Evaluation of renal parenchymal stiffness using shear wave elastography in Behçet’s disease without clinical renal involvement

Abstract

Rationale and objectives

Renal involvement in Behçet’s disease is uncommon but clinically relevant and may remain subclinical in the absence of abnormal renal function tests or urinalysis findings. Shear wave elastography (SWE) may provide quantitative information on renal parenchymal stiffness beyond conventional ultrasonographic parameters. To evaluate renal parenchymal stiffness using SWE in patients with Behçet’s disease without clinical, biochemical, or urinalysis evidence of renal involvement.

Materials and methods

This prospective case-control study included 29 patients with Behçet’s disease and 40 healthy controls. All participants underwent conventional renal ultrasonography and renal SWE using a standardized protocol. Renal length, width, cortical thickness, and right and left renal parenchymal stiffness values were recorded. Clinical characteristics, laboratory parameters, disease activity scores, organ involvement, and treatment status were analyzed in the Behçet’s disease group.

Results

Patients with Behçet’s disease had significantly higher right, left, and mean renal parenchymal stiffness values than healthy controls. Mean renal stiffness was 6.87 ± 1.39 kPa in the Behçet’s disease group and 4.87 ± 0.39 kPa in controls (p < 0.001). In contrast, renal length, width, and cortical thickness did not differ significantly between groups. Mean renal stiffness showed a positive correlation with erythrocyte sedimentation rate (r = 0.675, p < 0.001). In multivariable linear regression analysis, erythrocyte sedimentation rate remained independently associated with mean renal stiffness, while composite immunosuppressive treatment was associated with lower stiffness values. Exploratory ROC analysis showed good discriminatory performance of mean renal stiffness for differentiating patients with Behçet’s disease from controls.

Conclusion

Renal parenchymal stiffness is increased in patients with Behçet’s disease despite normal renal function, normal urinalysis, and preserved conventional ultrasonographic parameters. As a pilot study, these findings suggest that SWE may provide additional quantitative information on subclinical renal parenchymal alterations in Behçet’s disease; however, larger longitudinal studies are required to validate its clinical significance.

Supplementary Information

The online version contains supplementary material available at https://doi.org/10.1186/s12880-026-02666-9.

Introduction

Behçet’s disease, first described by the renowned Turkish dermatologist Hulusi Behçet is a chronic inflammatory vasculitis characterized by periods of relapse and remission [1], and exhibiting multisystemic involvement [2]. The disease typically presents with recurrent oral aphthous ulcers, genital ulcerations, and various skin lesions. While mucocutaneous findings are prominent, the disease can also affect the ocular, vascular, neurological, gastrointestinal, and articular systems. The clinical presentation and course of Behçet’s disease are quite heterogeneous, and the extent and severity of organ involvement can vary significantly among patients [3, 4]. Therefore, early diagnosis and a multidisciplinary approach are of great importance for the prognosis and quality of life of the disease.

Renal involvement in Behçet’s disease, while relatively rare compared to other organ involvements, is a clinically significant complication [5]. The spectrum of renal involvement is quite broad; it can present with different clinical manifestations such as asymptomatic urinary abnormalities, glomerulonephritis, renal vascular involvement, and amyloidosis [6]. Especially in the early stages, renal changes may be subclinical and undetectable by serum creatinine, glomerular filtration rate, or routine urine tests. This can lead to kidney damage progressing unnoticed until advanced stages [7]. Therefore, even in patients without clinically and biochemically significant renal involvement, it is important to investigate the presence of subclinical structural and functional changes in the kidneys.

Conventional renal ultrasonography (US) is a widely used, non-invasive and easily accessible imaging method for evaluating kidney morphology [8]. While it provides basic information about kidney size, parenchymal echogenicity, cortical thickness and structural features, it may not always reflect early parenchymal changes in clear morphological findings [9]. Shear wave elastography (SWE) is an ultrasound-based method that can quantitatively evaluate tissue stiffness and provide information about fibrosis, inflammation, and microstructural changes by measuring renal parenchymal stiffness [10, 11]. Therefore, renal elastography is becoming increasingly important as a potential imaging biomarker for evaluating subclinical kidney involvement that may not be revealed by conventional US, particularly during periods when clinical and laboratory findings have not yet become apparent. While the use of renal SWE in various chronic kidney diseases and systemic inflammatory conditions is becoming more prevalent in the literature [10, 12–14], there is limited data on the potential contribution of this method in patients with Behçet’s disease without significant renal involvement.

