acute renal failure in children
Introduction
Introduction to acute renal failure in children Acute kidney damage caused by any cause, within a few hours to several days, makes the nephron regulatory function decline sharply, can not maintain the balance of body fluid electrolytes and excretion of metabolites, leading to hyperkalemia, metabolic acidosis and acute uremia syndrome, Commonly known as acute renal failure (acuterenalfailure, ARF). Acute renal failure is a common clinical syndrome found in children of all ages. The etiology of ARF in each age group has its own characteristics. ARF can be divided into three types according to the cause of pre-renal, renal and post-renal. According to clinical manifestations, it can be divided into oliguria and non-oliguric type and high-decomposition type. If ARF can be diagnosed early and treated in time, renal function can be reversed to normal, otherwise chronic renal insufficiency remains. basic knowledge The proportion of illness: 5%-10% Susceptible people: young children Mode of infection: non-infectious Complications: pulmonary edema, cerebral edema, hyperkalemia, hyponatremia, congestive heart failure
Cause
Causes of acute renal failure in children
(1) Causes of the disease
APF can be divided into pre-renal (about 55%), renal (about 40%) and post-renal (about 5%).
Prerenal
As renal perfusion is reduced, GFR is reduced and acute renal failure occurs. Since the kidney itself has no organic damage, the renal function is restored after the cause is eliminated.
(1) low blood volume: such as major bleeding, gastrointestinal dysfunction (such as diarrhea, vomiting, gastrointestinal decompression), renal dysfunction (such as osmotic diuretic, diuretic, adrenal insufficiency), skin loss (such as burns, A lot of sweating), the third gap lost fluid (such as pancreatitis, peritonitis, large area damage with crush injury).
(2) decreased cardiac output: cardiogenic shock, congestive heart failure, pericardial tamponade, and massive pulmonary infarction.
(3) systemic vasodilation: allergic reactions, the use of antihypertensive drugs, sepsis and vasodilator overdose.
(4) systemic or renal vasoconstriction: anesthesia, major surgery, alpha adrenergic agonist or high dose dopamine, hepatorenal syndrome.
(5) Kidney self-regulation disorder: such as non-steroidal anti-inflammatory drugs, the application of angiotensin-converting enzyme inhibitor drugs.
2. Renal
GFR reduces tubule cell damage (acute tubular necrosis), glomerular, tubulointerstitial or vascular inflammation due to hypoperfusion or nephrotoxic substance damage, thrombosis leading to embolic renal vascular occlusion or vasomotor nephropathy .
(1) Acute tubular necrosis:
1 acute renal ischemia: such as trauma, burns, major surgery, major bleeding and severe salt loss, dehydration, acute hemoglobinuria, acute myoglobinuria, Gram-negative bacilli sepsis can cause renal ischemia, hypoxia and acute Renal tubular necrosis.
2 nephrotoxic substance damage: substances that cause renal tubular poisoning and necrosis are:
A. Exogenous: such as antibiotics (such as aminoglycosides, cephalosporins, tetracycline, amphotericin B, vancomycin, polymyxin, etc.); X-ray contrast agents; heavy metals (such as mercury, lead, Arsenic, antimony, etc.; chemotherapy preparations (such as cisplatin, methotrexate, mitomycin); immunosuppressants (such as cyclosporine); organic solvents (such as ethanol, carbon tetrachloride); insecticides; Fungicides; biological toxins (such as snake venom, scorpion venom, bee venom, raw fish gall, poison mites, etc.).
B. Endogenous: such as rhabdomyolysis, hemolysis, uric acid, oxalate, plasma cell disease cachexia (such as myeloma).
(2) acute glomerulonephritis and (or) vasculitis: acute streptococcal infection after nephritis, acute nephritis, pulmonary hemorrhagic nephritis syndrome, acute diffuse lupus nephritis, purpuric nephritis.
(3) acute interstitial nephritis: infection allergies, drug allergies (such as penicillin family, sulfa drugs, analgesics or non-steroidal anti-inflammatory drugs, etc.), caused by the infection itself (such as epidemic hemorrhagic fever, etc.).
(4) acute renal parenchymal necrosis: acute renal cortical necrosis, acute renal medullary necrosis.
