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The natural history of diabetic kidney disease includes glomerular hyperfiltration, progressive albuminuria, declining GFR, and ultimately, ESRD.
Metabolic changes associated with diabetes lead to glomerular hypertrophy, glomerulosclerosis, and tubulointerstitial inflammation and fibrosis.
Introduction It took more than three millennia from the first description of diabetes in 1552 BC to the recognition of an association between diabetes and kidney disease, but it took only several decades for diabetic kidney disease (DKD) to become the leading cause of ESRD in the United States (1,2).
This microvascular complication develops in approximately 30% of patients with type 1 diabetes mellitus (DM1) and approximately 40% of patients with type 2 diabetes mellitus (DM2) (2,3).
Kidney disease attributed to diabetes is a major but under-recognized contributor to the global burden of disease.
Between 19, the number of deaths attributed to DKD rose by 94% (10).
Segmental mesangiolysis is observed with progression of diabetes and thought to be associated with development of Kimmelstiel–Wilson nodules and microaneurysms, which often present together (29,30) (Figure 3).
Mesangial volume expansion is detectable within 5–7 years after DM1 diagnosis (14,25,27,28).
Achieving this goal will require characterization of new biomarkers, designing clinical trials that evaluate clinically pertinent end points, and development of therapeutic agents targeting kidney-specific disease mechanisms (, glomerular hyperfiltration, inflammation, and fibrosis).
Additionally, greater attention to dissemination and implementation of best practices is needed in both clinical and community settings.
The earliest consistent change is thickening of glomerular basement membrane, which is apparent within 1.5–2 years of DM1 diagnosis.
It is paralleled by capillary and tubular basement membrane thickening (14,25,26) (Figure 1).
Between the years 19, the overall prevalence of obesity in adults snowballed from 15% to 31% in the United States (8).