Acute renal failure was gradually recognized in the treatment of patients with crush syndrome in earthquakes and wars. In the Tangshan earthquake in 1976, 2%-5% of the injured were combined with crush syndrome and received diuretic and volume expansion treatment. 1990, the Iran earthquake, 154 people received dialysis treatment.
1.Definition: It refers to a renal insufficiency syndrome caused by multiple etiologies of rapidly declining renal function, clinically characterized by sudden oliguria and anuria, progressive azotemia, and disturbance of water-electrolyte acid-base balance.
2, morbidity: ARF is a common clinical syndrome, the morbidity accounts for about 5% of general hospital inpatient cases, ICU even up to 30%. According to the EDTA32 center statistics, the incidence of single organ failure (SOF) is 30-60 people/1 million population, with an average of 28.9 people/1 million population (>30% for severe cases), second only to acute respiratory failure, and the older the age, the higher the incidence. And regardless of whether ARF is the primary or secondary cause, the incidence of combined multi-organ failure (MODS) is ≥ 50%.
3, mortality: early statistics for 30-70%, the average 50%. The survival rate of SOF is 90%, while the survival rate of MODS is less than 20% (3 organs), such as 5 organ dysfunction is almost 0. Especially when combined with sepsis, the mortality rate is up to 74.5%; age > 60 years, the mortality rate of 70%.
4. Judgment criteria of ARF: clinically, the progressive increase of blood creatinine exceeds 44.2umol/L/d, and creatinine clearance rate (CCr) decreases to less than 50ml/min; in patients with original chronic renal insufficiency, CCr decreases by 15% from the original level can also be defined as acute renal failure.
Broadly speaking, acute renal failure can be divided into three major categories, including pre-renal acute renal failure, renal substantial (renal) acute renal failure, and post-renal acute renal failure. In some cases, the three types can be transformed into each other. If prerenal acute renal failure is not treated in time, it can develop into acute tubular necrosis in a few hours, and if postrenal acute renal failure is not released from obstruction as soon as possible, it can cause substantial renal acute renal failure in about 2 weeks, and the lesion will be further aggravated.
1, pre-Renal acute renal failure (pre-Renal ARF), also known as functional ARF, accounts for about 55-60% of ARF, the etiology is mainly.
(1) circulatory failure, pump failure caused by reduced cardiac output: due to various acute cardiovascular diseases, such as ischemic heart disease, valvular disease, pericardial disease, arrhythmia, hypercardia, and also such as acute renal artery occlusion, blunt abdominal trauma, renal arteriosclerosis, post-renal arteriography, nodular arteritis, acute renal vein embolism.
(2) Insufficient effective blood volume: blood loss, loss of body fluids, which can be lost through the gastrointestinal tract, kidneys, skin or wounds. Also such as burns, crush injuries, major surgical procedures, etc.
(3) Extracellular fluid redistribution: retention of body fluids in the third interstitial space, such as nephrotic syndrome and hepatorenal syndrome.
(4) Sudden rise or fall of blood pressure: ARF can be caused by sudden expansion of volume vessels, excessive hypotension or improper use of anesthetics, respiratory failure, etc. At this time, various vasoactive substances, PG, kinins, cardiac natriuretic agents, etc. lose their regulatory role for the kidney itself and blood pressure.
2, renal substantial acute renal failure: for various reasons involving the kidneys, called organic ARF, accounting for about 35-40% of ARF, clinically divided into four categories.
(1) Glomerular: primary or secondary acute and acute progressive glomerulonephritis due to various causes, such as crescentic nephritis, SLE, pulmonary hemorrhagic nephritis syndrome, allergic purpura nephritis, etc.
(2) Renal vascular: including renal microvascular and macrovascular lesions, such as malignant small arteriosclerotic nephropathy, acute bilateral renal cortical necrosis, acute renal artery embolism, renal vein thrombosis, arterial entrapment, etc. common in pathology obstetrics.
(3) Acute interstitial renal lesions: including allergic, such as drug-induced acute interstitial nephritis, severe infectious, metabolic, and tumor-induced interstitial infiltrative renal disease.
(4) Acute tubular necrosis: the most common type, accounting for 75% of renal ARF, i.e. ARF in the narrow sense. most common in disasters, the focus of this section.
(3) Post-renal acute renal failure: obstructive ARF, accounting for about 5% of ARF. The etiology is mainly due to urological stones, tumors compressing the renal pelvis and ureter, occupational lesions of the urinary system, prostate disorders and bladder rupture, which cause obstruction in or outside the ureter, bladder outlet or urethra.
