The lungs are one of the most commonly involved organs in uremia. Uremic pneumonia in the narrow sense refers to the symmetrical butterfly wing shadows radiating from the lung hilum to both sides on chest X-ray in uremic syndrome, which are mainly manifested by pulmonary edema.
The most common is dyspnea, mostly mild to moderate, characterized by the ability to lie down, with an incidence between 30% and 80%. Next is coughing, with an incidence of 50% to 65%, usually dry or with a small amount of white mucous sputum, and with a large amount of yellow pus sputum in case of combined infection. A small number of patients also experience bilateral lower chest distension.
The most common pulmonary complication of chronic renal failure is uremic pneumonia, also known as uremic lung, or uremic pulmonary edema, which is a clinical syndrome with pulmonary edema as the main pathological manifestation. Typical symptoms are coughing, coughing sputum, blood in sputum, dyspnea, still lying flat at night, and shortness of breath after activity.
The incidence of uremia still accounts for 50 to 100/1 million of the natural population, and the lung is one of the most commonly involved organs in uremia. The disease refers to the pathophysiological changes and clinical manifestations of the respiratory system in uremia, including pulmonary edema, pulmonary calcification, pleurisy pulmonary infarction, pulmonary fibrosis and pulmonary hypertension, and other symptoms, and patients can be affected regardless of gender.
I. Disease description
The lung is one of the most commonly involved organs in uremic syndrome. In the narrow sense of uremic pneumonia, the chest X-ray shows symmetrical butterfly-wing shadows radiating from the lung hilum to the sides, and the lesions are mainly manifested as pulmonary edema;
In a broader sense, uremic pneumonia refers to the pathophysiological changes and clinical manifestations of the respiratory system in uremia, including pulmonary edema, pulmonary calcification, pleurisy, pulmonary infarction, pulmonary fibrosis and pulmonary hypertension. The pulmonary manifestations of uremic pulmonary edema, also known as uremic pneumonia and chronic renal failure, are discussed below.
The most common pulmonary complication of chronic renal failure is uremic pneumonia, also known as uremic lung, or uremic pulmonary edema, which is a clinical syndrome with pulmonary edema as the main pathological manifestation.
Second, symptoms and signs
1, symptoms: its typical symptoms are coughing, coughing sputum, blood in sputum, dyspnea, still lying flat at night, shortness of breath after activity. In contrast, patients with early uremic pneumonia do not have obvious symptoms, with systemic symptoms caused by uremia. In some patients with atypical symptoms, pulmonary edema has become very obvious, but the symptoms of dyspnea and cough and sputum are very mild, so they are easily ignored. If interstitial lung fibrosis develops, there can be obvious dyspnea, and about half of the patients can be complicated by pleural effusion, mostly fibrinous exudate, a few are bloody.
2, signs: early uremic pneumonia patients can have no obvious signs, late stage can appear typical signs, shortness of breath, lip cyanosis, both lungs can be heard in the wet Madhuban Zu Zu case still woven
Disease etiology
The lungs are in a very important position in the whole body organs, on the one hand, the lungs are directly connected to the external environment and linked to the external environment. Therefore, the lung is subject to both the attack of external pathogenic factors and the influence of internal environmental changes, systemic diseases, can lead to changes in the respiratory system. In chronic renal failure, many infections, toxins, immune and other factors can adversely affect the lungs.
These factors include direct effects of bacteria, fungi, and viruses on the lungs, i.e., infections, and may also have indirect effects on the lungs, such as pulmonary edema due to sodium and water retention, i.e., uremic pneumonia. In chronic renal failure, pulmonary edema caused by sodium and water retention can directly cause lung damage, while in chronic renal failure, various toxins in the body can directly cause lung damage, and pathological processes that damage the kidneys can also cause changes in the lungs, such as scleroderma, Wegener’s granulomatosis, nodular disease and pulmonary-renal syndrome.
