Hypertension affects over 1 billion individuals worldwide (1, 2), with approximately 20–40% of patients ultimately developing chronic kidney disease (CKD) (3), and some progressing to end-stage renal disease requiring dialysis or transplantation (4). Early diagnosis and intervention for hypertension-related renal impairment remains a critical challenge (5). Conventional parameters such as serum creatinine and blood urea nitrogen often fail to reflect subtle structural alterations in early stages due to robust renal compensatory capacity, posing significant challenges for early diagnosis of hypertension-related nephropathy. The renal cortex, where functional nephrons are concentrated, is initially affected by pathological processes including renal arteriolar sclerosis and interstitial fibrosis secondary to hypertension (6). Therefore, precise assessment of alterations in renal cortical elasticity may provide critical information for early detection and monitoring of hypertension-related renal injury (7).

Shear Wave Elastography (SWE) has gained widespread application in hepatic fibrosis assessment, thyroid nodule differentiation, and breast lesion evaluation due to its non-invasive, quantitative, and real-time capabilities (8, 9). SWE reflects tissue stiffness by measuring shear wave propagation velocity within tissues. Compared to conventional ultrasonography, which primarily evaluates renal morphology and echogenic characteristics, SWE demonstrates superior sensitivity in detecting renal parenchymal elasticity and identifying pathological changes such as renal fibrosis and tissue remodeling (10). Previous literature has documented that SWE demonstrates excellent discriminatory capacity across different CKD stages, with elasticity parameters correlating with glomerular filtration rate (eGFR) and serum creatinine levels (11). However, research regarding SWE assessment of renal elasticity in hypertensive patients remains relatively limited, with insufficient standardized technical parameters and operational protocols. Additionally, multiple potential factors influence renal cortical elasticity, including patient age, blood pressure control status, and renal arterial perfusion, with their independent mechanisms of action not fully elucidated.

Although alterations in renal elasticity are intimately associated with tissue remodeling, whether specific elasticity value changes possess independent clinical diagnostic significance requires more comprehensive research support (12). The current clinical application of SWE in assessing hypertension-related renal damage remains exploratory, with considerable uncertainty regarding severity determination and progression trend through elasticity parameters (13). Therefore, integration of patient demographic information, laboratory parameters, and imaging data is essential for comprehensive analysis of clinical factors influencing renal cortical elasticity, establishing the foundation for precise SWE application in hypertensive patients.

This study aims to employ SWE technology for quantitative analysis of renal cortical elasticity in hypertensive patients and investigate its correlation with clinical characteristics and laboratory parameters, thereby preliminarily identifying independent clinical factors potentially influencing renal cortical elasticity. Through this investigation, we intend to provide preliminary data supporting the establishment of SWE-based assessment criteria for hypertension-related renal damage in future applications, while offering novel perspectives and methodologies for early intervention and personalized therapeutic approaches.

Hypertension is a common and frequently occurring disease in clinical practice, and long-term hypertension often affects the kidneys and eventually develops into hypertensive nephropathy (15). With the increasing incidence rate and mortality of hypertensive nephropathy, clinical attention to hypertensive nephropathy is gradually increasing (16). Due to the delayed and non-specific results of laboratory and imaging examinations, how to detect and intervene in the treatment of hypertensive nephropathy as early as possible is currently a major challenge in the medical field (17). Although renal biopsy is still the “gold standard” for this disease, in practical work, the proportion of hypertensive patients diagnosed with kidney damage through clinical laboratory examination and imaging examination is higher than that diagnosed by renal biopsy pathology (18). Due to the partial similarity in pathological characteristics between hypertensive nephropathy and various primary or secondary kidney diseases, this method also has certain limitations (19).

Conventional ultrasonography has established its role in hypertension prognosis, particularly through Doppler assessment of renal hemodynamics. The renal RI has been extensively validated as a marker of vascular damage in cardiovascular diseases and predictor of adverse outcomes in hypertensive patients (20, 21). In this study, there was no statistically significant difference in right renal artery trunk PSV and RI between the two groups (p > 0.05). Due to the fact that the selected case group in this study were all patients with simple hypertension, patients were only found to have elevated blood pressure during blood pressure measurement. These patients presented without characteristic hypertensive symptoms, and conventional ultrasound examination revealed no significant alterations in renal hemodynamics. Although our study did not demonstrate significant RI differences between groups, this finding is consistent with existing literature suggesting that RI changes may become apparent primarily in advanced stages of hypertensive nephropathy. Recent investigations have explored alternative Doppler parameters, such as the renal augmented velocity index, which may demonstrate superior sensitivity for detecting early vascular changes compared to traditional RI measurements in hypertensive populations (22).

