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Clinical manifestations of uremia

Dec 30, 2016
Water, electrolyte, acid-base metabolism disorders, metabolic acidosis and water, electrolyte balance disorder is the most common.
(1) metabolic acidosis in chronic renal failure uremia stage of human metabolism of acid products such as phosphoric acid, sulfuric acid and other substances due to renal excretion disorder and retention, can occur". Mild chronic acidosis, but most patients have few symptoms, such as arterial blood HCO3<15 mmol/L, can appear obvious loss of appetite, vomiting, weakness, deep breathing etc..
(2) the disturbance of water and sodium metabolism, mainly manifested as water sodium retention, or low blood volume and hyponatremia. When the renal function is not complete, the kidney's ability to adapt to the excessive sodium overload or over capacity is gradually decreased. Uremia patients such as unduly limiting water, can lead to excessive volume load, different degrees of common subcutaneous edema (eyelids, lower limbs) and / or effusion (pleural and abdominal), then prone to high blood pressure, left ventricular dysfunction (chest tightness performance, activity intolerance and even could not lie down at night) and brain edema. On the other hand, when patients with a lot of urine, and excessive water restriction, or concurrent vomiting, diarrhea and other gastrointestinal symptoms, and easily lead to dehydration. In clinical capacity overload is common, so patients in uremic intake should pay attention to proper control of water (except drinking water also includes soup, fruit, Rice porridge more food water), avoid excessive fluid replacement should be the treatment process, to prevent the occurrence of heart failure and pulmonary edema.
(3) potassium disorders: when GFR was reduced to 20-25ml/min or less, the renal excretion of potassium capacity decreased gradually, then prone to hyperkalemia; especially when excessive intake of potassium, acidosis, infection, trauma, such as gastrointestinal bleeding occurs, more prone to hyperkalemia. Severe hyperkalemia (serum potassium >6.5mmol/L) has a certain risk, the need for timely treatment and rescue (see hyperkalemia treatment). At the same time, due to lack of potassium intake, too much loss of gastrointestinal tract, the use of potassium excretion and other factors, there may be hypokalemia. The most common clinical manifestations are hyperkalemia, so patients with uremia should strictly limit the intake of food containing high potassium, and should regularly review the blood potassium.
(4) disturbance of calcium and phosphorus metabolism, mainly phosphorus and calcium deficiency. Chronic renal failure renal generation 1, 25- (OH) 2D3 decreased, intestinal calcium absorption is reduced; the target organ of 1, 25- (OH) 2D3 resistant, the renal tubular reabsorption of calcium decreased, in addition, hyperphosphatemia can make higher calcium phosphate product, promote the deposition of calcium phosphate, calcium induced ectopic and hypocalcemia. The food is rich in phosphorus, and the concentration of serum phosphorus is regulated by the absorption of phosphorus by the intestinal tract and the excretion of the kidney. When the decline in glomerular filtration rate, urinary P excretion decreased when phosphorus concentration increased gradually, hyperphosphatemia further inhibited 1, 25- (OH) 2D3 synthesis, exacerbation of hypocalcemia. Parathyroid gland secretes more PTH to maintain calcium. Causes of secondary hyperparathyroidism (PHPT).
Metabolism of protein, carbohydrate, fat and vitamin
CRF protein metabolism in patients generally showed protein metabolism disorder accumulation (azotemia), including urea, guanidine compounds, creatinine, indole, amines, phenols and molecular substances.
Urea excretion, urea accumulation in uremia, and fatigue, anorexia, vomiting, inattention, hypothermia and hemorrhagic tendency performance; arginine guanidino compounds normally mainly metabolized in the liver for urea, guanidine acetic acid and creatinine, urinary sepsis when urea and creatinine accumulation, and the fine amino acids can be through other channels for decomposition of methyl guanidine and guanidine arginine. Among them, methyl guanidine is the most toxic small molecule substance, and the accumulation in the body can reach 70 to 80 times the normal value, which is related to weight loss, red cell life span, vomiting, diarrhea and lethargy. Amine aliphatic amine can cause myoclonus, asterixis and hemolysis; polyamines (spermine, cadaverine and putrescine) can cause anorexia, nausea and vomiting and urinary protein, and can promote the dissolution of red blood cells, inhibition of erythropoietin production, promote the occurrence of pulmonary edema, ascites and edema of renal failure.
Abnormal glucose metabolism is mainly manifested in two cases of impaired glucose tolerance and hypoglycemia. Hyperlipidemia is very common, most of the patients showed mild to moderate hypertriglyceridemia, a small number of patients showed mild hypercholesterolemia, or both two. Vitamin metabolism disorders are common, such as increased serum vitamin A levels, vitamin B6 and folic acid deficiency.