In recent years, foreign scholars have reported that the common causes of uremia are diabetic nephropathy, hypertensive nephropathy, glomerulonephritis, polycystic kidney, etc., and most of the patients with diabetic nephropathy and hypertensive nephropathy are elderly, and most of these patients are combined with coronary heart disease, so they are more likely to have uremic pneumonia, i.e. uremic pulmonary edema. In contrast, patients with polycystic kidney generally do not show clinical symptoms until they are about 60 years old, so most of these patients are also elderly.
1.Increased permeability of alveoli-capillaries
(1) Small molecule substances: including urea, guanidine substances and amines. Urea is the largest content of a metabolic substance in body fluids, chronic renal failure in the middle and late stages, the serum concentration of urea gradually increased, the common clinical symptoms of uremia such as headache, weakness, nausea, vomiting, drowsiness, bleeding tendency, etc. are related to urea, but also diffuse damage to the alveolar-capillary membrane, so that its permeability increases, the longer the presence of urea in the body, the greater its toxicity.
Guanidine substances are metabolites of certain amino acids and creatinine, which are excreted from urine about 10g per day in normal people. In uremic patients, the serum level of creatinine rises, and the serum level of guanidine substances also rises in parallel. Amines include aliphatic amines, aromatic amines and polyamines. Both aliphatic and aromatic amines can inhibit the activity of certain enzymes and affect metabolism. Polyamines can promote erythrocyte lysis, inhibit erythropoietin production, inhibit Na+-K–ATPase and Mg++-ATPase activities, increase microcirculatory permeability, and promote the production of uremic pulmonary edema.
(2) Medium-molecular substances: These include hormones with normal structure but increased concentration, high concentration of normal metabolites, and lysis products of cells or bacteria. High concentrations of middle-molecule substances can cause peripheral neuropathy, inhibition of erythropoiesis, inhibition of various antibody production, and reduced cellular immune function, including parathyroid hormone (PTH), which has the most pronounced diffuse damage to alveolar-capillary membranes, and can also affect myocardial function and cardiomyocyte metabolism.
(3) Immunological factors: Since glomerular basement membrane and pulmonary capillary basement membrane have the same antigenic determinant clusters, the causes of uremia, such as chronic glomerulonephritis and nephrotic syndrome, can damage pulmonary capillary basement membrane and alter its permeability.
2, increased volume load The animal model of ligation of ureters producing acute renal failure showed pulmonary lesions, proving that the mechanism of occurrence depends on excess water. The increase in volume load due to low urine and urinary closure in uremic patients is the most important pathophysiological change and is one of the important reasons for the formation of pulmonary edema.
3. Decreased plasma colloid osmotic pressure Large amounts of proteinuria, malnutrition, and combined anemia cause a decrease in plasma colloid osmotic pressure, resulting in fluid leakage into the interstitium and causing interstitial edema. The regulation of fluid flow across the pulmonary capillaries is based on the Starling formula, i.e., the net water flow is determined by the interaction of the net water pressure difference across the membrane (△P), the colloid osmotic pressure difference across the membrane (△π), and the membrane filtration coefficient (Kf).
A certain balance between ΔP and Δπ is maintained during normal time, which is mainly regulated by the lymphatic system. Primary pulmonary edema occurs as a result of alterations in membrane Kf, where fluid leakage from the membrane increases beyond lymphatic drainage and fluid accumulates in the interstitial spaces of the lung tissue. Secondary pulmonary edema results from alterations in Δπ or ΔP, which cause fluid to enter the pulmonary interstitium within the pulmonary capillaries. Patients do not necessarily show excessive systemic fluid volume, but may have increased intracardiac and pulmonary wedge pressures.
4, left heart insufficiency In uremia, myocardial function is impeded and left heart insufficiency leads to elevated pulmonary capillary pressure, causing pulmonary edema and decreased pulmonary compliance. In the late stage of uremia, cardiovascular abnormalities on chest X-ray are not necessarily related to urea nitrogen (BUN) and creatinine (Scr), indicating that pulmonary edema formation is a combination of factors.
