Kidney damage in type 2 diabetes is highly heterogeneous and poorly captured by traditional markers such as albuminuria and eGFR. This Kidney International review discusses how deep endotyping — integrating clinical trajectory analysis, renal histopathology, and molecular profiling — can identify subgroups with distinct pathophysiology, enabling more targeted therapy selection.
Renal damage in type 2 diabetes (T2D) exemplifies a complex, multisystemic disorder with substantial heterogeneity in clinical trajectory, histopathology and molecular drivers. Traditional clinical markers, albuminuria and glomerular filtration rate, fail to capture this diversity since many patients follow atypical trajectories such as non-albuminuric progression, rapid eGFR decline or regression of albuminuria. Deep endotyping approaches integrating clinical dynamics, renal histopathology, and multi-omics profiling can define biologically distinct endotypes.
