chronic renal anemia
Introduction
Introduction to chronic renal anemia Anemia caused by chronic renal failure is called chronic renal anemia due to various organic kidney diseases. In the chronic renal failure, the exocrine and endocrine function of the kidney is reduced or lost. The pathogenesis of anemia is complicated. The clinical anemia is often masked by the primary kidney disease, especially in the early stage of the disease, which is easily ignored by clinicians. Application, patients with chronic renal failure have significantly prolonged survival, and chronic renal anemia is also more common. basic knowledge The proportion of illness: 0.0035% Susceptible people: no special people Mode of infection: non-infectious Complications: anemia, renal failure
Cause
Cause of chronic renal anemia
(1) Causes of the disease
Various organic kidney diseases can occur after the disease continues to progress, such as chronic glomerulonephritis, renal arteriosclerotic nephropathy, chronic pyelonephritis, diabetic nephropathy, polycystic kidney disease, kidney tuberculosis, etc. In patients with renal failure, blood urea nitrogen exceeds 17.8 mmol / L, and creatinine exceeds 354 mol / L, almost all anemia.
(two) pathogenesis
Renal excretion failure
(1) Hemodilution: Patients with chronic renal failure often have water and sodium retention and dehydration due to renal excretion of water and decreased sodium salt function. Therefore, red blood cells and hemoglobin often have a wide range of changes, when blood volume increases significantly. Produces blood dilution.
(2) Hemolysis: The application of 51Cr in the determination of erythrocyte half-life of uremic patients showed that the red blood cell life span was milder or moderately shorter than that of normal people, 20% of patients were significantly shortened, and linearly correlated with blood urea nitrogen level, determined by 32P method. In 13 patients with azotemia, the average red blood cell life was 66 days (normal 120 days). After effective dialysis treatment, the life span of red blood cells could be prolonged, indicating that the red blood cell survival period was shortened to the cause of red blood cells, which was related to the accumulation of uremic metabolic products. Erythrocytes are prematurely destroyed in the spleen to form extravascular hemolysis. The reasons are: decreased transaminase and membrane ATPase activity involved in the metabolism of pentose phosphate pathway, leading to abnormal metabolism of pentose branch and reduced glutathione production. Decreased, the anti-oxidation effect of erythrocyte membrane on drugs and chemical products decreased, the deformability decreased; the membrane ATPase activity decreased, the Na-K pump energy supply was insufficient, Na was retained in the cells, the erythrocyte osmotic fragility increased, the cells were spherical, and the spleen It is easy to be destroyed. In addition, it is currently noted that mechanical damage of red blood cells in uremic patients is another important cause of hemolysis. Uremia can be seen under electron microscope. The large number of renal microvascular fibrin deposits, the flow of red blood cells within the capillaries, distortion in the fibrin network, mechanical damage and destruction, microangiopathic hemolysis.
(3) Reduction of erythropoiesis: The decrease in erythropoiesis in uremic patients is related to the following factors:
1 erythroid progenitor cell proliferation and hemoglobin synthesis in erythrocytes are inhibited,
2 In vitro hematopoietic progenitor cell culture proved that the CFU-E and BFU-E numbers of uremic patients were lower than normal in their own serum, while the number in normal human AB serum was normal, and clinically effective peritoneal dialysis and hemodialysis improved patients. Anemia, indicating the presence of factors that inhibit erythropoiesis in the serum of uremic patients, including high, medium and low molecular weight peptides, lipids, terpenoids and parathyroid hormones, but this inhibitor is in vitro Hematopoiesis has an inhibitory effect, not only on red blood cells,
3 erythroid progenitor cells have reduced response to erythropoietin. Experiments have shown that the same dose of erythropoietin is administered to uremic patients and normal people. The increase in erythrocyte count in uremic patients is only 1/10 of that of normal people. It is related to the inhibition of harmful metabolites, and it has also been suggested that there may be specific erythropoietin inhibitors in the blood.
