Diabetic Nephropathy

Diabetic nephropathy is chronic kidney injury caused by sustained diabetes-related stress on the glomeruli. Persistent hyperglycaemia initially drives glomerular hyperfiltration: blood moves through the filtration units under abnormally high pressure. Advanced glycation end-products, oxidative stress and inflammation then damage the filtration barrier and surrounding renal tissue. Albumin normally remains in the bloodstream. As the barrier becomes more permeable, albumin begins to appear in the urine. This albumin leak can develop before the estimated glomerular filtration rate (eGFR) falls, so a normal serum creatinine does not exclude early kidney disease. With progressive nephron injury, eGFR declines and the kidneys become less able to regulate sodium, water, potassium and acid-base balance. Hypertension accelerates this process by adding pressure to already injured glomeruli. The resulting kidney disease can further worsen blood pressure through sodium retention and activation of the renin-angiotensin-aldosterone system (RAAS). That feedback explains why blood pressure, urinary albumin and eGFR must be followed together rather than treating any single result as the whole picture.