High blood sugar is one of the main characteristics of diabetes, and long-term high blood sugar can lead to gradual loss of kidney function, which may eventually develop into diabetes kidney disease (DN). The following is a detailed process of how high blood sugar can damage the kidneys step by step: High blood sugar can lead to an increase in the filtration rate of kidney balls, resulting in greater pressure on kidney balls, thereby undermining their structure and functioning. This damage is reflected in the thickening of the nephrocyte base membrane, the expansion of the membrane cell and the increase in the interplasm fibre, which eventually leads to the stratification of the renal ball.
2. Kidney tube damage: In addition to the kidney ball, high blood sugar can cause damage to the kidney tube. Renal tube pesetas are prone to collapse in a high blood sugar environment, leading to reduced renal tube weight absorption. In addition, high blood sugar can cause interflammation of kidneys and further damage to kidney function.
3. Oxidizing stress and inflammation responses: High blood sugar activates oxidizing stress and produces active oxygen (ROS), which causes damage to cell DNA, lipids and proteins and exacerbates cell damage. At the same time, the inflammation response will be activated by releasing a variety of cytogens, such as white cell vector-6 (IL-6) and tumour necrosis alpha (TNF-α), which further promote inflammation and fibrosis.
4. Angiological disorders: High blood sugar can also lead to renal vascular disorders, including small artery constriction and major artery expansion, which affects blood flow and kidney dynamics. This vascular functional impairment not only increases the pressure on the small renal ball, but may also cause high renal blood pressure, further exacerbating the kidney damage.
Metabolism change: High blood sugar can also cause a range of metabolic changes, such as an increase in vascular stressor II (Ang II), an increase in insulin sample growth factor-1 (IGF-1) and the accumulation of end-products of glucose cellide (AGEs). These metabolites not only directly damage kidney cells, but also exacerbate pathology by activation of different signal circuits.
6. Overaccumulation of extracellular matrices (ECM): In a high blood sugar environment, overaccumulation of ECM proteins leads to internal fibrosis of kidneys, which is one of the key pathological characteristics of diabetes mellitus. The extraordinary accumulation of ECM not only affects the kidney structure but also hinders normal cell function.
7. End-of-life kidney disease (ESRD): As the pathology process continues, it may eventually lead to end-of-life kidney disease (ESRD), when the patient may need dialysis or kidney transplant treatment. Untreated or controlled diabetes can cause kidney failure and increase cardiovascular and death risks.
Strict control of blood sugar levels is therefore essential to prevent and slow down the development of diabetes kidneys. The damage to the kidneys of high blood sugar can be effectively reduced through a reasonable diet, regular exercise, medication and regular examinations.
