These causative factors lead to abnormalities within various sections of the kidney, including glomeruli, tubules, interstitium, and vasculature.
Prolonged diabetes mellitus duration, inadequate blood sugar level control, and unaddressed hypertension are influential risk factors for the development of diabetic nephropathy. In a similar vein, a familial history of hypertension and cardiovascular incidents among immediate relatives also significantly heightens the risk of diabetic nephropathy. Contributing to this picture, factors like obesity, smoking, and hyperlipidemia enhance susceptibility to diabetic nephropathy. The cumulative presence of these risk factors, coupled with familial tendencies, suggests the potential implication of genetic factors.
During its initial stages, diabetic nephropathy doesn't present overt symptoms. The earliest sign emerges from persistent microalbuminuria. Over time, most untreated patients eventually experience hypertension and varying degrees of fluid retention.
In more advanced stages, patients might show uremia symptoms (e.g., nausea, vomiting, reduced appetite) earlier (i.e., at a higher glomerular filtration rate [GFR]) than those unaffected by diabetic nephropathy. This phenomenon could arise from the combined impact of diabetes-induced organ damage (e.g., neuropathy) and renal dysfunction, exacerbating the symptoms.
The progression of diabetic nephropathy encompasses multiple clinical phases: hyperfiltration, microalbuminuria, macroalbuminuria, nephrotic proteinuria, progressive chronic kidney disease, ultimately culminating in end-stage renal disease (ESRD).
Damage occurs across all parts of the kidney: the glomerulus, renal tubules, vasculature (including afferent and efferent renal arterioles), and the interstitium.
Diabetic Nephropathy Pathogenesis