Acute tubular necrosis
(Acute Tubular Nerosis ATN)
Etiology: two main types.
I. Nephrotoxicity: including endogenous and exogenous nephrotoxic substances
(A) Exogenous toxic substances
1, nephrotoxic substances: antibacterial drugs are the most common cause of ATN, accounting for about 70%
(1) Aminoglycosides are the most common (70%)
(2) Peptides: cephalosporins (I and II generation), vancomycin, mucomycin
(3) Amphotericin B
(4) Sulfonamides
Clinical characteristics: not much related to drug concentration but closely related to the dose of involvement, usually with a course of drug incidence of 10%.
(2) Contrast agents (2-20%)
Due to the high osmotic effect of iodine-containing contrast agents, hypovolemia and the use of diuretics can aggravate renal damage, which usually occurs a few hours to a few days after the examination.
(3) Immunosuppressive agents: cyclosporine, D-penicillamine, etc.
(4) Diuretics: mercury-containing diuretics, high-dose mannitol
(5) anti-tumor chemotherapy drugs: cisplatin, aminoglycoside, mitomycin, etc.
(6) organic toxins: organophosphorus pesticides, insecticides, rodenticides, methanol, toluene, etc.
(7) other: anesthetics, dextrose, glycerol injection, antiviral drugs, heroin, non-steroidal anti-inflammatory drugs.
(8) ACEI
2.Biotoxins: snake, bee, scorpion, black spider poisoning, fish bile poisoning, poisonous Qin.
3, heavy metals: gold, silver, copper, mercury, arsenic, lead, etc.
4.Microorganisms: toxin and its metabolites, severe bacterial infections, Staphylococcus aureus sepsis, Gram-negative bacillus sepsis, fungal infections, Legionella infections, epidemic hemorrhagic fever, etc.
High risk factors.
(1) Pediatrics and the elderly.
(2) Blood volume deficiency.
(3) Pre-existing chronic kidney disease.
(4) Concomitant use of diuretics.
(5) Hypercoagulable state.
(6) Excessive dose in a short period of time, excessive duration of treatment, repeated use of nephrotoxic substances.
(B) endogenous nephrotoxic substances
1, pigment toxicity.
(1) abnormal increase in body hemoglobin: acute intravascular hemolysis, allogeneic transfusion, hemolysis of immune diseases, poisoning, malaria, sericosis, black urine fever, etc.
(2) Skeletal muscle fracture lysis, trauma lasting coma resulting in myoglobinuria.
(3) Strenuous exercise, ischemia, myositis, hypokalemia “non-traumatic rhabdomyolysis”.
Mainly due to tubular blockage of the renal tubules and the direct toxic effect on the tubules.
2, electric shock injury: mainly due to renal vasoconstriction, renal ischemia, tubular blockage and direct toxic effects on tubules.
3.Other: hypercalcemia, light chain protein, and hyperuricemia in multiple myeloma.
2. Renal ischemia: more lasting and severe damage can occur on the basis of anterior renal ischemia
As mentioned above, reduced effective blood volume, reduced cardiac output or due to shock, reduced extracellular fluid volume, severe infection, acute gastrointestinal infection, shock pneumonia, severe acute pancreatitis, sepsis, epidemic hemorrhagic fever, leptospirosis and other prerenal factors can be used as initiating factors to cause ATN.
Pathogenesis
1. Renal tubular injury theory.
(1) Anti-leakage theory.
(2) renal tubular occlusion theory
2. Abnormal renal hemodynamic regulation theory
3. Cytokine action theory.
More and more cytokines are found to be involved in the pathogenesis of the whole process, including cell injury, regeneration, repair, protection, hemodynamic and renal function changes. Cytokines play two main roles.
(1) renal cell destruction: causing renal vasoconstriction, decreased renal blood flow, decreased glomerular filtration rate, and decreased urine output. In this case, it is mainly due to the increased secretion and release of vasoactive substances that cause vasoconstriction, such as renin-angiotensin II, endothelin, endothelium-derived vasodilator factor, thromboxane A2 and lipoxygenase metabolites (leukotrienes, oxygen free radicals).
(2) Protection of renal cells: promote renal tubular regeneration, repair and vasodilatation to increase renal blood flow and glomerular filtration rate. Such as PGI2, cardiac natriuretic, NO, EGF.
Pathology
Visual observation: the kidney increases in size. Surface pallor and increased weight.
Gross specimen: pale renal cortex is seen, indicating renal cortical ischemia, while the medulla is dark red, indicating renal medullary stasis. Causes.
