Chronic kidney disease (CKD) represents a global public health challenge with substantial implications for morbidity, mortality and healthcare resource utilisation. The formal definition and classification of CKD were established by the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (K/DOQI) in 2002 and subsequently refined by Kidney Disease: Improving Global Outcomes (KDIGO) [1,2]. CKD is defined as the presence of kidney damage or a reduced glomerular filtration rate below 60 mL/min/1.73 m² persisting for at least three months, irrespective of the underlying cause, with kidney damage frequently evidenced by albuminuria [3].

The epidemiological burden of CKD is considerable and continues to escalate. Global prevalence estimates indicate that approximately 13.4% of the population experiences CKD stages 1 through 5, with 10.6% manifesting the more advanced stages 3 through 5 characterised by moderate to severe reductions in kidney function [4]. In the Indian subcontinent, the mean prevalence of CKD stages 1 to 5 stands at 13.1%, with 6.7% of individuals affected by the more advanced stages, underscoring the urgent need for early detection and comprehensive risk-modification strategies [4].

The relationship between CKD and cardiovascular disease constitutes one of the most critical clinical paradigms in contemporary nephrology and cardiology. Diminished eGFR and the presence of albuminuria function as powerful, graded and independent predictors of cardiovascular and all-cause mortality [5]. CKD has been unequivocally established as an independent cardiovascular risk state, with risk increasing progressively as kidney function declines and albuminuria worsens [6]. Large collaborative meta-analyses have confirmed that reductions in eGFR and increases in albuminuria are associated with graded elevations in cardiovascular and all-cause mortality across diverse populations [7]. Patients with end-stage renal disease face an extraordinarily elevated risk of premature death, predominantly attributable to cardiovascular complications rather than renal failure per se.

The cardiovascular pathology associated with CKD differs in important respects from conventional atherosclerotic occlusive disease. While sharing features of atheromatous plaque formation and vessel stenosis, CKD-associated vasculopathy demonstrates additional characteristics including left ventricular hypertrophy, extensive vascular calcification affecting both the intimal and medial arterial layers, and increased vascular stiffness with reduced arterial compliance [8]. Medial arterial calcification transforms the arterial media into a rigid conduit, augmenting pulse-wave velocity and left ventricular afterload, and is accelerated by disturbances in calcium–phosphate homeostasis and elevated fibroblast growth factor 23 [8].

Given the magnitude of cardiovascular risk in CKD populations, there is a pressing need for reliable, accessible and cost-effective methods to detect subclinical atherosclerosis. Ultrasonographic measurement of intima-media thickness (IMT) in the common carotid and femoral arteries has been widely validated as a reproducible, non-invasive surrogate marker of systemic atherosclerotic burden, and importantly, femoral IMT changes may be more pronounced and occur earlier in the disease course than carotid changes in CKD [9]. Sonographically measured IMT is now regarded as a validated surrogate marker for atherosclerosis across diverse clinical contexts including diabetes mellitus, hypertension, hyperlipidaemia and CKD, and multiple case–control studies have documented significantly increased carotid IMT in CKD patients compared with controls [10,11,12]. The technique captures early atherosclerotic changes before luminal narrowing becomes hemodynamically significant, and standardised carotid IMT protocols have been codified by international consensus [13].

The prognostic value of IMT is well established. Meta-analyses demonstrate that increased carotid IMT independently predicts future myocardial infarction, stroke and cardiovascular death after adjustment for conventional risk factors [14], a relationship first demonstrated in landmark cohorts such as the Cardiovascular Health Study and the Atherosclerosis Risk in Communities (ARIC) study [15,16]. In CKD, carotid IMT and indices of arterial stiffness are independently associated with adverse cardiovascular outcomes [17]. However, the comparative assessment of carotid versus femoral IMT remains an evolving area; combined carotid and femoral ultrasound morphology screening has predicted cardiovascular events in general populations, suggesting complementary information from the two vascular beds [18].

