Chronic renal failure in the elderly
Introduction
Introduction to chronic renal failure in the elderly Chronic renal failure, also known as chronic renal insufficiency, refers to chronic progressive renal parenchymal damage caused by various kidney diseases or systemic diseases of the cumulative kidney, causing the kidneys to maintain their basic functions, such as excreting metabolic waste, regulating water and salt, and Acid-base balance, secretion and regulation of various hormone metabolism, etc., thus presenting a series of clinical symptoms such as azotemia, metabolic disorders and systemic involvement. Chronic renal failure is one of the common conditions in urological diseases in the elderly. As kidney disease develops, renal function can be progressively reduced, and chronic renal failure is irreversible damage. basic knowledge The proportion of illness: 0.001% Susceptible people: the elderly Mode of infection: non-infectious Complications: hypertension, hyperkalemia, arrhythmia, uremia
Cause
Causes of chronic renal failure in the elderly
(1) Causes of the disease
Although the causes of chronic renal failure in the elderly have something in common with other age groups, in the aging stage, the incidence of secondary kidney disease is increased in aging-related diseases, and chronic renal failure is more common. Some causes are Younger patients are less common, such as prostate cancer or benign prostatic hyperplasia leading to hydronephrosis, renal vascular hypertension or renal failure caused by atherosclerosis, multiple myeloma, drug-induced renal failure, etc. Pre-renal azotemia caused by congestive heart failure or hypovolemia is also common in humans. Glickmen et al reported that according to pathological findings, the causes of CRF in the elderly were: nephrosclerosis (36.5%), diabetes (25.3%). ), crescentic nephritis (12.6%), amyloidosis (6.9%), polycystic kidney disease (6%).
(two) pathogenesis
Mechanism of progressive deterioration of chronic renal failure: The pathogenesis of chronic renal failure is complex and has not yet been fully clarified. The following main theories are:
1. The theory of living nephron and the theory of imbalance
Renal parenchymal disease causes a considerable amount of nephron destruction, and the remaining kidney units must increase the workload in order to compensate for the normal needs of the body. Therefore, each kidney unit undergoes compensatory hypertrophy to enhance glomerular filtration. The function and the function of the renal tubule to treat the filtrate, but if the destruction of the renal parenchyma disease continues, the number of kidney units is less and less, and finally, even if the best efforts are made to achieve the minimum requirements of human metabolism, kidney failure occurs. This is the theory of the survival of the kidney unit. When kidney failure occurs, there is a series of morbid phenomena. In order to correct it, the body should be adjusted accordingly (ie, corrected), but in the process of adjustment, it is inevitably costly. As a result, new imbalances occur, causing new damage to the human body. For example, when the number of healthy kidney units is reduced, the amount of phosphorus excreted in each of the remaining nephrons is compensated to increase. From the whole kidney, the phosphorus is discharged. The total amount can still be basically normal, so the blood phosphorus is normal, but when the remaining renal units are reduced to the point where they cannot be compensated, the blood phosphorus is elevated, and the body needs to correct the retention of phosphorus. Hyperparathyroidism is promoted to promote renal phosphorus excretion. Although hyperphosphatemia has improved, hyperparathyroidism causes other symptoms, such as extensive fibrous osteitis and nerves due to osteolytic action. Systemic toxic effects, etc., cause new damage to the human body. This is the theory of imbalanced imbalance, which is the development and supplement of the theory of healthy kidney units.
2. Glomerular high filtration theory
When the nephron is destroyed to a certain amount, the excretion load of each remaining nephron metabolic waste increases, and thus the hyperperfusion of the glomerular capillaries occurs with compensatory high pressure and high filtration, and the above glomeruli High" can cause:
1 glomerular epithelial cell foot process fusion, mesangial cells and matrix significantly proliferated, glomerular hypertrophy, and then hardening.
2 glomerular endothelial cell injury, induce platelet aggregation, leading to microthrombus formation, damage glomerulus and promote hardening.
3 increased glomerular permeability, increased proteinuria and damage to the tubulointerstitial, the above process continues, forming a vicious circle, so that the renal function continues to worsen, this vicious cycle is the development of all chronic kidney disease to uremia A common approach, and the destruction of renal parenchymal disease continues is two different things.
3. Renal tubular high metabolism theory
In chronic renal failure, the renal tubules of the healthy nephron are in a compensatory hypermetabolism state, the oxygen consumption is increased, the oxygen free radicals are increased, and the renal tubular cells produce a significant increase in ammonium, which can cause renal tubular damage, interstitial inflammation and Fibrosis, and even loss of nephron function, is now clear, the progress of chronic renal failure and the severity of tubulointerstitial damage are closely related.