1, when renal blood flow decreases by 30-50%, the distribution of blood flow in the kidney changes significantly, and the small arteries entering the bulb in the outer 1/3 of the cortex are highly sensitive to vasoconstrictive substances, so renal cortical ischemia is serious. renal blood flow decreases during ATN, the glomerular filtration rate decreases, and tubular filtrate decreases, which helps prevent hypotensive perfusion and hypoxia-induced cell injury, which is the process of self-compensation after kidney injury.
2, near the medullary glomerulus out of the small arteries thicker, less resistance, relatively more blood flow into the medulla, the so-called “blood flow short circuit” phenomenon – bruising.
3, the external renal medulla oxygen tension is much lower than the cortical, so hypotension and local hypoxia cause kidney injury mainly in the medulla, especially the thick segment of the ascending branch of the medullary collaterals, ATN occurs.
4, intravascular erythrocyte aggregation causing vascular obstruction.
Light microscopy: early damage repair and lesion process can be observed to overlap and interleave, tubular epithelial cells swelling, degeneration, continuous necrosis and shedding, the lumen is filled with necrotic cells, tubular type and exudate.
Toxic-induced damage is mainly in the proximal tubule, where epithelial cells undergo degeneration but do not damage the basement membrane, and the disease process can regenerate and repair in about a week, with clinical entry into the polyuric phase. The ischemic type first damages the interlobular arteries, the lesions are in the distal tubules and the outer segment of the medullary collaterals, the lesions can involve all segments and collecting ducts in severe cases, the basement membrane can be shortened and ulcerated, causing back leak, interstitial edema, congestion and inflammation, which can affect the small veins, and the cells cannot be regenerated in the case of basement membrane rupture. The recovery time of ischemic type is long and even irreversible.
Clinical manifestations
The onset of the disease is rapid, systemic symptoms are obvious, and there are differences in performance due to different etiologies. Clinically, there are three types: oliguric type, non-oliguric type and hypermetabolic type.
Oliguric type ATN (OATN)
It accounts for 70% of the cases, with a non-medical etiology and pathological changes mostly due to renal ischemia. It is divided into oliguric or anuric phase, polyuric phase, and recovery phase. In the animal test, it is divided into the initiation period, maintenance period and recovery period. The initiation period corresponds to the first 6 hours after the initiation of renal injury, the maintenance period continues from 6 hours until renal function starts to recover, and the recovery period indicates that renal function has started to recover.
I. Oliguric phase or anuric phase
1.Decrease in urine output; <400ml/24h and <100ml/24h is called anuria. Renal ischemia can be oliguria in 1 day, and the latency period is about 1 week for those caused by toxic substances. The average duration of oliguria is 1-2 weeks, short can be a few hours, up to several months, more than 4 weeks to consider renal cortical necrosis or other aggravating factors, the longer the oliguria period, the worse the prognosis.
2. Progressive azotemia: Uremia can appear in various systems, including the digestive tract, cardiovascular, nervous system, hematological system, skeletal and endocrine system, among which the symptoms of the digestive system are the most common and the earliest to appear. It is accompanied by metabolite retention in the body and elevated blood creatinine, usually elevated 44.2-88.4umol/L/24h, and urea nitrogen elevated 3.6-7.1mmol/L/24h; if the elevated blood creatinine exceeds 176.8umol/L/24h and urea nitrogen exceeds 8.9mmol/L/24h, it is the hypermetabolic type.
Glomerular filtration rate decreased to <50ml/min.
3. Water-electrolyte and acid-base imbalance disorders.
(1) Water toxicity: dilutive hyponatremia occurs. Clinical manifestations include edema, weight gain, hypertension, acute left heart failure, pulmonary edema and cerebral edema, and in severe cases, headache, convulsions, coma and fundic edema.
(2) Hyperkalemia: weakness, bulging bowel, slowed heart rate, ventricular fibrillation, and in severe cases, cardiac arrest.
(3) Metabolic acidosis: clinical weakness, drowsiness, deep and fast breathing, and cardiac arrhythmia. In severe cases, convulsions, coma, respiratory paralysis, and cardiac arrest may occur.
(4) Hypocalcemia and hyperphosphatemia: It often occurs after 2 days of oliguria. Low calcium can cause convulsions, high phosphorus often no clinical symptoms.
(4) Cardiovascular system manifestations: hypertension, heart failure, arrhythmia, pericarditis.
5, bleeding tendency: gastrointestinal bleeding, diffuse intravascular coagulation.
