Role of Renal Doppler and Shearwave Elastography in Diabetic Nephropathy

Abstract

Background:

Diabetic nephropathy is a leading cause of chronic kidney disease and end-stage renal failure worldwide. Early detection of renal microvascular and parenchymal changes is crucial for timely intervention and risk stratification.

Objectives:

The objective is to evaluate the diagnostic utility of renal Doppler ultrasonography and shearwave elastography (SWE) in detecting and staging diabetic nephropathy, and to assess their correlation with biochemical markers of renal function.

Materials and Methods:

This prospective cross-sectional study included adult patients with type 2 diabetes mellitus, categorized based on albuminuria stages. Renal resistive index and pulsatility index were measured using Doppler ultrasound, while renal cortical stiffness was quantified using point SWE. Findings were correlated with estimated glomerular filtration rate (eGFR), serum creatinine, and urinary albumin–creatinine ratio.

Results:

Increased renal cortical stiffness and elevated Doppler indices were observed in patients with microalbuminuria and overt nephropathy compared to normoalbuminuric diabetics. SWE showed a strong inverse correlation with eGFR and a positive correlation with urinary albumin levels. Combined use of Doppler and elastography improved early detection of subclinical nephropathy with high diagnostic sensitivity.

Conclusion:

Renal Doppler and SWE are valuable non-invasive tools for early identification and functional assessment of diabetic nephropathy. Their integration into routine screening may enhance early detection, staging, and monitoring of renal involvement in diabetic patients.

INTRODUCTION

Diabetes mellitus is a global health epidemic, affecting over 500 million individuals worldwide, with numbers projected to rise sharply in the coming decades. Among the various complications associated with long-standing diabetes, diabetic nephropathy stands out as a major cause of morbidity and mortality. It is the leading cause of chronic kidney disease (CKD) and end-stage renal disease globally, accounting for more than 40% of new cases of dialysis initiation.[1] Despite the availability of clinical and biochemical tools for monitoring renal function, the insidious onset and slow progression of diabetic nephropathy often result in delayed diagnosis and missed opportunities for early intervention.[2]

Conventionally, the diagnosis and staging of diabetic nephropathy rely on serum creatinine levels, estimated glomerular filtration rate (eGFR), and urinary albumin excretion. However, these parameters often reflect renal damage only after significant nephron loss has occurred.[3] Microalbuminuria, while considered an early marker, may not be sufficiently sensitive or specific in certain clinical scenarios. Therefore, the demand for noninvasive imaging biomarkers that can detect structural and hemodynamic alterations in the kidneys at an earlier stage has become increasingly relevant in clinical nephrology.[4]

In recent years, renal Doppler ultrasonography has emerged as a valuable tool for assessing intrarenal blood flow dynamics. Parameters such as resistive index (RI) and pulsatility index (PI) provide indirect yet reliable estimates of microvascular resistance and vascular compliance within the renal parenchyma.[5] Elevated RI values have been associated with glomerulosclerosis, interstitial fibrosis, and impaired renal autoregulation – all of which are hallmarks of diabetic nephropathy. Furthermore, Doppler assessment offers the advantage of real-time, bedside evaluation without the risks of contrast or ionizing radiation.[4]

Parallel to Doppler, the evolution of elastographic imaging has added a new dimension to the functional assessment of the kidneys. Shearwave elastography (SWE) is a quantitative, ultrasound-based modality that measures tissue stiffness by analyzing the propagation speed of mechanically induced shear waves.[6] Increased renal cortical stiffness is believed to correlate with underlying histopathological changes such as fibrosis, tubular atrophy, and extracellular matrix deposition. These pathophysiologic features are characteristic of progressive diabetic nephropathy and may appear before overt changes in glomerular filtration or albuminuria occur.[7]

Several recent studies have explored the diagnostic and prognostic utility of renal elastography and Doppler techniques in various renal pathologies. However, limited data are available on their combined application in diabetic patients across different stages of nephropathy. It is imperative to evaluate whether these imaging modalities can serve as early, sensitive, and reproducible markers for detecting subclinical renal involvement in diabetes.

This study was undertaken to investigate the role of renal Doppler ultrasonography and SWE in assessing diabetic nephropathy. It aims to compare imaging parameters across different albuminuria-based stages, correlate them with renal function indices, and evaluate their potential as adjunct tools in the early detection, grading, and longitudinal monitoring of diabetic kidney disease.

MATERIALS AND METHODS

Study design and setting

This was a prospective cross-sectional observational study conducted over a 12-month period in the Department of Radiology, in collaboration with the Department of Nephrology and Endocrinology. Informed consent was obtained from all participants prior to enrolment.

