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  Chronic renal failure refers to a variety of kidney disease leading to progressive decline in renal function irreversible, until the loss of function arising from a series of symptoms and metabolic disorders consisting of clinical syndrome, referred to as chronic renal failure. Chronic end-stage renal failure is often said that uremia. Uremia is not an independent disease, but a variety of advanced clinical common kidney disease syndrome, chronic renal failure is the terminal stage of the emergence of a series of clinical manifestations of the syndrome. Clinical manifestations

  Water, electrolyte, acid-base metabolism disorders

  To metabolic acidosis and water, electrolyte balance disorders are the most common.

  (1) metabolic acidosis chronic renal failure uremic phase of the human body metabolism of acidic products such as phosphoric acid, sulfuric acid and other substances due to renal excretion barrier and retention, can occur "uremic acidosis." Mild chronic acidosis, the majority of patients with less symptoms, but if the arterial blood HCO3 <15 mmol / L, there may be significant loss of appetite, vomiting, weakness, deep breathing and so on.

  (2) water and sodium metabolism, mainly Shuinazhuliu, or hypovolemia and hyponatremia. Renal insufficiency, the kidneys on the sodium overload or excess capacity of adaptability gradually decreased. Uremic patients, such as unduly restrict water, can lead to excessive load capacity, common subcutaneous edema of varying degrees (eyelids, lower limbs) or / and body cavity effusion (pleural cavity, abdominal cavity), then prone to blood pressure, left Heart failure (manifested as chest tightness, decreased tolerance to activity even at night can not be supine) and cerebral edema. On the other hand, when the patient a lot of urine, but excessive restrictions on water, or concurrent vomiting, diarrhea and other gastrointestinal symptoms, but also easily lead to dehydration. Clinical capacity overload is more common, so patients with uremia in peacetime should pay attention to proper control of water intake (in addition to drinking water, including soup, porridge, fruits and other watery food), the process of diagnosis and treatment should avoid excessive Rehydration, to prevent heart failure pulmonary edema.

  (3) potassium metabolism: when the GFR down to 20-25ml / min or less, the renal potassium excretion capacity decreased, prone to hyperkalemia at this time; especially when excessive potassium intake, acidosis, infection, Trauma, gastrointestinal bleeding and other occurrences, more prone to hyperkalemia. Serious hyperkalemia (serum potassium> 6.5mmol / L) there is a certain risk, the need for timely treatment and rescue (see the treatment of hyperkalemia). Sometimes due to inadequate intake of potassium, gastrointestinal loss is too much, the application of potassium diuretics and other factors, can also occur hypokalemia. Clinical more common is hyperkalemia, so patients with uremia should be strictly limited to high potassium intake of food, and should regularly review the serum potassium.

  (4) calcium and phosphorus metabolism disorders, mainly for excessive phosphorus and calcium deficiency. Decreased 1,25- (OH) 2D3 in the kidneys during chronic renal failure and reduced calcium absorption in the intestinal tract; resistance to 1,25- (OH) 2D3 by target organs, reduced reabsorption of renal tubules, Phosphorus can increase the product of calcium and phosphorus to promote the deposition of calcium phosphate, causing ectopic calcification, blood calcium decreased. Food is rich in phosphorus, phosphorus concentration by the intestinal absorption of phosphorus and renal excretion to adjust. When the glomerular filtration rate decreased, urinary phosphorus excretion decreased, the phosphorus concentration increased gradually, high phosphorus further inhibition of 1,25 - (OH) 2D3 synthesis, increased hypocalcemia. Parathyroid compensatory secretion of more PTH to maintain serum calcium. Resulting in secondary hyperparathyroidism (referred to as hyperparathyroidism).

  Protein, carbohydrates, fats and vitamins metabolic disorders

  CRF patients protein metabolic disorders generally manifested as the accumulation of protein metabolites (azotemia), including urea, guanidine compounds, creatinine, amines, indole, phenols and middle molecular substances.

  Urea excretion, uremia in vivo accumulation of urea, may be associated with fatigue, anorexia, vomiting, inability to concentrate, lower body temperature, bleeding tendency and other performance-related; guanidine compounds under normal circumstances arginine metabolism in the liver mainly urea, Guanacetic acid and creatinine, urea, creatinine accumulation of urea, and arginine can be broken down into other ways for the methyl guanidine and guanidine arginine. Methyl guanidine is the most toxic of small molecules, the body up to 70 to 80 times the normal value, and weight loss, red blood cell life shortened, vomiting, diarrhea, drowsiness and many other clinical symptoms. Amine amine, cadaverine, putrescine) can cause anorexia, nausea, vomiting and proteinuria, and can promote erythrocyte lysis, inhibition of erythrocyte (erythrocyte), erythrocyte The formation of progesterone, promote renal edema, ascites and cerebral edema.