5, the effect of oxygen free radicals, adhesion molecules and cytokines Uremia due to the reduction of residual kidney units, creatinine metabolism and susceptibility to infection and other factors increase the production of oxygen free radicals, the patient’s systemic antioxidant capacity is significantly reduced, can not quickly and effectively remove these superoxide anions, resulting in the removal of foreign bodies at the same time, aggravating tissue damage. Among these factors, hypochlorous acid accelerates creatinine metabolism, and the metabolites formed can easily penetrate into cells and cause cytotoxic effects and tissue damage.
The lungs are hypersensitive to hypochlorous acid and play a major role in neutrophil-induced lung tissue damage. The use of biologically incompatible membranes during hemodialysis activates complement, causing leukocytes to accumulate in the pulmonary microcirculation and releasing various lysosomal enzymes, resulting in lung damage. It has also been demonstrated that leukocyte accumulation in the pulmonary microcirculation is associated with increased expression of adhesion molecules on its surface and increased leukocyte activity.
6, respiratory muscle disorders in uremia due to malnutrition, active vitamin D3 deficiency, hyperparathyroidism, malnutrition and other factors, resulting in muscle weakness and disuse, chest wall compliance changes, which affects lung function, as manifested by the maximum inspiratory pressure, maximum expiratory pressure and trans-diaphragmatic pressure are decreased.
7. Other factors Improper clinical management of water intake, metabolic acidosis and electrolyte disorders are also very likely to cause pulmonary edema.
IV. Pathophysiology
Grossly, both lungs are observed as diffuse rubbery hardness changes with weight gain. Microscopically, the lesions in the inner bands of both lungs are prominent, and the alveoli are found to contain protein-rich fibrinous aqueous solutions, sometimes with dense hyaline masses, which may have mononuclear cell infiltration, basement membrane of the alveoli and amyloid deposits of small vessels, and also pulmonary hemorrhage and iron-containing heme deposits, the latter of which may lead to fibrosis. 20% of cases have fibrinous pleuritis. With repeated prolongation of the disease, recurrent pulmonary edema and pulmonary calcification, pulmonary fibrosis is common on autopsy, with diffuse patchy changes in both lungs, or fibrous tissue replacing entire subsegments.
The pathology of uremic pneumonia is characterized by diffuse rubbery changes, or sclerosing edema, accompanied by an increase in lung weight. Microscopic changes are typical of pulmonary edema with dilated alveolar capillaries, bruising, thickened alveolar membranes, alveolar septal edema, and protein-rich fibrous exudate in the alveoli that is jelly-like and easily coagulated. In severe cases, there is hemorrhagic and fibrinous pulmonary edema, alveolar wall cell detachment, visible macrophage and monocyte infiltration, and sometimes hyaline membrane formation.
Recurrent uremic pulmonary edema causes interstitial fibrosis and intra-alveolar deposits of iron-containing hemoglobin. Approximately 20% are associated with fibrinous pleuritis. Uremic pulmonary edema differs from other forms of pulmonary edema in that its occurrence is generally thought to be associated with elevated levels of blood urea nitrogen and creatinine. Uremic toxin, a small molecule guanidine, is present in the blood of patients with uremia. This substance can lead to increased permeability of alveolar capillaries, resulting in spillage of protein-containing fluid into the alveoli and interstitium and the development of pulmonary edema.
Sodium and water retention is another cause of uremic pulmonary edema. In addition, elderly patients with uremia are mostly associated with left heart failure, which also plays an important role in the development and progression of uremic pulmonary edema. Decreased plasma colloid osmotic pressure, such as massive proteinuria, malnutrition, and anemia, leads to fluid leakage into the interstitium, causing interstitial pulmonary edema. The increase in free radicals in the body and the patient’s decreased systemic antioxidant capacity to rapidly and effectively eliminate these superoxide anions leads to increased tissue damage while removing foreign bodies.