(4) bleeding tendency: about 1/3 to 1/2 uremia patients can occur purpura, gastrointestinal and genitourinary tract bleeding, can make the original anemia worse, the main cause of bleeding is platelet dysfunction, uremia patients blood The metabolic wastes of retention are urea, uric acid, creatinine, phenols, thiosuccinic acid, etc. These products can reduce platelet adhesion, platelet factor III activity disorder, prolonged bleeding time, poor blood clot dysfunction and prothrombin consumption test. Abnormal, effective hemodialysis and peritoneal dialysis can correct platelet dysfunction. In addition, blood in the dialysis machine during hemodialysis, blood test before and after dialysis can aggravate blood loss.
(5) Nutritional deficiency:
1 iron deficiency: common in uremic patients after blood loss failed to timely iron; renal inflammatory injury caused by serum iron decreased, iron reuse decreased; aluminum ions in dialysate can interfere with iron and red blood cells; iron deficiency caused by the above reasons Can be complicated by hypopigmentation of small cell anemia.
2 folic acid deficiency: folic acid can be lost through peritoneal dialysis.
3 protein deficiency: low protein diet in patients with uremia, loss of appetite can reduce protein synthesis, affecting hemoglobin synthesis.
2. Renal endocrine failure
Renal endocrine function refers to its secreted erythropoietin (EPO), a polypeptide hormone with a relative molecular mass of 46,000 to 70,000. It is mainly caused by hypoxia-stimulated capillary endothelial cells in the peri-tubule, secreting human blood. Extrarenal organs such as the liver can also secrete a small amount of EPO, but most of the EPO in the human body is secreted by the kidney. EPO can promote the proliferation and differentiation of hematopoietic cells in all stages of the erythroid; promote hemoglobin synthesis; promote the maturation and release of reticulocytes, chronic There are two types of EPO reduction in blood in patients with renal failure.
(1) Relative reduction: refers to patients with iron deficiency anemia who are lower than the same level of anemia in patients with blood EPO higher than normal, seen in early and middle stage chronic renal failure patients.
(2) Absolute reduction: EPO in blood is significantly reduced to a low value. In patients with advanced renal failure, the renal functional nephron is destroyed, and the production of EPO is also significantly reduced. The reduction of EPO causes hematopoietic cells to proliferate and the differentiation ability is reduced. One of the main causes of renal anemia.
Prevention
Chronic renal anemia prevention
It is recommended that you can eat more water pipes to improve anemia, enhance immunity, balance nutrient absorption and other effects.
1. Replenishing blood and replenishing qi: Suitable for those who have no brilliance and lose ruddy, cold hands and feet.
2. Improve immunity: Protein is the most important nutrient for maintaining immune function and is the main component of white blood cells and antibodies.
3. Prevention: It is necessary to keep the patient's daily life, to maintain a good mood, to treat the disease correctly, and to establish confidence in the fight against the disease. Otherwise, the illness of the seven emotions may make the condition worse. Diet should be light, eat spicy and hot products.
Complication
Chronic renal anemia complications Complications, anemia, renal failure
Anemia, kidney failure.
Symptom
Chronic renal anemia symptoms Common symptoms Shortness of kidney failure Heart palpitations pale pale fatigue bleeding tendency
Patients can be seen with general anemia, such as: pale, fatigue, palpitations, shortness of breath and other symptoms, and anemia symptoms are often overshadowed by the symptoms of primary kidney disease and renal failure, only the original kidney disease progresses slowly, kidney failure symptoms are not Typically, anemia becomes an important symptom of patients with renal failure. The degree of anemia is not related to the primary disease of the kidney. It is roughly related to the degree of renal failure, but there are some exceptions in the case of renal anemia caused by polycystic kidney disease. The degree of anemia is often worse than other diseases. The renal anemia caused by light is mild, and the cause of EPO-producing cells is more related to the chronic failure of polycystic kidney disease.
Some patients have clinical bleeding tendency, such as skin bleeding, nasal, oral mucosal oozing, digestive tract or urinary tract bleeding.