Despite several studies evaluating carotid IMT in CKD, limited data are available comparing both carotid and femoral IMT simultaneously, particularly in the Indian population, and the role of femoral IMT as a marker of systemic atherosclerosis remains underexplored. The present study was therefore undertaken with the objectives: (i) to measure carotid and femoral arterial IMT in CKD patients and controls; and (ii) to compare the extent of atherosclerosis across different age groups of CKD patients with age-matched controls.

Study design and setting

This was a hospital-based cross-sectional study conducted in the Department of Radiodiagnosis, Bangalore Medical College and Research Institute (BMCRI), Bengaluru, over the period March 2024 to August 2025. Participants were drawn from patients presenting to the Department of Radiodiagnosis at Victoria Hospital and the Institute of Nephro-Urology, referred from hospitals attached to BMCRI. The study was reported in accordance with the STROBE recommendations for cross-sectional studies.

Participants

Patients aged over 18 years with CKD, defined per KDIGO criteria as an estimated glomerular filtration rate (eGFR) less than 60 mL/min/1.73 m² persisting for three or more months irrespective of the cause, and who were willing to provide informed consent, were eligible as cases. Subjects with normal serum creatinine and uric acid, without any known kidney pathology, who were referred for ultrasonography for causes other than renal or cardiovascular pathology, served as controls.

Patients who were unwilling to consent, those with acute kidney injury, coexistent congenital renal anomalies (horseshoe kidney, ectopic kidney, renal agenesis), a solitary kidney, or a radiological kidney pathology (polycystic kidney disease, medullary cystic kidney disease, renal cell carcinoma) were excluded. Controls with conditions likely to affect the study outcome, such as cirrhosis of the liver, obstructive uropathy or aortic compression, were also excluded. A consecutive sampling technique was employed, whereby all eligible patients presenting during the study period who met the inclusion criteria were enrolled until the desired sample size was achieved.

Sample size

The sample size was calculated on the basis of a previous study (Doğan et al.) that demonstrated a significant difference in carotid and femoral IMT between CKD patients and controls, in which femoral IMT was 0.436 ± 0.189 mm in cases and 0.645 ± 0.132 mm in controls. Assuming a minimum expected difference of 0.05 between the two groups, with a standard table value of 1.96 for a 95% confidence interval (Z_α), 0.84 for 80% power (Z_1−β), a pooled standard deviation (σ) of 0.161 and an effect size (d) of 0.05, the calculation yielded n = 163 per group. This was rounded to approximately 170 per group. Accordingly, 170 known cases of CKD and 170 normal subjects as controls were included, giving a total of 340 participants.

Imaging technique / protocol

All CKD cases underwent estimation of eGFR using the abbreviated Modification of Diet in Renal Disease (MDRD) equation (eGFR = 186 × [serum creatinine]^−1.154 × [age]^−0.203 × 0.742 [if female] × 1.210 [if black]) and were staged according to the KDOQI classification. A structured, pre-prepared case proforma was used to record demographic details, dietary habits, lifestyle, smoking and drug history, clinical history, physical examination and investigations including serum creatinine and urinary albumin.

All subjects were evaluated using a high-resolution ultrasound scanner (Samsung RS80 EVO and Mindray DC-80 systems) with a broadband linear-array (4–12 MHz) B-mode transducer, by a single experienced radiologist to eliminate inter-observer variability. The B-mode technique measures the distance between the lumen–intima and media–adventitia interfaces, a quantity validated histologically as a direct in-vivo measurement of the arterial intima-media complex [19], and was performed following the standardized far-wall, leading-edge measurement conventions recommended by international consensus [20]. Only the right common carotid artery and the right superficial femoral artery were evaluated in all subjects to maintain uniformity and reduce inter-side variability. The common carotid artery approximately 1 cm from its bifurcation, and the superficial femoral artery approximately 1 cm from its bifurcation, were standardised as the measurement sites. The screen image was magnified to improve measurement accuracy, and electronic calipers were aligned parallel to the arterial walls (Figures 1 and 2). Minimal probe pressure was maintained and alignment parallel to the vessel wall was ensured. Three separate measurements were recorded at fixed anatomical landmarks at each site and a mean value was calculated. Segments demonstrating focal atherosclerotic plaque were excluded from IMT measurement to ensure that only true intima-media thickness was assessed. Differences in IMT between CKD cases and controls across different age groups, and between stages of CKD, were compared.

