GBZ 79-2002 Diagnostic criteria for occupational acute toxic nephropathy

This standard specifies the diagnostic criteria and treatment principles for occupational acute toxic nephropathy. This standard applies to acute toxic nephropathy caused by occupational chemical substances in occupational activities. This standard can also be used as a reference for acute toxic nephropathy caused by other toxic substances in non-occupational activities. GBZ 79-2002 Diagnostic criteria for occupational acute toxic nephropathy GBZ79-2002 Standard download decompression password: www.bzxz.net

ICS 13.100
National Occupational Health Standard of the People's Republic of China GBZ79—2002
Diagnostic Criteria of Occupational Acute Toxic Nephropathy Issued on April 8, 2002
Implemented on June 1, 2002
Issued by the Ministry of Health of the People's Republic of China
Article 6.1 of this standard is recommended, and the rest are mandatory. This standard is formulated in accordance with the "Law of the People's Republic of China on the Prevention and Control of Occupational Diseases". In various occupational activities, exposure to some high-concentration and highly toxic chemicals in a short period of time may cause acute toxic nephropathy. At present, there are no clear standards at home and abroad for medical institutions to refer to for correct diagnosis and treatment. In order to protect the health of the contactors: effectively prevent and treat occupational acute toxic nephropathy, this standard is formulated based on the progress of clinical and laboratory research in recent years. Appendix A of this standard is an informative appendix.
This standard is proposed and managed by the Ministry of Health of the People's Republic of China. This standard was drafted by the Occupational Disease Research Center of Peking University Third Hospital, and the Occupational Disease Department of Shandong Provincial Hospital and the Institute of Occupational Disease Prevention and Control of Jilin Chemical Industry Company Staff Hospital participated in the drafting. The Ministry of Health of the People's Republic of China is responsible for interpreting this standard. Occupational acute toxic nephropathy diagnostic standard GBZ79-2002
Occupational acute toxic nephropathy refers to acute poisoning with kidney damage as the main manifestation caused by short-term exposure to large doses of chemical substances in occupational activities. 1 Scope
This standard specifies the diagnostic criteria and treatment principles for occupational acute toxic nephropathy. This standard applies to acute toxic nephropathy caused by occupational chemical substances in occupational activities. Acute toxic nephropathy caused by other toxic substances in non-occupational activities can also be used as a reference. 2 Normative references
The clauses in the following documents become the clauses of this standard through reference in this standard. For all dated referenced documents, all subsequent amendments (excluding errata) or revised versions are not applicable to this standard. However, parties to an agreement based on this standard are encouraged to study whether the latest versions of these documents can be used. For any undated referenced document, its latest version shall apply to this standard.
GB/T16180
3 Diagnostic principles
Diagnostic criteria for occupational acute chemical poisoning (general principles) Diagnostic rules for occupational acute latent chemical poisoning Evaluation of the degree of disability caused by work-related injuries and occupational diseases of employees Diagnosis can only be made based on the occupational history of short-term exposure to a large number of chemical substances, typical clinical manifestations of acute kidney injury, relevant laboratory test results and on-site labor hygiene investigation, and the exclusion of similar diseases caused by other causes. 4 Observation subjects
Those who are exposed to a large number of kidney poisons in a short period of time and have transient acute kidney damage are the subjects of acute toxic nephropathy observation.
