There is a saying that a fat destroys everything. Obesity, which has been officially defined as a chronic disease, also increases the risk of multiple diseases, or makes the primary disease worse and more difficult to treat. Today we will introduce 1 kind of exclusive injury that fat people may suffer, obesity-related glomerular disease. Help you to recognize the disease and thus strengthen your confidence in losing weight.
Obesity-related glomerulopathy, org for short. As the rate of obesity continued to grow rapidly, scholars began to pay attention to the close relationship between obesity and chronic kidney disease, and eventually found that obesity was an independent risk factor for kidney disease, thus formally defining ORG. Features of renal histological changes in this disease include glomerular or tubular hypertrophy, focal segmental glomerulosclerosis, or spherical sclerosis. In addition, inflammation, hemodynamic changes, insulin resistance, lipid metabolism disorders, etc., will also affect the occurrence and development of ORG.
The latest issue of the Journal of Obesity Review published a review article systematically reviewing the relevant mechanisms of ORG and concluding that the formation of ORG is mainly related to 7 factors. 1st, glomerular hyperfiltration, due to obesity, resulting in arteriole dilation, increased blood flow into the kidneys, resulting in increased pressure in the glomeruli, glomerular enlargement, cell hypertrophy and apoptosis occurs. At the same time, it will promote the absorption of sodium ions, cause angiotensin levels to rise, and increase the glomerular filtration rate. Moreover, obese people are prone to high blood pressure and diabetes, and these two diseases are risk factors for chronic kidney disease and increase kidney damage.
The second mechanism of obesity-associated glomerular disease formation is hyperactivation of the angiotensin system, causing hemodynamic changes. The third mechanism, insulin resistance, promotes chronic inflammation, causes apoptosis or hypertrophy, and causes glomerular sclerosis. The fourth mechanism is the change of renal units. The fifth mechanism is that fat cells secrete inflammatory factors, which have a toxic effect on cells, promote the formation of atherosclerosis, and affect the structure and function of the kidneys. The sixth mechanism is genetic influence. The seventh mechanism is environmental factors.
Obesity-associated glomerular disease, proteinuria is usually detected, and if left untreated, progression of proteinuria is slow and stable. However, about 30% of ORG patients will have more than 3.5 grams of protein in their urine per day, and some patients will have a daily urine protein level of more than 20 grams. Such patients are at higher risk of progressing to end-stage renal disease, that is, uremia. Most patients with ORG will have both hypertension and dyslipidemia.
To assess renal function in patients with ORG, in addition to quantitative urine protein testing, glomerular filtration rates are also required. Studies have shown that structural changes in the kidneys may occur before renal insufficiency or proteinuria appears, so a renal biopsy is needed if necessary. Changes in biomarkers such as kidney damage molecules and neutrophil gelatin-associated apolipoproteins are also a novel method for diagnosing ORG. In order to keep abreast of kidney changes, obese people also need to do ultrasonic elastography and MRI tests. In addition, color Doppler ultrasonography can help to understand hemodynamic changes within the kidneys.
The first important measure to deal with obesity-related glomerular disease is weight loss. Weight loss can effectively reduce proteinuria and reduce glomerular filtration rate. After using conventional methods, it is still difficult to control weight, and bariatric surgery needs to be considered to promote renal stabilization. The second measure is to use angiotensin blockers to delay the occurrence of uremia, but the clinical research of such drug therapy is limited and the effect remains to be seen. New hypoglycemic drugs, such as sodium-glucose cotransporter inhibitors, can help reduce weight loss, reduce insulin resistance, have the effect of protecting kidney function, and can reduce inflammation and reduce kidney fibrosis. Related studies have shown that metformin can restore normal expression of cells, reduce the release of pro-inflammatory factors and lipid accumulation. Therefore, obese diabetics can choose to use it under the guidance of a doctor. It has also been found that melatonin has the function of regulating the biological clock, and can be anti-inflammatory, antioxidant, thereby playing a role in improving kidney function, therefore, it can also be used as a therapeutic drug for ORG.
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