To the best of our knowledge, no previous study has specifically evaluated renal parenchymal stiffness using SWE in patients with Behçet’s disease without overt renal involvement. Therefore, this pilot prospective case-control study aimed to compare conventional renal ultrasonography and SWE findings between patients with Behçet’s disease and healthy controls, and to explore the relationship between renal stiffness and clinical or laboratory markers of disease activity.

Materials and methods

Study design and ethical approval

This prospective observational case-control study was conducted at a tertiary referral centre between January 2025 and February 2026. The study protocol was approved by the local institutional ethics committee (2024/158), and written informed consent was obtained from all participants before enrolment. The study was conducted in accordance with the principles of the Declaration of Helsinki.

Study population

Patients aged 18 years or older with a diagnosis of Behçet’s disease were consecutively evaluated for inclusion. Behçet’s disease was diagnosed according to the International Criteria for Behçet’s Disease (ICBD) [15]. Healthy volunteers with comparable age and sex distribution and no known systemic inflammatory disease, chronic kidney disease, or regular medication use were included as controls.

Exclusion criteria were known chronic kidney disease, estimated glomerular filtration rate < 60 mL/min/1.73 m², and abnormal urinalysis findings, including proteinuria or hematuria. Participants with renal masses, renal cysts likely to affect measurement, hydronephrosis, congenital renal anomalies, nephrolithiasis, urinary tract obstruction, previous renal surgery, active urinary tract infection, pregnancy, or inadequate ultrasonographic image quality for reliable shear wave elastography assessment were also excluded.

Demographic data, including age, sex, height, and weight, were recorded for all participants. In patients with Behçet’s disease, disease duration, comorbidities, smoking status, organ involvement, current treatments, and disease activity scores were documented. Clinical manifestations were assessed, including oral aphthosis, genital ulceration, cutaneous involvement, ocular involvement, vascular involvement, neurological involvement, pulmonary involvement, articular involvement, and gastrointestinal involvement. Pathergy test positivity was also recorded.

Treatment data included colchicine, azathioprine, systemic corticosteroids, anti-TNF agents, cyclosporine, anticoagulant therapy, antiaggregant therapy, and non-steroidal anti-inflammatory drug use. Composite immunosuppressive treatment was defined as the use of azathioprine, systemic corticosteroids, anti-TNF agents, cyclosporine, or any other recorded immunosuppressive treatment.

Disease activity was assessed using the Behçet’s Disease Current Activity Form (BDCAF). BDCAF is a disease activity index that evaluates the presence of clinical manifestations attributable to Behçet’s disease during the preceding four weeks, including oral aphthosis, genital ulcers, skin lesions, articular, ocular, vascular, neurological, and gastrointestinal involvement. In the present study, patients with at least one active BDCAF manifestation were classified as having active disease, whereas patients without any active manifestations were classified as inactive (remission). Patient-perceived disease activity was assessed using the Behçet’s Syndrome Activity Score (BSAS). BSAS is a patient-reported outcome measure scored on a scale from 0 to 100, with increasing scores reflecting greater perceived disease activity [16]. Serum creatinine, estimated glomerular filtration rate, erythrocyte sedimentation rate (ESR), C-reactive protein, and white blood cell count were recorded from the same clinical assessment period.

Ultrasonography and shear wave elastography protocol

All renal examinations were performed by a single radiologist with 5 years of experience in ultrasonography and shear wave elastography. The operator was blinded to the participants’ clinical group and laboratory findings at the time of the examination. All examinations were performed using the same ultrasound system and a standardised protocol. A Resona I9 ultrasound system (Mindray, Shenzhen, China) equipped with a convex transducer (SC6-1, 1–6 MHz) was used. Participants were instructed to fast for 6–8 h and to empty their bladder before the examination to minimise physiological variability and improve imaging conditions.

