Why do glomeruli harden? ——Analysis of pathological mechanisms and prevention and treatment strategies
Glomerulosclerosis is one of the core pathological characteristics of chronic kidney disease (CKD). In recent years, its incidence has increased significantly with changes in lifestyle and the aging of the population. This article combines the latest medical research and clinical data to analyze the causes, mechanisms and key points of prevention and treatment of glomerulosclerosis.
1. Definition and harm of glomerulosclerosis

Glomerulosclerosis is a pathological process in which glomerular capillary loops are gradually replaced by scar tissue, resulting in loss of filtration function. According to the "Global Kidney Disease Report 2023", approximately 40% of end-stage renal diseases are caused by glomerulosclerosis.
| glomerulosclerosis type | Proportion | Main causes |
|---|---|---|
| Focal segmental glomerulosclerosis (FSGS) | 35% | Genetic mutations, obesity, viral infections |
| diabetic nephrotic sclerosis | 45% | Long-term hyperglycemia and metabolic abnormalities |
| Hypertensive nephrosclerosis | 15% | uncontrolled high blood pressure |
2. Core pathogenesis
1.Hemodynamic abnormalities: High pressure within the glomerulus causes damage to endothelial cells and triggers collagen deposition.
2.Metabolic disorders: Hyperglycemia/hyperlipidemia environment promotes mesangial cell proliferation and ECM accumulation.
3.inflammatory response: TGF-β, IL-6 and other profibrotic factors continuously activate myofibroblasts.
| pathological stage | key features | time span |
|---|---|---|
| Early stage | Podocyte damage, proteinuria | 1-3 years |
| progress period | Mesangial matrix dilation, capillary occlusion | 3-5 years |
| terminal stage | Global sclerosis, loss of kidney function | 5-10 years |
3. Latest prevention and control progress (2023-2024)
1.Targeted drugs: SGLT2 inhibitors (such as empagliflozin) can reduce intraglomerular pressure by 30%.
2.gene therapy: RNA therapy targeting APOL1 high-risk genotypes has entered Phase III clinical trials.
3.early screening: Urinary exosome detection technology enables diagnosis to be advanced to the asymptomatic period.
| Interventions | efficient | Applicable stage |
|---|---|---|
| Blood pressure control (<130/80mmHg) | 68% | full cycle |
| RAAS inhibitors | 72% | Issue 1-2 |
| ketogenic diet intervention | 53% | Early days |
4. Patient management suggestions
1.Regular monitoring: Check urine microalbumin/creatinine ratio (UACR) every 3 months.
2.lifestyle: Daily sodium intake is limited to less than 2g, and BMI is controlled at 18.5-24.9.
3.risk aversion: Avoid NSAIDs drugs and unnecessary contrast agent examinations.
Conclusion:Glomerulosclerosis is the result of multiple mechanisms, and early intervention can delay the progression of the disease by more than 60%. In 2024, the New England Journal of Medicine pointed out that combining precision medicine and artificial intelligence prediction models, it is expected to reduce the conversion rate of end-stage renal disease by 40% in the next five years.
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