Examine
Chronic renal anemia check
Peripheral blood
(1) Red blood cells: Most of the renal anemia is positive cells, positive pigmented anemia, but it can also cause small cells or large cell anemia due to hemorrhage, hemolysis, etc. Reticulocytes are mostly in the normal range, sometimes slightly increased or Reduced, blood smear often sees a variety of shaped red blood cells and red blood cell debris such as spines, helmets, triangles, etc., also visible multi-staining and smear red blood cells, echinocyte is one of the characteristics of renal failure anemia, red blood cells carrying The ability of oxygen has not been significantly impaired in uremia, due to hyperphosphoremia and increased erythrophosphoric acid 2,3-diphosphoglycerate, which reduces the affinity of hemoglobin to oxygen. In addition, oxygenolysis can cause oxygenolysis. Moving away from the curve to the right, further reducing the affinity of hemoglobin and oxygen, is conducive to the release of oxygen in the tissue, the patient may be reduced by the organic phosphorus in the red blood cells after strong dialysis, the correction of body fluid acidosis can increase the affinity of hemoglobin and oxygen, resulting in tissue Temporary hypoxia leads to a series of symptoms, the so-called "dialysis imbalance syndrome", in addition, the proportion of hemoglobin A1 is increased Normal increased by 7.1% to 10%.
(2) white blood cells and platelets: white blood cell count and classification and platelets are mostly normal in renal anemia, but uremia itself and hemodialysis treatment can have a certain effect on the function of white blood cells and platelets, and granulocyte phagocytosis declines in uremia. The dialysis membrane can activate the complement to produce leukocyte stasis in the lungs, and the white blood cells in the blood are transiently reduced. The decrease of cellular immunity can make the patient easy to be infected, the platelet aggregation function, the adhesion function is reduced, the platelet factor III activity is abnormal, and in addition, the microvessels are concurrent. In the case of pathological hemolytic anemia, abnormal blood coagulation factors such as fibrin reduction can be seen.
2. Bone marrow
Basically normal, erythroid, granulocyte, megakaryocyte proliferation and immature cells in all stages of the proportion are in the normal range, in the late stage of uremia, bone marrow hyperplasia is observed, young red blood cells mature obstruction.
3. Iron metabolism
Serum iron is generally normal or slightly reduced. The iron metabolism may vary with the cause of renal dysfunction or comorbidities. For example, if combined with chronic infection, serum iron decreases, total iron binding capacity and iron saturation decrease. Combined bleeding or poor patient's appetite, if the food intake is too small, it may show iron deficiency anemia, serum iron decreases, total iron binding capacity increases, iron saturation decreases significantly, and vice versa, such as repeated blood transfusion, can lead to iron excess, red blood cells The level of pheromone and iron renewal rate are generally normal, and the utilization of iron by red blood cells is reduced in the late stage of uremia, but the primary kidney disease itself can change the above indicators and aggravate renal failure anemia.
4. Inosine clearance rate (Ccr)
The degree of anemia is roughly related to the degree of renal failure. The relationship between hemoglobin and creatinine and creatinine clearance (Ccr) is not obvious when the renal function is more than 70% of normal people, but when the renal function falls below 70% of the normal value. When Ccr is 240ml·min-1/1.73m2, hemoglobin is significantly correlated with Ccr; when Ccr<2ml·min-1/1.73m2, hemoglobin is not significantly correlated with Ccr.
5. Other
The bilirubin is generally normal, and the protoporphyrin in the red blood cells is normal or moderately elevated, but most of the increase is accompanied by a decrease in serum iron and a normal lactate dehydrogenase.
According to the condition, clinical manifestations and symptoms, physical signs are selected for ECG, B-ultrasound, X-ray and other examinations.
Diagnosis
Diagnosis and diagnosis of chronic renal anemia
diagnosis
Have a history of chronic kidney disease, combined with clinical manifestations, laboratory tests, can be diagnosed.
Differential diagnosis
1. Hemorrhagic anemia The incidence of bleeding in this disease accounts for 76%. It is more common in gastrointestinal bleeding and needs to be differentiated from hemorrhagic anemia.
2. Other chronic diseases are anemia.
