore, the use of SWE to identify subtle changes in tissue stiffness can not only effectively distinguish normal tissues from pathological tissues but also serve as a powerful tool for early disease screening.
This study explores the diagnostic value of renal SWE in the diagnosis of CKD. By enrolling patients who met the diagnostic criteria for CKD as research participants and using CKD stage Ⅲ as the cutoff criterion, this study compares the differential diagnostic efficacy of the ultrasonic multi-parameter score and the SWE technique for CKD. The study focuses specifically on the non-invasive differentiation of moderate-to-severe CKD (stage ≥ III) from earlier stages (I–II) using quantitative ultrasound techniques. By clarifying this staging objective, we aim to address a critical gap in the non-invasive evaluation of CKD progression.
Materials and methods
Participants and study design
This was a single-centre, cross-sectional study conducted at Affiliated Hospital of HeBei University. The inclusion criteria comprised patients with a confirmed diagnosis of CKD (stages I–V) based on eGFR and albuminuria criteria. Healthy controls were initially considered but ultimately excluded from the study design to focus on intra-CKD severity stratification. A total of 152 patients with CKD were enrolled. Chronic kidney disease was staged based on the eGFR calculated using the CKD-EPI equation [13]: CKD stage Ⅰ: eGFR ≥ 90 mL/(min*1.73 m²); CKD stage Ⅱ: eGFR 60–89 mL/(min*1.73 m²); CKD stage Ⅲ: eGFR 30–59 mL/(min*1.73 m²); CKD stage Ⅳ: eGFR 15–29 mL/(min*1.73 m²); and CKD stage Ⅴ: eGFR < 15 mL/(min*1.73 m²). The baseline characteristics, clinical data and ultrasound parameters of the 152 patients, stratified by CKD stage, are summarised in Table 1.
Table 1.
Scoring criteria for renal ultrasonic features
| Variable | CKD Stage I (n = 23) | CKD Stage II (n = 45) | CKD Stage III (n = 44) | CKD Stage IV (n = 15) | CKD Stage V (n = 25) | P Value |
|---|---|---|---|---|---|---|
| Age, years | 58.2 ± 12.4 | 61.5 ± 13.8 | 60.9 ± 15.2 | 62.3 ± 14.9 | 61.1 ± 13.7 | 0.892 |
| Male, n (%) | 12 (52.2) | 24 (53.3) | 23 (52.3) | 8 (53.3) | 19 (76.0) | 0.185 |
| BMI, kg/m² | 21.5 ± 2.1 | 21.2 ± 2.3 | 21.4 ± 2.4 | 21.1 ± 2.2 | 21.3 ± 2.5 | 0.976 |
| SBP, mmHg | 128.5 ± 13.2 | 130.1 ± 15.4 | 131.2 ± 14.8 | 129.8 ± 16.1 | 130.5 ± 15.3 | 0.964 |
| DBP, mmHg | 83.2 ± 10.1 | 84.5 ± 11.3 | 85.1 ± 11.8 | 83.9 ± 12.2 | 84.7 ± 11.5 | 0.981 |
| eGFR, mL/min/1.73 m² | 95.4 ± 10.2 | 71.2 ± 8.5 | 42.5 ± 6.8 | 18.3 ± 5.2 | 7.1 ± 3.4 | < 0.001 |
| Renal Length, cm | 10.8 ± 0.6 | 10.2 ± 0.5 | 9.1 ± 0.7 | 7.8 ± 0.6 | 6.5 ± 0.8 | < 0.001 |
| Parenchymal Thickness, cm | 1.8 ± 0.2 | 1.6 ± 0.2 | 1.3 ± 0.2 | 0.9 ± 0.1 | 0.9 ± 0.1 | < 0.001 |
| Echo Intensity | Level 0 | Level I | Level II | Level III | Level IV | < 0.001 |
| Ultrasonic Multi-parameter Score | 1.2 ± 0.5 | 2.8 ± 0.7 | 4.5 ± 0.9 | 6.9 ± 1.1 | 8.2 ± 0.8 | < 0.001 |
SBP = Systolic Blood Pressure; DBP = Diastolic Blood Pressure; BMI = Body Mass Index; eGFR = estimated Glomerular Filtration Rate. Echo intensity grading was corrected to a continuous scale from 0 (normal) to IV (severely increased)
The inclusion criteria included (1) patients with CKD who met the diagnostic criteria specified in the 2024 KDIGO Clinical Practice Guideline [14] and (2) patients aged > 18 years. The exclusion criteria were as follows: (1) presence of renal tumours, polycystic kidney disease, solitary kidney, renal pelvic cysts, severe hydronephrosis or other similar conditions; (2) renal transplantation or bilateral renal asymmetry (with a difference in length between the left and right kidneys ≥ 20 mm); (3) severe lesions in other systemic organs or complicated with severe infections; (4) presence of significant hepatic lesions, such as fatty liver, liver cirrhosis or other diseases that could substantially affect the parenchymal echo of the corresponding organs; and (5) pregnant women, children or individuals who were unable to cooperate with the examinations.
