, the prevalence of chronic kidney disease (CKD) is 11% The results of China's first large-sample epidemiological survey on chronic kidney disease show that chronic kidney disease in adult residents of Beijing presents a high prevalence and low awareness rate, in which the prevalence rate reaches 9.3%, while the patient's awareness rate of the disease is only 8.7%. Peking University Institute of Kidney Disease, Department of Nephrology of Peking University Hospital and Beijing CDC cooperated to adopt a multi-stage stratified random sampling method to monitor the indicators of kidney injury and related risk factors. After standardization according to the gender-age composition ratio of Beijing residents, the prevalence of albuminuria was found to be 5.6%, the prevalence of decreased renal function was found to be 1.7%, and the incidence of hematuria was found to be 3.5%. Accordingly, the prevalence of chronic kidney disease among adult residents of Beijing is 9.3%, which is similar to that of the United States and Northern Europe (6.5%-10%).
The awareness rate of chronic kidney disease is only 8.7%, which is only 1/5 of that in developed countries, and based on the current prevalence rate in Beijing, it is estimated that there are at least 120 million patients with chronic kidney disease in the country, and a conservative estimate is that 1% of them will develop kidney failure. According to the survey released by Kidney Disease Research Institute of Southeast University and Kidney Disease Research Institute of Cardiff University, 14.8% of the general hospitalized patients suffer from chronic kidney disease, of which 40% have no knowledge, and 29.5% of the non-kidney hospitalized patients over 65 years old suffer from chronic kidney disease. Domestic statistics on hospital outpatient clinics for patients with kidney disease and chronic renal insufficiency in the past five years show that 50% of patients who attended the clinic missed the best time for treatment. Global chronic kidney disease caused by end-stage renal failure is increasing at a rate of 8%.
DDFAO scanning technology does not use traditional imaging techniques to determine organic renal lesions. This is because although ultrasound can morphologically mark the degree of renal fibrosis, it is not able to obtain a diagnosis in the vast majority of fibrotic patients. A large number of renal units are damaged by the strong compensatory ability of the kidney and cannot be easily detected, which makes most patients with early renal fibrosis have no abnormal urinary proteins. Therefore, it is difficult to accurately detect the traces of early fibrosis in the clinic.DDFAO technology accurately obtains the biological activity status of renal tissues through electronic scanning. DDFAO provides a clear clinical guideline for the diagnosis of early renal fibrosis.
DDFAO system analyzes the activation state of RAAS system
Circulating RAAS only has short-term effects, and angiotensin II (AngII) produced by activation of circulating RAAS has the effects of vasoconstriction, aldosterone secretion, promotion of renal water and salt reabsorption, cardiac orthostatic changes, and cardiac arrhythmia, etc. Circulating RAAS accounts for about 10%~15% of the total RAAS in the body; tissue RAAS accounts for about 10%~15% of the total RAAS. Circulating RAAS only accounts for about 10%~15% of the total RAAS in the body; tissue RAAS activation produces AngII and so on can promote the proliferation of vascular wall hypertrophy, myocardial hypertrophy, fibrosis and intraglomerular hypertension; tissue RAAS accounts for as much as 85%~90% of the total RAAS.
Excessive activation of the renin-angiotensin-aldosterone system (RAAS) produced by renal tissue cells plays a key role in promoting renal fibrosis. Early diagnosis of renal fibrosis necessitates renal pathology, also known as renal biopsy, because renal biopsy is not indicated in patients with early asymptomatic fibrosis, and DDFAO improves the detection rate of renal fibrosis.
DDFAO electronic scanning addresses two key To Top
1, analysis of the causative factors of hypertension, especially for primary hypertension to distinguish the key factors;
2, analysis of the structural and functional status of the heart, brain, and kidneys of patients with hypertension; and the timely detection of damage to the target organs, as well as the timely treatment and control of its development.
Intra-glomerular high pressure due to systemic hypertension triggers glomerular inflammation, injury and sclerosis, and controlling high intra-glomerular pressure is an important measure to prevent progressive kidney damage.
The DDFAO system provides a set of biologically active parameters for all organs, tissues or glands involved in the RAAS system, providing information on target organ damage. It allows patients to benefit more from early intervention .
Imbalance between nutritional intake and consumption activates inflammatory processes
Cardiovascular disease is the leading cause of morbidity and mortality in diabetic patients, and atherosclerosis is the underlying basis of cardiovascular disease. The imbalance between nutrient intake and consumption causes an increase in glucose and free fatty acids entering the cell, resulting in acetyl coenzyme A overload, excessive superoxide production in the mitochondrial electron chain, and an increase in the reactive oxidation product ROS, which activates protein kinase-C and nuclear factor KB, activating the inflammatory process, which occurs in the endothelium of the vasculature, muscle, adipose, and pancreatic islet β-cells, respectively. cardiovascular lesions, insulin resistance and abnormal insulin secretion, respectively.