Study population

The study included 90 adult patients with known type 2 diabetes mellitus, aged between 35 and 70 years. Patients were stratified into three groups based on urinary albumin-creatinine ratio (UACR): normoalbuminuria (UACR <30 mg/g), microalbuminuria (UACR 30–300 mg/g), and macroalbuminuria (UACR >300 mg/g). Inclusion criteria were patients with a minimum diabetes duration of 5 years, stable blood pressure control, and availability of recent laboratory investigations. Exclusion criteria included patients with known CKD due to nondiabetic causes, obstructive uropathy, urinary tract infection, congenital renal anomalies, renal artery stenosis, cardiovascular instability, or those on nephrotoxic medications.

Clinical and laboratory evaluation

Detailed clinical history, including duration of diabetes, blood pressure, body mass index (BMI), and medication use, was recorded. Laboratory parameters included serum creatinine, eGFR calculated by the CKD-EPI equation, fasting blood glucose, glycated hemoglobin, and UACR. All investigations were performed within 1 week of the imaging studies to ensure clinical correlation.

Ultrasound and Doppler evaluation

Renal ultrasound was performed using a high-resolution Doppler-capable ultrasound machine equipped with a 3–5 MHz convex transducer. Bilateral kidneys were assessed in longitudinal and transverse planes for cortical echotexture, size, corticomedullary differentiation, and renal artery waveform patterns. Doppler measurements were obtained from segmental arteries at the upper, mid, and lower poles of each kidney. RI was calculated using the formula: RI = (peak systolic velocity– end diastolic velocity)/Peak Systolic Velocity. PI was also measured. The mean RI and PI values for each kidney were recorded, and the average of both kidneys was used for analysis.

SWE Assessment: Point SWE was performed using the same ultrasound system equipped with elastography software. Measurements were taken from the cortical region of each kidney, avoiding major vessels and renal pyramids. The patient was instructed to hold their breath during acquisition to minimize motion artifacts. A minimum of five valid measurements were taken from each kidney, and the median value was considered. Results were expressed in kilopascals (kPa) as an indicator of renal cortical stiffness.

Data Collection and Statistical Analysis: All imaging and laboratory data were entered into a structured database. Patients were grouped as per UACR classification, and mean values of RI, PI, and SWE were compared across the three groups. Correlation analysis was performed between imaging parameters and renal function markers (serum creatinine, eGFR, and UACR). Statistical analysis was carried out using Statistical Package for Social Sciences version 26.0. Continuous variables were expressed as mean ± standard deviation. One-way analysis of variance and post hoc Tukey tests were used for group comparisons. Pearson correlation was used to analyze associations, and a P < 0.05 was considered statistically significant.

RESULTS

A total of 90 patients with type 2 diabetes mellitus were enrolled and categorized into three groups based on UACR: Group A (normoalbuminuria, n = 30), Group B (microalbuminuria, n = 30), and Group C (macroalbuminuria, n = 30). The mean age was 56.4 years, with a male-to-female ratio of approximately 1.3:1. Across groups, increasing albuminuria was associated with higher serum creatinine, lower eGFR, and longer diabetes duration.

Table 1 demonstrates that patients with macroalbuminuria had significantly longer diabetes duration (P = 0.012) and higher blood pressure (P < 0.05) compared to normoalbuminuric patients, while age and BMI were comparable across groups. Progressive renal dysfunction was evident with rising serum creatinine and declining eGFR as albuminuria advanced (all P < 0.001).

Table 1.

Baseline clinical and renal function parameters

Parameter	Group A (n=30)	Group B (n=30)	Group C (n=30)	P
Demographics
Mean age (years)	55.2±7.8	56.7±8.1	57.3±7.3	0.324
Male/female	17/13	18/12	20/10	0.601
Diabetes duration (years)	6.4±2.1	8.2±2.8	10.1±3.2	0.012
BMI (kg/m2)	25.3±3.4	26.1±3.7	26.8±4.1	0.288
Systolic BP (mmHg)	128.6±12.3	136.4±14.2	144.2±15.6	0.015
Diastolic BP (mmHg)	79.2±8.4	83.1±9.2	86.5±10.1	0.021
Renal function
Serum creatinine (mg/dL)	0.78±0.18	1.02±0.31	1.48±0.52	<0.001
eGFR (mL/min/1.73 m2)	91.6±12.6	72.4±14.8	51.8±16.2	<0.001
UACR (mg/g)	18.3±7.2	122.6±62.4	624.4±412.8	<0.001

BMI=Body mass index, BP=Blood pressure, eGFR=Estimated glomerular filtration rate, UACR=Urinary albumin-creatinine ratio

Table 2 shows progressive and highly significant increases in all imaging parameters across albuminuria stages. Both Doppler indices (RI and PI) and cortical stiffness demonstrated stepwise elevation from normoalbuminuria through microalbuminuria to macroalbuminuria (all P < 0.001). Post-hoc analysis confirmed significant differences between all pairwise group comparisons. Bilateral symmetry was confirmed with no significant differences between right and left kidney measurements for any parameter. Gender-based subgroup analysis revealed no significant differences in imaging values between male and female participants.