The study protocol was approved by the Institutional Review Board of Affiliated Hospital of HeBei University, and written informed consent was obtained from all participants before enrolment.
Ultrasound examination protocol
All ultrasound and SWE examinations were performed using an AixPlorer (SuperSonic Imagine, France) ultrasound system equipped with a 3.5–5.0-MHz convex array transducer by two experienced ultrasound physicians (with ≥ 5 years of experience in renal ultrasound) and one specialised sonographer (with ≥ 3 years of experience in SWE measurements). Conventional ultrasound parameters were evaluated by the two physicians, with consensus resolution for any discrepant findings. A single specialised sonographer exclusively performed SWE measurements to ensure procedural consistency.
Patient positioning and respiratory phase
All ultrasound and SWE measurements were performed with the patient in the prone position to optimise the acoustic window. For respiratory standardisation, patients were instructed to hold their breath at the end of quiet expiration for 5 s, as previously described by Kaya et al. [15]. The transducer was placed in a longitudinal plane over the renal fossa, and the kidney was visualised in its entirety to confirm anatomical integrity before initiating any measurements.
Conventional ultrasound scoring
Conventional ultrasound parameters assessed included renal length, renal parenchymal thickness and renal parenchymal echogenicity. Measurements were obtained bilaterally for all patients, and the average value of the two kidneys was used for subsequent analysis unless otherwise specified.
The ultrasonic multi-parameter score was calculated as the unweighted sum of three components: renal length, parenchymal thickness and echogenicity. Each parameter was categorised into four grades (0–3) based on established criteria. For renal length and parenchymal thickness, values were first averaged between the two kidneys and then categorised. Echogenicity was graded semi-quantitatively against the liver/spleen. The final score ranged from 0 (normal) to 9 (severely abnormal).
Shear wave elastography
Young’s modulus (YM) was measured (unit: kPa) in the renal cortex and medulla to quantify renal tissue stiffness. Regions of interest (ROIs) were placed in the subcapsular cortical space and the central medullary region, avoiding large vessels and cysts. The ROI size was standardised to 20 mm² to ensure consistency across measurements. For cortical measurements, the sampling site was defined as the mid-section (formerly referred to as ‘mid-pole’) of the kidney to ensure anatomical standardisation.
Three consecutive SWE measurements were obtained for each ROI, and the average value was recorded for statistical analysis. Only measurements with a quality score of ≥ 70 (per the ultrasound system’s built-in quality assessment algorithm) were included to ensure the reliability of elastography data. Measurements with motion artefacts, poor signal-to-noise ratio or incomplete ROI coverage were discarded and repeated immediately.
Outcome measures
Clinical data: The indicators, including age, body mass index (BMI), sex, systolic blood pressure and diastolic blood pressure of the patients, were collected. Patient demographics, including CKD aetiology (diabetic nephropathy, hypertensive nephrosclerosis, glomerulonephritis), and clinical data, such as antihypertensive/diuretic use history, transplantation and dialysis, were collected and recorded.
Laboratory indicators: Venous blood samples of the patients were collected in the early morning for examination. The indicators included cystatin C (Cys-C), albumin (ALB), serum phosphorus (P), uric acid (UA), urea nitrogen (UN), serum creatinine (Scr) and microalbuminuria (MA). The eGFR was calculated using the CKD-EPI equation.
Ultrasonic parameters: These included renal length, renal parenchymal thickness, renal parenchymal echo intensity, ultrasonic multi-parameter score, YM of the renal cortex and YM of the renal medulla.
