Pathogenesis (disease development)
Diabetic nephropathy is a secondary disease of diabetes mellitus (diabetes). Due to inadequately controlled blood glucose metabolism, the clinical picture develops over many years (on average 15-30 years), and approximately 20-30% of all patients with diabetes develop it during their lifetime.
The exact pathophysiology of diabetic nephropathy is not yet fully understood. However, it is thought that hyperglycemic metabolic state and a combination of hemodynamic changes in renal blood flow (glomerular hypertension/high blood pressure), structural changes in the glomeruli (renal corpuscles) due to hyperglycemia, and various interactions between hormones such as angiotensin II and endothelin may ultimately lead to preterminal renal failure. Diabetic nephropathy initially manifests as thickening of the glomerular basement membrane. After prolonged damage, glomerulosclerosis (glomerular sclerosis; scarring of the glomeruli (renal corpuscles) as the final stage of the disease associated with renal tissue loss) then occurs.
Etiology (causes)
Biographic causes
- Genetic burden from parents, grandparents.
Behavioral causes
- Nutrition
- High protein diet
- Consumption of stimulants
- Tobacco (smoking)
Causes related to disease
- Dyslipidemia (lipid metabolism disorders).
- Hypertension (high blood pressure)
- Long-standing diabetes mellitus (diabetes).
Laboratory diagnoses – laboratory parameters that are considered independent risk factors.
- HbA1c (elevated)
- Microalbuminuria (excretion of small amounts of albumin (20 to 200 mg/l or 30 to 300 mg per day) in urine) – risk factors for the onset of albuminuria were male sex and elevated uric acid levels (hyperuricemia) in patients with type 2 diabetes mellitus