The DDFAO system predicts early cardiovascular risk
The pathogenesis of hypertension is not fully understood, and it is generally believed that, during renal ischemia, when there is a decrease in paraglomerular cells and/or blood pins in the glomerular paraglomerular apparatus, and an increase in potassium in the blood, dense plaque cells increase secretion of renin (a protein hydrolyzing enzyme), which enters the blood evidence loop and interacts with hepatic synthesis of angiotensinogen (angiotensin) (angiotensin) and other proteins in the bloodstream with the activating action of chloride-activating enzymes. Angiotensinogen (α-globulin) synthesized by the liver to form angiotensin I (10 peptides), angiotensin I through the pulmonary and renal circulation, under the action of converting enzyme, the formation of angiotensin II (8 peptides), the latter in turn, by the action of the enzyme stripped of aspartic acid is converted into angiotensin III (7 peptides). Angiotensin II! can cause a rise in blood pressure due to strong contraction of small peripheral arteries and intensification of the heart beat (angiotensin III has a weaker antihypertensive effect). They also act on the adrenocortical zona glomerulosa to induce an increase in aldosterone secretion, causing sodium retention and an increase in blood volume, which increases vascular sensitivity to vasoconstrictor responses such as those to theophyllamine and angiotensin II, but at the same time inhibits renin secretion. However, not all patients with hypertension have increased renin secretion. Examinations have shown that 54% to 64% of patients with hypertension have normal plasma renin activity, 2O% to 30% of patients have lower than normal, and about 16% of patients have higher than normal. In the pathogenesis of nephrogenic hypertension the renin-angiotensin-aldosterone system plays an important role, but apparently only explains part of the pathogenesis of hypertension. In addition the kidneys regulate blood pressure through the vasodilatory action of certain prostaglandins and pancreatic vasopressors.
At the same time, renal secretion of renin is increased. Renin converts angiotensinogen present in plasma to angiotensin I, which is converted to angiotensin II by angiotensin-converting enzyme. Angiotensin II has a strong vasoconstrictive effect, which can aggravate the spasm of small arteries throughout the body, causing hypertension, and can stimulate aldosterone secretion, causing sodium retention, further aggravating hypertension.
DDFAO Diagnosis of Early Insulin Resistance and Intervention of IGT To Top
Evaluating the link between activation of the RAAS system and insulin resistance in patients guides cardiovascular specialists to make a comprehensive diagnosis of patients with hypertension combined with diabetes mellitus, and allows them to assess the effectiveness of related treatments. Reduction of insulin resistance stage in some hypertensive patients. Risk due to beta-blockers. At present, the knowledge rate of diabetes in China is 33%, and the treatment rate is 27%; the knowledge rate of hypertension is 42%, and the treatment rate is 31%; the prevalence of adult diabetes is 5.5% . The HbA1c treatment compliance rate for diabetic patients is only 24%.
The secret of insulin resistance: fasting blood glucose mainly reacts to the status of basal islet secretion of β-cells and the degree of hepatic insulin resistance; post-loading blood glucose mainly reacts to the status of early-phase islet secretion function of β-cells and the degree of peripheral insulin resistance. Post-load glucose is a major predictor of death from cardiovascular disease. Cardiovascular disease complicates 25% of patients diagnosed with diabetes for the first time, and 50% of patients with diabetes for many years. Between 50 and 80% of patients with diabetes eventually die of cardiovascular disease. The American Cardiovascular Society recognizes that diabetes is a cardiovascular disease, and is the equivalent of coronary heart disease. The risk of cardiovascular disease in patients with diabetes is two to five times that of non-diabetic patients.
DDFAO clinical show through electronic scanning can be early detection of human body sugar metabolism disorders of compensatory stage, this IGT belongs to the reversible stage, 1/3 IGT patients can develop into type 2 diabetes mellitus, 1/3 can be maintained in the state of RGT, 1/3 can be transformed into normal glucose tolerance. Therefore, early intervention in IGT can reverse the progression of type 2 diabetes, and the most critical factor is to diagnose susceptible individuals early.