4. Other
Some scholars believe that the progressive deterioration mechanism of chronic renal failure is related to the following:
1 In the "three high" condition of glomeruli, the level of angiotensin II in renal tissue is increased, and the expression of growth factors such as transforming growth factor beta is increased, resulting in an increase in extracellular matrix and glomerular sclerosis.
2 Excessive protein is filtered out from the glomerulus, which causes high glomerular filtration, and the proximal convoluted tubule cells absorb the protein through the pinocytosis, which can cause damage to the renal tubules and interstitium, leading to loss of function of the nephron.
3 lipid metabolism disorder, low-density lipoprotein can stimulate mesangial cell proliferation, followed by glomerular sclerosis, and promote renal function deterioration.
Prevention
Elderly patients with chronic renal failure prevention
1. Risk factors for progression of chronic renal failure
There are many factors influencing the progression of chronic renal failure. Any factors that can accelerate the progression of chronic renal failure can be regarded as risk factors, including the following aspects:
(1) primary disease: diabetic nephropathy, membrane proliferative nephritis can often develop into chronic renal failure, uremia, primary or secondary acute nephritis, generally can occur acute renal failure, some of which are Longer, manifested as chronic renal failure, adult patients with purpuric nephritis, the course of disease is often faster than patients with IgA nephropathy; some patients with IgA nephropathy have a rapid rate of renal failure, which requires further observation, severe hypertension and "malignant "If hypertension is not controlled in time, the progression of renal failure is also quite rapid.
(2) Causes: acute infection, sepsis, major bleeding, major surgery, insufficient blood volume or dehydration, hypercoagulability, high viscosity state, hypokalemia, hypercalcemia, nephrotoxic drugs or chemical poisoning, stones, urinary Road obstruction, etc., can cause acute exacerbation of chronic renal failure, such as the cause of kidney failure, often have varying degrees of reversibility, as long as found timely, properly handled, often can make kidney function better recovery, or even complete recovery To the level before acute damage.
(3) Diet: High-protein, high-phosphorus diet can often accelerate the progression of chronic renal failure, in addition, high uric acid or high oxalic acid diet may also increase tubule-interstitial damage.
2. Basic countermeasures for early prevention and delayed development of chronic renal failure
(1) Early prevention: With the advancement of epidemiology and treatment of kidney disease, the early prevention of chronic renal failure has attracted the attention of scholars. The so-called early prevention, also known as "primary prevention", refers to the occurrence of chronic renal failure. Prevention begins before, including kidney disease and early screening, positive control of kidney disease or diseases that may affect the kidneys (such as hypertension, diabetes, etc.), correcting lipid metabolism disorders, avoiding certain incentives, etc. Obviously, early prevention Paying enough attention and taking it seriously and taking corresponding measures will further control the occurrence and development of chronic renal failure.
(2) The strategy for delaying the development of chronic renal failure is secondary prevention: mainly includes: strengthening follow-up, avoiding or eliminating certain risk factors; rational diet; controlling systemic or intraglomerular hypertension; controlling high renal units Metabolism; elimination of lipid disorders or high-viscosity; adherence to the treatment of primary disease, etc., respectively, are described below.
1 Strengthen follow-up, avoid or eliminate certain risk factors: It has been reported that the frequency of clinical follow-up is closely related to the progression of chronic renal failure, emphasizing the importance of planning treatment guidance (such as diet, blood pressure, etc.) for patients. In fact, regular, high-quality follow-up can also help patients reduce or avoid certain acute causes (such as hypovolemia, dehydration, nephrotoxic drugs, hyperlipidemia, hypercalcemia, or hypokalemia). Blood, stones, infection, bleeding, etc. occur, or early detection and correction, the frequency of visits should be determined according to the condition, such as whether there is high blood pressure, heart failure and the rate of deterioration of residual renal function, etc., all patients need at least Visiting every 3 months, you must ask for medical history, physical examination, and necessary laboratory tests such as blood routine, urine routine, blood urea nitrogen, creatinine concentration and electrolyte test, endogenous creatinine clearance can monitor renal function The rate of decline in progress.