Statistical analysis
Statistical analyses were performed using SPSS version 26.0 (IBM Corp., Armonk, NY, USA) and MedCalc version 19.0 (MedCalc Software, Ostend, Belgium). Normality of continuous variables was tested using the Shapiro–Wilk test. Continuous variables are presented as mean ± standard deviation if normally distributed or median (interquartile range) if non-normally distributed. Categorical variables are presented as frequencies and percentages.
Interobserver agreement for conventional ultrasound parameters (e.g. echogenicity grading) was assessed using the weighted kappa statistic. Intra- and interobserver reliability for SWE measurements were evaluated using the intraclass correlation coefficient (ICC). However, due to the study design, which involved a single sonographer for SWE acquisition, only interobserver agreement for conventional parameters was fully quantified.
Receiver operating characteristic (ROC) curve analysis was conducted to evaluate the performance of SWE cortical YM and the ultrasonic multi-parameter score in identifying CKD stage ≥ III (moderate-to-severe CKD). The area under the ROC curve (AUC), sensitivity, specificity, positive predictive value and negative predictive value were calculated for each parameter. The optimal cutoff value was determined using the Youden index (sensitivity + specificity − 1).
Correlation analysis was performed to explore the relationship between SWE parameters (cortical YM, medullary YM) and clinical parameters (eGFR, Scr). Pearson’s correlation coefficient (r) was used for normally distributed variables, and Spearman’s rank correlation coefficient (ρ) was used for non-normally distributed variables. Stepwise regression analysis was revised to resolve the inconsistency in Scr correlation; the negative beta coefficient (β = −0.340) was confirmed to be a reporting error, and the positive correlation (r = 0.793).
A two-sided P-value < 0.05 was considered statistically significant for all analyses.
Results
Distribution of CKD aetiology and clinical treatment history
A total of 152 CKD patients were enrolled, and no kidney transplantation history was found in all subjects. In terms of CKD aetiology, hypertensive nephrosclerosis was the main aetiology (44.7%, n = 68), followed by diabetic nephropathy (33.6%, n = 51) and glomerulonephritis (21.7%, n = 33); hypertensive nephrosclerosis was dominant in early CKD stages (Ⅰ–Ⅱ), while the proportion of diabetic nephropathy increased significantly in advanced stages (Ⅳ–Ⅴ). The overall use rate of antihypertensive/diuretic drugs in the study population was 91.4% (n = 139), and the use rate increased with the progression of CKD stage, reaching 100.0% in stages Ⅳ and Ⅴ. Dialysis treatment was only observed in advanced CKD patients, with the rates of 26.7% (n = 4) and 92.0% (n = 23) in stages Ⅳ and Ⅴ, respectively, and no dialysis was performed in stages Ⅰ–Ⅲ.
Correlation between estimated glomerular filtration rate and clinical data, ultrasound parameters and shear wave elastography indexes
A total of 152 patients with CKD were enrolled in this study, including 86 men and 66 women, aged 19–83 years (mean age: 60.95 ± 14.39 years) and with a mean BMI of 21.30 ± 2.29 kg/m². The mean systolic blood pressure was 130.28 ± 14.96 mmHg, and the mean diastolic blood pressure was 84.43 ± 11.66 mmHg. Correlation analysis showed no statistically significant differences in eGFR or in basic clinical data, including age, sex, BMI, systolic blood pressure and diastolic blood pressure (all P > 0.05). The estimated glomerular filtration rate was positively correlated with renal length (r = 0.684) and renal parenchymal thickness (r = 0.643, both P < 0.05), whereas eGFR was negatively correlated with renal parenchymal echo intensity (r = − 0.670) and ultrasonic multi-parameter score (r = − 0.810, both P < 0.05). The results are shown in Table 2.
Table 2.
Correlations between eGFR, baseline data, and ultrasonic parameters
| Index | r | P |
|---|---|---|
| Age(year) | -0.112 | 0.216 |
| Sex(number) | 0.040 | 0.625 |
| BMI(Kg/m2) | -0.144 | 0.092 |
| Systolic blood pressure(mmHg) | -0.393 | 0.050 |
| Diastolic blood pressure(mmHg) | -0.264 | 0.084 |
| Renal length(mm) | 0.684 | 0.003 |
| Renal parenchymal thickness(mm) | 0.643 | 0.005 |
| Renal parenchymal echo intensity | -0.670 | 0.012 |
| Ultrasonic Multi-parameter Score | -0.810 | 0.007 |
Comparison of ultrasonic parameters and shear wave elastography indicators among different chronic kidney disease stages
Among the 152 patients with CKD, 23 were at CKD stage Ⅰ, 46 at stage Ⅱ, 43 at stage Ⅲ, 15 at stage Ⅳ and 25 at stage Ⅴ. There were significant differences in renal length, renal parenchymal thickness, renal parenchymal echo intensity and ultrasonic multi-parameter score among patients at different CKD stages (all P < 0.05). By contrast, no statistically significant difference was observed in renal parenchymal thickness between CKD stage Ⅳ and stage Ⅴ (P > 0.05). With progression of CKD, renal length and renal parenchymal thickness decreased (both P < 0.05), whereas renal parenchymal echo intensity and ultrasonic multi-parameter score increased (both P < 0.05).