5 Diagnosis and classification criteria
5.1 Mild toxic nephropathy
Any patient with any two of the following manifestations:
Continued positive urine protein;
Soy sauce-colored urine, positive occult blood test; hematuria, test shows a large number of red blood cells in the urine; d
A large number of casts, or white blood cells, or a large number of renal tubular epithelial cells are found in the urine; Glomerular filtration rate (GFR) is continuously <80ml/min. e)
5.2 Moderate toxic nephropathy
Anyone with any two of the following manifestations:
a) Urine volume continuously <400ml/24h;
b) Urine specific gravity continuously <1.012, or urine osmotic pressure (Uosm) continuously <350mOsm/kgH2Oc) Urine sodium (UNa) continuously >40mmol/L, or filtered sodium excretion rate (FENa) continuously >2%;d) GFR continuously <50ml/min
e) Blood urea nitrogen (BUN) continuously >7.0mmol/L (>20mg/dl), or daily increase >3.5mmol/L (>10mg/dl);
f) Blood creatinine (Pcr) >177μmol/L (>2mg/dl), or daily increase >89μmol/L (>1mg/dl). 5.3 Severe toxic nephropathy
Anyone with any two of the following manifestations:
a) Urine volume continuously <200ml/24h;
b) GFR continuously <30ml/min
c) BUN continuously >21mmol/L (>60mg/dl), or daily increase >7.0mmol/L (>20mg/dl);d) Pcr continuously >430umol/L (>5mg/dl), or daily increase >177μmol/L (>2mg/dl);e) Blood potassium (Sk) continuously >6.0mmol/L (>6.0mEq/L); symptoms of uremia, such as nausea, vomiting, headache, drowsiness, mental depression, convulsions, coma, etc., and even complications such as f)
congestive heart failure, acute pulmonary edema, metabolic acidosis, hyponatremia, sepsis, etc. 6 Treatment principles
6.1 Treatment principles
Observation subjects
a) Immediately get out of contact with the poison. For poisons that can be absorbed through the skin, contaminated clothing should be removed and the skin should be washed with soap and clean water. For those with digestive tract invasion, gastric lavage should be performed immediately: and then they need to lie still and keep warm to rest. b) For those with systemic poisoning reactions, they can be treated according to the treatment routine of poisoning by this poison; during the treatment process, it is necessary to be careful to use drugs with strong kidney toxicity.
c) Carefully record the amount of fluid intake and output and closely observe the results of routine urine tests for 2 to 3 days: those with abnormalities need to undergo further kidney function tests.
6.1.2 Mild and moderate toxic nephropathy
In addition to the above treatment, the following measures can also be taken: a) Those with special antidotes can use them early, but the dose should be small each time: For poisons that can be removed by blood purification measures, this treatment can be used in the early stage of moderate poisoning patients. b) At the early stage, attention should be paid to preventing hypovolemia, relieving renal vascular obstruction, and improving renal microcirculation. c) Start diuretic treatment at an early stage.
d) Use adequate glucocorticoids at an early stage.
e) For patients with pigment proteinuria, alkaline drugs should be used at an early stage. Cellular intervention measures such as oxygen free radical scavengers, calcium channel blockers, and angiotensin converting enzyme inhibitors can help f)
delay the progression of the disease, but they need to be used at an early stage. 6.1.3 Severe toxic nephropathy
In addition to the above treatments, the following key points should be noted: Actively adopt blood purification therapy to prevent and treat uremia, hyperkalemia, water intoxication, etc., and can cooperate with detoxification treatment a)
accelerate the discharge of toxins.
b) Actively prevent and treat damage to other organ systems in the body caused by toxins and protect the functions of important organs. c) Actively prevent and treat infections and other complications; pay attention to reasonable nutritional supplements. d) During the oliguric phase, the fluid intake should be limited and diuresis should be performed correctly: during the polyuric phase, attention should be paid to maintaining the body's water and electrolyte balance. 6.2 Other treatments
6.2.1 Observation subjects
Those who have no obvious kidney damage and systemic poisoning symptoms after observation can return to their original jobs. 6.2.2 Mild toxic nephropathy
After recovery, the patient can work in the original job.
Moderate toxic nephropathy
After recovery, the patient can work normally, but should avoid contact with kidney poisons. 6.2.4: Severe toxic nephropathy
After recovery, the patient can work lightly and avoid contact with kidney poisons; if necessary, the treatment can refer to GB/T16180. Instructions for the correct use of this standard
See Appendix A (Informative Appendix).
