Chronic renal failure, also known as chronic renal insufficiency, is a clinical syndrome caused by chronic progressive renal parenchymal damage from various causes, resulting in significant atrophy of the kidneys and inability to maintain their basic functions, with clinical manifestations of metabolite retention, imbalance of water, electrolytes and acid-base balance, and systemic involvement, also known as uremia.
Chronic renal failure is referred to as chronic renal failure, due to the destruction of renal units and the reduction of renal excretory regulation and endocrine metabolic function, resulting in a series of symptoms, signs and complications of water and electrolyte, acid-base balance disorders. The cause of pediatric chronic renal failure is closely related to the age of the child at the time of the first detection of renal failure.
Chronic renal failure under 5 years of age is often the result of anatomical abnormalities, such as renal hypoplasia, abnormal renal development, urinary tract obstruction, and other congenital malformations; chronic renal failure after 5 years of age is dominated by congenital glomerular diseases such as glomerulonephritis, hemolytic uremic syndrome, or hereditary lesions such as Alport syndrome and renal cystic lesions.
In various chronic kidney diseases, as the disease deteriorates, the progressive destruction of renal units to the extent that the remaining functional renal units are insufficient to adequately excrete metabolic wastes and maintain a constant internal environment, resulting in urinary dysfunction and disturbances in the internal environment, including retention of metabolic wastes and toxic substances, disorders of water, electrolytes and acid-base balance, and a series of clinical symptoms, is called CRF (chronic renal failure).
Chronic renal failure
Severe chronic renal failure, called uremia, is not an independent disease, but a combination of symptoms that occur when kidney damage is caused by various etiologies and progressively deteriorates to the end stage, when renal function is close to about 10% of normal.
As renal function damage is a longer development process, different stages, with their different degrees and characteristics, should generally be divided into several stages according to the level of renal function.
Renal function compensatory stage
When the damage of renal function units does not reach 1/2 of the total, it does not produce elevated blood urea nitrogen and creatinine, metabolic balance in the body, and no symptoms appear (with blood (Scr) creatinine at 133-177 μmol/L (2 mg/dl)).
Renal insufficiency stage
The kidney function level drops below 50%, the blood creatinine (Scr) level rises above 177μmol/L (2mg/dl), the blood urea nitrogen (BuN) level rises >7.0mmol/L (20mg/dl), and the patient has symptoms such as weakness, loss of appetite, nocturnal urination, and mild anemia.
Renal failure stage
When endogenous creatinine clearance (Ccr) drops below 25ml/min, BuN level is higher than 17.9–21.4mmol/L (50~60mg/dl), Scr rises above 442μmol/L (5mg/dl), the patient develops anemia, rising blood phosphorus level, falling blood calcium, metabolic acidosis, water and electrolyte disorders, etc.
End-stage uremia
Ccr is below 10ml/min, Scr rises above 707μmol/L, acidosis is obvious, symptoms of various systems appear, and even coma.
Symptoms of disease Pay attention to the presence of nausea, vomiting, diarrhea, burning pain in the lower limbs that must be moved frequently, skin itching, bone pain, convulsions and signs of bleeding. Physical examination: pay attention to the respiratory rate and depth, the smell of ammonia, the mental status, the degree of anemia, the presence of muscle twitching, water loss, edema, oral mucosal ulcers, pericardial friction sounds, the blood pressure and the presence of signs of heart failure.
Disease etiology Note the presence of acute and chronic nephritis, acute and chronic pyelonephritis, small renal arteriosclerosis, renal tuberculosis, urinary tract obstruction, systemic lupus erythematosus, diabetes mellitus, gout, multiple myeloma and polycystic kidney, and a history of long-term use of antipyretic analgesics and exposure to heavy metals.
Points to note.
1, should strive to clarify the etiology of chronic renal failure, or at least should clarify whether the renal damage is mainly glomerular damage, or interstitial tubular lesions, or renal vascular lesions prominent, so that according to the clinical characteristics, treatment has a focus.
2. The reversible factors that contribute to the progressive development of renal function in chronic renal failure should be identified, such as infection, metabolic acidosis, dehydration, heart failure, rapid and low blood pressure reduction, etc.
3. Attention should be paid to finding certain factors that exacerbate the progressive decline of renal function in chronic renal failure, such as hypertension, hyperlipidemia, hypercoagulable state, high protein dietary intake, large amount of proteinuria, etc.
Disease pathology Mechanism of progressive glomerular damage: According to clinical observation, patients with uremia have a regular disease progression, which is a process of progressive deterioration. According to the above staging, when the patient enters the stage of renal insufficiency and the blood creatinine reaches the level of 442umol/L (5mg/dl), the average time to develop into end-stage uremia is 10.8 months. The main mechanisms are the following theories.
1. Glomerular hyperfiltration theory
It is believed that the important reason for the progression of uremia is due to the overfiltration of glomeruli in the residual kidney units, which eventually leads to successive glomerular sclerosis. It is known that when the renal parenchyma is reduced, as in partial nephrectomy, the individual glomerular filtration rate in the remnant kidney unit increases and the resistance of the small glomerular input and output arteries decreases, thus increasing the individual glomerular blood flow rate. At the same time, the resistance of the small input arteries is reduced to a greater extent than that of the small output arteries, contributing to an increase in the hydrodynamic pressure gradient across the glomerulus capillaries. These constitute an increase in the glomerular filtration rate (GFR) of the residual kidney unit, and the degree of increase correlates with the degree of parenchymal reduction, with an average increase of 40 to 50% if one side of the nephrectomy is removed, while the increase in GFR of the residual kidney is twice as large as normal after 80% of the parenchyma is removed.