6, Infection: about 50%, the most common sites are respiratory, urinary, blood, biliary tract and skin. Since the introduction of early prophylactic dialysis, deaths from acute pulmonary edema and hyperkalemia in uremic patients have decreased significantly, while infections have become an important cause of death in the oliguric phase.
7. Endocrine and metabolic abnormalities.
(1) Elevated levels of parathyroid hormone and calcitonin, reduced levels of thyroxine and sex hormones, and elevated levels of antidiuretic hormone, renin-angiotensin, growth hormone, and gastrin.
(2) Glucose metabolism: decreased glucose tolerance, insulin resistance phenomenon, elevated plasma insulin and glucagon levels.
(2) Polyuric phase
It refers to the period when the urine volume gradually increases progressively from little to more than normal, usually lasting 1-3 weeks. At this time, the urine volume is >400ml/24h, then it increases exponentially day by day, and after a week, it can be more than 3000ml/d, which is a sign of kidney function recovery. Early polyuria can still be high blood potassium, blood creatinine, urea nitrogen can still rise; with the development of the disease can appear hyponatremia and hypokalemia. Urine specific gravity is low.
At this time, it is easy to complicate infection, dehydration and hypotension, and gastrointestinal bleeding can still occur, which is not out of danger, and the mortality rate can be as high as 20%.
Third, the recovery period
The urine volume gradually returns to normal, the kidney function basically returns to normal, urea nitrogen and blood creatinine are also basically normal. Glomerular filtration function mostly recovers within 3-12 months, but tubular function recovers more slowly, and some of them last for more than a year, and can still have low specific gravity and low osmolality, and a few severe cases produce permanent kidney damage (chronic renal failure).
Non-oliguric type of ATN (NOATN)
Urine output is often >700ml/24h, with a mean of >1000ml/24h, while GFR remains low, with azotemia and renal tubular damage, commonly associated with long-term use of nephrotoxic agents, such as aminoglycoside antibiotics.
1. Incidence: about 30-60%, with an increasing trend in recent years, due to.
(1) increased awareness of the disease.
(2) abuse of nephrotoxic drugs.
(3) early use of diuretics, dopamine, mannitol, etc. to increase renal blood flow and urine volume in acute renal failure.
2. Clinical features: milder disease, faster recovery, less dialysis, fewer comorbidities, easy hypokalemia.
3.Pathogenesis.
(1) Inconsistent degree of damage in each unit.
(2) Impaired medullary hyperosmolarity formation.
(3) Weak bulb-tube feedback.
(4) tubular dysfunction precedes GFR reduction.
(5) Although GFR was not significantly reduced, water reabsorption in the filtrate was reduced, so there was no significant reduction in urine volume.
Hypercatabolic ATN
The acute tubular necrosis due to massive trauma, burn or crush injury, post-surgery, severe infection with high fever, sepsis, etc. is critical, and tissue metabolism and decomposition are extremely vigorous, resulting in rapid increase in blood urea nitrogen, blood creatinine and blood potassium, rapid decrease in blood HCO3-, and severe acidosis. The rate of tissue metabolism and decomposition products is much faster than the rate of residual renal function to remove toxic substances.
Causes: Increased secretion of certain bioactive peptides such as catecholamines, glucagon and PTH in the patient’s blood promotes tissue protein catabolism, making catabolism greater than synthesis, and protein synthesis in vivo is impaired.
The clinical symptoms of intoxication are severe, with prominent neurological symptoms, such as drowsiness, coma, seizures, hyperreflexia or hyporeflexia, and myoclonic convulsions. In critical cases, the disease is often complicated by respiratory tract, urinary tract, trauma and skin infections, and in severe cases, sepsis. The disease is often accompanied by multiple organ failure.
Laboratory tests
Blood tests: there may be mild to moderate anemia, red blood cells, hemoglobin and platelets in peripheral blood may be reduced, and white blood cells may be increased.
Second, urine examination.
1, urine volume is often <400ml/d.
2, specific gravity: urine specific gravity is mostly 1.010-1.015, early can be 1.018, recovery period is often lower than 1.020.
3, urine osmolality <350mOsm/kg, urine osmolality: blood osmolality <1.1/1.
4.Urinary routine analysis: a small amount of urine protein, a few red and white blood cells, epithelial cells and tubular type.
5.Urinary index determination.
(1) Increased urinary sodium content > 40 mmol/L (normal = 10 mmol/L), prenephrosis < 20 mmol/L.
(2) Fraction of filtered sodium excretion (FENa%): ATN>2, renal anterior <1.