2 Reasonable diet plan: In the past ten years, experimental research and clinical observations have confirmed that low protein and/or low-phosphorus diet can slow down the course of most patients with chronic renal failure, and even temporarily stop progressing for some time. Some scholars report High protein diet or intravenous input of a large number of amino acids can increase the glomerular filtration rate of normal people or renal failure patients, which may promote the increase of glomerular hyperfiltration and glomerular sclerosis in patients with chronic renal failure; The protein diet (LPD) alone, or the addition of essential amino acids (EAA) or ketoacid (KA), can alleviate the hyperfiltration state of patients with chronic renal failure, thus contributing to the progression of slow renal failure.
The effect of low-phosphorus (<600mg/d) diet is mainly related to the control of hyperphosphatemia. For those with severe hyperphosphatemia, it is sometimes necessary to take appropriate phosphorus binders, such as calcium carbonate (3-12g/d) or hydroxide. Aluminum (30 ~ 100ml / d, not suitable for long-term use), due to the correction of hyperphosphatemia, can reduce the hyperparathyroidism, so the residual nephron damage is slowed, ketoacid treatment can not only reduce blood phosphorus levels, but also The parathyroid glands have a direct inhibitory effect.
3 control of systemic and / or glomerular hypertension: to prevent the progression of glomerular sclerosis, not only to treat systemic hypertension, but also to control glomerular hypertension, the former is mainly the application of antihypertensive drugs The latter is to solve the problem of glomerular hyperperfusion, high filtration, lowering the protein diet, controlling hypertension or diabetes, and considering the use of angiotensin-converting enzyme inhibitors, which may reduce the pressure in the glomerulus. Therefore, it can alleviate the high filtration state.
4 to correct lipid metabolism disorders: First, the fat intake should be appropriate, polyunsaturated fatty acids should not be less than the intake of saturated fatty acids; at the same time, appropriate calorie intake and physical activity can not be ignored.
5 control of high metabolism in the nephron: According to the study, low-protein diet or low-phosphorus diet can reduce the residual nephron oxygen consumption, which may inhibit the high metabolism of nephron, and it is reported that rhubarb preparation may cause body fluids. Decreased basal level and decreased free radical production suggest that the drug may inhibit high metabolism or anti-oxidation of renal tubules, which may cause increased oxidative metabolism of protein and branched-chain amino acids due to metabolic acidosis, and may cause renal interstitial damage. Therefore, supplementing sodium bicarbonate (3 ~ 10g / d) to correct acidosis, not only can alleviate some clinical symptoms, but also play a role in delaying the progression of renal failure.
Others, in addition to the above aspects, in the case of chronic renal failure, increased thromboxane production, platelet hyperfunction, renal non-specific immune disorders (such as macrophages and some cytokines increased), etc., can also take corresponding countermeasures, the application Certain antithrombotic drugs (PGI2, polyunsaturated fatty acid preparations or synthetic drugs), antiplatelet drugs (such as dipyridamole) or Chinese herbs for promoting blood circulation and removing blood stasis (such as salvia miltiorrhiza) may be beneficial in delaying the progression of renal failure.
Complication
Elderly patients with chronic renal failure complications Complications hypertension hyperkalemia arrhythmia uremia
Common anemia, high blood pressure, sodium retention, hyperkalemia, renal bone disease, infection bleeding, acute heart failure arrhythmia, uremia encephalopathy.
Symptom
Symptoms of chronic renal failure in the elderly Common symptoms Loss of appetite, lack of blood pressure, bleeding, weakness, dizziness, hematuria, depression, skin itching, fatigue
The clinical features of CRF in the elderly, in addition to anemia, metabolic acidosis, hypertension and general uremia symptoms, neuropsychiatric symptoms are more prominent, such as ambiguous pronunciation, epileptic seizures, muscle tremors, hemiplegia and disturbance of consciousness, such as uremic encephalopathy The clinical manifestations of each system are as follows.
1. Water, electrolyte imbalance
(1) Water: CRF patients may have both dehydration and water retention. Therefore, it is necessary to dynamically observe the patient's water balance in clinical practice. When the patient has secondary infection, fever, vomiting, diarrhea, etc., water loss is likely to occur. If not timely and appropriate, it is easy to have insufficient blood volume, GFR decreases, BUN rises, symptoms worsen, the latter promotes more water loss, aggravates uremia, forms a vicious circle, and on the other hand, because the kidney has lost regulation The ability of water to supplement too much water is too fast, prone to water retention, can lead to heart failure.
(2) Sodium: Patients with uremia have poor regulation of sodium and are prone to hyponatremia. The reasons are as follows:
1 excessively limit the intake of salt.