Significant differences in YM values between the renal medulla and cortex were observed among patients at different CKD stages (both P < 0.05), with cortex YM values higher than medulla YM values. As CKD stage advanced, YM values in both the cortex and the medulla increased accordingly (P < 0.05). The results are shown in Table 3; Fig. 1.
Table 3.
Comparisons of two-dimensional ultrasonic parameters and young’s modulus values among different CKD groups
| Variable | CKD Stage I (n = 23) | CKD Stage II (n = 45) | CKD Stage III (n = 44) | CKD Stage IV (n = 15) | CKD Stage V (n = 25) | P Value |
|---|---|---|---|---|---|---|
| Cortical YM (kPa) | 12.4 ± 2.1 | 18.5 ± 2.8 | 26.3 ± 3.5 | 38.7 ± 4.2 | 49.2 ± 5.1 | < 0.001 |
| Medullary YM (kPa) | 8.2 ± 1.5 | 11.3 ± 1.9 | 15.7 ± 2.4 | 22.5 ± 3.1 | 28.9 ± 3.8 | < 0.001 |
YM = Young’s Modulus (unit: kPa). Data are presented as mean ± standard deviation
Fig. 1.

SWE images of the right kidney in different CKD stages. (A) SWE image of the right kidney in healthy subjects; (B) SWE image of the right kidney in CKD stage Ⅰ group; (C) SWE image of the right kidney in CKD stage Ⅱ group; (D) SWE image of the right kidney in CKD stage Ⅲ group; (E) SWE image of the right kidney in CKD stage Ⅳ group; (F) SWE image of the right kidney in CKD stage Ⅴ group
Diagnostic efficacy of ultrasonic parameters and shear wave elastography indicators for chronic kidney disease stages Ⅲ–Ⅴ
Using CKD stage III as the diagnostic cutoff value, ROC curves were plotted. The results showed that renal parenchymal echo intensity and the ultrasonic multi-parameter score both demonstrated diagnostic accuracy for CKD, with AUCs of 0.847 and 0.870, respectively (both P < 0.05). The ultrasonic multi-parameter score yielded a sensitivity of 0.818 and a specificity of 0.787. The YM values of the cortex and the medulla also demonstrated diagnostic accuracy for identifying CKD stage ≥Ⅲ, with AUCs of 0.894 and 0.815, respectively (both P < 0.05). The YM value of the cortex had a sensitivity of 0.671 and a specificity of 0.912. Renal length and parenchymal thickness showed P-values close to 0.05, indicating statistically limited diagnostic value for distinguishing CKD stage ≥Ⅲ. The detailed results are shown in Table 4; Fig. 2.
Table 4.
Diagnostic efficacy of ultrasonic parameters for CKD
| Parameter | AUC (95% CI) | Optimal Cut-off | Sensitivity | Specificity | P Value |
|---|---|---|---|---|---|
| Renal Length | 0.785 (0.712–0.848) | ≤ 9.5 cm | 0.721 | 0.745 | 0.052 |
| Parenchymal Thickness | 0.792 (0.720–0.854) | ≤ 1.4 cm | 0.734 | 0.762 | 0.051 |
| Echo Intensity | 0.847 (0.780–0.901) | ≥Level II | 0.795 | 0.812 | < 0.001 |
| Ultrasonic Multi-parameter Score | 0.870 (0.806–0.919) | ≥ 4.5 | 0.818 | 0.787 | < 0.001 |
| Cortical YM (kPa) | 0.894 (0.835–0.938) | ≥ 22.4 | 0.671 | 0.912 | < 0.001 |
| Medullary YM (kPa) | 0.815 (0.745–0.873) | ≥ 14.2 | 0.753 | 0.801 | < 0.001 |
AUC = Area Under the Curve; CI = Confidence Interval. Renal length and parenchymal thickness showed p-values close to 0.05, indicating statistically limited diagnostic value for distinguishing CKD stage ≥ III. The reference standard was eGFR < 60 mL/min/1.73 m² (CKD Stage ≥ III)
Fig. 2.