V. Diagnosis
Clinically, the possibility of uremic pneumonia should be considered in patients who have been clearly diagnosed with chronic renal failure, if symptoms such as coughing, coughing, blood in sputum or hemoptysis, dyspnea, etc. appear during the course of the disease, and wet bow target cushy for wo escape nightmare protection let down pyrene cowardly strain (pneumonia, Goodpasture syndrome, cardiogenic pulmonary edema, etc.) appear at the bottom of the lung.
Laboratory tests: laboratory tests: all the laboratory test manifestations of chronic renal failure can be seen, such as advanced complications of interstitial lung fibrosis, blood gas analysis can appear hypoxemia and metabolic acidosis manifestations, pathogenic examination is often negative, routine examination of pleural effusion as exudate.
(I) Other ancillary tests.
1, imaging The performance on the chest X-ray varies with the severity and duration of the disease and is divided into 4 stages.
(1)Pulmonary stasis stage: it shows enhanced pulmonary texture, enlarged hilar shadow, and hairy glass-like changes in the middle and lower lung fields.
(2) Interstitial pulmonary edema stage: the outer diameter of the bronchial and vascular cross-sections around the hilum are thickened and the edges are blurred, which is called the “cuff sign”, and Kerley B and A lines may appear.
(3) Alveolar edema stage: diffuse dotted shadows and fusion into large shadows.
(4) Interstitial lung fibrosis stage: most of the cords and reticular shadows in the lung fields.
(5) Other: pleural effusion, pericardial effusion, pleural thickening, pulmonary calcification and other signs may appear.
(2) Pulmonary function measurement Decreased lung volume and decreased diffusion function.
(B) The diagnosis of uremic pneumonia can be based on.
1, there must be severe renal disease, and the detection of renal function meets the criteria of uremic pneumonia.
2, mostly seen in those with oliguria, anuria, excessive water and sodium intake or inadequate dialysis ultrafiltration.
3.The most important clinical symptom is dyspnea, but can lie down.
4.X-ray chest film typically shows extensive small or large exudative shadows in both lower lungs, and can change rapidly in a short period of time.
5.The total white blood cell count and neutrophil ratio of blood test are not increased, sputum culture is not pathogenic bacteria, and the X-ray chest film is not consistent with infection.
6.Arterial blood gas analysis is hypoxemia and metabolic acidosis.
7. Pulmonary function tests showed the earliest and persistent decrease in diffusion function, with restrictive ventilation changes accounting for more than 51%.
8, Anti-infection effect is not obvious, hemodialysis efficacy is obvious.
(III) Examination
Laboratory tests: blood gas analysis shows metabolic acidosis. Hypoxemia. PaCO2 decreases or is normal in the early and mid-term. When PaCO2 is significantly elevated, it indicates critical condition.
Other auxiliary examinations.
1.Chest x-ray
(1) Imaging characteristics of the lungs.
①Diverse morphology: it can appear as butterfly wing, corn-like, isolated or diffuse small pieces, single or multiple large pieces, masses or multiple nodules and other kinds of shadows, typical butterfly wing shape is rare, accounting for about 4% to 10%, increased lung texture, coarse disorder is the most common, accounting for 71%.
②Variable density: density can be light or dense, uniform or mixed with multiple images.
③Variable location: it can reside in both sides or one lung, it can be located in the whole lung on both sides or in the middle and lower fields of both lungs, or it can be seen in the whole lung on one side or in a lobe lung segment. Overall impression: more right lung than left lung, more middle and inner band than outer band, more middle and lower lung lobes than upper lung lobes, and the lower lobe of the right lung is highly susceptible to invasion.
(4) Rapid change: After treatment with hemodialysis, cardiac strengthening and diuresis, the lung shadow can be significantly absorbed or completely dissipated in a short time with the improvement of renal and cardiac function.