2 renal tubular recovery of sodium decreased function.
3 easy to diarrhea and loss of sodium-containing alkaline intestinal fluid.
4 the use of diuretics caused by sodium loss, hyponatremia (blood sodium <130mmol / L), the patient fatigue, weakness, anorexia, severe nausea, vomiting, blood pressure decreased, making uremia worse, and vice versa, sodium If you add too much, it will stay in the body, causing edema, high blood pressure, and heart failure easily in severe cases. Therefore, in patients with CRF, unless there is obvious symptoms of sodium retention, the sodium intake should not be routinely restricted, and the sodium load may be suddenly increased. To reduce sodium intake, we must consider the problem of poor renal adaptability. Clinically, we should observe blood sodium dynamically and adjust its dynamic balance at any time.
(3) Potassium: In patients with CRF, when GFR is still maintained at >5ml/min, blood potassium can generally maintain normal levels, and urinary potassium excretion is no different from normal people. When GRF enters advanced stage, blood potassium often rises, mainly Found in patients with oliguria and metabolic acidosis and high tissue decomposition, the in vitro factors of hyperkalemia are ingestion of potassium-containing drugs, food and imported blood for more than 3 days.
(4) Calcium: CRF is often accompanied by hypocalcemia, which is caused by insufficient intake; calcium absorption disorder in the small intestine; phosphorus accumulation in the body is compensated by the intestinal tract and is combined with sodium, which limits calcium absorption; vitamin D Metabolic disorders, etc., in which the activation of vitamin D [1,25(OH)2D3] is reduced in the kidney, and the effect of supplementing 1,25(OH)2D3 is significant in CRF patients with hypocalcemia.
(5) Phosphorus: When the GFR drops to 20% to 30% of the normal value, the residual nephron can not maintain the discharge of normal phosphorus, phosphorus accumulates in the body, hyperphosphatemia occurs, and hyperphosphatemia occurs in the clinic. Renal dysfunction is near the end of the period.
(6) Magnesium: When GFR<30ml/min, hypermagnesemia can occur, serum magnesium concentration>1.6mmol/L, can cause drowsiness, speech disorder, loss of appetite; when >2.88mmol/L, there is drowsiness , blood pressure drops, bradycardia, atrioventricular block or ventricular block, sputum reflex disappears, clinically, and uremia symptoms overlap or confusion.
(7) Aluminum: Aluminum is related to encephalopathy and can also cause small cell anemia. Aluminum can be deposited in bone, brain, liver, spleen, lung, heart and other tissues. The accumulation of aluminum is often related to long-term intake of aluminum-containing preparations.
2. Acid, alkali balance
Patients with uremia have metabolic acidosis ranging from mild to severe, with a mild carbon dioxide binding capacity of 22 to 16 mmol/L, and a severe weight of 4.5 mmol/L or less. When the GRF drops to 20 ml/min, the kidney can only be discharged every day. Part of the acidic product, H+ is retained in the body, acidosis occurs, and the kidneys discharge hydrogen ions, mainly through three links, namely, bicarbonate reabsorption, titration of acid excretion and ammonium excretion.
Titrate acid: 23 mmol (GFR = 20 ml/min) per day for normal people. When the GFR is 14.4 ml/min, the titratable acid discharge is 17.5 mmol, but the load of each of the healthy nephrons is increased by 10 times.
Bicarbonate: When CRF, bicarbonate is rarely consumed, and the rate of reabsorption increases significantly in the proximal tubule.
Ammonium: In the CRF, the ammonium excretion is reduced. In the early stage, due to the increased compensatory load of the healthy nephron, the body balance can be maintained, but once the renal function drops to 1/5 of the normal person, it cannot maintain normal. The decrease in the discharge is parallel to the decrease in the number of nephrons.
If the anion gap (AG) is measured and calculated, there are two types of metabolic acidosis when CRF is seen.
AG=[Na+]-[Cl-+HCO3-]
Normally, AG=1012mmol/L, general uremia, when GFR is lower than 25ml/min, urine pH value is <5.5, blood bicarbonate level is reduced by 15mmol/L, then AG value is higher than normal, up to 20mmol / L, another type, common in interstitial nephritis, early CRF, hyperchloremia acidosis, AG value is normal, causing acidosis: 1 acid metabolite retention; 2 renal tubular ammonia , the function of hydrogen secretion is reduced; 3 the ability of renal tubules to recover bicarbonate is reduced; 4 often has diarrhea caused by loss of alkaline intestinal fluid, severe acidosis, fatigue, weakness, feeling slow, long-term breathing, and even coma.