The right kidney was evaluated in the left lateral decubitus position, and the left kidney was evaluated in the right lateral decubitus or supine position, according to the best acoustic window. Conventional B-mode US was performed first. Renal length was measured as the maximum bipolar length of the kidney. Renal width was measured on the short axis. Cortical thickness was measured from the outer renal capsule to the base of the medullary pyramid.

SWE was performed immediately after B-mode US in the same position. Participants were asked to briefly hold their breath during acquisition to reduce respiratory motion. The transducer was placed perpendicular to the renal capsule and aligned with the long axis of the kidney. Real-time SWE was performed under B-mode guidance using a split-screen display. A trapezoid elastography sampling box was positioned over the midportion of the renal parenchyma. Circular regions of interest measuring approximately 5–7 mm were placed in the renal cortex, avoiding the renal sinus, medullary pyramids, large vessels, and areas of artefact. Measurement depth was kept at approximately 4–6 cm from the skin surface whenever technically feasible. Excessive transducer compression was avoided throughout the examination.

The built-in quality control tools of the ultrasound system were used to ensure measurement reliability. Measurements were accepted only when the motion stability indicator showed 4–5 stars with a green signal. The reliability map was also used, and measurements were obtained from areas with a reliability index above 90% whenever possible. Five valid measurements were obtained from each kidney. Measurements with poor signal quality, unstable colour filling, or no reliable signal were discarded and repeated. The median of five valid measurements was recorded in kilopascals for each kidney. Measurements were considered reliable when the interquartile range-to-median ratio was < 0.30. Right and left renal stiffness values were recorded separately, and their average was used for analysis [17, 18]. An example SWE image demonstrating renal parenchymal stiffness measurement is presented in Fig. 1.

Fig. 1.

Representative SWE image of renal parenchymal stiffness assessment. Measurements were performed by placing regions of interest within the renal parenchyma. Data were accepted only when motion stability was optimal, defined as a green M-STB indicator with a stability score of 4–5 stars. Reliability map-guided measurements were obtained from areas showing an RLB index of at least 90%

Statistical analysis

Continuous variables were assessed for normality using the Shapiro–Wilk test and visual inspection of histograms and Q–Q plots. Normally distributed variables were presented as mean ± standard deviation, whereas non-normally distributed variables were presented as median and interquartile range. Categorical variables were expressed as numbers and percentages.

Between-group comparisons were performed using the independent-samples t test or Mann–Whitney U test for continuous variables, and Fisher’s exact test for categorical variables. Paired right and left renal measurements were compared using the paired-samples t test or Wilcoxon signed-rank test, as appropriate. Correlations between renal stiffness and clinical or laboratory variables in the Behçet’s disease group were evaluated using Spearman’s correlation analysis.

Given the limited sample size of the Behçet’s disease group, organ involvement and treatment-related subgroup analyses were considered exploratory. No adjustment for multiple comparisons was applied; therefore, these findings should be regarded as hypothesis-generating. Multivariable linear regression analysis was performed to explore factors associated with mean renal stiffness. To limit model complexity and reduce the risk of overfitting, the regression model was restricted a priori to four clinically relevant variables: disease duration, estimated glomerular filtration rate, ESR, and composite immunosuppressive treatment status. Nevertheless, given the small number of patients, the regression coefficients and subgroup findings should be interpreted as exploratory rather than confirmatory. Statistical significance was defined as a two-sided p value < 0.05.

Results

A total of 69 participants were included in the study, comprising 29 patients with Behçet’s disease and 40 healthy controls. The mean age was 43.8 ± 9.5 years in the Behçet’s disease group and 41.8 ± 7.0 years in the control group, with no significant difference between groups (p = 0.312). Sex distribution was also comparable, with 17 women and 12 men in the Behçet’s disease group and 23 women and 17 men in the control group (p = 0.981). Height and weight were similar between groups (both p > 0.05), indicating an overall balanced baseline demographic profile (Table 1).

Table 1.