(2) Pulmonary imaging typing
(1) Pulmonary stasis type: the most common clinical type, accounting for about 60% of the cases, manifesting as increased and blurred shadows in both lung halls and thickened lung texture.
(2) Interstitial pulmonary edema type: the hilar shadow is enlarged with indistinct margins, and the upper and lower lung textures are increased, thickened and blurred. The K line is present in about 13%, the B line in 7%, and the A line in 2% to 3%.
(3) Alveolar pulmonary edema type: Extensive small or large lamellar shadows in both lower lungs, with low density, continuous and blurred, typically butterfly wing-shaped. This type accounts for about 19% of the clinical cases.
④Interstitial lung fibrosis type: most of the striated and lattice-like shadows in the lung field, accounting for about 21% of the clinical cases.
⑤ Heart enlargement: alveolar and interstitial edema type is mostly seen in heart enlargement and heart failure, with heart:chest >0.5 accounting for 61% of cases.
⑥ pleurisy: small or moderate effusion, generally only blunting of the rib-diaphragm angle, accounting for 31% of clinical cases.
2, CT and MRI High-resolution CT and magnetic resonance imaging (MRI), which are now widely used clinically, can detect subclinical pulmonary edema in such patients with more specificity and sensitivity.
3, pulmonary function Patients with uremia have abnormal pulmonary function at an early stage, and 47% of them have abnormal pulmonary function.
When 47% of the patients have abnormal lung function, the chest X-ray is still normal, so it can be seen that the lung function test has certain significance for the early detection of lung invasion in patients with uremia.
The lung function test is important for early detection of lung invasion in uremic patients. Spirometry and expiratory volume and 1s expiratory volume were lower than expected. Patients with uremia have decreased pulmonary ventilation, diffusion function and large and small airway ventilation, as evidenced by decreased forceful expiratory volume in one second (FEV1%), maximum expiratory flow in 50% and 25% of spirometry (V25, V50), and decreased carbon monoxide diffusion.
The decrease in these pulmonary function parameters was negatively correlated with the increase in plasma urea nitrogen concentration. The most important change in carbon monoxide diffusion (DLCO), which decreases in the early stage of uremia, is the edema of alveolar membrane, the secondary interstitial fibrosis of the lung, which decreases the alveolar capillary area, and the decrease of hemoglobin in pulmonary capillaries in anemia, all of which are the pathological basis for the decrease of diffusion function. As the disease worsens, mixed ventilation dysfunction becomes obvious.
Differential diagnosis
Clinical differentiation must be made from bacterial pneumonia, bronchopneumonia, and bronchiectasis.
1, cardiogenic pulmonary edema Some scholars believe that left heart failure is an important pathogenic factor in uremic lung, and there are many factors affecting cardiac function in uremia. Some other scholars believe that there is still some difference between the two.
(1) Cardiogenic pulmonary edema.
①History of coronary heart disease, cardiomyopathy, etc.
(②Typically, there is chest tightness, shortness of breath, pain in the precordial region, coughing pink foamy sputum, sputum, inability to lie down, and early history of coughing while lying down and history of sitting down and breathing.
③ cyanosis is obvious, both lungs can be heard on auscultation of extensive dry and wet woven grass
④Electrocardiogram has specific changes related to the primary disease.
⑤ X-ray chest film is interstitial pulmonary edema in the early stage, followed by pulmonary hemorrhagic changes, and pulmonary stasis is mainly manifested by vascular anger and vascular margin blurring in the upper lung.
(6) Cardiac strengthening and diuretic treatment have obvious effects.
(2) Uremic pulmonary edema.
①Even though the pulmonary edema is severe, the symptoms such as cough and sputum are still mild.
(2) Except for deep breathing due to metabolic acidosis, shortness of breath is also mild, and the patient can still lie down.
③Hemoptysis is rare, and pink foamy sputum is rarely present.
④X-ray chest films of 40% of patients do not show cardiovascular abnormalities.