  Abnormal glucose metabolism mainly glucose tolerance and low blood sugar in two cases, the former more common, the latter rare. Hyperlipidemia is quite common, with most patients presenting with mild to moderate hypertriglyceridemia, a small number of patients presenting with mild hypercholesterolemia, or both. Vitamin metabolic disorders are quite common, such as serum vitamin A levels, vitamin B6 and folic acid deficiency.

  Cardiovascular system performance

  Cardiovascular disease is one of the major complications of CKD and the most common cause of death. Especially in end-stage renal disease stage (ie, uremic stage), cardiovascular disease mortality further increased (accounting for 45% -60% of uremic deaths). Recent studies have shown that uremic patients with cardiovascular adverse events and atherosclerotic cardiovascular disease than the general population of about 15-20 times higher.

  Chronic renal failure due to renal hypertension, acidosis, hyperkalemia, sodium and water retention, anemia and toxic substances such as the role of heart failure can occur, arrhythmia and myocardial damage, due to urea (and possibly Uric acid) stimulation, but also the occurrence of aseptic pericarditis, patients with precordial pain, physical examination and pericardial friction sound. Severe pericardial cavity in the presence of cellulose and bloody exudate. Vascular calcification and atherosclerosis in cardiovascular disease also plays an important role.

  Respiratory symptoms

  Patients with gas exhaled urine, which is due to bacterial decomposition of urea in the formation of ammonia in saliva reasons; body fluid can be shortness of breath, shortness of breath; acidosis in patients with slow and deep breathing, severe acidosis can be seen the specificity Kussmaul breathing (deep breathing). Excessive fluid, heart failure can cause pulmonary edema or pleural effusion; uremic toxins induced by alveolar capillary permeability increased pulmonary congestion can cause uremic pulmonary edema, pulmonary x-ray examination at this time there may be " Butterfly wing "levy, timely diuretic or dialysis The symptoms can be improved rapidly; cellulose pleuritis is caused by inflammation of urea stimulation; pulmonary calcification is the deposition of calcium phosphate in the lung tissue.

  Gastrointestinal symptoms

  Uremic patients digestive system is the earliest symptoms of loss of appetite or indigestion, exacerbations may occur when anorexia, nausea, vomiting or diarrhea. These symptoms may occur with the intestinal bacteria urease decomposition of urea into ammonia, ammonia-induced inflammation of the gastrointestinal tract mucosa and multiple small superficial ulcers and so on. In addition nausea, vomiting and central nervous system dysfunction. Gastrointestinal bleeding are more common, the incidence was significantly higher than normal, mostly due to gastric erosion or peptic ulcer.

  Blood system performance

  CRF patients with abnormal blood system mainly for renal anemia and bleeding tendency. Most patients are generally mild to moderate anemia, mainly due to the lack of erythropoietin, it is called renal anemia; such as accompanied by iron deficiency, malnutrition, bleeding and other factors can increase the degree of anemia. Late CRF patients with abnormal platelet function, bleeding tendency, such as subcutaneous or mucosal bleeding, ecchymosis, gastrointestinal bleeding, cerebral hemorrhage.

  Neuromuscular system symptoms

  Early symptoms may have insomnia, inattention, memory loss and so on. Uremia may have reaction indifferent, delirium, convulsions, hallucinations, coma, mental disorders. Peripheral neuropathy is also common, sensory neurological disorders more significant, the most common is the distribution of acral socks like the loss of feeling, but also may have numbness, burning or pain, deep reflex slow or disappear, and may have neuromuscular Increased excitability, such as muscle tremors, spasms, restless legs syndrome. The occurrence of these symptoms and the following factors: ① the accumulation of certain toxic substances may cause nerve cell degeneration; ② electrolyte and acid-base balance disorders; ③ renal hypertension caused by cerebral vasospasm, hypoxia and capillary permeability Increased, can cause brain cell degeneration and brain edema. Primary dialysis patients may occur dialysis imbalance syndrome, nausea, vomiting, headache, convulsions, mainly due to hemodialysis after intracellular fluid osmotic imbalance and cerebral edema, increased intracranial pressure caused.

  Bone lesions

  Renal osteodystrophy (ie, renal osteodystrophy) is fairly common and includes fibrocystic osteitis (high turnover bone disease), adynamic bone disease, osteomalacia (low turnover bone disease), and bone Osteoporosis. About 35% of skeletal X-ray findings were found in pre-dialysis patients, but bone pain, walking inconvenience, and spontaneous fractures were rare (less than 10%). The bone biopsy (bone biopsy) can be found in about 90% of abnormal, so the early diagnosis depends on bone biopsy.

  Fibrocystic osteitis is mainly due to high PTH caused, prone to bone salt melted, rib fractures. X-ray examination showed bone cystoid defects (such as phalanges, ribs) and osteoporosis (such as the spine, pelvis, femur, etc.) performance.

  Bone formation of poor, mainly with the blood PTH concentration is relatively low, some osteogenesis factors related to insufficient and thus not enough to maintain bone regeneration; dialysis patients such as long-term excessive use of active vitamin D, calcium and other drugs or dialysate calcium content High, it may make the blood PTH concentration is relatively low.


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