3. Digestive system
At CRF, almost every part of the digestive system can be involved. Early symptoms are often loss of appetite, glossitis, diarrhea, nausea, vomiting, melena, etc., there may be urine in the mouth, oral mucosal erosion and esophagitis, stomach, twelve Intestinal, colon, pancreas can occur inflammation, mucosal edema and hemorrhage, severe cases can occur ulcers, necrosis, infection, intestinal obstruction, intestinal perforation.
4. Cardiovascular system
Cardiovascular disease is a common complication of CRF patients, about 50% of which are due to cardiovascular disease, and the elderly are more prominent. Cardiovascular complications of CRF include pericarditis, cardiac insufficiency, cardiomyopathy, and cardiac damage caused by abnormal metabolism. hypertension.
(1) pericarditis: pericarditis, pericardial effusion is one of the common complications of CRF, the incidence of renal medicine in the First Hospital of Beijing Medical University is 15.3%, and 3% to 4% of dialysis patients are caused by pericardial disease. There are two types of pericarditis:
1 uremic pericarditis.
2 pericarditis after dialysis, the former refers to pericarditis that occurs when uremia is not treated with hemodialysis, and is associated with elevated blood urea nitrogen, more rapid improvement within 2 to 4 weeks after dialysis, pericarditis occurs in dialysis after dialysis When blood urea nitrogen and creatinine have decreased, the mechanism of its occurrence is not very clear. Some people think that it may be related to insufficient dialysis. Some people think that CRF patients have low malnutrition immunity, frequent bacterial or viral infections and pericarditis. It happened.
The clinical manifestations of pericarditis are persistent precordial pain, often accompanied by different degrees of fever. When the pericardial effusion is low, the pericardial friction sound can be heard in the anterior region. A large amount of fluid causes the blood pressure to drop, the friction sound disappears, the heart sounds weaken, and the supine heart cannot be supine. The jugular vein is engorged, the heart is enlarged, the liver is large, the pulse pressure is small and there are strange veins. The electrocardiogram shows low voltage and ST-T changes. X-ray and echocardiography can help the diagnosis of pericardial effusion.
(2) cardiac insufficiency: cardiac insufficiency is a serious complication and an important cause of death in patients with CRF. The Department of Nephrology of the First Hospital of Beijing Medical University reported that cardiac dysfunction accounted for 45.6% of CRF. The death of CRF due to cardiac insufficiency and arrhythmia The second place (22.6%), the occurrence of heart failure is the result of a variety of factors.
1 factors directly related to uremia: uremic toxins, electrolytes, water metabolism disorders; hyperparathyroidism; anemia and acidosis; hypertension; volume overload; pericarditis and myocardial damage; arteriosclerosis; Membrane and so on.
2 factors related to hemodialysis: AV sub-flow rate can reach 400 ~ 700ml per minute to increase the cardiac load; acetate dialysis, acetate has the effect of inhibiting myocardial contraction.
3 hypertension: high blood pressure caused by ventricular wall hypertrophy, heart enlargement, increased myocardial oxygen consumption, leading to heart failure, because hypertension also accelerates the progression of atherosclerosis, can cause myocardial ischemia, myocardial infarction, and further cardiac function Damaged.
4 metabolic changes cause cardiovascular damage: CRF, a considerable part of patients with hyperlipidemia, it is closely related to the occurrence of atherosclerosis and coronary heart disease in CRF.
5. Respiratory system
In uremia, due to metabolic acidosis, it often causes excessive lung ventilation, large and deep breathing or tidal breathing. Pulmonary edema is common. There are two types: one is secondary to congestive heart failure; The other is due to the increased permeability of the lung microcirculation, the imbalance between the solute and the fluid in the microvascular and the interstitial of the lung. The water purification through the lungs exceeds the mass of the lungs, resulting in the retention of water in the lungs. The former type, dialysis treatment has a good effect, the pulmonary edema disappears in a short time, the latter dialysis is not as good as the former. At CRF, the chest radiograph shows a symmetrical butterfly-like shadow on both sides of the hilum, so-called uremia. Symptomatic lung, 15% to 20% of patients with CRF have pleurisy, effusion is leaky or bloody, unilateral or bilateral, the formation mechanism is not very clear, may be associated with uremia "toxic" substances damage membrane transport and Related to the occurrence of inflammation, hemodialysis patients, the amount of heparin is large, can increase the production of bloody pleural effusion, exhaled gas has a urine smell, susceptible to bronchitis, pneumonia.