(5) renal vascular disease: necrotizing vasculitis, allergic vasculitis, malignant hypertension, renal artery thrombosis or embolism, bilateral renal vein thrombosis, sepsis can also cause disseminated intravascular coagulation (DIC), leading to acute Renal failure.
(6) Others: acute rejection of transplanted kidneys, etc.
3. Post-renal
Renal pelvic obstruction caused by renal pelvis obstruction, renal interstitial pressure increased, renal parenchyma was damaged by compression, after a long time, reflex makes renal vasoconstriction, kidney ischemic damage, if accompanied by secondary infection, Aggravate the damage.
(1) urethral obstruction: urethral stricture, congenital valve, phimosis, riding a cross injury, damage the urethra.
(2) bladder neck obstruction: neurogenic bladder, stones, cancer, blood clots.
(3) ureteral obstruction: congenital stenosis of the ureter, stones, blood clots or necrotic kidney tissue (nipple) shedding, tumor compression, retroperitoneal fibrosis.
(two) pathogenesis
The physiological functions of the kidney include excretion (filtration and reabsorption), regulation of water, electrolytes and acid-base balance, and endocrine metabolism. These functions are complementary and closely related, glomerular filtration rate (glomerular filtration rate, GFR) decreased to less than 50% of normal level, serum creatinine increased quickly >176mol/L (2.0mg/dl), BUN increased simultaneously, and caused imbalance of water, electrolytes and acid-base balance, acute uremia symptoms, namely ARF.
Pathological change
(1) Visual inspection: The kidney is enlarged and soft, and the medulla is dark red in the kidney, and the cortex is pale due to ischemia. The two are in sharp contrast.
(2) microscopic examination: acute renal failure due to different causes, pathological changes are also different, there may be changes in renal blood vessels, glomeruli, renal tubules and renal interstitial, acute tubular necrosis (ATN) It is divided into ischemic and toxic. The lesions of toxic ATN are limited to the proximal tubules, which are focally distributed. The necrotic tubular basement membrane is intact and the tubular epithelial regeneration is good. The ischemic ATN lesions may involve various segments. The renal tubules were diffusely distributed, the necrotic tubule basement membrane was broken, and the epithelial cells were poorly regenerated.
2. Pathogenesis
The pathogenesis of acute renal failure is very complicated. There are many factors involved. It is not fully elucidated. Different patients, different causes, conditions and stages have different pathogenesis. At present, acute renal failure caused by renal ischemia and poisoning. The pathogenesis of the disease has a variety of doctrines.
(1) Theory of acute tubular damage:
1 renal tubular leakage theory: renal tubule fluid through the broken basement membrane, back leakage into the interstitial, oppressing capillaries, further reducing renal blood flow, leading to oliguria or anuria, is now considered to be no tubule basement membrane break Back leaks can also occur.
2 tubular obstruction theory: renal tubular epithelial damage and swelling, various tubular obstruction, interstitial edema compression, can fill the renal tubules leading to oliguria, no urine.
3 The vulnerability of the thick wall segment (mTAL) and the proximal straight tube (S3): the fine balance between oxygen supply and aerobic in the outer marrow, mTAL and S3 cells in the marginal segment of hypoxia, ischemia In the absence of oxygen, it is more susceptible to injury, and the renal parenchymal ischemia is further aggravated by the feedback of the bulb.
(2) Intrarenal hemodynamic changes Theory: Because the pathological changes of ATN kidney tissue are mild, intrarenal hemodynamic changes are important mechanisms for the occurrence of acute renal failure, including:
1 renal blood flow decreased dramatically.
2 The mechanism of glomerular arterioles contraction is:
A. Renin-angiotensin activation.
B. Endothelin action.
C. Sympathetic excitation.
D. Prostaglandin action (PGI2/TXA2 imbalance).
E. Effect of oxygen free radicals on endothelial cells.
F. Others: catecholamines, antidiuretic hormone (ADH), platelet activating factor (PAF), and the like.
3 glomerular capillary endothelial cells are swollen.
4 glomerular ultrafiltration coefficient (kf) decreased.
5 intravascular coagulation.