According to the experiment, SNGFR = K1*PnF K1 = ultrafiltration coefficient and PnF = mean net ultrafiltration pressure. As can be seen from the above equation, the magnitude of these two values determines the size of SNGFR. k1 does not change much in residual renal unit glomeruli even when there is a large reduction in renal units, and PnF plays a decisive role in increasing SNGFR. the size of PnF in turn depends on the following three factors.
(i) capillary hydrostatic pressure difference (ΔP);
②Plasma protein concentration (CA);
(3) glomerular plasma flow (QA). When the renal unit is lost, the residual renal unit “compensates” or “adapts” and both △P and QA increase with each other, resulting in an increase in SNF. This hyperfiltration, although a compensatory effect, in turn, causes glomerular damage in the residual renal unit. For example, in 85% of nephrectomized animals, residual glomerular hypertrophy, epithelial cell exfoliation, progressive enlargement of the thylakoid zone and loss of capillary lumen elasticity are seen at 3 months, eventually leading to focal, segmental glomerulosclerosis.
On the other hand, increased capillary pressure and blood flow encourage macrophages to move outside the capillaries and into the thylakoid zone, all of which contribute to glomerulosclerosis. These changes cause further reduction of renal units, resulting in increased filtration rate of residual glomeruli, new lesions and new sclerosis, forming a vicious circle and worsening of the disease.
2. The doctrine of correctional imbalance
In uremia, certain humoral factors that cause toxic effects gradually increase in body concentration, not entirely due to reduced renal clearance, but a balanced adaptation of the body; but in the process of adaptation, there is a new imbalance, and so on and so forth, causing progressive damage to the body. For example, in uremia, GFR decreases, urinary phosphorus excretion decreases, and hyperphosphatemia occurs, stimulating the parathyroid glands to secrete PTH, which acts on the renal tubules to increase urinary phosphorus excretion, lowering blood phosphorus and restoring it to normal levels.
However, due to the high loss of renal function, PTH continues to rise at the extracellular fluid level, which still makes it difficult to correct hyperphosphatemia, while causing an increase in serum calcium product and an increase in intracellular calcium, resulting in extensive deposition of calcium and phosphorus in multiple systems throughout the body, including the kidneys themselves. When GFR decreases further, hyperphosphatemia occurs again. This cycle results in increasing plasma PTH levels and further destruction of the renal unit.
In uremia, serum and urinary natriuretic hormone levels are elevated, suggesting that reduced renal clearance is not the cause of its elevation and that probably increased in vivo production is the main factor. In uremia, GFR decreases, sodium excretion tends to decrease, and the residual renal units become compensated for hypertrophy, and osmotic diuresis caused by urea accumulation is no longer able to regulate sodium balance. PTH natriuretic hormone itself is not a “toxic” substance, but under the above circumstances, its level in the body increases continuously, forming a new “toxin”. “toxin”.
The doctrine of hyperfiltration, which explains the main cause of progressive glomerular damage in uremia, provides the theoretical basis for the prevention and treatment of uremia. The doctrine of correction of imbalance, focusing on the formation of uremia, the body imbalance, the production of certain excessive substances, can form uremic symptoms, treatment of these imbalances, can reduce the occurrence of symptoms, such as partial removal of parathyroid glands, or trying to control secondary hyperparathyroidism, is important to alleviate the symptoms of uremia.
3.The “toxin” theory
It is known that there are more than 200 substances in the body of uremic patients with elevated concentrations, which may have toxic effects, about 20 kinds. These substances have the following characteristics.
①The substance can be published chemical identification and quantitative determination.
②Higher than normal concentration levels in the body.
③High concentrations are associated with specific uremic symptoms.
④Experimentally confirmed similar toxic effects when the concentration of the substance is similar to the concentration in the body fluid of uremic patients.
Mechanism of progressive deterioration of chronic renal failure The mechanism is not fully understood. The deterioration of renal function is undoubtedly related to the activity of the underlying disease. However, although the underlying disease has ceased to be active, e.g., GFR has fallen to about 25% of normal, renal function continues to decompensate incessantly until uremia develops, and its decompensation is through a common pathway.
Most scholars now believe that when a certain number of kidney units are destroyed, the metabolic waste excretion load of the remaining “surviving” kidney units increases to maintain the normal needs of the body. As a result, glomerular capillary hyperperfusion, hyperpressure and hyperfiltration (glomerular “triple high”) occur compensatorily. The glomerular “triple high” can cause.
(1) fusion of glomerular epithelial cell pedicles, significant proliferation of thylakoid cells and stroma, glomerular hypertrophy, and subsequent sclerosis;
(2) Glomerular endothelial cell damage, inducing platelet aggregation, leading to microthrombosis, damaging the glomerulus and promoting sclerosis;
(3) Increased glomerular permeability, resulting in increased proteinuria and damage to the tubular interstitium. The above process continues, forming a vicious circle, making the kidney function deteriorate further. This is the common pathway for all chronic kidney diseases to develop into uremia.
Angiotensin II (AII) plays an important role in the progressive deterioration of renal failure. In the glomerular “three highs”, the activity of renin and angiotensin axis increases, and AⅡ is a powerful vasoconstrictor. Whether it is the systemic circulation of AⅡ that causes hypertension, or the local AⅡ increase in the kidney, it can lead to the increase of glomerular capillary pressure, causing glomerular hypertrophy and then glomerulosclerosis. In addition, AⅡ also causes the following effects independent of blood pressure.
