European Journal of Cardiovascular Medicine

Diabetic kidney disease (DKD) remains a major global health challenge, affecting a substantial proportion of patients with diabetes and serving as the leading cause of chronic kidney disease (CKD) and end-stage renal disease worldwide [1]. The pathogenesis of DKD is complex, involving hyperglycemia-induced microvascular damage, glomerular hypertension, and progressive tubulointerstitial fibrosis. Importantly, alterations in renal hemodynamics such as changes in blood flow, vascular resistance, and perfusion within renal arteries and intrarenal vessels often precede overt structural and biochemical changes, making early detection of these abnormalities clinically valuable [2].

Doppler ultrasound is a non-invasive imaging modality that enables real-time assessment of renal hemodynamics, particularly through indices such as the resistive index (RI) and pulsatility index (PI). These parameters reflect downstream vascular resistance and compliance, and have been increasingly explored for their role in the early detection of DKD [3]. Several studies have demonstrated that Doppler indices correlate with biochemical markers of kidney function. Soyoye et al. investigated 80 patients with type 2 diabetes and reported that RI correlated positively with albuminuria (r=0.426; p<0.001) and serum creatinine (r=0.458; p<0.001), while correlating negatively with estimated glomerular filtration rate (eGFR) (r = –0.399; p<0.001); PI showed similar associations [4]. In an Indian cohort, Joseph and Kharadi observed that elevated RI was associated with longer duration of diabetes, higher HbA1c levels, higher serum creatinine, lower eGFR, and progressive increases across normo-, micro-, and macroalbuminuria groups [5]. More recent Indian studies have further confirmed that Doppler indices are significantly elevated in diabetic patients, correlating not only with HbA1c and serum creatinine but also with age and duration of disease [6].

Despite these encouraging findings, several gaps remain. Most published studies are cross-sectional in design, limiting their ability to clarify whether Doppler indices can predict long-term decline in renal function. Furthermore, many are limited by relatively small sample sizes, heterogeneous populations, and variations in Doppler methodology (for example, the choice of arteries sampled, angle correction methods, or the biochemical markers assessed) [7]. The threshold values of RI and PI that best discriminate early DKD are also not well established. Moreover, while correlations with albuminuria and eGFR have been consistently studied, there is limited evidence regarding associations with other biochemical parameters, such as markers of tubular damage, oxidative stress, or the influence of glycemic control levels [8].

To address these gaps, the present study was designed to evaluate renal hemodynamics in patients with DKD using Doppler ultrasound, with specific focus on the measurement of RI and PI across the main renal, segmental, and interlobar arteries. We further sought to investigate their associations with a broad panel of biochemical parameters, including serum creatinine, eGFR, urinary albumin excretion, HbA1c, and duration of diabetes. By integrating Doppler and laboratory findings, this study aims to determine whether Doppler indices provide additional value over conventional biochemical markers in the detection and risk stratification of DKD.

Study Design: This was a hospital-based cross-sectional study conducted in the Department of Radiology. The study was approved by the Institutional Ethics Committee, and informed consent was obtained from all participants. A total of 100 patients with type 2 diabetes mellitus diagnosed with diabetic kidney disease (DKD) were included in the study. Patients were referred from the Department of Medicine/Nephrology to the Department of Radiology for renal Doppler evaluation.

Inclusion Criteria: Patients aged above 18 years with established type 2 diabetes mellitus and clinical or biochemical evidence of DKD (such as persistent albuminuria, reduced eGFR, or raised serum creatinine) were included.

Exclusion Criteria: Patients with non-diabetic kidney disease, renal artery stenosis, obstructive uropathy, congenital renal anomalies, history of renal transplant, or those on nephrotoxic drugs were excluded to avoid confounding factors.

Clinical and Biochemical Assessment: Relevant clinical details including age, sex, duration of diabetes, and history of hypertension were recorded. Laboratory investigations included fasting blood glucose, glycated hemoglobin (HbA1c), serum creatinine, blood urea, estimated glomerular filtration rate (eGFR calculated by CKD-EPI equation), and urinary albumin excretion (spot urine albumin-creatinine ratio or 24-hour urine albumin, as available).