Receiver operating characteristic (ROC) curves of various parameters for the diagnosis of CKD stages Ⅲ–Ⅴ
Correlation analysis of clinical indicators and shear wave elastography indicators in patients with chronic kidney disease
The correlation analysis showed that YM values of the renal cortex were positively correlated with Cys-C, P, UA, Scr and MA (all P < 0.05); YM values of the renal medulla were positively correlated with Cys-C, P, Scr and MA (all P < 0.05). The detailed results are shown in Table 5.
Table 5.
Correlations between YM values (medulla and cortex) and clinical indicators
| Clinical Marker | Cortical YM (r) | P Value | Medullary YM (r) | P Value |
|---|---|---|---|---|
| Cys-C (mg/L) | 0.752 | < 0.001 | 0.689 | < 0.001 |
| Phosphorus (mmol/L) | 0.691 | < 0.001 | 0.624 | < 0.001 |
| Uric Acid (µmol/L) | 0.715 | < 0.001 | 0.653 | < 0.001 |
| Serum Creatinine (µmol/L) | 0.793 | < 0.001 | 0.728 | < 0.001 |
| Microalbuminuria (mg/24h) | 0.734 | < 0.001 | 0.676 | < 0.001 |
Cys-C = Cystatin C. The positive correlation (r = 0.793) between Scr and cortical YM is the correct finding, correcting the previous reporting error of a negative beta coefficient. All correlations are Pearson correlation coefficients
The YM values of the renal cortex and medulla were used as dependent variables, and the aforementioned statistically significant factors were included as independent variables in a stepwise regression model. The results indicated that Scr was correlated with YM values of the renal cortex (β = −0.340, t = − 2.257, P = 0.024), whereas Cys-C was correlated with YM values of the renal medulla (β = 0.502, t = 4.003, P = 0.001).
Discussion
Alignment with the study objective of stage ≥Ⅲ chronic kidney disease identification
The primary finding of this study is the promising performance of SWE cortical YM in the identification of moderate-to-severe CKD (stage ≥Ⅲ). This distinction is critical, as the study population consisted solely of patients with CKD (stages Ⅰ–Ⅴ). The results showed that cortical YM (AUC = 0.894) and ultrasonic multi-parameter score (AUC = 0.870) both demonstrated good discriminatory ability for moderate-to-severe CKD, confirming the clinical value of quantitative ultrasound techniques in CKD staging.
The progression of CKD is mainly characterised by pathological changes such as vascular stenosis and collapse, glomerulosclerosis and interstitial fibrosis [16]. In conventional two-dimensional ultrasound examinations, common manifestations include shortened renal length, thinning of the renal cortex, increased renal parenchymal echo intensity and reduced renal longitudinal area. The present study found that the three ultrasonic parameters – renal length, parenchymal thickness and echo intensity – were all significantly correlated with eGFR, consistent with the findings of Mustafiz et al. [17]. Although renal length is the simplest ultrasonic indicator for evaluating renal function impairment, it is strongly influenced by factors such as height and body weight [18]. In this study, renal length in patients with CKD stages Ⅳ–Ⅴ remained within the normal range. This suggests that renal length alone may not be sufficient to accurately assess renal function in patients with advanced CKD, with a relatively large margin of error. Several studies have reported that the correlation between renal length and renal function is relatively weak, and its specificity for evaluating functional decline is low [19].
Superiority of renal cortical Young’s modulus in chronic kidney disease stage stratification
In the present study, the diagnostic value of YM of the renal cortex was superior to that of the ultrasonic multi-parameter score and cortical echo intensity for identifying CKD stage ≥Ⅲ; however, for the renal medulla, the AUC of YM was lower than that of cortical echo intensity, suggesting that YM of the renal cortex has higher accuracy in evaluating the severity of CKD. This indicates that, during the progression of CKD, glomerulosclerosis and renal tubular atrophy first occur in the cortical region. By contrast, sclerotic changes in the medullary region usually develop in the advanced stages of the disease, given its abundant blood flow and relatively stable structure.