* Ion analysis of the interstitium includes: sodium; potassium; chloride; magnesium; calcium; phosphorus; and iron
* Blood gas analysis of the interstitium includes: PH value of the interstitial fluid; HCO3-value; PaCO2-value; PO2-value; H+-value; SBE-value; and iSO2-value. values; interstitial small molecule free radical values; interstitial hydrogen peroxide free radical values; interstitial superoxide anion free radical values; interstitial hydroxyl radical values;
* Major neurotransmitters: pentraxin values; dopamine values; catecholamine values; acetylcholine values;
* Hormonal analyses of interstitial: interstitial cortisol values; aldosterone values; adrenomedullary hormone secretion values; interstitial anti Hormonal analysis of interstitium: cortisol value of interstitium; aldosterone value; adrenomedullary hormone secretion value of interstitium; antidiuretic hormone value of interstitium; adrenocorticotropic hormone value of interstitium;
* Biochemical indexes of interstitium: triglyceride value of interstitium; glutamic oxaloacetic transaminase ALT/glutamic albuminous aminotransferase AST value of interstitium; alkaline phosphatase ALP and glutathione GGT value of interstitium; glucose value of interstitium; cholesterol value of interstitium
Clinical analysis of the eight major systems of the human body in DDFAO:
1. respiratory system; 2. Digestive system; 3. Immune system; 4. Urinary system; 5. Skeletal system; 6. Cardiovascular system; 7. Endocrine system; 8. Neurological system;
Only 2% of the 80% of patients using ACEIs have their target dose met
Chinese experts on ACEIs*** knowledge was published in March 2007
Currently, before the clinical application of ARBs, patients are usually not given kidney levels. Renal level tests are not usually done on patients. For hypertensive patients, the application of ARB is far superior to ACEI in the prevention of stroke, and ARB has a vasoprotective effect.
The DDFAO system helps cardiovascular specialists to accurately select antihypertensive drugs that inhibit the RAAS system
Target organ damage as an intermediate end point is valuable for predicting future cardiovascular risk in patients with hypertension, and there are differences in the effects of different drug treatments. Clinical practice should select drugs with sufficient evidence-based medical evidence to minimize target organ damage as early as possible, leading to a favorable clinical prognosis. Maximize patient benefit from RAAS system-blocking drugs and improve the rate of antihypertensive compliance. Reduce the risk to patients due to inappropriate choice of antihypertensive drugs.
Hypertension combined with different factors when the combination of drug guidance program:
* Combination of stable coronary heart disease: β-blockers combined with CCB;
* Combination of metabolic syndrome: ACEI or ARB combined with CCB;
* Combination of heart failure: ACEI or ARB combined with β-blockers or diuretics;
* Elderly patients: CCB combined with diuretics.
* Beta-blockers are mainly used in patients with fast heart rate; beta-blockers can also be used in patients with intolerance to ACEI and ARB drugs; pregnant women; patients with sympathetic activation with hypertension; hypertensive patients with symptomatic angina pectoris and myocardial infarction. However, there is a side effect of cough.
* CCB is mainly used for people with high blood pressure; it has good anti-atherosclerotic effect.
* ARB can reduce cardiovascular risk events, through the action of the large blood vessels, small blood vessels and inhibit thrombosis and other pathways to reduce the risk of stroke, is not suitable for pregnancy hypertension.
* ACEI, ARB and other drugs have better anti-insulin resistance, protective effect on the kidneys,
Can reduce or reverse left ventricular hypertrophy, improve myocardial function, reduce glomerular intracapsular pressure, reduce MAU, etc., is not suitable for gestational hypertension; there is a side effect of dry cough.
* Nitrates are important drugs in angina pectoris.
* Diuretics are not suitable for patients with abnormal glucose tolerance, blood uric acid, hyperkalemia, renal insufficiency, and increased cholesterol;
* Beta-blockers are not suitable for patients with heart failure, asthma, dyslipidemia, bradycardia, and pregnant women;
* α-1 receptor blockers (represented by the drug pyrazosin hydrochloride) are mainly used for the control of hypertension in pregnancy
Effective screening for early liver fibrosis To Top
Liver fibrosis (Fibrosis) is the excessive deposition of fibrous connective tissue in the liver, and is the result of an imbalance between fibroplasia (Fibrogenesis, i.e., increased synthesis of extracellular matrix) and fibrolysis (i.e., degradation of extracellular matrix). Fibrolysis is the body's repair response to injury, and once the harmful factors are removed and the extracellular matrix components are restored, fibrolysis stops. Therefore, acute or transient liver disease, even if severe, does not lead to liver fibrosis. However, repeated or persistent chronic inflammation and necrosis of the hepatic parenchyma due to a variety of etiological factors can lead to persistent fibroplasia of the liver and the formation of hepatic fibrosis, and the forward development of hepatic lobular structure destruction and nodule formation, which becomes cirrhosis.
Detection methods of liver fibrosis
* Serological diagnosis of liver fibrosis; the accuracy of this test is not high, and it is not sensitive to early fibrosis of the liver
* Histopathological examination; it is the "gold standard" for the diagnosis of liver fibrosis and cirrhosis, but there are limitations because the lesions of chronic hepatitis are diffuse, but it is very easy to detect. Although chronic hepatitis lesions are diffuse, it is difficult to ensure that a sampling can reflect the whole picture of the liver, especially liver fibrosis and cirrhosis, fine needle negative pressure hepatic puncture is difficult to obtain enough specimens to bring certain difficulties in diagnosis. For drug evaluation, a dynamic series of liver biopsy histopathology should be performed.
* Clinical and imaging diagnosis; insensitive to early hepatic fibrosis