(i) It is involved in extracellular matrix (ECM) synthesis, and excessive accumulation of ECM leads to glomerulosclerosis;
②AII increases the expression of growth factors, inflammatory factors and fibrogenic factors such as transforming growth factor β1 (TGF-β1), platelet-derived growth factor (PDCF), interleukin-6 (IL-6), platelet-activating factor (PAF) and thromboxane A2 (TXA2), which is the determinant mediator that contributes to the development of glomerulosclerosis.
AII increases glomerular capillary blood pressure, which causes increased glomerular permeability and excessive protein filtration from the glomerulus, which is absorbed by proximal tubular cells through cytokinesis, and can cause tubular damage, interstitial inflammation and fibrosis, resulting in loss of renal unit function. Studies have shown that the uptake of albumin by proximal tubular cells in culture increases the expression of growth factors, inflammatory factors and fibrotic factors. Proteinuria is now considered to be an important factor in the progressive deterioration of renal failure.
In recent years, it is believed that the rate of deterioration of renal failure is genetically related, such as the angiotensin-converting enzyme gene has an important relationship with the rate of renal decompensation.
The disease is characterized by nausea and vomiting, dullness, foul-smelling urine in the mouth, excessive or scanty urination at night, edema, lumbago, weakness, fatigue, headache, irritability, epistaxis, lack of facial color, and nail fault in the skin, etc. The disease can be classified as “Guange”, “Drowning Poison” and “Void Labor” in Chinese medicine. The main clinical manifestations of the disease are “Guan Ge”, “Drowning Poison”, “Void Labor” and so on. The key to the pathogenesis is the lack of power of qi-transformation in the Sanjiao and the stagnation of dampness and toxicity; the disease is located in the kidneys and affects the five viscera and six internal organs. The disease is mostly critical and has a poor prognosis, manifesting itself as a disorder of yin and yang and mixed evidence of deficiency and reality.
Clinical manifestations In the early stage, the disease is often manifested only as symptoms of the underlying disease.
1. When the residual kidney unit cannot adjust to the requirements of the body, the symptoms of renal failure appear.
2, renal failure lesions are very complex, can involve all organs of the body, constituting uremia performance
3, dialysis can improve most of the symptoms of uremia, but some symptoms can persist or even worsen
Symptoms of each system.
1, gastrointestinal tract: is the earliest and most common symptoms
Performance: a. Anorexia (loss of appetite at the earliest)
b. nausea, vomiting, abdominal distension
c. tongue and mouth ulcers d. ammonia odor in the mouth
e. Upper gastrointestinal bleeding, etc.
2. Blood system.
a. Anemia: It is a necessary symptom for uremic patients. The degree of anemia is parallel to the degree of uremia (renal function), and the decrease of erythropoietin (EPO) is the main cause.
b. Bleeding tendency: may be manifested as skin and mucous membrane bleeding, associated with increased platelet destruction and prolonged bleeding time, which may be caused by toxins and can be rapidly corrected by dialysis
c. Leukocyte abnormalities: reduced chemotaxis, phagocytosis and bactericidal ability, prone to infection, which can be improved after dialysis
3, cardiovascular system: is the most common cause of death in renal failure
a. Hypertension: most patients have varying degrees of hypertension
Volume dependent + renin dependent
It can cause atherosclerosis, left ventricular hypertrophy and heart failure
b. Heart failure: often manifestations of cardiomyopathy, water and sodium retention; hypertension; uremic cardiomyopathy, etc.
c. Pericarditis: uremic or due to inadequate dialysis, mostly hemorrhagic, usually a late manifestation
d. Atherosclerosis: rapid progression, more so in those with hemodialysis, can occur in coronary arteries, cerebral arteries, and peripheral arteries throughout the body Mainly due to hyperlipidemia and hypertension
4. Neurological and muscular system manifestations.
a. Early stage: fatigue, insomnia, lack of concentration, etc.
b. Late stage: peripheral neuropathy, sensory nerves are more significant than motor nerves
c. Dialysis imbalance syndrome: too rapid reduction of urea nitrogen, imbalance of intra- and extracellular osmotic pressure, resulting in increased intracranial pressure and cerebral edema, manifesting nausea, vomiting, headache, and convulsions in severe cases.
5. renal bone disease: a general term for the skeletal changes in uremia
a. Can cause spontaneous fractures
b. Rarely seen with symptoms, such as bone pain, walking difficulties, etc.
6. Respiratory manifestations.
a. Deep and long breathing in acidosis
b. Uremic bronchitis, pneumonia (butterfly wing), pleurisy, etc.
7. Skin symptoms: skin pruritus, urea cream deposition, uremic facies, which cannot be improved by dialysis
8. Endocrine disorders.
a. Decrease in hormones produced by the kidneys
b. Hormones degraded in the kidney can rise
9. Easy to be complicated by serious infection: fever is not as obvious as in normal people when infected
10. Metabolic disorders and other.
a. Hypothermia: body temperature is lower than normal by about 1oC (should be considered when estimating fever), basal metabolic rate often decreases
b. Abnormal glucose metabolism: general patients: reduced glucose tolerance; diabetic patients: insulin dosage should be reduced (degradation is reduced)
c. Abnormal lipid metabolism: TC is normal
d. Hyperuricemia: GFR <20, impaired clearance of uric acid, rare occurrence of gouty arthritis
Diagnostic tests 1. Blood routine, platelets, bleeding and clotting times, prothrombin time, blood urea nitrogen, creatinine, uric acid, carbon dioxide binding capacity, blood gas analysis, blood glucose (fasting, 2h after meal), blood lipids, serum potassium, sodium, chloride, calcium, phosphorus, magnesium, alkaline phosphatase, plasma protein, protein electrophoresis, urine routine, urine specific gravity, 24h urine protein quantification, 24h urine potassium, sodium, chloride, calcium, phosphorus Urea nitrogen, creatinine, uric acid quantification, endogenous creatinine clearance, morning urine osmolality measurement.
