Uraemia is a general term for a series of symptoms that occur in the late stages of renal failure. The main symptoms of chronic renal failure are poisoning caused by the accumulation of harmful substances and anemia and bone disease caused by decreased kidney hormones. The most common early symptoms are nausea, vomiting, loss of appetite and other gastrointestinal symptoms. After entering the advanced uremia stage, the whole body system will be affected, and serious conditions such as heart failure, mental disorders, and coma may occur, which are life-threatening. In the past, uremia was considered an incurable disease. Since the 2000s, dialysis and kidney transplant surgery have been implemented, which has significantly extended the life span of uremia patients.
During the uremia stage, in addition to the above-mentioned further aggravation of water, electrolyte, acid-base balance disorders, anemia, bleeding tendencies, hypertension, etc., there may also be symptoms caused by dysfunction of various organ systems and substance metabolism disorders. The clinical manifestations are described below.
(1) Nervous system symptoms
Nervous system symptoms are the main symptoms of uremia. In the early stages of uremia, patients often have symptoms such as dizziness, headache, fatigue, and decreased understanding and memory. As the condition worsens, irritability, muscle tremors, and twitching may occur; eventually it may progress to indifference, lethargy, and coma. The occurrence of these symptoms is related to the following factors: ① The accumulation of certain toxic substances may cause nerve cell degeneration; ② Electrolyte and acid-base balance disorders; ③ Cerebral vasospasm, hypoxia and capillary permeability caused by renal hypertension Increased levels can cause degeneration of brain nerve cells and brain edema.
(2) Digestive system symptoms
The earliest symptom of the digestive system of patients with uremia is loss of appetite or indigestion; when the condition worsens, anorexia, nausea, vomiting or diarrhea may occur. The occurrence of these symptoms may be related to the fact that the urease of bacteria in the intestine decomposes urea into ammonia, and ammonia stimulates the gastrointestinal mucosa, causing inflammation and multiple superficial small ulcers. Patients often suffer from gastrointestinal bleeding. In addition, nausea and vomiting are also related to dysfunction of the central nervous system.
(3) Cardiovascular system symptoms
Patients with chronic renal failure may suffer from renal hypertension, acidosis, hyperkalemia, sodium and water retention, anemia and toxic substances, etc. As a result, heart failure, arrhythmia, and myocardial damage may occur. Due to the stimulating effect of urea (and possibly uric acid), aseptic pericarditis can also occur, and the patient has precordial pain; pericardial friction rub is heard during physical examination. In severe cases, fibrin and bloody exudates may appear in the pericardial cavity.
(4) Respiratory system symptoms
During acidosis, the patient breathes slowly and deeply. In severe cases, Kussmaul breathing, a characteristic of acidosis, can be seen. The breath exhaled by the patient smells like urine. This is due to bacteria decomposing urea in the sleeping fluid to form ammonia. Severe patients may develop pulmonary edema, fibrinous pleurisy or pulmonary calcification and other lesions. Pulmonary edema is related to heart failure, hypoalbuminemia, sodium and water retention and other factors. Fibrinous pleurisy is inflammation caused by urea stimulation; pulmonary calcification is caused by the deposition of calcium phosphate in lung tissue.
(5) Skin symptoms
Skin itching is a common symptom in patients with uremia, which may be caused by stimulation of skin receptors by toxic products; some people think that it is related to secondary thyroid disease It is related to hyperparathyroidism, because removal of the parathyroid glands can immediately relieve this painful symptom. In addition, the patient's skin was dry, flaky, and tan. Changes in skin color were previously thought to be due to an increase in urinary pigment, but examination using an absorption spectrophotometer proved that the skin pigment was mainly melanin. In exposed areas of skin, minor bruises can cause skin ecchymosis. Since sweat contains a high concentration of urea, there are white crystals of urea at the openings of sweat glands, which is called urea cream.
(6) Substance metabolism disorders
1. Impaired glucose tolerance: Uremic patients have impaired glucose tolerance, and their glucose tolerance curve is similar to that of patients with mild diabetes, but this change is not sensitive to exogenous insulin. The possible mechanisms that cause impaired glucose tolerance are: ① Reduced insulin secretion; ② In uremia, the basal level of growth hormone secretion is increased, so the antagonizing effect of insulin is strengthened; ③ The binding disorder between insulin and target cell receptors makes the effect of insulin somewhat limited. Weakened; ④ The activity of liver glycogen synthase is reduced, causing liver glycogen synthesis disorder. It is currently believed that the main cause of the above changes may be the toxic effects of urea, creatinine and medium molecular weight poisons.
2. Negative Nitrogen Balance Negative nitrogen balance can cause wasting, cachexia, and hypoalbuminemia in patients.
Hypoalbuminemia is one of the important causes of renal edema. Factors causing negative nitrogen balance include: ① The patient's protein intake is restricted or protein intake is reduced due to anorexia, nausea and vomiting; ② Certain substances such as methylguanidine can enhance tissue protein catabolism; ③ Infections may occur Leading to increased protein decomposition; ④ protein loss due to bleeding; ⑤ loss of a certain amount of protein in urine, etc.