Figure 1. High-resolution B-mode ultrasound of the right common carotid artery in longitudinal view, demonstrating the standardized far-wall intima-media thickness measurement. The lumen–intima and media–adventitia interfaces form the characteristic double-line pattern, and electronic calipers positioned parallel to the vessel wall measure a normal carotid intima-media thickness of 0.08 cm (0.8 mm).

Figure 2. High-resolution B-mode ultrasound of the right superficial femoral artery in longitudinal view, showing the same electronic-caliper technique applied at the femoral site, with a normal femoral intima-media thickness of 0.06 cm (0.6 mm).

Statistical analysis

Data were analysed using SPSS software version 31.0. Normality was assessed using the Shapiro–Wilk test. Continuous variables were expressed as mean ± standard deviation. The independent-samples t-test was used to compare means between two groups, and one-way ANOVA (with post-hoc Tukey test where applicable) was used for comparisons across multiple groups. The chi-square test was used for categorical variables, and the paired t-test was used for within-group comparison of carotid and femoral IMT. Multivariable linear regression analysis was performed to identify independent predictors of IMT. A p value of <0.05 was considered statistically significant. All 340 enrolled participants completed clinical evaluation and ultrasonographic assessment and were included in the analysis, with no losses.

A total of 340 participants were included, comprising 170 CKD cases and 170 controls. The two groups were well matched demographically: the mean age was 54.76 ± 7.92 years in cases and 53.95 ± 7.59 years in controls (p=0.335), and the sex distribution was comparable (p=0.743), with the majority of participants in the 50–60-year age band. Age-group distribution did not differ significantly between groups (chi-square p=1.000). These findings are summarised in Table 1.

Table 1. Demographic characteristics of CKD cases and controls.

Table 2. Renal profile and distribution of CKD stage.

Among the CKD cases, Stage 3 constituted the largest subgroup (44.7%), followed by Stage 4 (32.9%) and Stage 5 (22.4%). Serum creatinine was significantly higher and eGFR significantly lower in CKD cases than in controls (both p<0.001), confirming the expected renal profile of the case group (Table 2).

Mean carotid and femoral IMT were both markedly and significantly higher in CKD cases than in controls. Mean CIMT was 1.85 ± 0.40 mm in cases versus 0.86 ± 0.09 mm in controls, and mean FIMT was 1.69 ± 0.37 mm in cases versus 0.74 ± 0.08 mm in controls (independent t-test, both p<0.001). Within both cases and controls, CIMT remained significantly higher than FIMT on paired comparison (both p<0.001) (Table 3; Figure 7). Representative case images illustrate this increased intima-media thickness at both the carotid and femoral sites in CKD patients (Figures 3 and 4).

Figure 3. B-mode ultrasound of the right common carotid artery in a 50-year-old man with Stage 3b CKD, showing increased carotid intima-media thickness (~0.8 mm) with no discrete atherosclerotic plaque.

Figure 4. B-mode ultrasound of the right superficial femoral artery in the same Stage 3b CKD patient, showing correspondingly increased femoral intima-media thickness (~0.8 mm).

Both carotid and femoral IMT increased progressively across CKD stages, from Stage 3 through Stage 5, with the highest values in Stage 5 (one-way ANOVA, CIMT and FIMT both p<0.001) (Table 4; Figure 8). The contrast between a near-normal carotid wall in earlier-stage disease and a markedly thickened complex in advanced disease is illustrated in Figures 5 and 6. A parallel progressive increase was observed with longer duration of CKD, the highest values occurring in the group with more than five years of disease (both p<0.001) (Table 5; Figure 9).