2.Immunological examination
3.Other tests: fundus, electrocardiogram and ultrasound of both kidneys, renal nuclear examination, chest X-ray, abdominal plain film and bone film if necessary.
4.Stage of renal insufficiency
①Compensation stage: kidney unit damage not more than 50%, GFR 50~80ml/min, Scrl 33~177μmol/L, no clinical symptoms;
②Decompensated stage: GFR50-20ml/min, Scr186-442μmol/L, clinical symptoms such as weakness, mild anemia and loss of appetite;
③Renal failure stage: GFRl0～20ml/min, Scr451～707μmol/L, the patient has severe anemia, metabolic acidosis, water-electrolyte metabolism disorder;
④Uremic phase: GFR<10ml/min, Scr>707μmol/L, clinically aggravated metabolic acidosis and prominent symptoms of all systems.
Treatment plan
Conventional treatment
1.Care according to the nursing routine of kidney disease.
2. Pay attention to the mental and respiratory conditions, any rhinorrhea or skin or mucous membrane bleeding. Those with mental abnormalities or convulsions or convulsions must prevent self-injury, and those in coma should be cared for according to the coma care routine.
3. Diet treatment.
①Give low protein, high calorie, vitamin-rich diet. Use eggs, milk and other high-quality protein, daily intake: 25-35g/d of protein for endogenous creatinine clearance >lOml/min, blood urea nitrogen 10.7-25.1mmol/L, blood creatinine 265.2-618.8μmol/L; endogenous creatinine clearance 5-lOml/min, blood urea nitrogen 25.1-36mmol/L, blood creatinine 618.8～884μmol/L, give 20～25g/d of protein, and keep the daily caloric energy above 146kJ(35kcal)/kg preferably.
(②Oral administration of essential amino acids at a dose of 0.1-0.2g/(ks?d) in 3-5 divided doses with water while on a low-protein diet. 250ml/d can be given intravenously for a short period of time for those with severe gastrointestinal symptoms.
③Low-protein diet plus α-keto acid treatment, take Kai Tong as an example: 3/d, 1.6-3.2g/time, pay attention to review blood calcium concentration, contraindicated in hypercalcemia. The staple food should be wheat starch with vegetable protein removed. In the absence of severe hypertension and obvious edema, urine volume >1000ml/d, salt 2~4g/d, potassium intake is not strictly limited.
4.Chinese herbal medicine treatment. For those who have Yang deficiency, it is advisable to strengthen the spleen and kidney, and tonify both qi and blood, and add Xianmao, Epimedium, Cuscuta and other Yang-aiding drugs; for those who have spleen and kidney failure and dampness, it is advisable to lightly percolate and benefit dampness, and flatly tonify the spleen and kidney. The Chinese medicine rhubarb is effective in delaying the progression of renal function in chronic renal failure.
5. Pay attention to water and electrolyte balance. If there is water loss or hyponatremia, it should be corrected in time. For high blood phosphorus and low blood calcium, give 1g of calcium carbonate, 3/d or oral 1,25 dihydroxyvitamin D3, 0.25-0.5μg/d, and adjust the dose according to the blood calcium concentration.
6. In mild acidosis, compound citrate solution (1000ml containing 140g of citrate and 98g of sodium citrate) can be taken, 40-90ml/d, in 3 doses. If the carbon dioxide binding capacity <13.5mmol/l (30 volume %) and there are symptoms of acidosis, use 5% sodium bicarbonate 200ml IV, or 11.2% sodium lactate lOOml diluted to 600ml IV. If edema is obvious and blood pressure is too high, use 3.64% aminobutriol (THAM) 200ml IV.
7. Those with infectious factors should be actively controlled by antibiotics.
8, can try adsorbent, such as oxidized starch 30-50g / d, divided internal; medicinal charcoal 40g / d, divided internal, has the effect of reducing blood urea nitrogen.
9, urine less, edema obvious people available furosemide (tachyphylaxis) 40 ~ 100mg sedation, 1/6 ~ 8h, or butylamine lmg, 1/6 ~ 8h. But prohibit potassium-protective diuretics, so as not to aggravate hyperkalemia.
10, obvious hypertension with antihypertensive drugs, to choose A-CEI mainly, such as mercaptomethoproline (25-100mg, 3/d), enalapril (5-10mg, 1/d), benazepril (5-20mg, 1/d), the principle of medication as acute nephritis, antihypertensive should not be too fast, excessive, to maintain diastolic blood pressure at 13.3kPa (100mmHg) is appropriate, should not reduce The urine volume should not be reduced, and the occurrence of hyperkalemia should be observed.
In cases of heart failure, digitalis preparations can be used, but the dose should be reduced by 1/2 to 1/3 compared to the usual amount. severe anemia can be treated with erythropoietin, subcutaneous injection 2-3 times/week, 1500-3000 U/time. In case of bleeding, blood transfusion is appropriate. In case of nausea and vomiting, metoclopramide (Gastrofluan), domperidone (morpholine) or chlorpromazine (Dormantine) can be used.