Cardiovascular system performance
Cardiovascular disease is one of the major complications and the most common cause of death in patients with CKD. Especially in the stage of end-stage renal disease (that is, uremia stage), the mortality rate of cardiovascular disease (45%-60%) was increased. A recent study found that uremic patients with adverse cardiovascular events and atherosclerotic cardiovascular disease than the general population is about 15-20 times.
Chronic renal failure due to renal hypertension, acidosis, hyperkalemia, sodium and water retention, anemia and toxic substances, etc., can occur heart failure, arrhythmia and myocardial damage, because urea (possibly uric acid) stimulation, can also have sterile pericarditis, patients with precordial pain. Physical examination time and pericardial friction sound. In severe cases, the presence of fibrin and bloody exudate. Vascular calcification and atherosclerosis also play an important role in cardiovascular disease.
Respiratory symptoms
The patient's exhaled breath has the smell of urine, which is due to bacteria in saliva urea formation because of excessive ammonia; body fluids can appear shortness of breath, shortness of breath and slow; patients with respiratory acidosis and deep, serious when can see the particularity of Kussmaul respiratory acidosis (deep breath). Fluid overload, cardiac dysfunction can cause pulmonary edema or pleural effusion; by alveolar capillary permeability increase induced by uremic toxins, can cause pulmonary congestion and pulmonary edema at "uremia, chest X-ray can appear" butterfly wing "sign, timely diuresis can rapidly improve the symptoms of dialysis or fibrinous pleurisy is urea; stimulation of inflammation; pulmonary calcification is caused by calcium phosphate deposition in lung tissue.
Gastrointestinal symptoms
The earliest symptom of digestive system in patients with uremia is loss of appetite or indigestion, anorexia can exacerbations, nausea, vomiting or diarrhea. The occurrence of these symptoms may be the intestinal bacteria and urease resolve urea into ammonia, ammonia stimulates gastric mucosal inflammation and multiple superficial ulcer etc.. In addition, nausea and vomiting are also associated with dysfunction of the central nervous system. Gastrointestinal bleeding is more common, the incidence is significantly higher than that of normal people, mostly due to gastric mucosal erosion or peptic ulcer.
Blood system performance
The abnormal blood system of CRF patients mainly showed renal anemia and bleeding tendency. Most of the patients were generally mild and moderate anemia, the reason is mainly due to lack of erythropoietin, called renal anemia; factors such as iron deficiency, malnutrition, bleeding, can aggravate the degree of anemia. Advanced CRF patients have abnormal platelet function, bleeding tendency, such as subcutaneous or mucosal bleeding, bruising, gastrointestinal hemorrhage, cerebral hemorrhage etc..
Symptoms of neuromuscular system
Early symptoms may have insomnia, lack of concentration, memory loss, etc.. In may have indifferent reaction, delirium, convulsions, hallucinations, coma, mental disorders etc.. Peripheral neuropathy is common, sensory neuropathy is more obvious, the most common is the kind of feeling of loss distribution of acral socks, also can have numbness, burning or pain, deep reflex, and neuromuscular excitability increase, such as muscle tremors, spasm, restless legs sign. The occurrence of these symptoms is related to the following factors: some toxic substances accumulation may cause degeneration of nerve cells; the electrolyte and acid-base balance disorders; cerebral vasospasm in renal hypertension induced by hypoxia, and increased capillary permeability, can cause brain cell degeneration and brain edema. The dialysis patients may suffer from dialysis disequilibrium syndrome, such as nausea, vomiting, headache, convulsion, and so on, mainly due to the imbalance of the osmotic pressure of the cells and the brain edema and intracranial pressure.
Skeletal lesions
Renal osteodystrophy (i.e. renal osteodystrophy) is quite common, including osteitis fibrosa (high turnover bone), bone formation (adynamic bone disease), bad osteomalacia (low turnover bone disease) and osteoporosis. In the pre dialysis patients with skeletal X-ray found abnormal about 35%, but the pain, walking inconvenience and spontaneous fracture is rare (less than 10%). Bone biopsy (biopsy) of about 90% can be found abnormal, so early diagnosis depends on bone biopsy. Osteitis fibrosa is mainly due to PTH caused by excessive, prone to bone salts, rib fracture. X-ray examination showed bone cystic defect (such as bone, rib) and osteoporosis (such as the spine, pelvis and femur) performance.
Bone formation and the occurrence of adverse blood PTH concentration is relatively low, some osteogenic factor deficiency, which is not enough to maintain bone regeneration; high dialysis patients such as excessive application of active vitamin D, calcium and other drugs or dialysate calcium content, may make the blood concentration of PTH is low.

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