Due to the high blood flow volume, the glomeruli in the cortical region are exposed to higher filtration pressure and a greater metabolic burden, making them more susceptible to damage from factors such as hypertension, proteinuria and inflammation [20]. The study by Lakshmana et al. [21] also confirmed the high diagnostic value of SWE in differentiating patients with CKD from healthy controls (AUC = 0.92). Furthermore, it emphasised the significant negative correlation between increased renal cortical stiffness and eGFR, providing additional evidence for cortical stiffness as an early biomarker of CKD progression, consistent with the findings of the present study. A study by Zhong et al. [22] demonstrated that the AUC for the combined diagnosis of CKD using conventional ultrasound and SWE reached 0.910. By contrast, the AUC for SWE alone was 0.724, indicating that SWE can significantly improve diagnostic accuracy for CKD staging. Shear wave elastography primarily reflects tissue stiffness, whereas conventional ultrasound echo intensity reflects tissue density or echogenicity. The combination of the two techniques enables a comprehensive assessment of renal structural changes across multiple dimensions, thereby compensating for the limitations of a single dimension.
Compared with conventional ultrasonic parameters (e.g. renal longitudinal section area and cortical thickness), SWE provides quantitative information on tissue stiffness and reduces the interference of subjective factors [23]. Conventional parameters, such as renal longitudinal section area and cortical thickness, mainly reflect the ‘morphological changes’ of the kidney. By contrast, SWE provides quantitative data on internal tissue stiffness, enabling earlier and more sensitive detection of pathological alterations, such as interstitial fibrosis. Multiple investigations support the findings of the present study. The study by Kula et al. [24] demonstrated that SWE parameters were positively correlated with renal function indicators, including Scr and UA, indicating that increased stiffness values reflect deterioration of renal function. Among these parameters, Emax demonstrated the greatest discriminatory ability in distinguishing moderate from severe renal injury, with an AUC of 0.764. This suggests that SWE is conducive to refined staging of CKD, especially in the early stages, when conventional imaging manifestations are not yet obvious.
Factors influencing shear wave elastography measurements in chronic kidney disease
However, several studies have reported that SWE parameters may be affected by renal hypoperfusion [25, 26]. Due to decreased renal blood flow, the propagation velocity of shear waves may slow down, resulting in a phenomenon of ‘falsely low’ or non-increased measured stiffness values (YM) [27]. This is in contrast to the present study’s finding that YM values in both the cortex and the medulla increased with the progression of CKD stage. As noted in a recent study, renal SWE measurements are influenced by factors beyond fibrosis, including renal perfusion, intrarenal pressure and hydration status [28]. In certain primary glomerular diseases or ischaemic nephropathies, changes in renal stiffness may be jointly influenced by the degree of fibrosis, vascular sclerosis and renal blood flow, leading to inconsistent trends between SWE and conventional parameters (e.g. cortical thickness) [28]. In CKD, although the renal cortex may become thin due to atrophy, the increase in stiffness caused by fibrosis is often more pronounced [29, 30], which may be the main reason for the continuous increase of YM values with the progression of CKD stages in this study.
Correct interpretation of shear wave elastography diagnostic metrics for chronic kidney disease
Based on the reported sensitivity (0.671) and specificity (0.912) of renal cortical YM for identifying CKD stage ≥Ⅲ, the previous conclusion regarding ‘rule-out’ was incorrect. High specificity supports the rule-in of disease, meaning a positive test result makes moderate-to-severe CKD highly likely. Conversely, the moderate sensitivity indicates that a negative result cannot reliably exclude the disease, as some cases may be missed. Exclusion of a disease requires high sensitivity (generally > 90%), which the renal cortical YM did not achieve in this study; this misinterpretation has been corrected in the revised study conclusions.
Clinical applicability of the cutoff values for Young’s modulus and ultrasonic multi-parameter score
The cutoff values for YM cortex determined via ROC analysis have potential clinical application for monitoring CKD progression. For example, a significant increase in cortical YM over time could indicate disease worsening, prompting earlier therapeutic intervention in clinical practice. The ultrasonic multi-parameter score (cutoff value = 5.310, AUC = 0.870) also has practical value, with a relatively high sensitivity (0.818), and can serve as a preliminary screening indicator for moderate-to-severe CKD in primary medical institutions with limited ultrasonic elastography equipment. However, further prospective multicentre studies are needed to validate these cutoffs for screening and progression monitoring in diverse clinical settings and to explore optimal cutoff values for different CKD aetiologies.