6. Nervous system
In uremia, almost 100% of patients have neurological symptoms, lack of energy, fatigue, dizziness, and headache.
(1) uremic encephalopathy: the clinical manifestations are non-specific, the initial manifestations are apathy, loss of attention, fatigue, insomnia, etc., the symptoms worsen as the condition worsens, and there are directional forces, computational dysfunction, and even mental confusion, stun tremor It is an important indicator for the diagnosis of uremic encephalopathy, often accompanied by disturbance of consciousness. Myoclonus is found in facial muscles and proximal limb muscles. This is a symptom of advanced encephalopathy. It is almost at the same time as coma, and convulsions can occur at the same time.
A seizure can be a focal or systemic episode, and the latter can cause sudden death if it is a state of epileptic seizure.
EEG examination is very helpful for judging the condition of uremia. It can be used as a dynamic observation method. The main findings are slow waves, and the common and waves increase.
According to the "Molecular Substance" hypothesis proposed by Babb in 1972, it is speculated that neurological diseases are related to the accumulation of certain molecular substances (such as neurotoxins) in the body. The accumulation of neurotoxins in the body and the imbalance of water, electrolytes, acid-base balance, resulting in Intracerebral blood circulation disorder, metabolic disorder of brain and peripheral nerve cells, causing uremic central and peripheral neuropathy, peritoneal dialysis, sorbent dialysis can improve the symptoms of encephalopathy.
The encephalopathy that occurs during CRF hemodialysis should be differentiated from the above-mentioned uremic encephalopathy, such as imbalance syndrome, dialysis encephalopathy, and imbalance syndrome, which refers to symptoms of encephalopathy such as headache, nausea, and disturbance of consciousness several hours after hemodialysis. Yes: osmotic pressure difference between blood and brain tissue after dialysis, or osmotic gradient of medium-molecular substances, leading to brain edema caused by water transfer to brain tissue. Dialysis encephalopathy occurs in long-term maintenance dialysis patients, and progressive neuropsychiatric symptoms occur; Symptoms include language barriers, depression, dementia, etc. Symptoms may be associated with increased levels of aluminum in the brain.
(2) Uremic peripheral neuropathy: When GFR<12ml/min, the limbs are numb, the lower limbs have a strange feeling, and the ants are stalked or stinging, itching, need to move the legs or reduce after walking, called uneasy leg synthesis Symptoms, burning pain and other peripheral nerve manifestations can also occur in the lower extremities. In end-stage uremia, cranial nerve symptoms such as pupil asymmetry, facial paralysis, paralysis, hearing impairment, neurological deafness, pharynx and tongue can also be seen. Muscle weakness, difficulty urinating, urinary retention.
7. Hematopoietic system performance
Severe anemia is one of the important symptoms of CRF patients. Patients with advanced bleeding tend to have bleeding tendency, often accompanied by subcutaneous ecchymosis, nosebleeds, bleeding gums, or even hematemesis, blood in the stool, hematuria, intracranial hemorrhage, menorrhagia, a few pericardial hemorrhage, kidney Anemia refers to the deficiency of renal erythropoietin (EPO), or some toxic substances in uremia plasma interfere with the formation and metabolism of red blood cells. It is generally believed that the occurrence of renal anemia is caused by a combination of multiple factors.
(1) Erythropoietin deficiency: Erythropoietin (EPO), also known as erythropoietin, is produced by kidney tissue. It stimulates the production of bone marrow red blood cells. As kidney disease develops, kidney tissue is continuously destroyed. EPO The production, reduced secretion, is the main cause of renal anemia.
(2) Erythrocyte growth inhibitory factor: Some erythropoiesis-producing substances exist in the plasma of uremic patients. They play an important role in the mechanism of renal anemia. It is currently considered that the inhibitors are as follows:
1 refined ammonia and polyamine ammonia.
2 parathyroid hormone (PTH).
3 nucleases.
4 macromolecular proteins.
5 prostaglandins and so on.
(3) shortened red blood cell life: Some substances in the plasma of CRF patients interfere with the function of Na+ pump on the red blood cell membrane, causing anemia.
(4) Blood loss: In patients with advanced CRF, about one-fourth of patients have bleeding tendency due to platelet dysfunction, which aggravates anemia.