(3) Renal failure index (RFI) ATN>2, renal anterior <1, mainly based on the principle of increased urinary sodium concentration and decreased urinary creatinine/blood creatinine ratio during ATN.
(4) urine creatinine: blood creatinine <20:1, this ratio reflects the ability of renal tubular reabsorption of water filtered out from the glomerulus, because creatinine will not be reabsorbed by the renal tubules, so the lower the concentration of urine creatinine, the worse the ability of renal tubular reabsorption of water.
C. Renal function measurement.
Blood urea nitrogen and blood creatinine are significantly elevated. Glomerular filtration rate (GFR) decreases, which is often inferred clinically from endogenous creatinine clearance (Ccr) (normal is 80-120 ml/min?1.73m2)
IV. Blood biochemical measurements.
1. High blood potassium: >5.2mmol/L (normal value is 3.5-5.2mmol/L), elevated by about 0.3mmol/L per day during oliguric period.
2.Low blood sodium: <130mmol/L (normal value is 135-145mmol/L).
3, low calcium: <2.2mmol/L (normal value is 2.2-2.7mmol/L), high phosphorus >1.6mmol/L (normal value is 0.6-1.6mmol/L).
4. Metabolic acidosis: CO2CP <20mmol/L (normal value is 22-31mmol/L), blood PH <7.35.
V. Renal imaging.
Including B ultrasound, abdominal plain film, CT, radionuclide scan, angiography to identify acute renal vascular disease, urography, etc. Retrograde imaging is feasible if necessary. It can understand the size of the kidney, the presence of stones, effusion, calcification, obstructive masses, and help to identify chronic renal failure, post-renal acute renal failure, enlargement of both kidneys in ARF, and reduction of both kidneys in chronic renal failure. If acute renal artery embolism or renal vein thrombosis is suspected, color Doppler, nuclide scan, MRI and angiography are feasible and performed only when necessary.
VI. Indications for renal biopsy.
(1) The etiology is not known.
(2) exclude acute glomerulopathy, acute interstitial nephritis, vasculitis syndrome.
(3) Anuria or oliguria for more than 4 weeks.
(4) Know the prognosis of the disease.
Diagnosis of ATN
1. a history of the primary disease causing ATN
2. clinical presence of oliguria and dramatic deterioration of renal function
3, low urine specific gravity, <1.015; decreased urine osmolality, urine osmolality: blood osmolality <1.1; urine sodium >40 mmol/L; FENa>2,RFI>2; blood creatinine: urine creatinine <20; urine BUN: blood BUN <8.
Differential diagnosis points of ATN
I. Differentiation of chronic renal failure.
1, history of chronic diseases such as recurrent swelling, proteinuria, hematuria, hypertension or diabetes mellitus.
2, with polyuria and increased nocturia.
3, with clinical manifestations of chronic renal failure uremia, such as severe anemia, pruritus, renal bone disease and lesions of the nervous system.
4, the volume of both kidneys is reduced, but in diabetic nephropathy, renal amyloidosis and polycystic kidney the volume of the kidneys may not be reduced or even increased.
Differentiation from pre-renal azotemia
1, history of hypovolemia or circulatory failure, increased urine volume after volume expansion and diuresis.
2.Low urine and high specific gravity, urine specific gravity >1.020; urine osmolality >500mOsm.
3, low urine and low urinary sodium <20 mmol/L, FeNa <1, RFI <1.
4, urine creatinine: blood creatinine > 40, urinary urea nitrogen: blood urea nitrogen > 8.
5, central venous pressure <6mmH2O, ATN normal or elevated.
C. Differentiation from post-renal urinary tract obstruction
1, signs of urinary tract obstruction without ATN etiology.
2, sudden anuria; alternating anuria and polyuria in a short period of time is characteristic.
3, often with renal colic and percussion pain in the renal area; massive fluid accumulation in the kidney and enlarged kidneys
4. insignificant changes in urinary routine.
5, imaging examination.
IV. Differentiation from other renal parenchymal ARF
(A) Acute glomerulonephritis
1, no history of primary ATN.
2, manifestations of other systemic diseases, such as SLE and pulmonary hemorrhagic nephritis syndrome, massive proteinuria, tubularity, and aberrant red blood cells.
3, oliguria, edema, hypertension.
4, different changes in urinary indicators.
5, renal biopsy pathology showing crescentic nephritis changes.
(B) acute interstitial nephritis
1, a history of allergy due to drugs or other things.
2, fever, rash, abdominal pain, arthralgia in the course of the disease.
