Definition of renal anemia
Many patients with chronic kidney disease will gradually develop pallor, pale eyelids and nail beds, fatigue and sleepiness, mental weakness, significantly reduced activity endurance, dizziness, headache, tinnitus, blurred vision, poor concentration, panic, chest tightness and breathlessness, loss of appetite, nausea and constipation as the disease slowly progresses, so be extra cautious that you may have renal anemia.
Renal anemia refers to anemia caused by various factors that cause insufficient production of erythropoietin (Epo) in the kidneys or some toxic substances in the plasma of uremia that interfere with the production and metabolism of red blood cells, and is a common complication of chronic renal insufficiency to the end stage. The degree of anemia is often correlated with the degree of renal decompensation.
According to the WHO (World Health Organization) recommended diagnostic criteria for anemia, anemia is diagnosed at age >15 years with hemoglobin <130 g/L in men, <120 g/L in adult non-pregnant women, and <110 g/L in adult pregnant women. This criterion is also referred to for renal anemia. Usually most patients with chronic kidney disease, reaching stage 3, develop anemia.
Pathogenesis of renal anemia
Red blood cells, also known as erythrocytes, are the most numerous type of blood cell in the blood. In healthy people, the life span of red blood cells is about 120 days, but in uremic patients, due to the presence of uremic toxins, the life span of red blood cells is about 90 days. Red blood cells transport oxygen to all parts of the body tissues, and then transport metabolites from all parts, so they are an indispensable “transport team” in our body. Hemoglobin and iron are the main substances that make up red blood cells. In simple terms, anemia is a decrease in the concentration of hemoglobin and the number of red blood cells in the blood that function normally. A decrease in hemoglobin causes a decrease in oxygen transport, which is the basis for the survival of all cells in the body, so all tissues and organs in the body become deprived of oxygen when anemia occurs.
The ability of a healthy person to maintain a stable hemoglobin concentration and red blood cell count, neither too much nor too little, is dependent on the body’s own regulation, which requires the appropriate hormones to transmit information to the bone marrow, the blood-producing organ. Erythropoietin (EPO) is the “messenger” responsible for transmitting hematopoietic information. When the body is deficient in this hormone, the bone marrow reduces blood production, resulting in anemia. The kidneys are the organ that produces this hormone. When the kidney function decreases, EPO production decreases and anemia gradually develops. Therefore, patients with renal failure need exogenous supplementation of erythropoietin.
As the saying goes, if there is no hematopoietic material, the bone marrow will not make enough red blood cells for us, and even if it does, its morphology will not be normal, some are large and some are small. Abnormal morphology makes red blood cells less functional and more susceptible to destruction. The production of red blood cells requires a number of important substances, including amino acids, fats, carbohydrates, as well as iron and growth factors: folic acid and vitamin B12. Since patients with uremia usually have an appetite disorder that causes a deficiency of hematopoietic materials, additional iron and folic acid supplements and, in special cases, vitamin B12 supplements are sometimes required depending on clinical needs. Too little of these hematopoietic materials will not work, and too much will cause toxicity, so regular blood tests are needed to guide the dosage of supplementation.
In addition, some systemic diseases can also cause anemia. For example, excessive menstruation in female patients; blood loss during dialysis and frequent blood tests in hemodialysis patients; hyperparathyroidism; peptic ulcers and hemorrhoids; chronic infections and occupational diseases; certain blood disorders such as aplastic anemia and leukemia; hypersplenism in liver cirrhosis, etc.
Clinical symptoms of renal anemia
How do you know that you have renal anemia? As the name implies, renal anemia requires two factors: chronic kidney disease and anemia.
Kidney disease has been called the “invisible killer”, and many patients are diagnosed with “uremia” at the time of consultation and lose the chance of treatment. The official definition of chronic kidney disease is structural or functional damage to the kidney lasting more than 3 months with or without a decrease in glomerular filtration rate; or a glomerular filtration rate of less than 60 ml/min/1.73 m2 for more than 3 months with or without kidney damage. It sounds too complicated for patients to consult nephrology if they have back pain, edema, poor nausea, weakness, urinary urgency and frequency, painful urination, increased nocturia, decreased urine volume, deepened urine color such as thick tea, hematuria, foamy urine, etc. The doctor will determine whether you belong to the chronic kidney disease population based on the examination results and treatment effects. Patients with certain chronic diseases, such as hypertension, diabetes, gout, recurrent urinary stones, recurrent urinary tract infections, polycystic kidney, and patients who take oral painkillers and herbal medicines for a long time should also visit the nephrology department regularly to evaluate whether there is secondary kidney damage. Once you are in the management of chronic kidney disease, you will need to follow up with a regular nephrology clinic (preferably with a regular doctor) and your doctor will perform the appropriate tests and treatment according to the stage you are in.