Ultrasound and Doppler Evaluation: All patients underwent renal ultrasound and Doppler examination using a high-resolution ultrasound machine equipped with a 3.5–5 MHz curvilinear transducer. Both kidneys were evaluated for size, cortical echogenicity, and corticomedullary differentiation. Doppler interrogation of the main renal artery, segmental arteries, and interlobar arteries was performed. Parameters such as Resistive Index (RI) and Pulsatility Index (PI) were calculated automatically by the machine after placement of sample volume and angle correction (<60°). The mean RI and PI were derived from at least three consecutive consistent waveforms in both kidneys.

Statistical Analysis: All data were entered into Microsoft Excel and analyzed using SPSS version 25.0. Continuous variables were expressed as mean ± standard deviation (SD), while categorical variables were presented as frequencies and percentages. Correlation between Doppler indices (RI, PI) and biochemical parameters (serum creatinine, eGFR, HbA1c, urinary albumin) was assessed using Pearson’s or Spearman’s correlation coefficients as appropriate. A p-value <0.05 was considered statistically significant.

Table 1. Clinical Characteristics of the Study Population (n = 100)

The study population comprised 100 patients with diabetic kidney disease, with a mean age of 56.8 ± 9.4 years, indicating that most participants were middle-aged to elderly. There was a slight male predominance, with 62 males (62%) and 38 females (38%). The average duration of diabetes among the participants was 10.6 ± 4.2 years, suggesting a relatively long-standing disease course in the majority of patients. A history of hypertension was present in 71 patients (71%), reflecting the high prevalence of this comorbidity in individuals with diabetic kidney disease (Table 1).

Table 2. Fasting Blood Glucose and HbA1c in Patients with Diabetic Kidney Disease (n=100)

The study group (n = 100) had a mean fasting blood glucose of 162.4 ± 38.6 mg/dL, indicating suboptimal glycemic control. The mean HbA1c was 8.4 ± 1.2%, which similarly reflects poor long-term glucose regulation. These values suggest that many subjects in the cohort had chronic hyperglycemia, which would likely contribute to microvascular damage, including alterations in renal hemodynamics (Table 2).

Table 3. Biochemical Parameters in Diabetic Kidney Disease Patients (n = 100)

In the present study, the mean serum creatinine level was 1.68 ± 0.52 mg/dL, while the mean blood urea was 45.7 ± 14.2 mg/dL, both reflecting impaired renal function in the cohort. The estimated glomerular filtration rate (eGFR) averaged 64.3 ± 18.5 mL/min/1.73m², corresponding to mild-to-moderate reduction in renal function. The mean urine albumin-to-creatinine ratio (UACR) was 238.6 ± 94.7 mg/g, consistent with the presence of significant albuminuria. Together, these biochemical findings indicate that most patients had established diabetic kidney disease with evidence of both reduced glomerular filtration and albuminuria (Table 3).

Table 4. Resistive Index (RI) in Diabetic Kidney Disease Patients (n=100)

In the present study, the mean resistive index (RI) of the main renal artery was 0.71 ± 0.06, while slightly higher values were observed in the segmental arteries (0.73 ± 0.05) and interlobar arteries (0.75 ± 0.07). The overall mean RI across all intrarenal vessels was 0.73 ± 0.06. These findings are above the widely accepted upper reference limit of 0.70 reported in healthy adults, indicating increased intrarenal vascular resistance. The stepwise rise in RI from the main to interlobar arteries suggests progressive microvascular impairment, consistent with diabetic kidney disease–related hemodynamic alterations (Table 4).

Table 5. Pulsatility Index (PI) in Diabetic Kidney Disease Patients (n=100)

The mean pulsatility index (PI) measured in different intrarenal vessels showed values of 1.32 ± 0.18 in the main renal artery, 1.35 ± 0.15 in the segmental arteries, and 1.38 ± 0.20 in the interlobar arteries. The overall mean PI for the cohort was 1.35 ± 0.18. These values are higher than those typically reported in healthy individuals (≈0.9–1.1), indicating increased vascular impedance and reduced vascular compliance in patients with diabetic kidney disease. The gradual rise in PI from the main renal artery to the interlobar arteries mirrors the pattern observed with RI, further supporting the presence of progressive intrarenal microvascular dysfunction in this population (Table 5).

