Best Hospital for Kidney Disease

Email US:763363721wxn@gmail.com   Call Us:0086-15176446195

The main clinical manifestations of chronic renal failure

Dec 28, 2016
At different stages of CRF, the clinical manifestations are also different. In CRF the compensation period and decompensation stage, patients without any symptoms, or only weak, backache, nocturia and other mild discomfort; a few patients may have loss of appetite, metabolic acidosis and mild anemia. CRF metaphase, these symptoms become more obvious. In the late stage of uremia, acute heart failure, severe hyperkalemia, gastrointestinal bleeding, central nervous system disorders, and even life-threatening. 1 chronic disorders of water and electrolyte metabolism. In renal failure, acid-base imbalance and electrolyte metabolism disorders are common. In this kind of metabolic disorders, metabolic acidosis and sodium and water balance disorders are the most common.
(1) metabolic acidosis in mild to moderate chronic renal failure (GFR>25ml / min, Scr<350 or mol / L) patients, some patients due to decreased reabsorption of hydrogen ion barrier tubular secretion or renal tubular HCO3-, and normal anion gap hyperchloremic metabolic acidosis, i.e. renal tubular acidosis. When GFR is reduced to <25ml / min (ScI). >350350 mol / L), renal failure metabolites such as phosphoric acid, sulfuric acid and other acidic substances due to renal excretion disorder and retention can occur hyperchloraemia of (or chloremia of) high anion gap metabolic acidosis, namely uremia acidosis". Most patients can tolerate mild chronic acidosis, but if arterial blood HCO3-<15mmol / L}, can have obvious symptoms such as anorexia, vomiting, weakness, deep breathing etc.. The above symptoms may be due to the inhibition of the activity of enzymes in the body.
(2) the disturbance of water and sodium metabolism: the balance of sodium and water is mainly manifested in the retention of sodium and water, and sometimes can be manifested as 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. The retention of sodium and water can be manifested as different degrees of subcutaneous edema or (or) fluid accumulation in the body, which is common in clinical practice. Low blood volume mainly manifested as hypotension and dehydration.
Causes of hyponatremia, which can cause the lack of sodium (true hyponatremia), but also because of too much water or other factors caused (hypokalemia), while the latter is more common, the clinical situation and treatment are completely different, so attention should be paid to the differential.
(3) potassium metabolism disorder: when the GFR from 20 to 25ml / min or lower, 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 / 1) there is a certain risk, the need for timely treatment and rescue. 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.
(4) disturbance of calcium and phosphorus metabolism: calcium deficiency and excessive phosphorus. The lack of a variety of factors and calcium activated calcium intake, vitamin D deficiency, hyperphosphatemia, metabolic acidosis and so on, there was lack of calcium hypocalcemia. The concentration of serum phosphorus was regulated by the absorption of phosphorus by the intestinal tract and the excretion of the kidney. When the glomerular filtration rate decreased and the urine excretion decreased, the serum phosphorus concentration increased. The blood phosphorus concentration and high calcium combined into calcium phosphate deposition in soft tissue, serum calcium decreased, and inhibition of proximal tubule 1, 25 (OH) vitamin D3 (2 ossification in three alcohol), stimulation of parathyroid hormone (PTH). In early renal failure, serum calcium, phosphorus can be maintained in the normal range, and usually do not cause clinical symptoms, only in the middle and late stage of renal failure (GFR<20ml / min) occurs when hyperphosphatemia, hypocalcemia. Hypocalcemia, hyperphosphatemia, active vitamin D deficiency can cause secondary hyperparathyroidism (PHPT) and renal osteodystrophy. (5) magnesium metabolism disorder: when GFR<20ml / min, due to the reduction of renal excretion of magnesium, often mild mild magnesium. Patients often have no symptoms. However, the use of drugs is still not containing magnesium, such as magnesium containing antacids, laxative etc.. Magnesium deficiency can also occur, associated with inadequate intake of magnesium or excessive use of diuretics.
2 protein, carbohydrate, fat and vitamin metabolism disorders
The protein metabolism disorder of CRF patients is generally manifested as the accumulation of protein metabolites (including the level of serum albumin) and the decrease of serum and tissue essential amino acids. These metabolic disorders were mainly related to the increase of protein decomposition and / or synthesis, negative nitrogen balance and renal excretion disorder.
Abnormal glucose metabolism is mainly manifested in two cases of impaired glucose tolerance and hypoglycemia. Impaired glucose tolerance is associated with elevated glucagon and insulin receptor dysfunction, which may be characterized by an increase in fasting plasma glucose levels and postprandial blood glucose levels, but generally less often in patients with symptoms. Hyperlipidemia is common in patients with chronic renal failure, most patients showed mild to moderate hypertriglyceridemia, few patients showed mild hypercholesterolemia, or some combination of the two; some patients plasma very low density lipoprotein (VLDL), apolipoprotein a[LP (a)] level elevated high density lipoprotein (reduce the level of HDL).
Vitamin metabolism disorders in CRF patients are quite common, such as elevated serum vitamin A levels, vitamin B6 and folic acid deficiency, often associated with inadequate dietary intake and decreased activity of some enzymes.
3 cardiovascular manifestations of cardiovascular disease is one of the main complications and the most common cause of death in patients with CKD. Especially in the stage of end-stage renal disease, the mortality rate was further increased (45%_60%). A recent study found that uremic patients with adverse cardiovascular events and atherosclerotic cardiovascular disease than the general population of about 15 to 20 times. In the United States, the annual mortality rate of the central vascular disease in the general population is 0.27%, while that of hemodialysis patients is as high as 9.5%, which is about 35 times that of the former.