Table 2.

Imaging parameters across albuminuria groups

Parameter	Group A (n=30)	Group B (n=30)	Group C (n=30)	P
Doppler indices
RI	0.59±0.03	0.66±0.04a	0.74±0.05a,b	<0.001
PI	0.92±0.12	1.16±0.15a	1.38±0.18a,b	<0.001
SWE
Cortical stiffness (kPa)	12.4±1.1	16.7±1.8a	22.9±2.3a,b	<0.001

^aSignificantly different from Group A (P<0.001), ^bSignificantly different from Group B (P<0.001). No significant differences were observed between right and left kidneys for any imaging parameter (P>0.05 for all comparisons). Similarly, no significant gender-based differences were detected in RI (male 0.67±0.06 vs. female 0.68±0.07, P=0.744) or cortical stiffness (male 17.4±2.8 kPa vs. female 17.7±3.1 kPa, P=0.693). kPa=Kilopascal, RI=Resistive index, PI=Pulsatility index, SWE=Shearwave elastography

Table 3 demonstrates strong and statistically significant correlations between all imaging parameters and established renal function markers. RI and SWE showed particularly robust inverse correlations with eGFR (r = −0.72 and r = −0.71 respectively, both P < 0.001) and positive correlations with serum creatinine and UACR (all r > 0.60, P < 0.001). Duration of diabetes correlated significantly with both RI (r = +0.58) and SWE (r = +0.62), suggesting cumulative renal vascular and parenchymal injury over time.

Table 3.

Correlation between imaging parameters and renal function markers

Correlation	Coefficient (r)	P
RI
RI versus serum creatinine	+0.66	<0.001
RI versus eGFR	−0.72	<0.001
RI versus UACR	+0.69	<0.001
RI versus diabetes duration	+0.58	<0.001
PI
PI versus serum creatinine	+0.61	<0.001
PI versus eGFR	−0.68	<0.001
PI versus UACR	+0.64	<0.001
SWE
SWE versus serum creatinine	+0.64	<0.001
SWE versus eGFR	−0.71	<0.001
SWE versus UACR	+0.69	<0.001
SWE versus diabetes duration	+0.62	<0.001

eGFR=Estimated glomerular filtration rate, UACR=Urinary albumin-creatinine ratio, SWE=Shearwave elastography, RI=Resistive index, PI=Pulsatility index

Table 4 presents diagnostic performance metrics for individual and combined imaging approaches. For detecting macroalbuminuria, SWE demonstrated superior sensitivity (90.1%) compared to RI (86.7%), though both showed good diagnostic accuracy (85.7% vs. 82.5%). For predicting reduced eGFR (<60 mL/min/1.73 m²), the combined use of RI and SWE achieved the highest diagnostic performance with sensitivity of 91.1%, specificity of 83.2%, overall accuracy of 87.1%, and AUC of 0.93—superior to either modality used alone.

Table 4.

Diagnostic performance of imaging modalities

Imaging modality	Outcome	Sensitivity (%)	Specificity (%)	Accuracy (%)	AUC
For macroalbuminuria detection (mg/g)
RI	UACR >300	86.7	78.3	82.5	0.89
SWE	UACR >300	90.1	81.4	85.7	0.91
For reduced eGFR prediction
RI alone	eGFR <60	79.3	76.0	77.6	0.85
SWE alone	eGFR <60	84.6	78.4	81.3	0.88
RI + SWE combined	eGFR <60	91.1	83.2	87.1	0.93

AUC=Area under the curve, eGFR=Estimated glomerular filtration rate (mL/min/1.73 m²), UACR=Urinary albumin-creatinine ratio, SWE=Shearwave elastography, RI=Resistive index

DISCUSSION

Diabetic nephropathy is a progressive microvascular complication of diabetes mellitus and remains a leading cause of CKD and end-stage renal failure globally. Despite widespread use of biochemical markers such as serum creatinine, eGFR, and albuminuria for disease detection and monitoring, these parameters often fail to detect early-stage renal damage. In recent years, imaging modalities like renal Doppler and SWE have gained increasing attention for their non-invasive, functional, and reproducible assessment of renal vascular and parenchymal changes in diabetic kidney disease.[8,9] It was observed that patients with higher levels of albuminuria exhibited significantly longer diabetes duration and higher blood pressure, both known contributors to the progression of renal injury. Renal function markers, including serum creatinine and eGFR, showed clear trends, with deterioration becoming evident as albuminuria advanced from normo-to macroalbuminuria. These trends provided clinical validation of the underlying progressive renal impairment.[10,11]

