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Life sciences · Journal article
Frontiers in Medicine · October 22, 2026
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Kidney outcomes vary substantially among people with similar body mass index (BMI), and conventional measures of obesity do not specify the adipose compartments that lie closest to the kidney or the biological state of those tissues. Human imaging, physiological studies, and paired-tissue analyses now permit a more anatomically explicit account of kidney adiposity. Perirenal adipose tissue (PRAT), renal sinus adipose tissue (RSAT), and intrarenal lipid are distinct constructs and should not be collapsed into a single ‘fatty kidney’ construct. This critical narrative review examines kidney adiposity at the obesity–CKD interface using a claim-conditioned translational evidence continuum spanning association, partial independence from systemic adiposity, prospective association, human mechanistic support, treatment-associated depot remodeling, depot–renal response linkage, causal mediation, and treatment-effect modification. Selected kidney-associated fat measures are associated with albuminuria, filtration, intrarenal haemodynamics, and CKD status, and some signals persist after adjustment for BMI or visceral adipose tissue. In paired tissue from healthy kidney donors, PRAT and RSAT show distinct metabolic and immune profiles. However, much of the human evidence derives from cohorts enriched for type 2 diabetes, which limits extrapolation to non-diabetic obesity-associated CKD. Acquisition, segmentation, normalisation, external validation, and clinically useful thresholds also remain unsettled. Intervention studies show that selected kidney-associated fat measures can change with lifestyle or sodium-glucose cotransporter-2 inhibition, whereas major kidney-outcome trials often did not measure kidney-adiposity compartments. These parallel observations do not establish that depot remodeling mediates renal protection. Compartment-resolved assessment of kidney adiposity should therefore be regarded as a research strategy rather than a clinical classification. Its future value depends on incremental prognostic or decision information beyond eGFR, albuminuria, and validated CKD risk models, and on direct testing of whether depot modification contributes causally to kidney response.