Diabetes is a worldwide epidemic that has led to widespread macro and microvascular complications associated with it including chronic kidney disease. Diabetic nephropathy is a major kidney-related complication resulting from diabetes characterized by the presence of pathological quantities of urine albumin excretion, diabetic glomerular lesions, and loss of glomerular filtration rate leading to kidney failure with potentially life-threatening consequences. It slowly damages the kidney’s delicate filtering system which is responsible for removing waste products and extra fluid from the body through urine. Worldwide, it is also called diabetic kidney disease which is end-stage renal failure. In kidneys, nephrons filter waste products and excess water from the bloodstream and further excrete them in the urine. The glomerulus, a group of blood vessels in the nephron’s filtering function is affected due to high blood sugar resulting in kidney failure and high blood pressure. About 25% of people with type 1 and type 2 diabetes eventually develop kidney disease associated with increased cardiovascular mortality and risk increases with the duration of the disease. The main risk factors are hypertension, overweight, smoking, glycaemic control, high blood pressure, and dyslipidemia. Early stages of diabetic nephropathy often show any symptoms but as the condition worsens, sign and symptoms include-
- Swelling of the hands, feet, and face
- Trouble sleeping or concentrating
- Poor appetite
- Itching (end-stage kidney disease)
- Drowsiness (end-stage kidney disease)
- Abnormalities in the hearts’ regular rhythm
- Muscle twitching
Diabetic nephropathy can be classified into different stages based on the values of urinary albumin excretion i.e. microalbuminuria and macroalbuminuria. This condition can be primarily screened and diagnosed by the amount of albumin in the urine test. The main complication of diabetic kidney disease is pulmonary edema, hyperkalemia, anemia, and dialysis or a kidney transplant for survival. Cellular signaling pathways including diacylglycerol (DAG)-protein kinase C (PKC) pathway, advanced glycation end-products (AGE), polyol pathway, hexosamine pathway, and oxidative stress are activated by excess intracellular glucose leading to the development of glomerulosclerosis. Pathology and pathophysiology of this chronic disease involve the significant role of DNA methylation, non-coding RNAs, and histone modifications. Novel urinary biomarkers such as α-1 microglobulin, β-1 microglobulin, nephrin, neutrophil gelatinase-associated lipocalin (NGAL), beta-trace protein (beta TP), microRNA-130b (miR-130b), and cystatin C are identified in the patients who are at risk of developing kidney damage. The most suitable way to treat diabetic nephropathy is by preventing microalbuminuria from progressing to macroalbuminuria, blocking angiotensin receptors, maintaining a healthy lifestyle, blocking the renin-angiotensin-aldosterone (RAAS) system, treating your diabetes, and lipid-modifying statin therapy. Diet is a key factor for diabetic nephropathy patients including a proper amount of fat to prevent malnutrition. A protein-deficient diet and limited saturated fatty acid consumption are advised by the nutritionists.
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