Diabetic kidney disease: Radiological assessment and clinical correlations

Table 1 Histological classes of diabetic kidney disease

Histologic class	Glomerular	Tubulointerstitial	Vascular
Class I	Isolated thickening of the GBM. Minimal or absent mesangial alterations[18]	Normal or tubular hypertrophy (secondary to hyperfiltration)	Normal or mild arteriolar hyalinosis (more common in the efferent arteriole)[17]
Class II	Diffuse mesangial matrix expansion, mild (IIa) or severe (IIb). Absence of nodular lesions (Kimmelstiel-Wilson) and global glomerulosclerosis < 50%[18]	Focal tubular atrophy and interstitial fibrosis (correlated with the severity of mesangial expansion). Glycogen accumulation in tubular epithelial cells (Armanni-Ebstein lesions)[19]	More evident arteriolar hyalinosis, often involving both afferent and efferent arterioles[17]
Class III	Presence of at least one Kimmelstiel-Wilson nodular lesion. Nodules are acellular and PAS-positive. Global glomerulosclerosis < 50%[19]	Moderate-to-severe IFTA. Infiltration of inflammatory cells[19]	Marked arteriolar hyalinosis. Atherosclerosis of interlobular arteries (characteristic of DKD, but not specific)[17,20]
Class IV	Diffuse global glomerulosclerosis > 50%. The most advanced form of diabetic glomerulosclerosis, with widespread involvement of all remaining glomeruli[18]	Severe and diffuse IFTA (a key predictor of progression to end-stage renal disease[19]	Extensive vascular sclerosis and vascular wall hypertrophy[20]

This table summarizes the histopathological classification of diabetic kidney disease, highlighting the progressive glomerular, tubulointerstitial, and vascular alterations that characterize each class. Class I is defined by isolated glomerular basement membrane thickening with minimal mesangial involvement and usually mild or absent vascular changes. Class II is marked by diffuse mesangial expansion, mild (IIa) or severe (IIb), accompanied by early tubulointerstitial injury and more evident arteriolar hyalinosis. Class III is characterized by the appearance of Kimmelstiel-Wilson nodules and moderate-to-severe interstitial fibrosis and tubular atrophy, together with marked arteriolar involvement. Class IV represents the most advanced stage, defined by diffuse global glomerulosclerosis affecting more than half of the glomeruli, extensive interstitial fibrosis and tubular atrophy, and widespread vascular sclerosis. GBM: Glomerular basement membrane; IFTA: Interstitial fibrosis and tubular atrophy; DKD: Diabetic kidney disease; PAS: Periodic acid-Schiff.