SWE represents an emerging ultrasonic technique that has garnered significant attention in renal disease evaluation. SWE can detect the hardness of the renal cortex and reflect its biomechanical changes (23). In our study, the YM in the right renal cortex of the simple hypertension group was higher than that of the healthy control group, indicating that hypertension may lead to an increase in renal cortex hardness (24). In hypertensive patients, although no significant changes were found in renal anatomy, hemodynamics, and physiological function, the cortical hardness of the kidneys has already changed, which is consistent with previous research results (25). This may be because when patients have long-term high blood pressure, it can lead to damage to renal vascular endothelial cells. On the one hand, the walls of renal arterioles thicken, and on the other hand, the renin angiotensin aldosterone system is activated. The glomeruli have mild hypoxic ischemic pathological changes, and occasionally segmental glomerular fibrosis (26, 27). At this time, renal damage caused by hypertension is mainly manifested as benign glomerular arteriosclerosis. Although focal glomerular fibrosis has occurred, the kidneys can maintain relatively constant renal blood flow and renal capillary hydrostatic pressure through a series of compensatory adjustments, so there will be no changes in renal structure and function due to blood pressure fluctuations in the short term. If patients do not receive timely and effective intervention at this time, the severity of kidney involvement will progressively worsen and eventually develop into uremia (28, 29). Therefore, this research result has significant clinical implications.

In this study, the strong positive correlation between hypertension duration and cortical stiffness, with hypertension duration identified as an independent predictor of renal cortical Young’s modulus, indicates that SWE may serve as a valuable biomarker for monitoring subclinical disease progression. Regarding the underlying pathophysiology, hypertension-induced renal damage represents a progressive pathological process. Early hypertensive nephropathy manifests as benign arteriolosclerosis (30, 31), characterized by renal arterial intimal thickening, subsequent vessel wall hypertrophy with luminal narrowing, mild glomerular ischemic changes, and focal glomerular and tubular atrophy. This progression perpetuates a pathological cycle wherein renal damage exacerbates hypertension severity, which subsequently accelerates further renal deterioration. In the late stage, malignant glomerular arteriosclerosis develops, characterized by glomerular consolidation and sclerosis, renal interstitial fibrosis, arteriolar fibrinoid necrosis or thrombosis, and associated pathological changes (32). Concurrently, renal tissue stiffness progressively increases throughout this pathological continuum. Multiple investigations have demonstrated the clinical utility of elastography in various renal pathologies, establishing its role as a non-invasive assessment tool for tissue mechanical properties. Leong et al. validated SWE’s capability to quantify renal tissue stiffness, demonstrating superior performance compared to conventional ultrasound parameters in detecting CKD (33). Chen et al. demonstrated significant correlations between renal stiffness measured by SWE and histopathological renal fibrosis, suggesting elastography’s utility as a surrogate marker for early fibrosis detection (34). Similarly, investigation by Leong et al. found that SWE accurately detects chronic renal histopathological changes, including glomerular sclerosis, interstitial fibrosis, and tubular atrophy (35). These findings support our observation that SWE can detect subclinical renal changes before conventional parameters become abnormal.

The absence of significant correlations between renal cortical Young’s modulus and several conventional renal parameters in our study warrants detailed discussion. The lack of correlation with renal volume measurements suggest that morphological changes may lag behind biomechanical alterations in early renal disease. The non-significant relationship between cortical stiffness and conventional Doppler parameters (PSV and RI) in our cohort reflects the limitations of hemodynamic assessments in detecting early renal damage. This finding is consistent with study demonstrating that RI measurements remain within normal ranges during initial stages of renal pathology, only becoming elevated with advanced vascular changes (36). Our results suggest that elastographic measurements may provide superior sensitivity for detecting early pathological changes compared to conventional hemodynamic parameters. Additionally, the absence of correlation between cortical Young’s modulus and serum biomarkers (blood urea nitrogen, creatinine, and uric acid) in our study population reflects the preserved renal function in early hypertensive disease. This observation is particularly significant, as it demonstrates SWE’s ability to detect subclinical renal alterations before conventional functional markers become abnormal. Limitations of this study: (1) The single-center design and limited sample size may restrict generalizability and statistical power, necessitating larger multi-center studies for validation; (2) There is a lack of comparison between hypertensive nephropathy groups in this study; (3) The study population comprised exclusively early-stage hypertensive patients with suboptimal pharmaceutical control, without comparison to populations achieving target blood pressure ranges following therapeutic intervention; (4) The involvement of two different ultrasound operators, despite their comparable expertise in elastography techniques, introduces potential inter-operator variability that may influence measurement consistency; (5) We did not systematically analyze the potential effects of antihypertensive medications on renal stiffness measurements or evaluate the impact of blood pressure variability on elastographic findings; (6) This study lacks direct biochemical assessment of RAS activation markers, such as urinary angiotensinogen, which would provide mechanistic validation for the observed correlation between hypertension duration and renal cortical stiffness. These limitations should be considered when interpreting our findings and designing future investigations in this field

In summary, for patients with simple hypertension, although routine clinical screening has not yet found any damage to renal structure and physiological function, the hardness of the right renal cortex has changed. And the duration of hypertension is an independent influencing factor. Clinically, SWE could be integrated into routine hypertensive patient evaluation as an early screening tool, with hypertension duration serving as a key consideration for patient selection given its role as an independent predictor of renal cortical stiffness, enabling risk stratification, personalized monitoring, and earlier therapeutic interventions when conventional biomarkers remain normal. The technique’s ability to prompt more aggressive blood pressure management, earlier nephrology consultation, and enhanced monitoring protocols, combined with its seamless incorporation into existing ultrasound examinations with minimal additional cost and time burden, positions elastography as a valuable auxiliary diagnostic tool that represents a paradigm shift toward earlier, more sensitive detection of hypertensive renal involvement, ultimately offering clinicians an evidence-based approach for optimizing patient care through timely intervention and personalized management strategies.