(3) Cytological mechanism:
1TP depletion through: increase intracellular free calcium; activate phospholipase A2; activate calpain; induce depolymerization of actin F and other pathways to change the cytoskeleton, damage cells, ATP depletion is the central link of ATN.
2 vasoactive substances: mainly involved in endothelin, NO, platelet activating factor (PAY) and renin-angiotensin-aldosterone system (RAS system), the total role is to contract renal blood vessels and damage renal tubular epithelial cells.
3 renal tubule structure and function abnormalities: various factors cause destruction of the cytoskeleton, loss of cell polarity, destruction of the proximal tubule brush border, cell-to-cell tight junction and cell-matrix adhesion loss, plus the formation of various casts Factors such as the destruction of the structure and function of the renal tubules.
4 The role of apoptosis: There are two apoptosiss in ARF pathology, the first apoptosis occurs immediately after renal injury, and the second occurs in the recovery phase of ARF, which plays an important role in the occurrence and recovery of ARF. .
5 The role of growth factors: At the time of ARF, the immediate reactive genes c-fos, egr-1 expression was up-regulated, epidermal growth factor EGF, IGF-1, FGF, HGF isletin increased, mainly in cell regeneration, tissue repair Works in the middle.
Prevention
Prevention of acute renal failure in children
First, there must be a reasonable amount of protein intake. The metabolites in the human body are mainly derived from the protein components in the diet. Therefore, in order to reduce the workload of the remaining kidneys, the protein intake must be compatible with the excretion ability of the kidneys.
For example, when the serum creatinine is 170-440 micromoles/liter, the protein is preferably 0.6 grams per kilogram of body weight per day. If there is a large amount of proteinuria, an additional 1.5 grams of protein may be added for every 1 gram of urine protein lost.
When the serum creatinine exceeds 440 mol/L, the protein intake should be further reduced to a total of no more than 30 g per day.
However, it must be emphasized that if blindly pursuing restrictions on protein intake, it will lead to malnutrition, decreased physical fitness, and poor results.
Second, in order to maximize the use of the ingested protein, it is not allowed to be converted into energy consumption, and a low-protein diet must be supplemented with energy.
At least 35 kilocalories per kilogram of body weight per day, mainly supplied by sugar, can eat fruit, sugar products, chocolate, jam, honey and so on.
Third, it is worth noting that some foods meet the previous conditions, such as egg yolk, meat pine, animal offal, dairy products, bone marrow, etc., but they are not suitable for consumption because of their high phosphorus content, because the storage of phosphorus can promote The function of the kidneys is further aggravated.
In order to reduce the amount of phosphorus in food, fish, meat, potatoes, etc. should be cooked before cooking.
Fourth, the amount of salt should be determined according to the condition. If you have high blood pressure or edema, you should use a low-salt diet, 2 grams of salt per day.
Fifth, drugs excreted by the kidney may also damage the kidneys, such as gentamicin, sulfa antibiotics, penicillin, indomethacin, paracetamol, and hormones and contrast agents.
In addition, if you have high blood pressure, diabetes, and infection, you should also guard against kidney damage caused by these diseases.
Complication
Complications of acute renal failure in children Complications pulmonary edema cerebral edema hyperkalemia hyponatremia congestive heart failure
Excessive volume complicated with congestive heart failure and pulmonary edema, arrhythmia, gastroenteritis or stress ulcers with gastrointestinal bleeding, convulsions, coma and behavioral changes, but also pleural effusion, ascites, brain edema, high potassium Blood, low calcium, hyponatremia, hypertension and co-infection.
1. Pulmonary edema (pulmonary edema) refers to the formation of imbalance and imbalance of reflux in the lungs for some reason, so that a large amount of tissue fluid can not be absorbed by the pulmonary lymph and pulmonary vein system in a short time, from the extravasation of the pulmonary capillaries, accumulation In the alveolar, interstitial and bronchioles, resulting in severe ventilation and ventilation problems, clinical manifestations of extreme dyspnea, sitting breathing, cyanosis, sweating, paroxysmal cough with a lot of white or pink The color foam is sputum, the lungs are full of symmetrical wet squeaky sounds, and the X-ray chest radiograph shows the blunt-like blushing shadows of the two lungs. In the late stage, there may be shock or even death. In the early stage of arterial blood gas analysis, there may be low O2, low CO2 partial pressure, and serious O2 deficiency, CO2 retention and mixed acidosis are one of the clinical critical illnesses.