Appendix A
(Informative Appendix)bZxz.net
Instructions for the correct use of this standard
A.1 This standard is mainly applicable to the diagnosis and treatment of acute toxic damage to the kidney caused by work or production contact, which causes chemical substances to invade the body in a relatively large amount in a relatively short period of time; it is also applicable to mechanical obstruction of the renal tubules caused by chemical substances (such as pigment protein casts, crystals, etc.), or acute kidney damage caused by its immune mechanism (such as acute interstitial nephritis, Goodpasture's nephritis syndrome, etc.). Acute toxic nephropathy caused by environmental factors or drugs can refer to this standard. This standard can also be used as a reference for the diagnosis and treatment of secondary acute kidney damage caused by various non-specific systemic pathological conditions caused by other diseases, such as hypoxia, shock, cardiopulmonary dysfunction, etc. A.2 Common occupational poisons with direct kidney toxicity include: a.a. Heavy metals or metalloid compounds, such as cadmium, mercury, chromium, lead, bismuth, uranium, platinum, arsenic, phosphorus, etc. b. Hydrocarbon compounds, such as chloroform, carbon tetrachloride, trichloroethylene, ethylbenzene, tea, gasoline, etc. c. Phenols, such as phenol, cresol, resorcinol, etc. d. Pesticides, such as organic mercury, organic arsenic, organic chlorine, organic phosphorus, organic fluorine, paraquat, etc. e. Other compounds, such as synthetic dyes, glycols, acrolein, oxalic acid, pyridine, morphine, etc.
Common occupational poisons with indirect renal toxicity are mainly chemical substances that can cause acute intravascular hemolysis or generate denatured globin bodies, such as arsine, antimonide, telluride, copper salts, nitro and amino compounds of benzene, chlorpyrifos, phenylhydrazine, coal tar derivatives, etc., which can cause hemoglobin casts to block the renal tubules; some compounds can form crystals or myoglobin casts in the renal tubules, which can also cause renal tubular blockage and even acute tubular necrosis. Many environmental factors and drugs also have direct or indirect renal toxicity, and differential diagnosis should be paid attention to. A.3 The incubation period of this disease is usually several hours to tens of hours, so the observation period is at least two days. A.4 In addition to general clinical manifestations, the main observation items are urine volume and urine routine examination (including color, specific gravity, pH value, protein and urine sediment examination, and urine osmotic pressure measurement if conditions permit); if the above examinations are abnormal but have recovered on their own after reexamination, it is transient renal damage; if the above indicators continue to be abnormal, occult blood test or further examination of various renal function indicators such as urine sodium, filtered sodium excretion rate, blood creatinine, urine creatinine, glomerular filtration rate, etc. should be performed. A.5 Mild toxic nephropathy should be differentiated from urinary tract infection. In addition to symptoms and signs, bacteria found in urine often have an important role in indicating infection.
A.6 Currently, the most commonly used and sensitive renal function indicators are: (1) Urine osmotic pressure (Uosm) Urine osmotic pressure or osmotic concentration is an observation indicator of urine concentration, so it can be used to reflect the reabsorption capacity of the renal tubules. Although urine specific gravity measurement also has this function, it is easily affected by the properties of the solute and its molecular weight. For example, the presence of protein and sugar can increase urine specific gravity. Urine osmotic pressure is only related to the number of solute particles, but not to their size. Therefore, it can more accurately reflect the functional status of the renal tubules than specific gravity. At present, instruments such as freezing point osmometers and vapor pressure osmometers are often used for measurement. They are convenient and fast, and the results are more objective and reliable. Under normal circumstances, Uosm is usually >500mOsm/kgH2O. If Uosm is <350mOsm/kgH2O, it often indicates renal tubular function damage. (2) Urine sodium (UNa) When the renal tubules function normally, hypertonic hyponatremia is excreted. Therefore, UNa under normal circumstances will not exceed 20mmol/L. When the renal tubules are damaged, their water absorption and sodium retention functions are significantly reduced, so hypotonic hypernatremia is excreted. At this time, UNa is usually >40mmol/L. Therefore, urine sodium determination can reflect the functional status of the renal tubules and help to distinguish between prerenal azotemia and acute tubular necrosis.