Baseline demographic characteristics of controls and patients with Behçet’s disease

Variable	Control (n = 40)	Behçet’s disease (n = 29)	p value
Age, years	41.8 ± 7.0	43.8 ± 9.5	0.312
Height, cm	167.7 ± 7.5	166.9 ± 8.1	0.779
Weight, kg	74.0 ± 14.2	71.5 ± 12.9	0.499
Sex, female/male	23 (57.5%) / 17 (42.5%)	17 (58.6%) / 12 (41.4%)	0.981

Renal ultrasonography and elastography findings

Renal parenchymal stiffness was significantly higher in patients with Behçet’s disease than in healthy controls. Right parenchymal stiffness was 7.10 ± 1.45 kPa in the Behçet group and 4.81 ± 0.46 kPa in the control group (p < 0.001). Similarly, left parenchymal stiffness was significantly higher in the Behçet group than in controls (6.65 ± 1.53 kPa vs. 4.93 ± 0.51 kPa, p < 0.001). The average of right and left renal stiffness values were also significantly increased in patients with Behçet’s disease compared with controls (6.87 ± 1.39 kPa vs. 4.87 ± 0.39 kPa, p < 0.001) (Fig. 2).

Fig. 2.

Comparison of mean parenchymal stiffness values between patients with Behçet’s disease and healthy controls. Boxes represent the interquartile range, horizontal lines indicate medians, whiskers indicate the data range, and dots represent individual participants

In contrast, no significant differences were observed between the groups in renal length, width, or cortical thickness (Table 2).

Table 2.

Renal ultrasonography and elastography parameters represent the average of right and left kidney measurements

Variable	Control	Behçet’s disease	p value
Parenchymal stiffness, kPa	4.87 ± 0.39	6.87 ± 1.39	< 0.001
Length, mm	110.6 ± 10.0	106.6 ± 7.5	0.124
Width, mm	47.9 ± 7.4	48.2 ± 5.9	0.878
Cortical thickness, mm	9.26 ± 0.53	9.17 ± 0.62	0.474

Clinical characteristics of patients with Behçet’s disease

In the Behçet’s disease group, the median disease duration was 9.00 years (IQR, 7.00–18.00). The mean serum creatinine level was 0.81 ± 0.17 mg/dL, and the mean estimated glomerular filtration rate was 98.17 ± 12.75 mL/min/1.73 m². Median ESR and C-reactive protein levels were 11.00 mm/h (IQR, 6.00–24.00) and 0.30 mg/dL (IQR, 0.30–0.50), respectively.

All patients had oral aphthosis. Genital ulceration was present in 22 patients (75.9%), cutaneous involvement in 16 (55.2%), ocular involvement in 11 (37.9%), vascular involvement in 9 (31.0%), articular involvement in 14 (48.3%), and pathergy positivity in 13 (44.8%). Clinical characteristics, organ involvement patterns, and treatment status of the Behçet’s disease group are summarised in Table 3.

Table 3.

Clinical characteristics, organ involvement, and treatment status in patients with Behçet’s disease

Variable	Behçet’s disease (n = 29)
Disease duration, years	9.00 (7.00–18.00)
Creatinine, mg/dL	0.81 ± 0.17 (0.41–1.10)
GFR, mL/min/1.73 m²	98.17 ± 12.75 (65.00–119.00)
ESR, mm/h	11.00 (6.00–24.00)
CRP, mg/dL	0.30 (0.30–0.50)
WBC, ×10³/µL	7.30 (6.30–8.90)
BSAS	37.31 ± 18.06 (10.00–78.00)
BDCAF activity status, active/inactive, n (%)	16 (55.2%) / 13 (44.8%)
Any comorbidity	16 (55.2%)
Smoking	11 (37.9%)
Oral aphthosis	29 (100.0%)
Genital ulcer	22 (75.9%)
Skin involvement	16 (55.2%)
Ocular involvement	11 (37.9%)
Vascular involvement	9 (31.0%)
Neurological involvement	2 (6.9%)
Pulmonary involvement	1 (3.4%)
Articular involvement	14 (48.3%)
Gastrointestinal involvement	1 (3.4%)
Positive pathergy	13 (44.8%)
Any systemic involvement	26 (89.7%)
Colchicine	25 (86.2%)
Azathioprine	12 (41.4%)
Systemic corticosteroid	10 (34.5%)
Anti-TNF	3 (10.3%)
Cyclosporine	0 (0.0%)
Composite immunosuppressive treatment	18 (62.1%)
Anticoagulant	3 (10.3%)
Antiaggregant	4 (13.8%)
NSAID	2 (6.9%)