11, dialysis therapy: those who have the conditions should be implemented in a timely manner.
12.Allogeneic kidney transplantation: those who have indications and conditions to receive transplantation, and those who are properly selected by the recipient and donor immunity can be performed.
Micronized Chinese medicine infiltration therapy treatment
In the treatment of chronic renal failure, “micro-Chinese medicine infiltration therapy” is used for treatment. Micro-Chinese medicine infiltration therapy is actually a systematic treatment of micro-Chinese medicine infiltration therapy to interrupt the process of kidney fibrosis, which guides the formulation and implementation of medication and treatment measures for kidney failure patients based on the latest kidney disease diagnosis theory. Its core technology is to micronize the Chinese medicine for kidney disease and then evenly distribute it in the two kidney areas and infiltrate it with the micronization therapy instrument.
The treatment of kidney failure micro-chemical Chinese medicine infiltration therapy and combined with western medicine symptomatic treatment, if necessary, hemodialysis or peritoneal dialysis treatment, but this is only an auxiliary measure, is not the key to treatment. Summarize the process of kidney failure treatment can be broadly divided into four parts, which are divided as follows.
1, treatment of chronic renal failure, the first is the treatment of the cause of the disease
The treatment for the cause is to treat kidney failure from the “source”. The cause of kidney failure is due to various causes of deformation and damage to the intrinsic cells of the kidney. Take glomerular renal failure as an example, we can explain our treatment method: glomerular disease is an immune disease, its pathogenesis is often triggered by antigen or antibody binding to form immune complexes, and deposited in the glomerulus (immune complexes). With the involvement of inflammatory mediators (e.g., complement, interleukins, reactive oxygen species, etc.), it finally leads to glomerular injury. In the therapeutic practice, the following measures are taken.
1.Dilate renal arteries to increase the effective perfusion of glomeruli, tubules and interstitium, accelerate the supply of damaged cells i, and relieve their hypoxic state.
2.Dilate the systemic arteries to reduce and relieve the systemic hypertensive state, especially to reduce the glomerular intra-glomerular pressure and reduce the glomerular hypercritical state.
3.By accelerating the supply, avoiding the endothelial cells from being activated to inhibit the formation of microchemical tethering.
4.Inhibit the chemotaxis and infiltration of a series of inflammatory factors by accelerating the blood velocity and through adequate supply to stop the abnormal release of already activated inflammatory cells.
The reality of clinical observation is that through the implementation of the above four therapeutic measures, the normal metabolic function of the glomerulus is activated, and when the glomerular condition improves, the function of the whole kidney also improves
2, treatment of chronic renal failure, followed by treatment for the pathogenic process
The development process of chronic renal failure is also the process of gradual reduction of effective kidney units and continuous loss of kidney function. In this process, both kidneys gradually atrophy, a large number of glomerulosclerosis, tubular-interstitial fibrosis. Therefore, the process of renal failure is also the process of deepening renal fibrosis. Interrupting the process of renal fibrosis is important to effectively control the progression of the disease to uremia.
Although some research institutions have pointed out that some Chinese medicines are effective in blocking the process of renal fibrosis, not many of them are really applied to clinical practice. The drugs used in our hospital are a series of Chinese medicines that have been micronized. The activity of Chinese medicine increases after micronization treatment, and many drug components that are difficult to function under traditional conditions can also function adequately.
3.Treatment of chronic renal failure, again for the treatment of symptoms
Chronic renal failure patients with clinical symptoms, mostly related to water-electrolyte and acid-base balance imbalance; another kidney failure symptoms related to uremic toxins. Symptom-specific treatment can improve the disorder of internal environment, regulate the imbalance of renal balance and improve the quality of life of kidney failure patients.
Microchemical Chinese medicine infiltration therapy in the treatment of kidney failure, the specific approach is.
1.For the treatment of renal anemia, one of the common symptoms of renal failure
By using recombinant human erythropoietin (Rhepo, hereinafter referred to as EPO), the active substance of traditional Chinese medicine, to treat renal anemia. Clinical observation shows that the effect is very significant. This therapy is universally applied to patients with anemia. Generally speaking, renal failure patients, especially maintenance hemodialysis patients, lose small amounts of blood over a long period of time, which causes the loss of some hematopoietic materials, such as iron and folic acid. In order to make EPO fully effective, some hematopoietic raw materials should be replenished before using EPO. the active substance of Chinese medicine is rich in more than ten kinds of trace elements, including iron and folic acid, which can fully meet the need of improving anemia condition.
2.For the treatment of hypertension in renal failure
Hypertension is a reversible condition, for which we pay great attention to catch this link in the process of treating chronic renal failure. The long-term tightening state of renal blood vessels is the key cause of renal hypertension, so the most important and effective means of treating hypertension is direct vasodilation. We found in the clinical process that there are a large number of vasodilating factors in the microprocessed Chinese medicine play a synergistic role to make the blood vessels become relaxed, so it relieves the renal hypertension caused by insufficient diastole and excessive tension of blood vessels, and strongly relieves the symptoms of renal failure patients.