When you reach a certain stage of chronic kidney disease, you should be alert to the occurrence of anemia (see the previous article for the causes). How to find out you are anemic? When you wake up in the morning and look at yourself in the mirror, do you have pale face and lips, cracked tongue, dry hair, thinness, lethargy, flat nails (anti nail), lusterless and easy to break; the work you are usually able to do is now incompetent, the endurance of activities is significantly reduced, dizziness, headache, tinnitus, blurred eyes, concentration is not good; sometimes there is also panic, chest tightness and breathlessness, with frequent attacks of angina pectoris in patients with coronary heart disease; there are Many patients also suffer from loss of appetite, indigestion, nausea, constipation, or even “xerophagia”. If you suspect that you have anemia, you can visit a hospital for a routine blood test. Based on the diagnostic criteria for anemia, your doctor will determine whether you have “renal anemia” and how to treat it.
Treatment goals and monitoring (based on the consensus on the diagnosis and treatment of renal anemia of the Nephrologist Branch of the Chinese Medical Association)
I. Laboratory indicators to assess anemia.
(1) Complete blood count: including hemoglobin, red blood cell indicators [including mean red blood cell volume (MCV), mean red blood cell hemoglobin volume (MCH), mean hemoglobin concentration (MCHC)], white blood cell count, and platelet count.
(2) Reticulocyte count.
(3) Iron reserve and iron utilization indicators: including serum ferritin concentration, transferrin saturation.
(4) Vitamin B12, folic acid, bone marrow pathology and other items can be examined when the condition requires.
(2) When to perform routine blood tests.
(1) Whenever clinical symptoms, signs or other medical indicators suggest anemia, hemoglobin should be measured promptly.
(2) For patients without a history of anemia and not treated with erythropoietin: for chronic kidney disease stage 1~3, measure hemoglobin at least once every 6 months; for chronic kidney disease stage 4~5, those who have not started dialysis treatment, measure hemoglobin at least once every 3~6 months; for chronic kidney disease stage 5 and dialysis patients, measure hemoglobin at least once every 1~3 months.
(3) Patients with a history of anemia, receiving erythropoietin therapy, dialysis or the initial phase of maintenance dialysis therapy should increase the frequency of measurement; patients with chronic kidney disease stage 3 to 5 receiving erythropoietin therapy and not receiving dialysis and peritoneal dialysis therapy should have their hemoglobin measured at least once every 3 months; patients with chronic kidney disease stage 5 receiving hemodialysis should have their hemoglobin measured at least once a month.
(4) Patients with chronic kidney disease receiving stable erythropoietin therapy should have their iron status monitored at least once every 3 months.
(5) Non-dialysis patients with chronic kidney disease stages 3-5 who are not receiving erythropoietin therapy should have their iron status monitored once every 3 months and should be evaluated first for iron status when anemia develops.
(6) Maintenance hemodialysis patients not receiving erythropoietin therapy should have their iron status monitored once every 3 months.
(7) The frequency of iron status monitoring should be increased when the following conditions occur to decide whether to start, continue or stop iron therapy: when erythropoietin therapy is started; when the dose of erythropoietin is adjusted; when bleeding is present; when the efficacy of intravenous iron therapy is monitored; when there are other conditions that cause changes in iron status, such as uncontrolled co-inflammatory infections.
III. Target values for anemia treatment.
(1) Hemoglobin >110 g/L (Hct> 33%), but >130 g/L or more is not recommended.
(2) Ferritin 100-500ug/l and transferrin saturation >20% in peritoneal dialysis patients.
Having written so much, in fact, I just want to say that the monitoring items performed for the treatment of renal anemia are complex and the treatment goals that need to be achieved by different patients need to be individually formulated, so the best way is to follow the advice of the doctor in charge and the specialist nurse and have the laboratory tests on time in order to adjust the treatment plan in time.