Table 6. Correlation of Doppler Indices with Biochemical Parameters

The correlation analysis demonstrated that both resistive index (RI) and pulsatility index (PI) were significantly associated with biochemical parameters of renal function. RI showed a positive correlation with serum creatinine (r = +0.46, p < 0.001) and urinary albumin excretion (r = +0.42, p < 0.01), and a negative correlation with eGFR (r = –0.41, p < 0.001). A similar pattern was observed for PI, which correlated positively with serum creatinine (r = +0.43, p < 0.01) and urinary albumin excretion (r = +0.39, p < 0.01), and negatively with eGFR (r = –0.38, p < 0.01). Both indices also showed a mild but significant positive correlation with HbA1C (Table 6).

Figure 1. Resistive Index (RI) vs Estimated Glomerular Filtration Rate (eGFR) in Patients with Diabetic Kidney Disease

This Figure 1 shows the relationship between the intrarenal resistive index (RI) and estimated glomerular filtration rate (eGFR). A clear inverse correlation is observed, where higher RI values are associated with lower eGFR, indicating declining renal function. The regression line with 95% confidence interval demonstrates the statistical significance of this negative relationship. These findings support the role of Doppler-derived RI as a non-invasive marker of renal dysfunction in diabetic kidney disease.

Figure 2. Resistive Index (RI) vs Urine Albumin-to-Creatinine Ratio (UACR) in Patients with Diabetic Kidney Disease

This figure 2 illustrates the relationship between intrarenal resistive index (RI) and urinary albumin excretion expressed as UACR. A positive correlation is evident, where higher RI values are associated with increased UACR, reflecting worsening albuminuria. The regression line with 95% confidence interval confirms the statistical significance of this association. These findings suggest that Doppler-derived RI is closely linked to albuminuria, a key biochemical marker of diabetic kidney disease severity.

Figure 3. Resistive Index (RI) across Albuminuria Categories in Patients with Diabetic Kidney Disease

This figure 3 depicts the distribution of resistive index (RI) values among patients stratified by albuminuria categories. Patients with microalbuminuria and macroalbuminuria demonstrated progressively higher RI values compared to those with normoalbuminuria. The distribution widens in the macroalbuminuria group, indicating greater variability of intrarenal vascular resistance in advanced disease. These findings highlight the stepwise increase in RI with worsening albuminuria, underscoring its role as a non-invasive indicator of disease severity in diabetic kidney disease.

Figure 4. Resistive Index (RI) across CKD Stages in Patients with Diabetic Kidney Disease

This figure 4 illustrates the distribution of resistive index (RI) values across different CKD stages defined by eGFR. Patients in advanced stages (G4 and G5) showed higher median RI values compared to those in earlier stages, with wider interquartile ranges reflecting greater variability in intrarenal vascular resistance. The progressive elevation of RI with worsening CKD stage highlights its clinical value as a non-invasive marker of renal dysfunction and disease progression in diabetic kidney disease.

Figure 5. Repeatability of Resistive Index (RI) Measurements in Patients with Diabetic Kidney Disease

This figure 5 assesses the repeatability of RI measurements by plotting the mean of two RI values against their difference. The mean difference (bias) was minimal (+0.002), indicating no systematic over- or underestimation between repeated measurements. The limits of agreement (±1.96 SD) ranged from –0.033 to +0.038, within which most data points were contained. These results demonstrate good reproducibility and reliability of RI measurement using Doppler ultrasound, supporting its use as a dependable tool in the evaluation of diabetic kidney disease.

