Diabetic nephropathy is a type of kidney damage that affects people with diabetes. Over time, high blood sugar levels can damage the kidneys’ filtering system, leading to a progressive decline in kidney function. This condition is a common cause of chronic kidney disease and can eventually lead to end-stage renal disease (ESRD), requiring dialysis or kidney transplantation.
The pathophysiology of diabetic nephropathy involves hyperglycemia-induced damage to renal glomeruli, resulting in increased albumin excretion, glomerulosclerosis, and a decline in glomerular filtration rate (GFR). The damage is primarily due to prolonged exposure to high glucose levels, leading to oxidative stress, inflammation, and changes in the glomerular extracellular matrix.
Diabetic nephropathy often presents with microalbuminuria, which can progress to macroalbuminuria. As the disease progresses, patients may experience hypertension, edema, and an increased risk of cardiovascular events. Monitoring urine albumin levels is crucial for early detection and management.
Management of diabetic nephropathy focuses on controlling blood glucose levels, managing blood pressure, and reducing proteinuria. Angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) are commonly used to protect kidney function. Lifestyle modifications, including a low-protein diet and smoking cessation, are also recommended.
Diabetes mellitus leads to diabetic nephropathy by causing chronic hyperglycemia, which damages the small blood vessels in the kidneys. This damage reduces the kidneys' ability to filter waste from the blood and can eventually lead to kidney failure.
Diabetic nephropathy is a major contributor to the development of chronic kidney disease (CKD). As kidney function deteriorates due to nephropathy, patients become at risk for CKD progression to end-stage renal disease (ESRD), requiring more intensive management such as dialysis.