⑤ The basic pathological lesion is fibrinous exudate, and its pulmonary stasis changes are vasodilatation of the whole lung.
⑥Anti-infective therapy, cardiac and diuretic therapy are ineffective, while dialysis therapy is effective.
2, pulmonary infections Patients with chronic renal failure are mostly accompanied by reduced immune function, coupled with anemia and metabolic acidosis, which make the body’s defense factors impaired and vulnerable to various infections, with viral and bacterial infections of the lungs bearing the brunt.
(1) There is fever, worsening cough, coughing purulent sputum, and worsening shortness of breath.
(2) Dry and moist woven grass can be heard on auscultation of the lungs
(3) Routine blood tests reveal elevated total white blood cell count and elevated neutrophil ratio.
(4) C-reactive protein measurement is significantly elevated.
(5) Sputum culture can obtain positive results, and anti-infection treatment according to drug sensitivity test is obvious.
3, pulmonary tuberculosis Uremic patients with pulmonary tuberculosis is about 20%, and 2-3 months after receiving dialysis in the late stage of uremia is a good period for tuberculosis.
(1) Atypical symptoms: due to immune deficiency, there can be no afternoon hypothermia, or high fever that is not effective against general antibiotics. Symptoms such as night sweats, decreased appetite, and wasting are often masked by symptoms of the primary disease, and tuberculin tests are often falsely negative.
(2) Blood sedimentation is significantly accelerated, up to 100mm/h. Sputum smear or culture, Mycobacterium tuberculosis can be detected, with a positive rate of 20%-30%. The positive rate of sputum nucleus PCR detection can be significantly increased.
(3) X-ray chest film may not have typical TB manifestations, CT examination has some significance.
(4) Experimental anti-tuberculosis treatment is effective.
4, pulmonary hemorrhage – nephritis syndrome The late stage of this syndrome into the uremic phase is no longer distinguishable, but the early and middle stage has its own characteristics.
(1) The disease is mostly seen in males under 16 years of age.
(2) Intermittent recurrent hemoptysis with varying amounts of hemoptysis.
(3) Ferritin-containing macrophages can be found in the sputum.
(4) Pulmonary function shows restrictive ventilation dysfunction; decreased diffusion function; and decreased arterial partial pressure of carbon dioxide, indicating hyperventilation.
(5) X-ray chest film shows diffuse granular or nodular shadows in both lungs; the shadows may be wandering, with clear apical lung areas.
(6) Blood test is positive for anti-glomerular basement membrane (GBM) antibody.
VII. Therapeutic measures
Phentolamine
1.Conventional treatment Mainly treat the primary disease, improve renal function, oxygen therapy. When combined with pulmonary infection, sensitive and non-nephrotoxic antibiotics can be used, and penicillin family antibiotics are generally applied. In case of heart failure, half or 1/3 amount of digitalis preparation or vasodilator such as phentolamine can be given as 5% glucose 250ml + phentolamine 10mg, 1 time/d, intravenously.
2.Optimal program for hemodialysis treatment, can obtain rapid results.
3.Rehabilitation treatment Patients with chronic renal failure often have a long course of illness and recurring disease, and are prone to tension, anxiety, pessimism, depression and other emotions, which can rapidly aggravate the disease, so family members should pay attention to communication with patients to eliminate tension. Inpatients should pay attention to cooperate with medical staff to facilitate the recovery of the disease. They should build up confidence to overcome the disease, realize that life, old age, sickness and death are the natural laws of life, face the disease bravely and exert subjective initiative. During hospitalization, they should actively learn about the disease from doctors, understand the nature and pathological process of the disease, cooperate with doctors to do special tests such as kidney puncture biopsy, etc. They can also read books about kidney disease and learn about protective and recuperative knowledge to achieve the best treatment effect.