Continuous variables are presented as mean ± SD (minimum–maximum) or median (IQR), according to distribution. Categorical variables are n (%)

Correlation between renal elastography and clinical/laboratory parameters

Mean renal parenchymal stiffness showed a positive correlation with ESR in the Behçet’s disease group (r = 0.675, p < 0.001). No significant correlations were found with disease duration, serum creatinine, estimated glomerular filtration rate, C-reactive protein, white blood cell count, BDCAF activity status, or BSAS (Table 4).

Table 4.

Spearman correlations between mean renal elastography values and clinical/laboratory parameters in patients with Behçet’s disease

Variable	r	p
Disease duration	-0.142	0.463
Creatinine	0.042	0.830
GFR	0.192	0.318
ESR	0.675	< 0.001
CRP	-0.273	0.152
WBC	-0.162	0.402
BDCAF	-0.040	0.839
BSAS	-0.038	0.853

Exploratory subgroup analyses

In exploratory subgroup analyses, mean renal parenchymal stiffness was higher in patients with comorbidities, including hypertension, diabetes mellitus, heart failure, or hypothyroidism, than in those without comorbidities (7.35 ± 1.21 kPa vs. 6.28 ± 1.40 kPa, p = 0.038). Patients receiving composite immunosuppressive treatment had lower mean renal parenchymal stiffness than those not receiving such treatment (6.43 ± 1.25 kPa vs. 7.59 ± 1.34 kPa, p = 0.031).

Average right-left renal parenchymal stiffness did not differ significantly according to ocular involvement, articular involvement, pathergy positivity, smoking status, colchicine use, azathioprine use, or systemic corticosteroid use. Patients with vascular involvement had numerically higher values than those without vascular involvement, although this difference did not reach statistical significance (7.40 ± 0.80 kPa vs. 6.63 ± 1.54 kPa, p = 0.087) (Additional File 1).

Multivariable linear regression analysis

A multivariable linear regression model was constructed to identify independent factors associated with average right-left renal parenchymal stiffness in patients with Behçet’s disease. The model included disease duration, estimated glomerular filtration rate, ESR, and composite immunosuppressive treatment status. The overall model was statistically significant (R² = 0.652, adjusted R² = 0.594, p < 0.001).

In this model, ESR was independently associated with average right-left renal parenchymal stiffness (B = 0.080, standardised β = 0.663, 95% CI 0.048 to 0.111, p < 0.001). Composite immunosuppressive treatment was also associated with lower stiffness values (B = − 1.094, standardised β = −0.390, 95% CI − 1.811 to − 0.376, p = 0.004). Disease duration and estimated glomerular filtration rate were not independently associated with renal parenchymal stiffness.

Exploratory ROC analysis

Exploratory ROC analysis demonstrated good discriminatory performance of mean renal parenchymal stiffness for differentiating patients with Behçet’s disease from healthy controls. Mean renal parenchymal stiffness yielded an AUC of 0.907 (95% CI 0.801–0.988). An optimal exploratory of ≥ 5.50 kPa provided 82.8% sensitivity and 100.0% specificity (Fig. 3).

Fig. 3.

Exploratory ROC analysis of mean parenchymal stiffness for differentiating patients with Behçet’s disease from healthy controls. AUC was 0.907 (95% CI 0.801–0.988), and the optimal exploratory was ≥ 5.50 kPa

Discussion

The main finding of this prospective case-control study is that patients with Behçet’s disease who had no clinical, biochemical, or urinalysis evidence of renal involvement nevertheless demonstrated significantly higher renal parenchymal stiffness on SWE than healthy controls. In contrast, conventional US parameters, including renal length, width, and cortical thickness, were not significantly different between groups. These findings suggest that increased renal stiffness may reflect subtle renal parenchymal alterations that are not detected by conventional ultrasonography or routine renal laboratory tests.