4.Treatment for the recovery of renal function in patients with chronic renal failure
Through the treatment for the cause, pathogenesis and symptoms, the condition can be effectively relieved and controlled, but for kidney failure patients, just controlling the condition is not enough. Because a large number of kidney units in the body of kidney failure patients are damaged and fibrosis or sclerosis, both kidneys or single kidney atrophy, especially in the uremic period, only about 10% of the remaining kidney units, if you can not repair the thousands of necrotic kidney units, the remaining kidney units are still “overload” work, over time, inevitably Inevitably, lesions will also appear. This is the reason why many patients are not cured for a long time and their condition is recurrent. The only effective way to solve this problem is to repair the damaged kidney units so that they can regain their metabolic capacity.
Health Tips
Diet.
1. The focus of dietary treatment is to limit protein intake to reduce nitrogen retention. However, care should be taken to ensure adequate calories and sufficient essential amino acids. The amount of protein intake for each patient should be flexible according to its muscle research clearance rate.
2, adhere to a high quality low protein diet, low phosphorus, low salt, high calories; avoid aggravating factors, moderate cold, avoid wind and cold; avoid external sensation, infection, diet with moderation.
Prevention.
1, to avoid overexertion and strong mental stimulation;
2, prevent infection, remove the foci of infection to reduce the cause of deterioration
3, have smoking and alcohol addiction should be quit;
4, with swelling, hypertension, significant proteinuria and a little action will aggravate the symptoms, are recommended to bed rest.
Attention.
1, good oral care, reduce irritation, prevent oral ulcers, affect eating.
2, the patient has headache, insomnia, irritability, the room light should be dark, in order to facilitate the patient to rest, if necessary, use sedatives, can take Valium, etc.
3, high blood pressure, blood pressure should be measured regularly, according to the condition of the antihypertensive drugs, and to adhere to the regular intake.
4.When there is bleeding, use hemostatic drugs according to the doctor’s requirements.
5. Pay attention to the protection of the skin to prevent abrasions and bedsores.
6.If the condition is serious, send to hospital for hemodialysis or peritoneal dialysis treatment in time.
Contraindications for patients with chronic renal failure
A. Prevent over-supplementation.
Chinese medicine says “deficiency is tonic, the real is diarrhea”, we should follow the principle of “no deficiency is not tonic”, “what is lacking is tonic”, for the lack of body, can be supplemented, but must be supplemented in moderation. Otherwise, it will cause imbalance of yin and yang in human body. At the same time, you should know that medicine is not as good as food, medicine is three parts poisonous, can use food tonic do not use medicine tonic.
Second, to prevent excess heat.
Some patients with chronic renal failure have a big appetite in autumn, often resulting in excess caloric intake, fat accumulation and “autumn fat”. Because obesity can bring many diseases, so chronic renal failure patients in the autumn diet can not indulge in appetite, pay attention to moderation.
Third, pay attention to balanced nutrition.
According to the Dietary Guidelines for Chinese Residents, food should be varied, with cereals as the mainstay, and coarse and fine food. A single food cannot supply the body with comprehensive nutrition, such as cereals mainly supply calories and vitamin B1; beans and soy products mainly supply plant protein; vegetables and fruits mainly supply vitamin C, inorganic salts and dietary fiber; animal food mainly supplies high-quality protein, fat, vitamins, etc.
Fourth, avoid digestive tract diseases.
Autumn weather from hot to cool, the human body in order to adapt to this change, physiological metabolism has also changed. The ancient doctors of China put forward the idea of “autumn should be warm”, that is to say, chronic renal failure patients should avoid eating cold food in autumn, should eat more warm food, so as to help protect the gastrointestinal, to prevent diarrhea, dysentery, loose stools and other gastrointestinal diseases.
In addition to diet, patients with chronic renal failure must be guided by a specialist in the standardization of medication, the principle of medication is: less and more precise, to safe and effective prevail. It is important to go to a regular hospital to treat the disease, and the medication must be under the guidance of a specialist, and all kinds of advertisements, clinics and charity clinics should be treated calmly, and it is better not to use them. [1] Related information
Uremic toxic substances: generally divided into small molecules (molecular weight < 500dal), medium molecules (molecular weight 500 ~ 5000dal) and large molecules (molecular weight > 5000dal) three categories. Large molecules of toxic substances, the most from the attention of the urea, guanidine.
A large molecule substances
(1) Urea: In uremia, one of the largest metabolites in the body fluid. When its serum concentration is quite high, it can cause headache, weakness, nausea, vomiting, drowsiness, bleeding tendency, etc. The toxicity of urea is related to the length of its existence, and its metabolite cyanate can cause carbamylation of proteins, which has an important relationship with the symptoms of uremia.
(2) guanidine: guanidine is a metabolite of certain amino acids and creatinine, injecting animals with large amounts of methylguanidine, a series of symptoms similar to uremic syndrome can occur. Methylguanidine is positively charged and easily binds to negatively charged phospholipids in cells, accumulates in cells and forms cytotoxicity. The production level of methylguanidine is parallel to that of creatinine. When the urine volume is less than 400 ml/d, both plasma and urinary methylguanidine rise. Guanosuccinic acid is less toxic than methylguanidine and is excreted in the urine of a normal person at about 10 mg per day, which can increase fivefold in uremia. The effects of guanidinosuccinic acid are.
①Inhibit the adhesion and aggregation of platelets, and have inhibitory effect on platelet factor III.
②Promote autohemolysis.
③Inhibit lymphocyte function.
④ Causes impairment of enzyme activity in brain tissue.