(3) Filtered sodium excretion rate (FEN) It ​​is defined as the total amount of sodium excreted in the urine per unit time as a percentage of the total amount of sodium filtered through the glomerulus during that period of time. This indicator not only includes the urine sodium factor, but also contains functions such as blood sodium, blood creatinine, urine creatinine, and glomerular filtration rate. Therefore, the result is more objective and reliable. It is currently recognized as the best indicator to reflect renal tubular function. The calculation formula is:
Urine sodium concentration (mmol/L)
FENa (%) =
Blood sodium concentration (mmol/L)
Urine creatinine concentration (ml/dl or umol/L)
Blood creatinine concentration (ml/dl or μmol/L) Under normal circumstances, FENa <1%. If this value is >2%, it indicates renal tubular dysfunction. (4) Endogenous creatinine generation rate (Ccr) This indicator is used to judge the glomerular filtration capacity based on the clearance of a certain metabolite generated in the body. It does not require the injection of exogenous reference substances, so it is simpler and easier to use. Creatinine is the dehydration and dephosphorylation product of high-energy creatinine phosphate. The amount of creatinine generated is very constant. Under normal circumstances, it is completely excreted through urine. Except for a very small amount (<5%) that can be excreted by the renal tubules, most of it is filtered out through the glomerulus and is not reabsorbed by the renal tubules. Therefore, its clearance rate can better reflect the glomerular filtration capacity. The calculation formula is as follows:) 1.73 (m2)
Urine creatinine concentration (mg/dl or μmol/L) 24-hour urine volume (ml) Ccr (ml/min) =
Serum creatinine concentration (mg/dl or μmol/L) 1.73 is the body surface area of ​​an adult with a standard weight of 70 kg 24X60 (min)
s (m2)
S is the body surface area of ​​the subject, which can be obtained by looking up the table based on height and weight; it can also be calculated according to the following formula: S=[height (cm)×0.0061+weight (kg)×0.0128]-0.15291.73/S is roughly 1. This value is slightly less than 1 for those who are overweight, and slightly greater than 1 for those who are underweight. The normal value of Ccr is 80ml/min～120ml/min. If this value is continuously lower than the normal value by more than 50%, the possibility of acute renal insufficiency may be considered; if this value is less than 25% of the normal value, it indicates that acute renal failure has occurred. A.7 The focus of the treatment of this disease is on the prevention and treatment of acute renal failure. The key is to block the relevant pathways of disease progression early before the onset of acute renal insufficiency. The measures routinely used in clinical practice include: reasonable infusion and timely replenishment of blood volume, administration of microvascular dilators to relieve renal vascular spasm and improve renal microcirculation, adequate diuresis to facilitate the discharge of toxins and metabolic waste in the body, early and sufficient use of glucocorticoids, and active application of blood purification therapy, among which blood purification therapy has a significant effect on the removal of harmful substances in the blood. Generally speaking, hemoperfusion (HP) is more effective in removing exogenous toxins. Although plasma exchange (PE) can also effectively remove harmful substances in the blood, it uses too much blood and is difficult to be widely used. Various dialysis techniques such as hemodialysis (HD) and peritoneal dialysis (PD) have a better effect on removing metabolic waste and exogenous harmful substances with a molecular weight of <50kd. For various toxic nephropathies, especially when acute renal dysfunction has occurred, it is a treatment method that takes both the symptoms and the root cause into consideration. This standard relaxes the conditions for the use of blood purification therapy and advocates its early use, that is, when it is judged that there is acute moderate toxic nephropathy. In addition to being used for treatment purposes, it also becomes a preventive means to delay the occurrence of toxic nephropathy, which is expected to play a good role in improving prognosis.6 The most commonly used and sensitive renal function indicators are: (1) Urine osmotic pressure (Uosm) Urine osmotic pressure or osmotic concentration is an observation indicator of the degree of urine concentration, so it can reflect the reabsorption capacity of the renal tubules. Although urine specific gravity measurement also has this function, it is easily affected by the properties of the solute and its molecular weight. For example, the presence of protein and sugar can increase urine specific gravity: Urine osmotic pressure is only related to the number of solute particles, but not to their size. Therefore, it can more accurately reflect the functional status of the renal tubules than specific gravity. At present, instruments such as freezing point osmometers and vapor pressure osmometers are often used for measurement, which is convenient and fast, and the results are more objective and reliable. Under normal circumstances, Uosm is usually >500mOsm/kgH2O. If Uosm is <350mOsm/kgH2O, it often indicates renal tubular function damage. (2) Urinary sodium (UNa) When the renal tubules function normally, hypertonic hyponatremic urine is excreted, so UNa under normal circumstances will not exceed 20mmol/L: When the renal tubules are damaged, their water absorption and sodium retention functions are significantly reduced, so hypotonic hypernatremic urine is excreted, and UNa at this time is often >40mmol/L. Therefore, urine sodium determination can reflect the functional status of the renal tubules and help to distinguish between prerenal azotemia and acute tubular necrosis.