3, elevated blood and urine eosinophils, elevated blood IgE, and sterile pusuria.
4, renal biopsy pathology shows interstitial renal changes.
(C) Identification of renal vascular hypertension
1, malignant hypertension (renal artery trunk and branch stenosis)
(1) Prevalent in adolescents, no family history, rapid onset, systolic blood pressure >200 mmHg.
(2) Hypertensive encephalopathy (cerebral hemorrhage), pulmonary edema, acute left heart failure.
(3) Characteristic ocular changes: sudden loss of visual acuity or blindness, optic papilla edema, protein exudate.
(4) Continuous vascular murmurs can be heard in the upper abdomen or lumbar region.
(5) The patient’s two kidneys are unequal in size, with a difference of >1.5 cm in length and diameter.
(6) Renal arteriography and fractional renal function, plasma renin measurement can determine the diagnosis.
2.Acute renal artery occlusion
(1) History of wind heart disease is often present: diastasis, atrial fibrillation, history of IEE or aortic surgery, history of lumbar and abdominal trauma, aortic or renal artery sclerosis, aneurysm, arteritis.
(2) sudden onset, episodes of severe and persistent pain in the lower back and abdomen, vomiting, fever.
(3) Sudden decrease in urine output with ARF manifestations.
(4) Increased blood leukocytes, urine protein, LDH, and serum glutathione transaminase.
(5) r-renal angiography of the affected kidney does not appear, renal arteriogram.
3.Bilateral renal vein thrombosis
(1) The presence of high-risk factors: such as severe dehydration, nephrotic syndrome hypercoagulable state, intrarenal blood flow stagnation, tumor invasion of the renal vein wall.
(2) Sudden onset, episodes of severe and persistent pain in the lower back and abdomen, vomiting, fever.
(3) Sudden decrease in urine output and the development of ARF.
(4) Enlargement of both kidneys.
(5) Imaging examination.
Treatment of ATN
Principles: targeting the cause, early prevention, early treatment, early medication and preventive dialysis
I. Prevention and treatment of the underlying cause: two main types of measures are taken to correct systemic circulatory hemodynamic disorders and to avoid the application and treatment of various exogenous or endogenous nephrotoxic substances.
II. Treatment of the incipient phase.
The incipient phase refers to a transitional period between pre-renal azotemia and established ATN, when the urine osmolality: blood osmolality is between 1.1 and 1.4. If the urine osmolality: blood osmolality is <1.1, the diagnosis of ATN is confirmed and the treatment is based on the oliguric phase. Treatment measures in the initial stage are as follows.
1.Diuretics to maintain urine output
(1) 20% mannitol 100-200ml intravenous push or drip, observe 1-2h, if the urine volume increases more than 17ml/h, it means the patient has insufficient blood volume.
(2) Mannitol plus tachyphylaxis (4mg/kg) intravenous drip, observe 1-2h, if not effective, tachyphylaxis can be doubled to 8mg/kg intravenous push, if the urine volume increases, it indicates that the course of the disease is in the prerenal stage or non-oliguric ARF; if the urine volume does not increase, then establish ATN and discontinue diuretics.
Mechanism of action.
(1) Decrease renal vascular resistance, resulting in increased renal blood flow and increased glomerular filtration rate.
(2) Reduce NaCl reabsorption by medullary collaterals, impede medullary hyperosmolarity and diuresis, reduce renal tubular obstruction, and achieve prevention of ARF, reversal of ARF, and conversion of oliguric type to non-oliguric type ARF.
2.Application of vasoactive drugs
(1) Small dose of dopamine (0.5-2.0ug/kg.min) intravenously can dilate blood vessels, improve renal blood flow and increase glomerular filtration rate, thus producing diuretic effect. Use within 24 hours of onset.
(2) Calcium channel antagonist (CCB): dilates renal blood vessels and causes moderate solute diuretic effect, which can prevent ischemic renal failure and convert oliguric type to non-oliguric ARF.
(3) Angiotensinase inhibitors (ACEI) and angiotensin II receptor blockers (ARB): can cause vasodilation, decreased renal vascular resistance, increased renal blood flow, increased glomerular filtration rate, and increased urine output.
(4) Prostaglandins (PGs).
(i) PGE2 and PGI2 cause renal vasodilatation.
(ii) Inhibition of water and sodium reabsorption and increase in urine output.
(3) Promote the secretion and release of renin from dense spots.
(5) Cardiac natriuretic (ANP): powerful diuretic and vasodilatory effects.
(i) dilate the small glomerular inlet arteries, while contracting the small outlet arteries, increase intracapillary pressure, and increase GFR.