Table 3. Comparison of mean carotid (CIMT) and femoral (FIMT) intima-media thickness between CKD cases and controls, with within-group comparison. Between-group comparison by independent t-test; within-group (CIMT vs FIMT) comparison by paired t-test.

Table 4. Mean CIMT and FIMT across CKD stages among cases (one-way ANOVA).

Table 5. Mean CIMT and FIMT by duration of CKD among cases (one-way ANOVA).

Figure 5. B-mode ultrasound of the right common carotid artery in a 60-year-old woman with Stage 4 CKD, long-standing hypertension and diabetes, showing a markedly thickened carotid intima-media complex (~1.4 mm) approximately 1 cm proximal to the carotid bulb.

Figure 6. B-mode ultrasound of the right common carotid artery in a patient with Stage 3 CKD, showing a normal-thickness intima-media complex (0.05 cm; 0.5 mm), illustrating the near-normal arterial wall that may be seen in milder, earlier disease.

Figure 7. Mean carotid (CIMT) and femoral (FIMT) intima-media thickness in CKD cases versus controls. Both measurements were markedly higher in CKD cases than in controls, and within each group the carotid measurement exceeded the femoral (independent and paired t-tests, all p<0.001) (data from Table 3).

Figure 8. Mean carotid (CIMT) and femoral (FIMT) intima-media thickness across CKD stages 3 to 5, showing a progressive stage-wise increase with the highest values in Stage 5 (one-way ANOVA, both p<0.001) (data from Table 4).

Figure 9. Mean carotid (CIMT) and femoral (FIMT) intima-media thickness by duration of CKD, showing a parallel progressive increase with the highest values in patients with more than five years of disease (one-way ANOVA, both p<0.001) (data from Table 5).

Table 6. Association of hypertension, diabetes and BMI category with intima-media thickness.

Table 7. Diabetes and smoking subgroup comparison of CIMT and FIMT (one-way ANOVA; CIMT p<0.001 and FIMT p<0.001 for each subgroup set).

Table 8. Association of biochemical parameters with CIMT and FIMT in CKD cases and controls (independent t-test).

Table 9. Multivariable linear regression: independent predictors of intima-media thickness.

Conventional risk factors showed significant univariate associations with IMT. Hypertension and diabetes were each associated with higher CIMT and FIMT (independent t-test, both p<0.001), and increasing BMI category was associated with a stepwise increase in IMT (ANOVA, both p<0.001) (Table 6). In subgroup analyses, diabetic and non-diabetic CKD cases had substantially higher IMT than diabetic and non-diabetic controls, and CKD smokers had higher values than both control subgroups (ANOVA, all p<0.001) (Table 7). The greatest values were consistently observed when these risk factors coexisted with CKD, indicating an accelerating rather than an independent effect.

Biochemical parameters were analysed directly against IMT. HbA1c, total cholesterol, LDL cholesterol and triglycerides showed positive associations with higher CIMT and FIMT, whereas HDL showed an inverse association; CKD patients consistently exhibited higher IMT across all biochemical categories (all p<0.001), with relatively little variation within CKD subgroups, suggesting a ceiling effect of vascular damage (Table 8).

On multivariable linear regression, age (β=0.492, p<0.001) and eGFR (β=−0.385, p<0.001) emerged as the independent predictors of IMT, age being positively and eGFR negatively associated with arterial wall thickness. The conventional risk factors (hypertension, diabetes, BMI and smoking) and biochemical abnormalities, although significant on univariate analysis, did not retain independent significance and were interpreted as confounding or accelerating variables (Table 9; Figure 10).

Figure 10. Standardised β coefficients from multivariable linear regression, identifying age (β=+0.492) and eGFR (β=−0.385) as the independent predictors of intima-media thickness; age is positively and eGFR negatively associated with arterial wall thickness (both p<0.001) (data from Table 9).