(1) hypertension and left ventricular hypertrophy: the majority of patients with varying degrees of high blood pressure, mostly due to sodium retention, renin angiotensin increased or / and some of the factors that contribute to diastolic blood vessels. High blood pressure can cause arteriosclerosis, left ventricular hypertrophy and heart failure. The internal fistula, which is caused by anemia and hemodialysis, can result in high cardiac output state, increase left ventricular load and left ventricular hypertrophy.
(2) heart failure: the most common cause of death in patients with uremia. With the deterioration of renal function, the prevalence of heart failure increased significantly, up to 65% ~. Most of the reasons are related to water sodium retention, hypertension and uremia. Paroxysmal dyspnea, pulmonary edema and other symptoms, not supine with acute left heart failure, but there is generally no cyanosis.
(3) uremic cardiomyopathy: the etiology may be related to the retention of metabolic waste and anemia and other factors; some patients may be associated with coronary atherosclerotic heart disease. The occurrence of arrhythmia was related to myocardial injury, hypoxia, electrolyte disturbance and accumulation of uremic toxins.
(4) pericardial disease: pericardial effusion is common in patients with CRF, about the causes and uremic toxin, hypoproteinemia, heart failure and other factors, a few cases may also be related to factors such as infection and hemorrhage. The light can be asymptomatic or have low heart sound blunt, far away, a few cases may also have pericardial tamponade. Pericarditis can be pided into uremia and dialysis related; the former is relatively rare, the clinical manifestations and general pericarditis is similar to that of idealism for bloody pericardial effusion.
(5) vascular calcification and atherosclerosis: in recent years, due to the abnormal distribution of hyperphosphatemia, calcium and vascular protective proteins (such as fetuin A) deficiency caused by vascular calcification, also plays an important role in cardiovascular disease. Atherosclerosis often progresses rapidly, and the degree of pathological changes in hemodialysis patients is higher than that before dialysis. In addition to the coronary arteries, cerebral arteries and systemic peripheral arteries also occur in atherosclerosis and calcification.
4 respiratory symptoms or fluid overload acidosis may have shortness of breath, shortness of breath, severe acidosis can cause deep breathing. Excessive body fluid, cardiac insufficiency can cause pulmonary edema or pleural effusion. The alveolar capillary permeability increase induced by uremic toxins, can cause pulmonary congestion and pulmonary edema "in uremia, chest X-ray can appear" butterfly wing "sign, timely diuresis or dialysis can rapidly improve the symptoms.
5 gastrointestinal symptoms are loss of appetite, nausea, vomiting, mouth of urine. Gastrointestinal bleeding is more common, the incidence is significantly higher than that of normal people, mostly due to gastric mucosal erosion or peptic ulcer, especially the former is the most common.
6 the hematological manifestations of CRF, the patients with abnormal blood system mainly for 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 with bleeding tendency, the causes and the decrease of platelet function, advanced CRF patients may also have coagulation factor VIII deficiency. Mild bleeding can occur subcutaneous or mucosal bleeding, ecchymosis, or gastrointestinal bleeding may occur, such as cerebral hemorrhage.
7 early symptoms of neuromuscular system symptoms may be fatigue, insomnia, lack of concentration, etc.. Personality changes, depression, memory loss, and reduced judgment. Uremia often 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, and muscle atrophy and weakness. The initial dialysis patients can produce dialysis disequilibrium syndrome, mainly blood urea nitrogen decreased too fast, resulting in intracellular and extracellular fluid osmotic pressure imbalance, caused by increased intracranial pressure and brain edema, nausea, vomiting, headache, severe convulsions. Long term hemodialysis patients sometimes "dialysis dementia", and dialysis water aluminum content too much due to aluminium poisoning related.
8 endocrine disorders mainly include: renal endocrine disorders: such as 1, 25, 2 (OH) vitamin D3 and erythropoietin deficiency and renal renin angiotensin II excessive; hypothalamic pituitary endocrine disorders such as prolactin, melanophore hormone, luteinizing hormone (.MSH) luteinizing hormone (FSH), follicle stimulating hormone (LH), adrenocorticotropic hormone (ACTH) levels increased; endocrine function disorder of the peripheral: most of the patients had secondary hyperparathyroidism (elevated plasma PTH), some patients (about 1/4) slightly reduced levels of thyroxine; other disorders, such as insulin receptor hypogonadism is quite common.
9 bone lesions of renal osteodystrophy (i.e. renal osteodystrophy) is quite common, including osteitis fibrosa (high conversion osteopathy), bone formation, poor osteomalacia (low turnover bone disease) and osteoporosis. In the pre dialysis patients with skeletal X-ray found abnormal about 35%, and the emergence of bone 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 high PTH caused by the excessive osteoclastic activity, causing bone salts, increased bone resorption, bone collagen matrix damage, and substituting fibrous tissue, fibrous cystic osteitis, prone to rib fracture. X-ray examination showed bone cystic defect (such as bone, rib) and osteoporosis (such as the spine, pelvis, femur etc.) 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.
Osteomalacia is mainly due to the lack of ossification of three alcohol or aluminum poisoning caused by bone tissue calcification, resulting in excessive accumulation of calcified bone tissue; adult spine and pelvis to perform the earliest and prominent, there may be bone deformation.
Dialysis related amyloidosis bone disease (DRA) occurs only in dialysis after many years, may be due to beta 2 microglobulin amyloid deposition in bone by X-ray with cystic change in carpal bone and femoral head, femoral neck fracture can occur spontaneously.

Contact the Health Information Center

Phone: 0086-15176446195 | TTY: 0086-15176446195 | Email: 763363721wxn@gmail.com | Hours: 8:00 a.m. to 22:00 p.m. China time