The use of Doppler ultrasonography revealed consistent increases in intrarenal resistive and pulsatility indices as renal involvement progressed. These indices reflect altered microvascular compliance, glomerular capillary hypertension, and reduced perfusion—all pathophysiological hallmarks of diabetic nephropathy.[12] Importantly, these Doppler changes were noted even before severe declines in eGFR occurred, indicating their potential value in early detection of subclinical disease. The bilateral symmetry of Doppler findings reinforced the diffuse nature of diabetic renal involvement and further supports the utility of averaging values from both kidneys for diagnostic accuracy.[13]

SWE, which quantifies renal cortical stiffness, demonstrated even stronger differentiation across stages of nephropathy. Increased cortical stiffness correlates with histological features such as interstitial fibrosis, tubular atrophy, and extracellular matrix expansion.[14] These structural alterations are often irreversible and have traditionally required invasive biopsy for detection. The ability of SWE to non-invasively reflect these changes represents a major advancement in diabetic renal imaging. The modality also showed excellent reproducibility between kidneys and consistency across genders, suggesting broad applicability across patient subgroups.[15]

Correlative analysis revealed that both Doppler and elastography parameters were significantly associated with established biochemical indicators of renal dysfunction. RI and cortical stiffness increased in tandem with serum creatinine and albuminuria, while exhibiting strong inverse relationships with eGFR. These associations reinforce the pathophysiological relevance of the imaging findings and underscore their diagnostic validity.[16]

Interestingly, duration of diabetes showed a significant positive correlation with both Doppler and SWE values, suggesting that these imaging markers not only reflect current renal status but also accumulate longitudinal impact.[17] This further supports their role in long-term monitoring and risk stratification of diabetic patients. Additionally, when evaluated for diagnostic performance, SWE outperformed Doppler in detecting advanced nephropathy, although combining both modalities yielded the highest predictive accuracy. This highlights the synergistic potential of integrating vascular and parenchymal imaging in clinical protocols.[18,19]

The ability of these imaging techniques to detect subclinical nephropathy is particularly important, as early intervention can delay or even reverse disease progression. Moreover, these tools are noninvasive, widely available, cost-effective, and free of nephrotoxic contrast agents – making them ideal for routine use in diabetic care settings. Their integration into existing diabetic nephropathy screening algorithms could complement biochemical testing and significantly improve early detection, staging, and monitoring of renal damage.

Limitations of the study

Despite its strengths, this study has several limitations. It was conducted at a single tertiary care center, and while the sample size was adequate, larger multi-centric studies are needed for external validation. The use of 2D point SWE, although reliable, may not fully capture heterogeneous fibrosis distribution across renal cortices. In addition, histopathological confirmation through renal biopsy was not performed, which limits direct correlation between imaging biomarkers and microscopic structural damage. Finally, the cross-sectional nature of the study restricts conclusions about temporal progression; longitudinal follow-up is needed to determine the prognostic value of these parameters over time.

CONCLUSION

This study highlights the clinical value of renal Doppler ultrasonography and SWE as effective noninvasive tools for assessing diabetic nephropathy. Both modalities demonstrated strong correlation with established biochemical markers and provided early insight into vascular and parenchymal alterations even before advanced renal impairment occurred. The integration of Doppler and elastography into routine diabetic screening protocols may enhance early diagnosis, improve disease staging, and support timely therapeutic interventions aimed at slowing renal decline. A comprehensive summary of the study methodology and its key clinical impacts is provided in Table 5.

Table 5.

Summary of study methodology and key clinical findings

Parameter	Details
Study design	Prospective cross-sectional study; 90 patients with type 2 diabetes evaluated over 12 months
Patient Groups	Group A: Normoalbuminuria (n = 30)
	Group B: Microalbuminuria (n = 30)
	Group C: Macroalbuminuria (n = 30).
Methods Used	Renal Doppler: Measured Resistive Index (RI) and Pulsatility Index (PI).
	SWE: Measured renal cortical stiffness (kPa).
	Correlated with: Serum creatinine, eGFR, and UACR
Key Results (RI)	Normo: 0.59 vs. Micro: 0.66 vs. Macro: 0.74 (P < 0.001)
Key Results (PI)	Normo: 0.92 vs. Micro: 1.16 vs. Macro: 1.38 (P < 0.001)
Key Results (Stiffness)	Normo: 12.4 kPa vs. Micro: 16.7 kPa vs. Macro: 22.9 kPa (P < 0.001)
Correlations	RI vs eGFR: r = -0.72 (P < 0.001)
	SWE vs eGFR: r = -0.71 (P < 0.001)
Diagnostic Accuracy	Combined RI + SWE for eGFR < 60: Sensitivity 91.1%, Specificity 83.2%, AUC 0.93
Clinical Impact	Enables earlier intervention and better monitoring in diabetic patients

Conflicts of interest

There are no conflicts of interest.

Funding Statement

No external funding. Work carried out with departmental resources.