The present study was undertaken to evaluate the subclinical atherosclerotic burden in patients with CKD by ultrasonographic assessment of carotid and femoral arterial IMT, and to compare these measurements with age-matched controls. The findings demonstrate that CKD patients have significantly increased carotid and femoral IMT relative to controls, with a clear stage-wise increase across progressive CKD, supporting the concept that CKD is a major accelerator of subclinical atherosclerosis. The primary objective was achieved: mean carotid IMT (1.85 ± 0.40 vs 0.86 ± 0.09 mm) and mean femoral IMT (1.69 ± 0.37 vs 0.74 ± 0.08 mm) were markedly higher in CKD patients than in controls. These findings are in agreement with previous case–control studies. Ajiboye et al. reported significantly higher carotid IMT in CKD patients than controls, while Margekar et al. and Lawal et al. found similar elevations, confirming that CKD is associated with increased subclinical vascular disease [10,11,12]. The magnitude of IMT elevation in the present cohort exceeded that of several earlier reports, which may reflect a relatively larger proportion of patients with advanced CKD and a higher cumulative burden of CKD-related vascular injury. The demonstration of significantly increased femoral IMT alongside carotid IMT is clinically important. Although carotid IMT has traditionally received greater attention as a surrogate marker of atherosclerosis, femoral IMT is increasingly recognised as an important marker of systemic vascular disease. Doğan et al. and Kato et al. demonstrated that femoral arterial involvement may be pronounced in CKD and can contribute meaningful additional information about generalised atherosclerotic burden [9,21]. The present study therefore strengthens the concept that vascular changes in CKD are widespread and affect multiple arterial beds rather than being confined to a single territory. One of the most important findings is the clear progressive increase in both carotid and femoral IMT with advancing CKD stage, with the highest values in Stage 5 and a parallel increase with longer disease duration. This stage-wise pattern suggests a dose–response relationship between worsening renal dysfunction and increasing atherosclerotic burden. As renal function declines, the vasculature is exposed to an escalating burden of uraemic toxins, oxidative stress, endothelial dysfunction, chronic inflammation, anaemia, calcium–phosphate imbalance and neurohormonal dysregulation, which together accelerate intimal thickening, smooth-muscle proliferation, arterial stiffness and calcification. This result is supported by studies such as Wang et al. and Yilmaz et al., which demonstrated worsening vascular parameters with declining kidney function [22,23]. Although some earlier reports, such as Margekar et al., did not identify significant stage-wise differences [11], the present study provides stronger evidence of a progressive trend, suggesting that vascular thickening does not simply occur early and plateau but may continue to increase with worsening CKD severity. The study also demonstrated that CKD patients had higher IMT than age-matched controls across all age groups, indicating that CKD contributes to accelerated vascular ageing independent of chronological age. Although IMT increased physiologically with age in both groups, the absolute values were consistently higher in CKD patients. Studies by Bots et al. and Groothoff et al. have similarly shown that CKD is associated with disproportionately increased vascular thickening beyond the physiological effect of age [24,25]. This pattern implies that even younger CKD patients may harbour significant subclinical atherosclerosis, and that the absence of advanced age should not lead to underestimation of cardiovascular risk. Multivariable linear regression identified age and eGFR as the major independent predictors of IMT, with age positively and eGFR negatively associated with arterial thickening. This establishes that the severity of renal dysfunction itself is independently associated with vascular structural change, even after accounting for other variables. Similar observations have been made by Recio-Mayoral et al. and Kestenbaum et al., who showed that renal impairment is strongly associated with adverse vascular parameters independent of conventional risk factors [26,27]. In contrast, traditional risk factors such as hypertension, diabetes, BMI and smoking, although significant on univariate analysis, did not retain independent significance, implying that CKD-related pathophysiological mechanisms exert an overriding influence on arterial wall remodelling in this group. The markedly increased IMT observed in CKD can be explained by several interconnected mechanisms. A central mechanism is endothelial dysfunction, an early and critical event driven by reduced nitric oxide bioavailability, increased asymmetric dimethylarginine, oxidative stress and chronic uraemic toxin exposure, as