Table 2 Practical imaging approach in diabetic kidney disease

Clinical scenario	First-line imaging (clinical practice)	Key parameters to assess	Clinical decision impact	Advanced techniques (research/selected cases)	When to consider advanced imaging
Initial DKD assessment (new diagnosis of diabetes + albuminuria or declining eGFR)	B-mode US + color doppler	Kidney length (9-12 cm normal); cortical thickness (> 7 mm normal); echogenicity (grade 0-III); RI (< 0.70 normal); CMD preservation	Exclude alternative diagnoses (obstruction, masses, cysts); establish baseline renal size; identify vascular abnormalities	DWI-MRI, BOLD-MRI	Atypical presentation, rapid progression, young patient, consideration for clinical trial enrollment
Routine monitoring (stable DKD, predictable progression)	B-mode US (annually or when clinically indicated)	Progressive cortical thinning; increasing echogenicity; loss of CMD; changes in kidney size	Confirm expected progression; detect unexpected changes requiring further investigation	None typically indicated	N/A
Rapid/unexplained eGFR decline (> 5 mL/minute/1.73 m2/year or > 25% drop)	US + doppler. If inconclusive: Non-contrast CT	Hydronephrosis; renal artery stenosis (RI asymmetry > 0.05); stones, masses; perinephric abnormalities	Identify treatable causes: Obstruction, RAS, AKI superimposed on CKD	CT angiography (if RAS suspected and intervention considered), MRI with DWI (if AIN suspected)	High clinical suspicion for renovascular disease or acute interstitial nephritis; surgical/interventional planning needed
Discordant clinical findings (albuminuria without retinopathy, hematuria, rapid onset, age < 40 years)	US; consider nephrology referral + kidney biopsy	Assess for non-diabetic kidney disease: Asymmetric kidneys; cortical scarring; masses	Imaging alone insufficient; biopsy often required for definitive diagnosis	Multiparametric MRI (if biopsy contraindicated or to assess fibrosis burden pre-biopsy)	Biopsy contraindicated (bleeding risk, anticoagulation), need to quantify fibrosis non-invasively
Pre-dialysis planning (stage 4-5 CKD, eGFR < 30 mL/minute/1.73 m2)	US (bilateral kidney assessment + vascular mapping for access)	Kidney size (often < 9 cm); severe echogenicity; vascular anatomy (cephalic/basilic veins); arterial inflow	Dialysis modality selection, vascular access planning (AVF vs AVG)	Venography or US elastography (vessel compliance assessment)	Complex vascular anatomy, previous failed access, central venous stenosis suspected
Post-transplant DKD surveillance (transplant recipients with recurrent DKD)	US + doppler of allograft	Allograft size; cortical thickness; RI; exclude hydronephrosis/collections	Monitor allograft function, exclude rejection vs recurrent DKD	Protocol allograft biopsy (gold standard); DWI-MRI or elastography (if biopsy contraindicated)	Rising creatinine, new proteinuria, need to distinguish rejection from recurrent disease
Research/clinical trial setting (characterizing early DKD, treatment response monitoring)	Multiparametric MRI (DWI, BOLD, T1 mapping, ASL) or CEUS	ADC values; cortical/medullary R2; T1 relaxation times; perfusion parameters; tissue stiffness	Quantify subclinical damage, monitor response to novel therapies (SGLT2i, GLP-1 RA, endothelin antagonists)	Photon-counting CT, MR elastography, AI-based texture analysis	Specialized research centers, clinical trials, biomarker development studies
Complications (suspected papillary necrosis, emphysematous pyelonephritis, infected cyst)	Non-contrast CT (first-line for complications)	Gas in renal parenchyma; filling defects; perinephric stranding; abscess formation	Urgent intervention (drainage, antibiotics, possible nephrectomy)	Contrast-enhanced CT (only if eGFR > 30 and potential surgical benefit outweighs risk)	Severe infection requiring source control, surgical planning

This table provides practical, expert opinion-based recommendations for imaging selection in diabetic kidney disease (DKD) across common clinical scenarios. First-line imaging reflects widely available techniques appropriate for routine clinical practice in most centers. Advanced techniques are generally reserved for research applications, clinical trial enrollment, or highly selected cases where conventional imaging is inadequate or contraindicated. Clinical decision impact describes how imaging findings influence patient management. The framework emphasizes the central role of ultrasonography as the primary imaging modality for DKD, with judicious use of advanced techniques when clinical circumstances warrant additional investigation beyond standard care. Recommendations are based on expert consensus, acknowledging that local availability, expertise, and healthcare system resources will influence individual practice patterns. DKD: Diabetic kidney disease; eGFR: Estimated glomerular filtration rate; US: Ultrasonography; CMD: Corticomedullary differentiation; BOLD: Blood oxygen level-dependent; MRI: Magnetic resonance imaging; DWI: Diffusion-weighted imaging; N/A: Not applicable; RAS: Renal artery stenosis; CT: Computed tomography; RI: Resistive index; AKI: Acute kidney injury; CKD: Chronic kidney disease; AIN: Acute interstitial nephritis; AVF: Arteriovenous fistula; AVG: Arteriovenous graft; ASL: Arterial spin labeling; CEUS: Contrast-enhanced ultrasound; ADC: Apparent diffusion coefficient; GLP-1 RA: Glucagon-like peptide-1 receptor agonist; SGLT2i: Sodium-glucose cotransporter-2 inhibitor; AI: Artificial intelligence.