(ii) Sodium diuretic effect, affecting renal tubular reabsorption.
(iii) cytoprotective effect, which increases renal ATP synthesis, reduces energy expenditure and promotes cell repair.
④Antagonize vasoconstrictor active substances.
3, other treatment: intra-abdominal decompression: in patients with hepatorenal syndrome or nephrotic syndrome, a large amount of ascites causes intra-abdominal hypertension, resulting in renal and splenic ischemia and decreased glomerular filtration rate. Reducing intra-abdominal pressure can improve blood flow to the kidneys and improve renal function.
Third, the treatment of oliguric phase.
1, strict control of water and sodium intake: is the most important part of the treatment of acute renal failure. After correcting the patient’s original fluid deficiency, we should adhere to the principle of “quantity out for quantity in”.
Daily fluid intake (ml) = previous day’s urine volume + apparent water loss + 400 ml
For every 1℃ increase in body temperature, increase the amount of rehydration fluid by 100ml.
Monitoring indicators
①Body weight: generally, it is required to drop 0.2~0.3kg per day. If the body weight does not decrease or even increases, it indicates water and sodium retention; if the body weight drops >0.5kg/d, it indicates insufficient rehydration.
②Blood sodium: <130mmol/L indicates excessive fluid intake; >145mmol/L indicates insufficient fluid intake.
③Blood pressure: elevation should be noted for excessive body fluid.
2, diet and nutrition: provide low salt, high quality low protein, high calorie and high vitamin diet. Protein 0.6g/kg.d, high metabolic type 1.0~1.2g/kg.d, provide total calories 126~188kJ (30~45Cal)/kg body weight per day, minimum intake of carbohydrate 100g; for multi-organ dysfunction high metabolic ARF, deep venous puncture should be infused with high energy nutrition solution.
Objectives of nutritional therapy.
(i) to reduce the negative nitrogen balance and maintain the normal structural composition of the organism.
② restore the biochemical and water-electrolyte acid-base balance of plasma and tissues and reduce uremic toxins; ③ improve the physiological function and immunity of the organism.
If the patient is on dialysis treatment, the daily calories, proteins and other components of food may not be strictly limited.
3. Correction of water, electrolyte-acid-base balance
(1) Prevention and control of hyperkalemia: It is an important cause of death in acute renal failure. First of all, the intake of potassium-containing foods and drugs should be strictly limited; actively controlling infection, removing lesions and necrotic tissues, correcting metabolic acidosis, increasing sufficient calories and reducing endogenous protein decomposition can reduce the occurrence of hyperkalemia. Severe elevation >6.5mmol/L and widened QRS wave changes on ECG should be treated urgently with.
① 10% calcium gluconate 10-20 ml intravenously and slowly. May counteract the cardiotoxic effects of high potassium.
②5% NaHCO3100-200ml intravenously to correct metabolic acidosis and intracellular transfer of potassium ions, with rapid onset of action, but can cause water and sodium load, use with caution in cardiac insufficiency.
③50％ glucose 50ml+insulin 10u intravenously, promote glycogen synthesis to transfer potassium ions to the cells.
④11.2% sodium lactate 40-200ml intravenously.
⑤ Dialysis therapy: the above measures can only last for 2-6 hours, and dialysis is required to completely solve the problem.
Mild hyperkalemia (5.2-6.0mmol/L) only requires close observation and restriction of potassium intake, and cation exchange resin therapy can also be tried: 50g/d of sodium type exchange resin, divided into 3-4 times orally, and add 25% sorbitol 20ml to induce diarrhea, which can remove potassium ions in the intestine.
(2) Treatment of hyponatremia and hypernatremia: hyponatremia is mostly dilutive, and hypertonic saline intravenous drip needs to be given for symptoms of water toxicity, and hemodialysis can quickly remove excessive water. If it is hypernatremia, the amount of rehydration can be relaxed.
(3) Treatment of hypocalcemia and hyperphosphatemia: asymptomatic hypocalcemia does not need to be treated, and temporary intravenous calcium supplementation can be given when symptoms appear; moderate to severe hyperphosphatemia can be given 10-30 ml of aluminum hydroxide gel, which can be given orally three times a day.