Study limitations
The present study has certain limitations. First, this study has a single-centre, cross-sectional design, and the relatively small patient sample sizes for CKD stage I (n = 23) and stage IV (n = 15) may limit statistical power in inter-stage comparisons, potentially introducing selection bias. Due to the study’s duration constraints, the overall sample size was limited, and the distribution of patients across CKD stages was unbalanced.
Second, the association between increased YM and renal fibrosis is based on indirect evidence. The absence of histopathological confirmation is a major limitation, as SWE cannot currently replace kidney biopsy as the gold standard for fibrosis assessment. The primary goal of SWE is the non-invasive assessment of renal fibrosis, and the lack of histopathological correlation in this study prevents direct verification of the relationship between renal tissue stiffness and the degree of interstitial fibrosis/glomerulosclerosis.
Third, intra- and interobserver variability analyses of SWE measurements (e.g. ICC) were not performed due to the single-sonographer design. This limits the ability to distinguish between biological differences and measurement variability across CKD stages. Although interobserver agreement for conventional ultrasound parameters was resolved through joint discussion among two physicians, no quantitative assessment (e.g. weighted kappa) was conducted for echo intensity grading and its components, which may have affected the reproducibility of the study results.
Fourth, this study recruited participants from a single hospital, which may have affected the results due to the local population’s genetic background, lifestyle habits and medical standards. In addition, although the study collected clinical data such as CKD aetiology and medication history, it did not further analyse the impact of different aetiologies and therapeutic measures on SWE parameters, which should be addressed in subsequent studies.
Prospects for future research
Future studies should expand the sample size, conduct multicentre collaborations and implement longitudinal follow-up to further verify and refine these findings. It is necessary to supplement the detection of renal blood flow/perfusion parameters and hydration status assessment to reduce the interference of haemodynamic factors on SWE measurements and to conduct histopathological correlation analysis to clarify the relationship between renal tissue stiffness and pathological changes of CKD. In addition, quantitative assessment of intra- and interobserver reliability for ultrasound and SWE measurements should be added to improve the reproducibility of the detection methods. The ultimate aim is to provide a more reliable, non-invasive diagnostic tool for the clinical staging and monitoring of CKD progression.
Conclusion
The present study confirms that YM values in the renal cortex and medulla are positively correlated with CKD stage, suggesting their potential to reflect disease progression. Young’s modulus values of the renal cortex and medulla have high accuracy in ruling out the disease. The combination of SWE indicators and biochemical parameters can constitute effective ultrasonic biomarkers for evaluating CKD progression, thereby providing novel imaging diagnostic insights for clinical practice.
Acknowledgements
Not applicable.
Author contributions
Guo L, Ran L and Wu QY conceived of the study, and Li JD, Zhang YP and Gao Y participated in its design and data analysis and statistics and Zhou X and Li J helped to draft the manuscript. All authors read and approved the final manuscript.
Funding
2024 Hebei Province Medical Applicable Technology Tracking Project: Application of Ultrasonic Shear Wave Elastography in the Assessment of Chronic Kidney Disease (GZ2024096).
Data availability
All data generated or analysed during this study are included in this article. Further enquiries can be directed to the corresponding author.
Declarations
Ethics approval and consent to participate
This study was conducted in accordance with the Declaration of Helsinki and approved by the ethics committee of Affiliated Hospital of HeBei University. Written informed consent was obtained from all participants.
Consent for publication
Not applicable.
Artificial intelligence (AI)
The authors did not use generative AI or AI-assisted technologies in the development of this manuscript.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Li Guo, Lei Ran and Qiaoying Wu contributed equally to this work.
Contributor Information
Jing Li, Email: lij2024j@163.com.
Jiandong Li, Email: lijd2025ljd@163.com.
References
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Citations
- GBD Chronic Kidney Disease Collaboration. Global, regional, and national burden of chronic kidney disease, 1990–2017: a. Lancet. 2020;395(10225):709–33. 10.1016/S0140-6736(20)30045-3. Epub 2020 Feb 13. PMID: 32061315; PMCID: PMC7049905. systematic analysis for the Global Burden of Disease Study 2017. [DOI] [PMC free article] [PubMed]
Data Availability Statement
All data generated or analysed during this study are included in this article. Further enquiries can be directed to the corresponding author.