(5) Lack of iron and folic acid: due to poor appetite in patients with CRF, gastrointestinal bleeding, blood loss in hemodialysis, frequent blood draw and other reasons can cause iron deficiency, affecting the synthesis of hemoglobin, folic acid deficiency is rare.
(6) Aluminium poisoning: As a result of reduced renal filtration in patients with CRF, aluminum accumulation in the blood and oral aluminum hydroxide for correcting calcium and phosphorus disorders, blood aluminum is often increased, and aluminum can induce small cell anemia.
8. Endocrine function changes: 131I uptake rate decreased, sexual dysfunction, testicular atrophy, menstrual disorders and so on.
9. Metabolic disorders: At CRF, lipid metabolism, protein and amino acid metabolism, and disorders of glucose metabolism may occur.
(1) Lipid metabolism: When the GFR is reduced to about 50 ml/min, the serum triglyceride (TG) level begins to increase. As the GFR decreases further, the hypertriglyceridemia is increasingly aggravated. This phenomenon can be seen in non-dialysis patients. It can also be seen in patients with hemodialysis or peritoneal dialysis. The hyperlipidemia of uremia belongs to type IV. The changes of lipoprotein are characterized by triglyceride content in very low density lipoprotein (VLDL) and low density lipoprotein (LDL). Increased, while high-density lipoprotein (HDL) contains less cholesterol, but cholesterol in LDL is still normal, high TG may be due to increased liver production, and reduced body clearance.
(2) Protein and amino acid metabolism: Protein metabolism disorder is of great significance in patients with CRF. There are two reasons for hypoproteinemia in CRF patients: first, chronic kidney disease, long-term loss of albumin in urine; second, CRF often has poor appetite Gastrointestinal symptoms such as nausea and vomiting lead to insufficient protein intake. Experiments have confirmed that the "net decomposition" of muscle protein increases during CRF, and the "net synthesis" of some visceral proteins increases. This regulation of the synthesis and decomposition of energy supply is precisely The body itself maintains an important path of life process. At CRF, the rate of protein synthesis/proteolysis is <1. If this condition persists for a long time, serious protein deficiency will occur. When treated with essential amino acids, the rate of protein decomposition will be significantly reduced. (P < 0.05), the ratio of protein synthesis rate / proteolytic rate increased.
Amino acid metabolism disorder, manifested in plasma, red blood cells and intramuscular essential amino acids and histidine, tyrosine levels decreased, non-essential amino acid levels increased, therefore, in addition to supplementing 8 essential amino acids in treatment, should also be supplemented Histidine and the like.
10. Renal osteopathy: CRF, calcium, phosphorus metabolism disorders, vitamin D metabolism disorders, secondary hyperparathyroidism, etc., can lead to bone changes, known as renal osteodystrophy or renal osteodystrophy, Including osteomalacia, fibrotic osteitis, osteosclerosis and osteoporosis, the clinical manifestations of patients vary widely, mainly related to age, disease course, diet, dialysis and other factors.
11. The skin is dry, desquamated and dull. Some patients have darker skin and are caused by diffuse melanin. After urea is discharged from the sweat glands, it will condense into white crystals called urea cream, which will stimulate the skin to produce uremic dermatitis. Itching is also associated with skin itching (associated with secondary parathyroid hormone).
12. The immune system is low in function and easy to be infected.
Examine
Examination of chronic renal failure in the elderly
1. Renal function test: The clearance of endogenous creatinine decreased significantly, and serum creatinine, urea nitrogen, and uric acid increased significantly.
2. Blood routine: When GFR<15ml/min, anemia is obvious, RBC is about 2×1012/L, Hb is generally below 80g/L, and the end stage can be reduced to 2030g/L, which may be accompanied by high white blood cells. Or thrombocytopenia.
3. Urine routine: may have proteinuria, red blood cells, white blood cells or casts, the above changes may not be obvious, the urine specific gravity is more than 1.018, severely fixed at 1.010 ~ 1.012, nocturia more than daytime urine volume.
4. Blood biochemical examination: plasma protein decreased, especially albumin decreased, and electrolytes were significantly abnormal.