(4) Treatment of metabolic acidosis: If plasma carbon dioxide binding capacity and HCO3 are mildly reduced (>15mmol/L), they can be left untreated; plasma carbon dioxide binding capacity and HCO3 should be supplemented with sodium bicarbonate or sodium lactate intravenously if they are between 15-8mmol/L. After correction of acidosis, the concentration of free calcium ion in blood decreases, which can easily cause hand and foot convulsions. 10-20 ml of 10% calcium gluconate can be given intravenously. Patients with severe acidosis (plasma carbon dioxide binding capacity <8mmol/L) should be treated with dialysis immediately after emergency treatment with alkaline supplementation.
4. Treatment of heart failure: It is one of the main causes of death in acute renal failure. The treatment principle is basically the same as that of conservative internal medicine. Acute heart failure is the result of excess water and sodium in the body, expansion of extracellular volume and increased cardiac load, at this time the diuretic effect is poor, so the treatment is based on vasodilatation and reducing preload, nitroglycerin, sodium nitroprusside and other drugs can be used. Dialysis treatment is the most effective treatment.
5, the treatment of gastrointestinal bleeding: acute renal failure, often due to a decrease in the number of platelets or dysfunction, increased capillary fragility and thrombinogen generation disorders, and other reasons, resulting in obvious bleeding tendency, in serious cases, can lead to gastrointestinal hemorrhage, causing death. The treatment principle is similar to that of general gastrointestinal hemorrhage, including gastric mucosal protective agents, proton pump inhibitors, growth inhibitors, etc. Blood transfusion is required for severe bleeding. Dialysis is effective for uremic hemorrhage. Certain acid-control drugs excreted through the kidneys (such as cimetidine, ranitidine, etc.) require dose reduction for long-term application.
6, prevention and control of infection: all systems can be combined with infection in the oliguric phase, and the mortality rate is high. It is necessary to reasonably choose antibacterial drugs that are non-toxic or less toxic to the kidney according to the results of bacterial culture and drug sensitivity test, and adjust the dose according to the renal function. Severe infections should be given immune support therapy to reduce the mortality of infection.
7, dialysis therapy: dialysis can enable patients to pass the oliguric period, improve uremic symptoms, pulmonary edema, correct water intoxication, hyperkalemia and metabolic acidosis, ensure the smooth implementation of nutritional therapy, and reduce mortality. Prophylactic dialysis should be advocated to help reduce the complications of acute renal failure and improve the prognosis.
Commonly used dialysis techniques include conventional intermittent hemodialysis, peritoneal dialysis and continuous hemodialysis. The specific choice should be based on the technical capacity of the medical unit, the economic conditions of the patient, and the clinical needs of the patient’s condition. Generally speaking, peritoneal dialysis is suitable for elderly, children, patients with poor vascular conditions, unstable cardiovascular conditions, and active bleeding; however, peritoneal dialysis has limited solute clearance, affects abdominal breathing, and is not suitable for patients with hypermetabolic type and pulmonary edema. Continuous hemodialysis is more appropriate for hypermetabolic types or multi-organ dysfunction, but is costly.
Hemodialysis is the preferred dialysis therapy for acute renal failure, which has an impact on cardiovascular stability and is prone to complications such as bleeding, hypoxemia and imbalance syndrome during dialysis. Dialysis indications.
(i) acute pulmonary edema.
②High potassium >6.5 mmol/L.
③Metabolic acidosis with CO2CP<13mmol/L and PH<7.25.
④SCr>442ummol/L (5mg/dl) or BUN>21.4mmol/L (60mg/dl).
⑤ hypercatabolic state: BUN rising >10.7mmol/L (30mg/dl) per day and potassium rising >1mmol/L per day.
(⑥Anuria for 2 days or oliguria for more than 4 days.
(7) Oliguria for more than 2 days with any one of edema, hyperkalemia, cardiac insufficiency and uremic symptoms.
IV. Treatment of the polyuric phase.
In the early polyuric phase, many complications of uremia still exist, and the treatment principles of oliguric phase can still be followed, but it must be noted that
1, unless there is electrolyte loss according to, generally not rehydration.
2.For those who need rehydration, the intake can be 1/3 to 2/3 of the output volume (usually 500 to 1000ml less than the output volume), and try to supplement from the gastrointestinal tract to help shorten the polyuric phase.
3. For those who have been on dialysis, dialysis should be stopped only when SCr<354ummol/L and the patient is free from uremic state.
4. Protein intake can be increased appropriately to facilitate recovery.
V. Treatment during the recovery period: No special treatment is generally required, regular follow-up of renal function and avoidance of nephrotoxic drugs. Glomerular filtration function is mostly recovered within 3 months, but tubular function recovery is usually slower, often taking more than a year, so patients may still have polyuria, nocturia and low specific gravity urine and other manifestations of tubular insufficiency in the short term.