(3) Amines: including fatty cyclamines, aromatic cyclamines and polyamines. High concentrations of fatty amines (1-methylamine, 2-methylamine, 3-methylamine, etc.) can cause myoclonus, fluttering tremor and hemolysis, and can also inhibit the activity of certain enzymes. Aromatic cyclamines (amphetamines, tyramine) have inhibitory effects on brain tissue chlorination process, succinate oxidation and dopa carboxylase activity.
Polyamines include spermidine, sperm, putrescine and cadaverine. High concentrations of polyamines can cause anorexia, nausea, vomiting and proteinuria, and can promote erythrocyte lysis, inhibit erythropoietin production, inhibit Na+-ATPase and Mg2+-ATPase activities, and also increase the permeability of microcirculation and promote the production of uremic lung, acute pulmonary edema, ascites and cerebral edema.
II. Medium molecular substances
The application of techniques such as chromatography confirms that 8 to 9 clear peaks can be found in the plasma of uremic patients, and in severe patients, peak number 7 is particularly pronounced. The peritoneal clearance of urea is about 4 to 6 times lower than that of artificial membranes for hemodialysis, but the peritoneal clearance of medium-molecular substances is higher than that of artificial membranes. Although the rate of decline in urea nitrogen was slower in peritoneal dialysis patients, the relief of neurological symptoms was superior to that of hemodialysis, supporting the view that medium-molecular substances are toxicogenic. Mesomolecular toxicants may include.
(i) High concentrations of normal metabolites.
(2) Hormones with normal structure and increased concentration.
(3) Peptides produced by disorders of cellular metabolism.
④Cellular or bacterial lysis products.
High depth medium molecular substances can cause peripheral neuropathy, uremic encephalopathy, inhibition of erythropoiesis, inhibition of insulin activity, inhibition of antibody production, impairment of platelet function, low cellular immune function, sexual dysfunction and atrophy of exocrine glands.
Third, the role of PTH
Uremic patients often have secondary parathyroid hyperplasia and elevated levels of parathyroid hormone (PTH) in the blood. The causes may be due to elevated blood phosphorus; resistance of bone to the calcifying effects of PTH; and altered vitamin D metabolism.
The “toxin” effects of PTH are manifested in the following ways.
(1) Changes in the electroencephalogram due to elevated PTH. Motor nerve conduction velocity is slowed. Increased Ca2+ content in the brain.
(2) Elevated PTH levels are one of the most important causes of anemia. The main pathway is due to PTH’s ability to inhibit erythropoiesis, reduce erythrocyte survival, and cause bone calcium freeing and bone marrow fibrosis.
(3) Effects of PTH on the myocardium. The heart is one of the important target organs of PTH, which can affect cardiac function and cardiomyocyte metabolism.
Principles of medication for renal failure
1, early mild cases can be used A, and pay attention to control the amount of fluid intake, supplement vitamins and energy, maintain electrolyte and acid-base balance;
2, severe cases should be timely, early dialysis treatment, dialysis can choose peritoneal dialysis to maximize the protection of residual kidney function; pay attention to complications such as hypertension, anemia, proteinuria, etc., try to correct the damage to the kidney by reversible factors; if necessary, daily dialysis, and blood and human albumin transfusion;
3, combined with infection can be selected according to the specific situation in the C drugs;
4.When combined with hypertension, you can use the drugs in item A or C;
5. In case of combined heart failure, cardiac drugs such as cetiran may be given; 6. In case of combined bleeding, drugs in item A or C may be used.
Chronic renal failure is easily misdiagnosed
Mr. Wu has been suffering from “gastritis” for 5 years, and after the Spring Festival, he suddenly had gastric bleeding again, and his condition did not improve significantly after treatment, but still bleeding intermittently. The Zhengzhou hospital did a systematic examination for him and found that Mr. Wu was suffering from chronic renal failure.
Chronic renal failure is a serious disease that affects multiple systems throughout the body, and sometimes, it is easy to misdiagnose because the symptoms of a system are particularly prominent.
Why does the digestive system appear abnormal when you are suffering from kidney disease? This is because when the kidney function is damaged, the toxin discharge in the urine is reduced, the toxin in the blood will increase, and the toxin discharge from the digestive tract will also increase. The mucosa of the digestive tract is stimulated by the toxin, which causes superficial inflammation and ulcers in the mucosa of the stomach and duodenum, and even causes hemorrhage in the upper gastrointestinal tract. Clinically, it is often seen that patients with chronic renal failure see gastroenterology for a long time, and gastroscopy does have lesions, unbeknownst to them, which is one of the complications of chronic renal failure.
In the early stage of chronic renal failure, most patients have no symptoms and blood abnormalities are not obvious, only manifesting as hypertension, proteinuria and mild elevation of serum uric acid level. Wu Xianming reminds that it is important to keep a close eye on these suspicious conditions to avoid misdiagnosis.
The only way to detect kidney failure early is to do kidney function tests. For GI reactions due to kidney disease, the most important thing should be timely treatment of kidney failure. Gastrointestinal symptoms that have appeared should be closely observed and patients should be advised to eat easily digestible and non-irritating food. Patients with loss of appetite, nausea and vomiting should be put on bed rest.
What are the treatment measures for pediatric chronic renal failure
The management of pediatric chronic renal failure requires monitoring of the pediatric clinical (physical examination and blood pressure) and laboratory tests including hemoglobin, electrolytes (hyponatremia, hyperkalemia, acidosis), blood urea nitrogen and creatinine measurements, calcium and phosphorus levels, and alkaline phosphatase activity. Parathyroid endocrine levels and bone X-rays should be checked regularly for early detection of osteotropic disorders. Chest radiographs and cardiac ultrasound may be useful in understanding cardiac function. Nutritional status can be monitored by regular checks of serum albumin, zinc, iron conversion, folic acid and iron levels.