(3) Filtered sodium excretion rate (FEN) It ​​is defined as the total amount of sodium excreted in the urine per unit time as a percentage of the total amount of sodium filtered through the glomerulus during that period of time. This index not only includes the urine sodium factor, but also contains functions such as blood sodium, blood creatinine, urine creatinine, and glomerular filtration rate. Therefore, the result is more objective and reliable. It is currently recognized as the best index to reflect renal tubular function. The calculation formula is:
Urine sodium concentration (mmol/L)
FENa (%) =
Blood sodium concentration (mmol/L)
Urine creatinine concentration (ml/dl or umol/L)
Blood creatinine concentration (ml/dl or μmol/L) Under normal circumstances, FENa <1%. If this value is >2%, it indicates renal tubular dysfunction. (4) Endogenous creatinine generation rate (Ccr) This index is based on the clearance of a certain metabolite generated in the body to judge the glomerular filtration capacity. It does not require the injection of exogenous reference substances, so it is simpler and easier. Creatinine is the dehydration and dephosphorylation product of high-energy creatinine phosphate. The amount produced is very constant and is completely excreted through urine under normal circumstances. Except for a very small amount (<5%) that can be excreted by the renal tubules, most of it is filtered out through the glomerulus and is not reabsorbed by the renal tubules. Therefore, its clearance rate can better reflect the filtration capacity of the glomerulus. The calculation formula is as follows:) 1.73 (m2)
Urine creatinine concentration (mg/dl or μmol/L) 24-hour urine volume (ml) Ccr (ml/min) =
Serum creatinine concentration (mg/dl or μmol/L) 1.73 is the body surface area of ​​an adult with a standard weight of 70 kg 24X60 (min)
s (m2)
S is the body surface area of ​​the subject, which can be obtained by looking up the table based on height and weight; it can also be calculated according to the following formula: S=[height (cm)×0.0061+weight (kg)×0.0128]-0.15291.73/S is roughly 1. This value is slightly less than 1 for those who are overweight, and slightly greater than 1 for those who are underweight. The normal value of Ccr is 80ml/min～120ml/min. If this value is continuously lower than the normal value by more than 50%, the possibility of acute renal insufficiency may be considered; if this value is less than 25% of the normal value, it indicates that acute renal failure has occurred. A.7 The focus of the treatment of this disease is on the prevention and treatment of acute renal failure. The key is to block the relevant pathways of disease progression early before the onset of acute renal insufficiency. The measures routinely used in clinical practice include: reasonable infusion and timely replenishment of blood volume, administration of microvascular dilators to relieve renal vascular spasm and improve renal microcirculation, adequate diuresis to facilitate the discharge of toxins and metabolic waste in the body, early and sufficient use of glucocorticoids, and active application of blood purification therapy, among which blood purification therapy has a significant effect on the removal of harmful substances in the blood. Generally speaking, hemoperfusion (HP) is more effective in removing exogenous toxins. Although plasma exchange (PE) can also effectively remove harmful substances in the blood, it uses too much blood and is difficult to be widely used. Various dialysis techniques such as hemodialysis (HD) and peritoneal dialysis (PD) have a better effect on removing metabolic waste and exogenous harmful substances with a molecular weight of <50kd. For various toxic nephropathies, especially when acute renal dysfunction has occurred, it is a treatment method that takes both the symptoms and the root cause into consideration. This standard relaxes the conditions for the use of blood purification therapy and advocates its early use, that is, when it is judged that there is acute moderate toxic nephropathy. In addition to being used for treatment purposes, it also becomes a preventive means to delay the occurrence of toxic nephropathy, which is expected to play a good role in improving prognosis.6 The most commonly used and sensitive renal function indicators are: (1) Urine osmotic pressure (Uosm) Urine osmotic pressure or osmotic concentration is an observation indicator of the degree of urine concentration, so it can reflect the reabsorption capacity of the renal tubules. Although urine specific gravity