Behçet’s disease is a chronic multisystem vasculitis with heterogeneous clinical expression. Although mucocutaneous, ocular, vascular, neurological, gastrointestinal, and articular involvement are more frequently emphasized, renal involvement has also been described and may occur through different mechanisms [2, 19, 20]. The reported renal spectrum includes isolated urinary abnormalities, glomerulonephritis, AA amyloidosis, renal vascular lesions, interstitial nephritis, and drug-related nephrotoxicity. In a large Korean cohort [21], hematuria and proteinuria were identified in a subset of patients with Behçet’s disease, and elevated ESR was associated with these urinary abnormalities; among biopsied patients, IgA nephropathy was the most frequent histopathological diagnosis. These findings are clinically relevant because they indicate that renal involvement in Behçet’s disease is heterogeneous and does not conform to a single dominant renal phenotype. The present study adds a different dimension to this literature by showing that patients without conventional evidence of renal involvement may nevertheless exhibit increased renal parenchymal stiffness.

The absence of significant differences in renal size and cortical thickness further supports the potential value of SWE as a complementary imaging method. Conventional renal US remains useful for assessing kidney morphology, obstruction, focal lesions, cortical thickness, and parenchymal echogenicity, but it has limited sensitivity for early inflammatory, microvascular, interstitial, or fibrotic changes [18, 22, 23]. In our cohort, B-mode US did not reveal significant morphologic differences between patients with Behçet’s disease and controls, whereas SWE showed a clear increase in renal parenchymal stiffness. This finding suggests that SWE may provide quantitative information on renal parenchymal alterations that are not apparent on conventional ultrasonography. However, the biological and clinical significance of these stiffness changes remains uncertain.

Several mechanisms may explain the increased renal stiffness observed in Behçet’s disease. Systemic inflammation may promote endothelial activation, microvascular dysfunction, and altered intrarenal perfusion, all of which are relevant to the pathophysiology of Behçet’s disease [5, 6]. Subtle interstitial oedema, cellular infiltration, extracellular matrix remodelling, or early fibrotic change may also contribute. However, increased stiffness should not be interpreted as direct evidence of fibrosis alone, because renal SWE values are also influenced by perfusion, interstitial pressure, anisotropy, renal architecture, measurement depth, and technical factors [10, 12, 13]. Thus, the increased stiffness probably reflects a composite effect of inflammatory, vascular, and microstructural alterations.

The positive correlation between mean renal stiffness and ESR is one of the most informative findings of this study. ESR has previously been associated with urinary abnormalities in Behçet’s disease [21], and in our cohort it was the only laboratory variable independently associated with renal stiffness in multivariable analysis. This pattern supports an inflammation-linked interpretation of the SWE signal. By contrast, no significant associations were found between renal stiffness and serum creatinine, estimated glomerular filtration rate, C-reactive protein, white blood cell count, BDCAF activity status, or BSAS. One possible explanation is that renal SWE may reflect a more chronic or smouldering tissue-level effect that is better captured by ESR than by single-point renal function tests or short-term clinical activity scores. Another possibility is that the relatively small sample size limited the statistical power to detect weaker associations. Nevertheless, these findings suggest that renal stiffness in Behçet’s disease should not be viewed simply as a surrogate for routine renal function.

The finding that patients receiving composite immunosuppressive treatment had lower renal stiffness values than those not receiving such treatment is also noteworthy. One possible interpretation is that systemic immunosuppression attenuates inflammatory or vascular processes that contribute to increased parenchymal stiffness. This would be consistent with current treatment principles in Behçet’s syndrome, in which immunosuppressive and biologic therapies are used to control major organ inflammation and reduce the risk of long-term damage [2, 3]. However, this observation should be interpreted cautiously. The present study was not designed to evaluate treatment effects, treatment exposure was not randomized, and therapeutic decisions likely reflected disease phenotype, severity, organ involvement, and clinician preference. This finding should be regarded as hypothesis-generating and should be tested in longitudinal studies evaluating changes in renal stiffness before and after treatment modification.