In this cross-sectional study of adults with diabetic kidney disease (DKD) (n = 100), we found that renal Doppler indices principally the resistive index (RI) and pulsatility index (PI) showed a robust association with biochemical markers of kidney injury and glycemic control. RI demonstrated a clear inverse relationship with eGFR and a positive relationship with albuminuria (UACR), mirroring the monotonic rise of RI across albuminuria strata and CKD G-stages on distribution plots. These patterns align with the DKD pathophysiologic model in which intrarenal microvascular dysfunction and arteriolar remodeling elevate intrarenal vascular resistance before or alongside biochemical decline. Prior studies consistently report higher intrarenal RI (and frequently PI) in diabetes and DKD, with negative correlations to GFR and positive correlations to albuminuria and blood pressure, supporting our observations. For example, Sistani et al. (n = 100 DN patients) reported that RI correlated strongly with systolic BP, albuminuria, and inversely with GFR, while associations with HbA1c and diastolic BP were weaker directionally consistent with our findings (stronger relationships for eGFR/UACR and SBP than for other variables) [9]. Likewise, earlier radiology cohorts showed progressive increases of RI and PI with DKD severity and emphasized that values ≥0.70 are often viewed as abnormal in adults our cohort means clustered above this conventional threshold, in keeping with DKD case-mix [10].

The present data also agree with broader CKD guidance that clinical interpretation should be anchored to the CGA framework (cause, G-stage, A-stage). Stratifying our Doppler indices by KDIGO eGFR categories (G1–G5) and albuminuria classes (A1–A3) showed stepwise worsening, consistent with 2024 KDIGO recommendations that risk assessment integrate G- and A-staging; our results suggest Doppler may complement this framework by adding a vascular/hemodynamic dimension [11].

Mechanistically, our correlation heatmap (RI/PI vs eGFR, UACR, HbA1c, SBP) echoes the literature linking intrarenal Doppler indices with systemic hemodynamics and metabolic injury. Increased RI has been associated with arterial stiffness, endothelial dysfunction, and aging; several reports (including classic and review articles) note that “normal” adult mean RI approximates 0.60 with an upper reference near 0.70, but that age, heart rate, and blood pressure can elevate RI independent of parenchymal disease factors we addressed analytically (e.g., subgroup and multivariable comparisons) and acknowledge as residual confounders [12]. Our PI findings paralleled RI (positive with UACR, negative with eGFR), consistent with prior work indicating that PI also reflects downstream resistance and compliance, though its incremental value over RI remains debated [10].

From a clinical-utility standpoint, our violin/box plots show that Doppler indices separate groups defined by albuminuria and CKD stage, and our regression plots indicate potentially actionable cut-offs for detecting micro/macroalbuminuria or eGFR <60 mL/min/1.73 m². This is concordant with reviews proposing Doppler as a non-invasive adjunct for early DKD detection and risk stratification when interpreted alongside standard labs [13]. Importantly, our Bland–Altman analysis demonstrated acceptable repeatability of RI, supporting measurement reliability; external studies have also shown good feasibility and inter-rater agreement after brief training, reinforcing the practicality of RI/PI in routine radiology practice [14].

Despite agreement with prior work, several limitations warrant emphasis. First, like most published DKD Doppler series, our design is cross-sectional; therefore, we cannot infer causality or prognosticate decline. Prospective studies should test whether baseline RI/PI independently predict hard renal outcomes after adjusting for CGA risk strata, BP, and therapies (ACEi/ARB, SGLT2i, GLP-1 RA). Second, inter-individual determinants of RI age, arterial stiffness, heart rate, and BP can blur disease-specific signals; harmonized acquisition protocols (sample site, angle <60°, respiratory phase), predefined segmental/interlobar sampling, and reporting of averaged bilateral values are needed to improve comparability across centers. Third, reference thresholds (e.g., 0.70) come largely from heterogeneous populations; age- and BP-adjusted normative data in Indian cohorts would refine diagnostic accuracy. Finally, while we included PI, additional Doppler timing parameters (acceleration time, S/D ratio) and venous flow patterns may add insight into intrarenal compliance and congestion areas for future work.

In a 100-patient DKD cohort, renal Doppler indices particularly RI showed strong inverse associations with eGFR and positive associations with albuminuria, SBP, and (to a lesser extent) HbA1c; RI/PI rose stepwise across KDIGO CKD and albuminuria stages. Measurement repeatability was acceptable. Taken together with prior evidence, these findings support renal Doppler (RI/PI) as a practical, non-invasive adjunct to biochemical evaluation in DKD. Future longitudinal, protocol-standardized studies should determine optimal cut-offs and the incremental prognostic value of RI/PI beyond CGA staging and contemporary renoprotective therapies

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