measurement also has this function, it is easily affected by the properties of the solute and its molecular weight. For example, the presence of protein and sugar can increase urine specific gravity: Urine osmotic pressure is only related to the number of solute particles, but not to their size. Therefore, it can more accurately reflect the functional status of the renal tubules than specific gravity. At present, instruments such as freezing point osmometers and vapor pressure osmometers are often used for measurement, which is convenient and fast, and the results are more objective and reliable. Under normal circumstances, Uosm is usually >500mOsm/kgH2O. If Uosm is <350mOsm/kgH2O, it often indicates renal tubular function damage. (2) Urinary sodium (UNa) When the renal tubules function normally, hypertonic hyponatremic urine is excreted, so UNa under normal circumstances will not exceed 20mmol/L: When the renal tubules are damaged, their water absorption and sodium retention functions are significantly reduced, so hypotonic hypernatremic urine is excreted, and UNa at this time is often >40mmol/L. Therefore, urine sodium determination can reflect the functional status of the renal tubules and help to distinguish between prerenal azotemia and acute tubular necrosis.
(3) Filtered sodium excretion rate (FEN) It ​​is defined as the total amount of sodium excreted in the urine per unit time as a percentage of the total amount of sodium filtered through the glomerulus during that period of time. This index not only includes the urine sodium factor, but also contains functions such as blood sodium, blood creatinine, urine creatinine, and glomerular filtration rate. Therefore, the result is more objective and reliable. It is currently recognized as the best index to reflect renal tubular function. The calculation formula is:
Urine sodium concentration (mmol/L)
FENa (%) =
Blood sodium concentration (mmol/L)
Urine creatinine concentration (ml/dl or umol/L)
Blood creatinine concentration (ml/dl or μmol/L) Under normal circumstances, FENa <1%. If this value is >2%, it indicates renal tubular dysfunction. (4) Endogenous creatinine generation rate (Ccr) This index is based on the clearance of a certain metabolite generated in the body to judge the glomerular filtration capacity. It does not require the injection of exogenous reference substances, so it is simpler and easier. Creatinine is the dehydration and dephosphorylation product of high-energy creatinine phosphate. The amount produced is very constant and is completely excreted through urine under normal circumstances. Except for a very small amount (<5%) that can be excreted by the renal tubules, most of it is filtered out through the glomerulus and is not reabsorbed by the renal tubules. Therefore, its clearance rate can better reflect the filtration capacity of the glomerulus. The calculation formula is as follows:) 1.73 (m2)
Urine creatinine concentration (mg/dl or μmol/L) 24-hour urine volume (ml) Ccr (ml/min) =
Serum creatinine concentration (mg/dl or μmol/L) 1.73 is the body surface area of ​​an adult with a standard weight of 70 kg 24X60 (min)
s (m2)
S is the body surface area of ​​the subject, which can be obtained by looking up the table based on height and weight; it can also be calculated according to the following formula: S=[height (cm)×0.0061+weight (kg)×0.0128]-0.15291.73/S is roughly 1. This value is slightly less than 1 for those who are overweight, and slightly greater than 1 for those who are underweight. The normal value of Ccr is 80ml/min～120ml/min. If this value is continuously lower than the normal value by more than 50%, the possibility of acute renal insufficiency may be considered; if this value is less than 25% of the normal value, it indicates that acute renal failure has occurred. A.7 The focus of the treatment of this disease is on the prevention and treatment of acute renal failure. The key is to block the relevant pathways of disease progression early before the onset of acute renal insufficiency. The measures routinely used in clinical practice include: reasonable infusion and timely replenishment of blood volume, administration of microvascular dilators to relieve renal vascular spasm and improve renal microcirculation, adequate diuresis to facilitate the discharge of toxins and metabolic waste in the body, early and sufficient use of glucocorticoids, and active application of blood purification therapy, among which blood purification therapy has a significant effect on the removal of harmful substances in the blood. Generally speaking, hemoperfusion (HP) is more effective in removing exogenous toxins. Although plasma exchange (PE) can also effectively remove harmful substances in the blood, it uses too much blood and is difficult to be widely used. Various dialysis techniques such as hemodialysis (HD) and peritoneal dialysis (PD) have a better effect on removing metabolic waste and exogenous harmful substances with a molecular weight of <50kd. For various toxic nephropathies, especially when acute renal dysfunction has occurred, it is a treatment method that takes both the symptoms and the root cause into consideration. This standard relaxes the conditions for the use of blood purification therapy and advocates its early use, that is, when it is judged that there is acute moderate toxic nephropathy. In addition to being used for treatment purposes, it also becomes a preventive means to delay the occurrence of toxic nephropathy, which is expected to play a good role in improving prognosis.7 The treatment of this disease focuses on the prevention and treatment of acute renal failure. The key is to block the relevant pathways of disease progression before acute renal insufficiency occurs. The measures routinely used in clinical practice include: reasonable infusion and timely replenishment of blood volume, administration of microvascular dilators to relieve renal vascular spasm and improve renal microcirculation, adequate diuresis to facilitate the discharge of toxins and metabolic waste in the body, early and sufficient use of glucocorticoids, and active use of blood purification therapy, among which blood purification therapy has a significant effect on the removal of harmful substances in the blood. Generally speaking, hemoperfusion (HP) is more effective in removing exogenous toxins. Although plasma exchange (PE) can also effectively remove harmful substances in the blood, it uses too much blood and is difficult to be widely used. Various dialysis techniques such as hemodialysis (HD) and peritoneal dialysis (PD) have a better effect on removing metabolic waste and exogenous harmful substances with a molecular weight of <50kd. For various toxic nephropathies, especially when acute renal dysfunction has occurred, it is a treatment method that takes both the symptoms and the root cause into consideration. This standard relaxes the conditions for the use of blood purification therapy and advocates its early use, that is, when it is judged that there is acute moderate toxic nephropathy. In addition to being used for treatment purposes, it also becomes a preventive means to delay the occurrence of toxic nephropathy, which is expected to play a good role in improving prognosis.7 The treatment of this disease focuses on the prevention and treatment of acute renal failure. The key is to block the relevant pathways of disease progression before acute renal insufficiency occurs. The measures routinely used in clinical practice include: reasonable infusion and timely replenishment of blood volume, administration of microvascular dilators to relieve renal vascular spasm and improve renal microcirculation, adequate diuresis to facilitate the discharge of toxins and metabolic waste in the body, early and sufficient use of glucocorticoids, and active use of blood purification therapy, among which blood purification therapy has a significant effect on the removal of harmful substances in the blood. Generally speaking, hemoperfusion (HP) is more effective in removing exogenous toxins. Although plasma exchange (PE) can also effectively remove harmful substances in the blood, it uses too much blood and is difficult to be widely used. Various dialysis techniques such as hemodialysis (HD) and peritoneal dialysis (PD) have a better effect on removing metabolic waste and exogenous harmful substances with a molecular weight of <50kd. For various toxic nephropathies, especially when acute renal dysfunction has occurred, it is a treatment method that takes both the symptoms and the root cause into consideration. This standard relaxes the conditions for the use of blood purification therapy and advocates its early use, that is, when it is judged that there is acute moderate toxic nephropathy. In addition to being used for treatment purposes, it also becomes a preventive means to delay the occurrence of toxic nephropathy, which is expected to play a good role in improving prognosis.
Tip: This standard content only shows part of the intercepted content of the complete standard. If you need the complete standard, please go to the top to download the complete standard document for free.