The elderly due to age-related atherosclerosis and other reasons, the regulatory function is reduced, while the renal blood flow is reduced, creatinine clearance can be reduced to half of normal, the metabolism and excretion of drugs is reduced, the half-life of drugs is prolonged, drug accumulation poisoning is likely to occur, so in the use of drugs should follow medical advice, and carefully read the instructions to prohibit drugs that damage the kidneys. The early treatment of chronic renal failure is important to delay the development of the disease and improve the prognosis of patients.
For mid- to late-stage chronic renal failure, dietary and pharmacological treatment can also lead to symptom relief and delayed dialysis. In the application of non-dialysis therapy, nutritional therapy needs to be used as the basis, together with the application of drugs to delay chronic renal failure. For patients with significant azotemia, intestinal catheterization or oral adsorption therapy can be added. There is also the use of Chinese medicine bath therapy, Chinese medicine external application method, etc., which needs to be further explored. Patients with chronic renal failure, especially those with uremic pneumonia, should rest, and their exercise is exercise on the basis of rest, consider practicing tai chi, etc., and should not do strenuous exercise.
1.Hemodialysis Adequate dialysis, which can remove excess water and urotoxins and symptom relief, is the most basic and important clinical treatment at present. The recovery of ventilation function after dialysis is earlier than the recovery of diffusion function, especially the recovery of small airway ventilation function is fast, which may be related to the easy remission of small airway edema and the slower remission of alveolar edema. In China, it was reported that the indexes of pulmonary function improved significantly after 2 months of hemodialysis.
2, peritoneal dialysis Uremic patients should generally use this type of dialysis sparingly, because when the implantation of peritoneal dialysis fluid > 3L, the diaphragm is elevated, causing pulmonary complications such as collapse of the lower lobe of the lung, pulmonary atelectasis, pneumonia, pleural effusion, etc., which directly affect lung function, especially the most obvious decline in diffusion function. If the volume of abdominal dialysis fluid and intra-abdominal pressure are carefully controlled, the lung function also improves significantly after 3 months of dialysis.
3, kidney transplantation The history of kidney transplantation for nearly 40 years, has become an important means of treatment of uremia.
(1) Favorable factors for recovery of cardiopulmonary function after kidney transplantation.
(1) The recovery of urinary function is favorable to the stability of the body’s internal environment and the improvement of cardiopulmonary function.
(2) Improvement of anemia, increase of red blood cell count and recovery of oxygen carrying capacity.
③Pre-existing hypertension returns to normal.
④Corrected calcium and phosphorus metabolism disorder.
(2) Unfavorable factors for the recovery of cardiopulmonary function after kidney transplantation.
(①The application of high-dose hormones and immunosuppressive drugs easily induces pulmonary infection.
(2) Carbon monoxide diffusion function in lung function is difficult to recover after transplantation. The most likely explanation is that, prior to transplantation, pulmonary fibrosis has progressed due to repeated episodes of pulmonary edema, and this fibrosis can further reduce the residual air volume of the transplant recipient.
4.Other treatments
(1) Prevention and control of pulmonary infections.
①Anti-viral treatment can be used antiviral flush, 1 to 2 bags, 3 times/d, orally; Banlangen flush, 1 to 2 bags, 3 times/d, orally; Ribavirin tablets 0.2g, 3 times/d, orally; other anti-viral drugs used, pay attention to whether there is nephrotoxicity.
②According to the drug sensitivity test, the anti-infective drug can be ceftriaxone (ceftazidime), 1~2g, intravenous injection, 1 time/d, which can be applied routinely as long as the liver function is normal. Erythromycin, rifampin, cefoperazone, ampicillin (ampicillin, piperacillin, etc. are applied in regular doses when renal function is mildly impaired, and should be applied in reduced doses when renal function is moderately impaired or above.
(2) Strengthen nutrition and prevent anemia: low protein, low phosphorus diet; supplement with adequate essential amino acids and vitamin classes. Essential amino acid therapy is 0.1~0.2g per kg body weight per day, divided into 3~4 oral doses. Vitamin B and vitamin C should be supplied in regular amounts, while vitamin B6 should be supplied in large amounts. Give blood transfusion if necessary.