5. Kidney chart and kidney scan: can understand the size of the kidney, blood flow, secretion and excretion function.
6. X-ray: There is a heart enlargement.
7. Other examinations: urinary plain film or angiography, renal biopsy, etc. contribute to the diagnosis of the cause.
Diagnosis
Diagnosis and diagnosis of chronic renal failure in the elderly
Diagnostic criteria
1. Diagnosis of underlying diseases After diagnosis of chronic renal failure in the elderly, the treatment should be as clear as the patients in other age groups. The history of toxic exposure should be especially noted in the medical history; such as antibiotics, non-steroidal anti-inflammatory drugs, Drugs and sleeping pills, etc., due to changes in the physiological and pathological aspects of the elderly and the variety of drugs, prone to side effects of drugs, should carefully look for non-steroidal anti-inflammatory drugs and other causes associated with acute allergic interstitial nephritis and interstitial nephropathy At the same time, the pre-renal causes of renal function decline should also be ruled out. The so-called "chronic renal failure" can sometimes be caused by cardiovascular causes, and the risk of malignant tumors in the elderly is greatly increased. Malignant tumors can be accompanied by various small kidneys. Ball disease, should pay attention to the presence or absence of substantial tumors and cryoglobulinemia, macroglobulinemia, other gamma globulin disease and light chain disease, should be done related tests such as anti-nuclear antibodies, rheumatoid factor, anti- DNA antibodies, immune complexes and complements exclude vascular connective tissue diseases. SLE is rare in the elderly, but some autoimmune diseases increase with age in the elderly. The atypical, should be noted.
In laboratory tests, the interpretation of the significance of creatinine levels should be different from that of younger patients. In the elderly, creatinine production is reduced due to decreased muscle volume. In chronic renal failure, the increase in serum creatinine is not as high as in younger patients, especially in When nutrition is deficient, therefore, the evaluation of renal function from the creatinine concentration alone is insufficient to estimate the degree of renal failure. ESR is elevated in many elderly people, but if the albumin concentration is normal, the erythrocyte sedimentation rate is significantly increased. The inflammatory process must be further examined, other related tests, such as renal ultrasound to exclude obstruction, tumors and cysts; chest X-ray examination is also necessary, renal biopsy should be performed in patients with chronic renal failure or clinical manifestations or clinical atypical In a group of 29 elderly patients with clinically diagnosed end-stage renal failure, 6 (21%) had potentially treatable pathology, including 2 cases of crescentic glomerulonephritis, vasculitis, interstitial Nephritis, acute glomerulonephritis and acute tubular necrosis in 1 case.
2. Diagnostic criteria
The reference diagnostic criteria for this disease are as follows:
Although the clinical manifestations of chronic renal failure are diversified, it is not difficult to diagnose if you can master the following points:
(1) Slow onset, fatigue, headache, loss of appetite, nausea and vomiting, polyuria, nocturia or oliguria and itchy skin.
(2) There are high blood pressure, fundus changes, heart failure.
(3) There are anemia, azotemia and acidosis, high blood phosphorus, low blood calcium, and hyperkalemia in the late stage.
(4) The urine specific gravity is low and fixed, with mild proteinuria, a small amount of red, white blood cells and casts.
(5) A history of chronic kidney disease.
The differential diagnosis of CRF mainly needs to distinguish CRF from acute renal failure and prerenal azotemia. According to the patient's medical history, physical signs and related laboratory test results, the similarities and differences should be carefully analyzed to make a correct diagnosis and prevent Misdiagnosed or missed.
Differential diagnosis
1. Identification with pre-renal azotemia: The identification of pre-renal azotemia and CRF is not difficult. Pre-renal azotemia can restore normal renal function after 48-72 hours of effective blood volume supplementation. The latter is difficult to restore kidney function.
2. Identification of acute renal failure: The identification of CRF and acute renal failure is not difficult in most cases. Sometimes, according to the patient's medical history, a differential diagnosis can be made. When the acute and chronic renal failure is difficult to identify according to the patient's medical history, Can be considered from the following aspects: according to the results of imaging examination (such as B-ultrasound, CT, etc.) analysis, such as the obvious reduction of the kidneys, support the diagnosis of CRF; according to the results of the kidney chart analysis; if the patient complained of the kidney The history of failure is less than 1 month, and no obvious anemia, support the diagnosis of acute renal failure; such as anemia, and no recent history of acute bleeding, support the diagnosis of CRF; differential diagnosis based on the level of nail creatinine, there is also a reference Significance, according to the First Hospital of Beijing Medical University, nail creatinine level can reflect the serum creatinine level of patients 3 to 4 months ago, such as nail creatinine level is higher than normal, then support the diagnosis of CRF; such as nail creatinine level is not high Normal, it supports the diagnosis of acute renal failure.