emphasised by Yilmaz et al. and Recio-Mayoral et al. [23,26]. Chronic low-grade inflammation, with elevated interleukin-6, tumour necrosis factor-alpha and C-reactive protein, is a further major contributor; Stenvinkel et al. described the inflammatory milieu of uraemia as a key mediator of cardiovascular injury that stimulates vascular smooth-muscle proliferation and arterial wall thickening [28]. Oxidative stress also plays a major role, with increased reactive oxygen species and reduced antioxidant defences promoting lipid peroxidation and endothelial injury, as demonstrated by Himmelfarb et al. [29]. Disordered mineral metabolism—hyperphosphataemia, secondary hyperparathyroidism, elevated fibroblast growth factor 23 and reduced calcification inhibitors—promotes vascular calcification and stiffness, as shown by Palit and Kendrick and Karohl et al. [30,31]. Finally, uraemic toxin accumulation, including indoxyl sulphate, contributes substantially to endothelial dysfunction and vascular calcification, as demonstrated by Barreto et al. [32]. Together these mechanisms explain why CKD functions as more than a simple comorbidity, creating a pro-atherogenic, pro-calcific and pro-inflammatory vascular environment. The clinical implications are considerable. Cardiovascular disease is the leading cause of morbidity and mortality in CKD, and CKD confers cardiovascular risk independent of traditional factors; Sarnak et al. and Matsushita et al. established CKD as a powerful independent cardiovascular risk state with risk increasing as eGFR declines and albuminuria worsens [6,7]. Because increased IMT is associated with future myocardial infarction, stroke and cardiovascular death—each 0.1 mm increment in carotid IMT conferring a significant rise in event risk [14]—the substantial IMT elevations observed here signal a markedly increased future cardiovascular burden. These results support the value of IMT assessment for early cardiovascular risk stratification in CKD, and indicate that surveillance should intensify as CKD advances. Management of CKD should therefore extend beyond preservation of renal function to include aggressive cardiovascular risk reduction through control of blood pressure, glycaemia and lipids, smoking cessation, and correction of mineral-metabolism abnormalities. STRENGTHS AND LIMITATIONS The study has several strengths. It included an adequate sample size with equal numbers of CKD patients and controls, improving statistical robustness, and used age-matched controls to reduce confounding by age, a major determinant of IMT. Assessment of both carotid and femoral IMT allowed a broader evaluation of systemic vascular involvement than reliance on a single site, and the use of a standardised ultrasonographic protocol with all measurements performed by a single experienced radiologist enhanced methodological consistency. The demonstration of a clear stage-wise increase in IMT adds important evidence to an area where prior literature has been inconsistent. Certain limitations should be acknowledged. The cross-sectional design precludes conclusions regarding causality or the temporal sequence between CKD progression and IMT increase. As a single-centre study, generalisability may be limited, and the absence of longitudinal follow-up meant that the relationship between elevated IMT and future cardiovascular events could not be assessed. Plaque burden and plaque morphology were not evaluated, and detailed assessment of biochemical mediators such as C-reactive protein, fibroblast growth factor 23, parathyroid hormone, oxidative-stress markers and uraemic toxin levels was not performed, limiting direct mechanistic correlation.

Patients with chronic kidney disease have significantly increased carotid and femoral intima-media thickness compared with age- and sex-matched controls, indicating early and progressive subclinical atherosclerosis. A statistically significant progressive increase in both carotid and femoral IMT was observed with advancing CKD stage and longer disease duration, with the highest values in Stage 5 disease. Hypertension, diabetes, increased body mass index, smoking and adverse biochemical profiles were associated with higher IMT on univariate analysis and exerted an accelerating effect, but did not emerge as independent predictors on multivariable analysis, which identified age and eGFR as the principal independent determinants. Carotid IMT was consistently higher than femoral IMT in both groups, suggesting the carotid artery may be a more sensitive site for detecting early change, while femoral IMT provided a valuable additional marker of systemic atherosclerosis. Early identification of increased IMT in CKD patients may aid cardiovascular risk stratification and facilitate timely preventive intervention; overall, CKD remains the predominant factor driving vascular pathology, with traditional risk factors further enhancing these changes.

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