Treatment of renal anemia
Since renal anemia occurs not simply because of a decrease in erythropoietin secretion by the kidneys, there are many other factors to consider. Many uremic dialysis patients will be combined with other diseases that can cause anemia, such as infection, gastrointestinal bleeding, hypersplenism, and malignant tumors. Therefore, the treatment of anemia should be comprehensive, meticulous and individualized.
I. Finding the cause of anemia.
In addition to insufficient erythropoietin production due to decreased renal function, other causes of anemia include iron deficiency, combined inflammatory diseases, chronic blood loss, hyperparathyroidism, fibrous osteitis, aluminum toxicity, hemoglobinopathy, vitamin deficiency, multiple myeloma, malignancy, malnutrition, hemolysis, inadequate dialysis, application of ACEI/ARB and immunosuppressive agents, hypersplenism, and Erythropoietin antibody-mediated pure red blood cell aplastic anemia (PRCA), and other conditions. Therefore, timely consultation, your specialist nurse and doctor will help you analyze the cause of anemia and treat the cause.
II. Drug treatment.
Do not misuse blood-supplementing drugs, and must strictly grasp the indications of various drugs.
Most uremic dialysis patients need exogenous supplementation of erythropoietin, and the dose, frequency and route of medication should be adjusted according to the changes in hematocrit. Usually hemodialysis patients can choose between intravenous and subcutaneous administration (intravenous application requires larger doses). Subcutaneous injection is easy to learn and convenient to operate, so it is mostly used for peritoneal dialysis patients. When the hematocrit exceeds the target line, do not stop using erythropoietin, but slowly reduce the dose. Because the life span of erythrocytes in uremic patients is 60-90 days, the hematocrit will not change much at the beginning of discontinuation, but when these erythrocytes age and die, and no new erythrocytes are produced, the hematocrit will drop rapidly, so uremic patients must not discontinue erythropoietin on their own, but must adjust the dose under the guidance of a doctor.
Due to the decreased appetite of uremic patients, eating less, the gastrointestinal tract has limited absorption and utilization of iron in food, in addition, the life span of uremic toxin red blood cells is shorter than that of healthy people, so most of them will suffer from iron deficiency. In peritoneal dialysis patients, oral iron is applied in most cases for the convenience of the patient due to the lack of open venous access (hemodialysis patients can be given directly intravenously by access during dialysis). If the hematocrit continues to decrease and iron deficiency is evident, the physician may also recommend the use of intravenous iron at the hospital. Both insufficient and excessive iron can affect health and therefore require monitoring and guidance from a health care provider.
Vitamin B12 and folic acid are indicated for the treatment of megaloblastic anemia and most dialysis patients are not deficient in these two elements, but if a uremic patient has a combination of digestive disorders, there is a risk of malabsorption of these two elements. Doctors and nurses will treat patients accordingly based on their blood work and the results of vitamin B12 and folic acid tests.
Androgens can also be used as an anti-anemia treatment. However, the drug can cause masculinization (beard growth, hairiness, acne, thickening of the voice, menstrual disorders, etc.), hypertension, hyperkalemia, sodium retention, and prostate disorders, limiting its use in renal anemia. Most guidelines also do not recommend its use in the treatment of renal anemia.
III. Blood transfusion.
The main advantage of blood transfusion is its ability to rapidly reduce or correct anemia, and it is particularly useful in patients with rapidly declining hematocrit. When treating chronic anemia, transfusion of red blood cells should be avoided as much as possible when the condition permits, to reduce the risk of transfusion reactions. Patients who are suitable for organ transplantation should avoid transfusion of red blood cells when their condition permits to reduce the risk of allergic sensitization. Therefore the indications for blood transfusion must be properly grasped.
IV. Dietary care.
It is better for anemic people not to drink tea because iron in food, in the form of 3-valent colloidal iron hydroxide, enters the digestive tract. By the action of gastric juice, high-valent iron is transformed into low-valent iron before it can be absorbed. But tea contains tannic acid, easy to form insoluble iron tannate after drinking, thus hindering the absorption of iron. Secondly, milk and some drugs that neutralize stomach acid will hinder the absorption of iron, so try not to eat with iron-containing foods. Iron-rich foods include pig liver, pig blood, lean meat, dairy products, beans, rice, apples, and green leafy vegetables, which can be supplemented on a case-by-case basis. Vitamin C can promote the conversion of high-valent iron to low-valent, so it can be supplemented with meals to promote the absorption of iron.