1, the diet of chronic renal failure When the pediatric glomerular filtration to less than 50% of normal, the growth rate of children decreases, the main reasons for this are insufficient intake of calories. It is not known what the appropriate caloric intake is in renal insufficiency, but as much as possible, the caloric intake is comparable or higher than the age group of that child. Dietary caloric intake can be increased with unrestricted carbohydrates such as sugar, jam, bee dense, glucose polymers, and fats such as medium chain triglyceride oil, provided the patient can tolerate them.
When urea nitrogen is above 30 mmol/L (80 mg/dl) the patient may experience nausea, vomiting and anorexia, which may be relieved by restricting protein intake. Because children in renal failure still need a certain amount of protein for growth, so give protein 1.5g/(kg・d), and should be given high-quality protein (eggs and lean meat) containing a large amount of essential amino acids, such as eggs, milk, followed by meat, fish, chicken and poultry. Milk is too high in phosphorus and should not be used more than necessary. Food such as glucose and peanut oil should be used to supplement calories. Due to insufficient intake or dialysis loss, children with renal insufficiency may have water-soluble vitamin deficiency and must be routinely supplemented. If there is a deficiency of iron, zinc and other trace elements must also be supplied, fat-soluble vitamins such as A, E and K do not need to be supplemented.
2, the treatment of water and electrolytes in pediatric renal insufficiency, rare to limit the amount of intake, because there and the brain “thirst center” to regulate, unless the development of end-stage renal failure, then need to use dialysis. In most children with renal insufficiency, a normal sodium balance can be maintained with an appropriate diet. In some patients with renal insufficiency due to anatomical abnormalities, if a large amount of sodium is lost by urine, the sodium must be supplemented by diet; conversely, if the patient has hypertension, edema or congestive heart failure, the sodium must be restricted, sometimes in combination with tachyphylaxis, 1-4 mg/(kg/24h).
If renal function deteriorates further, dialysis treatment is required. Hyperkalemia can be treated with dietary potassium control and oral alkaline or potassium reducing resin (sodium polystyrene sulfonate, Kayexalate). Pediatric renal insufficiency almost always has acidosis, which generally does not require treatment, unless serum bicarbonate is below 20 mmol/L, which must be corrected with sodium bicarbonate.
3, renal osteodystrophy is often complicated by renal osteodystrophy when there is hyperphosphatemia, hypocalcemia, increased parathyroid endocrine levels and increased serum alkaline phosphatase activity. Serum phosphorus levels generally rise when the glomerular filtration rate falls below 30% of normal. Serum calcium decreases secondary to hyperparathyroidism. Hyperphosphatemia can be controlled with a diet low in phosphorus, or with calcium bicarbonate or antacids taken orally to promote phosphorus excretion from the intestine. Aluminum toxicity is also a concern in the pediatric population and serum aluminum levels must be monitored regularly. In severe renal insufficiency, vitamin D (Vit. D) deficiency can be combined with vitamin D. Vit. D is used for persistent low blood calcium, rickets on X-ray and increased serum alkaline phosphatase activity.
4, anemia Most patients with a stable hemoglobin of 60-90g/L (6-9g/dl) do not require blood transfusion, if hemoglobin is below 60g/L then carefully enter 10ml/kg of red blood cells (a small amount can reduce the risk of blood circulation overload.) .
5. Hypertension For hypertensive emergencies, sublingual nifedipine or intravenous injection of diazoxide, i.e., hypotensiveazine (5 mg/kg, extreme amount of 300 mg, injected within 10 seconds) can be administered. In severe hypertension complicated by blood circulation overload, tachyphylaxis (2-4mg/kg at a rate of 4mg/min) can be given. In case of renal insufficiency, sodium nitroprusside must be applied with caution, as thiocyanate may accumulate. In short, we should strive for early diagnosis and removal of the cause, if found too late, although the cause is removed, the damage to the kidney tissue is difficult to recover.
If the cause is urinary tract obstruction, appropriate surgical treatment should be done, but the child is often in poor renal function and cannot tolerate too much surgery, so nephrostomy or suprapubic cystostomy can be done first to facilitate drainage. If there is persistent or intermittent pyuria, the infection should be actively controlled and followed up and reviewed. For patients with end-stage renal disease or difficult-to-recover renal failure, chronic hemodialysis (artificial kidney, also known as long-term intermittent hemodialysis) has been applied in recent years, enabling many patients to continue to survive or return to normal life.
The current long-term regular dialysis, usually 2 to 3 times a week, can be performed at night while sleeping. In children treated with chronic hemodialysis, the development of secondary sexual characteristics and weight gain are not significantly affected, and only height is slightly affected. In recent years, the implementation of chronic hemodialysis has been transferred from hospitals to patients’ homes in foreign countries, and the duration of dialysis in children has been as long as 4 to 5 years.
Peritoneal dialysis has also been used for chronic renal failure, mainly in the intraperitoneal cavity with a long-term fixed catheter and daily dialysis on a regular basis, and can also be performed in the home according to medical advice. The ultimate goal of pediatric end-stage renal failure treatment is kidney transplantation. In foreign countries, the success rate of kidney transplantation in children over 5 years of age is the same as that of adults, and effective chronic hemodialysis is required prior to kidney transplantation (to keep the child alive while waiting for a suitable donor kidney) or after rejection.