Our findings are also consistent with the growing literature on renal SWE as a non-invasive method for assessing renal parenchymal injury. Previous studies and meta-analyses have evaluated SWE in chronic kidney disease, diabetic kidney disease, hypertensive nephropathy, renal fibrosis, and renal allografts, reporting altered stiffness values in diseased kidneys compared with healthy controls [14, 22, 24]. A meta-analysis of biopsy-proven renal fibrosis suggested that SWE may have diagnostic value for the assessment of renal fibrosis, although substantial methodological heterogeneity was observed across studies [13]. This heterogeneity is particularly important in native kidney elastography, as stiffness values may vary according to ultrasound platform, transducer type, acquisition depth, region of interest placement, renal anisotropy, breath-holding technique, hydration status, blood pressure, and renal perfusion [12, 14]. Therefore, absolute cut-off values should not be generalized across devices, populations, or protocols without external validation.

In recent years, SWE has gained increasing attention as a quantitative and non-invasive imaging technique that provides additional information beyond conventional ultrasonography. By enabling objective assessment of tissue stiffness, it may contribute to the detection of subtle parenchymal alterations before structural changes become apparent [25–28]. The growing clinical experience with SWE supports its potential as a complementary imaging biomarker, and the present findings suggest that it may also provide promising information in the assessment of clinically silent renal changes in Behçet’s disease. Further studies using standardized acquisition protocols, harmonized measurement techniques, and clearly defined reference ranges are needed to improve reproducibility and support the development of consensus-based recommendations for clinical use.

This study has several limitations. First, the modest sample size and single-centre design may limit generalizability. Although the regression model was restricted to four clinically relevant variables, some risk of overfitting remains; therefore, the regression and subgroup findings should be considered exploratory. Second, histopathological confirmation was not available, and the biological basis of increased renal stiffness could not be definitively established. Third, hydration status and blood pressure were not objectively assessed, and residual confounding related to these factors cannot be excluded. Fourth, although all examinations were performed by a single blinded operator, intraobserver and interobserver reliability were not evaluated. In addition, standardized reference values for renal SWE have not yet been established, and stiffness measurements are device- and protocol-dependent, which may limit the comparability and generalizability of our findings. Finally, the cross-sectional design precludes conclusions regarding the prognostic significance of increased renal stiffness.

Conclusion

In conclusion, renal parenchymal stiffness was significantly increased in patients with Behçet’s disease despite normal renal function, normal urinalysis, and preserved conventional ultrasonographic parameters. The association between renal stiffness and ESR suggests that the observed SWE changes may be related to subtle inflammation-associated renal parenchymal alterations. However, in the absence of histopathological or longitudinal validation, these findings should not be interpreted as evidence of definite subclinical renal involvement. Although these findings support the potential value of SWE as an adjunctive tool for early renal assessment in Behçet’s disease, larger longitudinal studies with standardized protocols and clinical outcome correlation are required before routine clinical use can be recommended.

Supplementary Information

Below is the link to the electronic supplementary material.

Abbreviations

AUC

Area under the curve

BSAS

Behçet’s Syndrome Activity Score

CRP

C-reactive protein

ESR

Erythrocyte sedimentation rate

ICBD

International Criteria for Behçet’s Disease

ROC

Receiver operating characteristic

SWE

Shear wave elastography

Author contributions

V.B. and N.D. contributed to the conceptualization and design of the study. N.D. contributed to data curation and statistical analysis. A.G.U. performed the ultrasonography and shear wave elastography examinations and was responsible for data acquisition. E.I. and S.Y. contributed to clinical evaluation, patient selection, and data interpretation. N.D. and A.G.U. drafted the original manuscript. All authors critically revised the manuscript for important intellectual content, approved the final version, and agree to be accountable for all aspects of the work. All authors read and approved the final manuscript.

Funding

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Data availability

The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.

Declarations

Ethics approval and consent to participate

This study involving human participants was conducted in accordance with the ethical principles of the Declaration of Helsinki. Ethical approval was obtained from the Institutional Clinical Research Ethics Committee of Inonu University Faculty of Medicine (approval number: 2024/158). Written informed consent was obtained from all participants prior to their inclusion in the study.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.