(3) Reduce cardiac load and improve pulmonary edema symptoms.
(1) Restrict the intake of water and sodium.
(2) Diuretic application: use furosemide (tachyphylaxis) at a dose of 20-80mg and then increase if the effect is not satisfactory. Thiazide and potassium retention diuretics are not effective.
Cardiotonic application: There has been controversy over the application of digitalis, most scholars believe that its clinical application still has the necessity of other drugs that cannot be replaced, digitalis toxin and digoxin with a short half-life should be used, and attention must be paid to the toxic reactions of digitalis.
④vasodilator application: can improve the clinical manifestations of pulmonary edema, clinical use of phentolamine (benzamazoline), sodium nitroprusside, nitrates.
(⑤ Other substances: Aminophylline, Chuanxiong, Danshen and other drugs have been reported to improve uremic pulmonary edema.
(4) Symptomatic treatment.
①Central non-anesthetic cough suppressants are preferred, such as dextromethorphan tablets, dextromethorphan syrup, coughzine tablets, and white glucosamine cough suppressant tablets.
②Phlegm-suppressing drugs are suitable for those whose sputum is thick and not easy to be coughed out, such as aminoglutethimide (Mucosolvan) and diacylcysteine.
③Oxygen should be administered according to the condition of respiratory difficulty.
VIII. Complications
Pleural effusion, respiratory distress, pulmonary edema, left heart failure, etc. may be complicated.
IX. Prognosis and prevention
Prognosis: Uremic pneumonia in the elderly with comorbidities mostly has a poor prognosis. Prevention: Prevention of uremic pneumonia should be done firstly by prevention of uremic pneumonia. Clinical prevention is aimed at healthy people and asymptomatic patients, firstly for patients with diabetes, hypertension, polycystic kidney, systemic lupus erythematosus, urinary tract obstruction should take primary and secondary preventive measures, health counseling for these patients, i.e. counseling individuals to change their behavioral lifestyle, reduce risk factors and stop the occurrence and development of the disease. These include.
① Health screening of high-risk groups, regular review of urine routine and kidney function, and early detection of disease.
② Eliminate risk factors for the deterioration of chronic renal failure such as infection, heart failure, dehydration or improper treatment.
③Adhere to the etiological treatment of chronic renal failure, such as chronic nephritis, lupus nephritis, purpura nephritis, IgA nephropathy, hypertensive nephropathy, diabetic nephropathy, etc. need to adhere to long-term treatment.
The kidneys’ ability to excrete metabolites decreases in chronic renal failure, and toxins accumulate in the body, which are basically metabolites of protein, so protein intake should be restricted, but too much restriction of protein intake can cause malnutrition, resulting in hypoproteinemia, so for patients with chronic renal failure to carry out nutritional therapy, it is appropriate to use high-efficiency Therefore, for patients with chronic renal failure, nutritional therapy should be carried out, preferably with high-efficiency proteins, such as eggs, milk, fish, lean meat, etc., and less vegetable proteins (such as soy products), ensure sufficient calories, and supplement vitamin C and vitamin B.
⑤ Prohibit or cautiously use drugs that are harmful to kidney function.
⑥If you notice a decrease in urine volume, an increase in edema, or an increase in nocturia, you should go to the hospital promptly.
(7) For patients with definite uremia who develop dyspnea, cough, inability to lie down and blood in sputum, consider combined uremic pulmonary edema and go to hospital immediately to avoid delay.
X. Epidemiology
Chronic renal failure occurs on the basis of various chronic renal parenchymal diseases and progresses slowly. According to statistics, chronic renal failure occurs in about 1 person per 10,000 people per year, and the incidence of uremic pneumonia can be as high as 60% or more in uremic patients, of which older uremic patients are more likely to develop uremic pneumonia.