In uremia, a large amount of urea can leak into the intestinal cavity from the blood. Intestinal bacteria can decompose urea and release ammonia. After the ammonia is transported to the liver by the blood, it can be synthesized into urea or non-essential amino acids, the latter of which is beneficial to the body. Therefore, some people believe that the protein intake of uremic patients can be lower than that of normal people, even lower than 20g per day to maintain nitrogen balance, but protein with higher nutritional value must be given, that is, nutrients rich in essential amino acids. In recent years, some people think.
In order to maintain the nitrogen balance of uremic patients, the protein intake should not be significantly different from that of normal people; and it is believed that excessive restriction of protein intake simply for the purpose of reducing blood urea nitrogen can cause Excessive consumption of one's own protein is therefore harmful rather than beneficial to the patient. 3. In patients with hyperlipidemia and uremia, the main reason is that the lipoprotein (pre-β-lipoprotein) required for the liver to synthesize triglycerides is increased, so the production of triglycerides is increased; it may also be due to the reduced activity of lipoprotein lipase It causes the clearance rate of triglycerides to decrease, so it is easy to form hypertriglyceridemia. This change may be related to the accumulation of methylguanidine.
The cause and pathogenesis of uremia
In uremia, nitrogen-containing metabolites and other toxic substances cannot be excreted and accumulate in the body. In addition to causing disorders of water, electrolyte and acid-base balance, And can cause lesions in multiple organs and systems.
1． Digestive system: The accumulated urea in the body is discharged into the digestive tract, and ammonia is formed in the intestine through the action of bacterial urease, which can stimulate the gastrointestinal mucosa, cause fibrinous inflammation, and even form ulcers and bleeding. The range of lesions is wide, ranging from the oral cavity, esophagus to the rectum. Urotoxic esophagitis, gastritis and colitis are more common. Patients often have symptoms such as nausea, vomiting, abdominal pain, diarrhea, and blood in the stool.
2. Heart and lung diseases: Hypertension caused by water and sodium retention, renal ischemia, and increased renin secretion can cause heart failure if it acts on the heart for a long time. Excessive penetration of urea in the blood into the pericardium and pleura can cause fibrinous pericarditis and fibrinous pleurisy, and pericardial and pleural friction sounds can be heard during auscultation. Heart failure can cause pulmonary edema. The discharge of blood urea from the respiratory tract can cause respiratory inflammation, and sometimes a transparent membrane may be formed along the alveolar walls; the permeability of pulmonary capillaries increases, and a large amount of fibrin and monocytes leak out of the alveolar cavity, with few neutrophils, which is called It is uremic pneumonia.
3． The main changes in the hematopoietic system are anemia and bleeding. Causes of anemia: ① Insufficient production of erythropoietin when severe renal tissue damage occurs. ② Metabolites accumulated in the body, some such as phenol and its derivatives, can inhibit the hematopoietic function of the bone marrow. Other poisons such as guanidine and its derivatives can shorten the survival life of red blood cells, accelerate red blood cell destruction and cause hemolysis. ③Excessive loss of transferrin from urine, causing iron transport disorders in the body.
Uraemic patients often have a tendency to bleed, manifesting as gum bleeding, epistaxis, gastrointestinal bleeding, etc. Causes of bleeding: ① Toxic substances inhibit bone marrow and reduce platelet production. ② Some patients do not have a reduced platelet count, but have a tendency to bleed. This may be due to platelet dysfunction caused by guanidine toxic substances in the blood, weakening platelet cohesion and reducing the release of platelet factor 3.
4. Skeletal system Hypocalcemia is common in urea. This may be due to: ① The kidney's function of excreting phosphate decreases, so the phosphate concentration in the blood increases and the calcium concentration decreases. ② The phosphate accumulated in the body combines with the ingested calcium in the intestine to form insoluble calcium phosphate, which reduces calcium absorption and increases excretion. ③1,25-dihydroxycholecalciferol is the active form of vitamin D that promotes calcium absorption in the intestines and is synthesized in the kidneys. In chronic kidney disease, the synthesis of 1,25-dihydroxycholecalciferol is impaired, causing calcium malabsorption in the small intestine and causing hypocalcemia.
Reduced blood calcium during long-term uremia can cause hyperparathyroidism, thus causing widespread decalcification of bone tissue, which is called renal osteodystrophy (renal osteodystrophy). Its shape is related to osteomalacia (osteomalacia). Similar to osteitis fibrosa cystica. The clinical use of 1,25-dihydroxycholecalciferol and its similar drugs is very effective in treating these calcium metabolism disorders related to renal diseases.
5. Skin: The skin of patients with uremia is often grayish-yellow and itchy. The color of the skin is related to anemia and the accumulation of urochrome in the skin. Urea accumulated in the body can be excreted through sweat glands, forming a crystalline powder on the skin surface called urea cream, which is commonly seen on the face, nose, cheeks, etc. The cause of itching is unclear, but it may be related to the stimulation of nerve endings by urea.