2. Congestive heart failure (CHF) refers to a pathology in which cardiac output is insufficient to maintain tissue metabolism due to systolic and/or diastolic dysfunction in the presence of moderate venous return. status.
3. Stress ulcer is an acute gastric mucosal lesion that occurs in severe trauma, severe systemic infection, extensive burns, shock, multiple organ failure and other serious stress reactions, and is one of the common causes of upper gastrointestinal bleeding.
4. There is a potential cavity between the visceral and parietal layers of the pleura, called the pleural cavity. Under normal circumstances, the width of the pleural cavity between the two layers of pleural cavity is about 10 ~ 20m, containing the slurry, about 0.1 ~ 0.2ml per kilogram of body weight, usually colorless, transparent, lubrication pleura, its exudation and resorption In equilibrium, any factor causes an increase in exudation and/or a decrease in reabsorption, ie, accumulation of fluid in the pleural cavity, resulting in pleural effusion.
5. Blood potassium above 5.5mmol/L is called hyperkalemia, and >7.0mmol/L is severe hyperkalemia. Due to hyperkalemia, there is often no or very few symptoms and sudden cardiac arrest, should be detected early, early prevention.
6. Hyponatremia only indicates that the serum sodium ion concentration is lower than the normal level, and it is not necessarily true that the sodium content of the body is decreased. According to the rapid onset, it can be divided into acute hyponatremia and chronic hyponatremia. The former refers to serum sodium ion concentration below normal level within 48 hours, otherwise it is chronic hyponatremia.
7. Under normal conditions, there is a small amount of liquid (usually less than 200ml) in the abdominal cavity of the human body, which will lubricate the intestinal peristalsis. Any pathological condition leads to an increase in the amount of fluid in the peritoneal cavity. When it exceeds 200 ml, it is called ascites.
8. In the absence of antihypertensive drugs, systolic blood pressure 139mmHg and / or diastolic 89mmHg, according to blood pressure levels, high blood pressure is divided into 1, 2, and 3. Systolic blood pressure 140mmHg and diastolic blood pressure <90mmHg are listed as simple systolic hypertension. The patient has a history of hypertension and is currently using antihypertensive drugs. Blood pressure, although lower than 140/90mmHg, should also be diagnosed as hypertension.
Symptom
Symptoms of acute renal failure in children Common symptoms Hypokalemia Hypermetabolic acidosis Fatigue Lack of urinary Chronic renal insufficiency Neonatal response Low hypocalcemia Nitrogenemia Hyperkalemia
1. oliguric acute renal insufficiency
Can be divided into oliguria, diuretic period, recovery period, the boundaries of children are often not obvious.
(1) oliguria: ARF, especially acute tubular necrosis, often has a significant oliguria, lasting about 10 to 14 days.
1 oliguria: neonatal urine volume <1ml / (kg · h), infants <200ml / d, preschool age <300ml / d, school age <400ml / d is oliguria, such as <50ml / d No urine.
2 azotemia: blood BUN, Cr increased, and due to the accumulation of toxins in the body caused by systemic systemic symptoms, such as anorexia, nausea, vomiting, hematemesis, lethargy, irritability, anemia.
3 sodium retention: systemic edema, elevated blood pressure, and pulmonary edema, cerebral edema, heart failure and other performance.
4 electrolyte disorder: hyperkalemia, can be expressed as irritability, nausea, vomiting, lethargy, numbness of the limbs, chest tightness, belching, slow heart rate, arrhythmia, ECG T wave high tip, QRS wave widening, etc., hyponatremia There may be a lack of expression, poor response, nausea, vomiting and even convulsions, high phosphorus and hypocalcemia, hand and foot sputum, convulsions, etc.
5 metabolic acidosis: manifested as fatigue, lethargy, flushing, nausea, vomiting, deep breathing, and even coma, shock and so on.
6 endocrine and metabolic changes: elevated PTH, decreased calcitonin (CT); decreased T3, T4, normal TSH; decreased erythropoietin; increased activity of ADH and renin-angiotensin-aldosterone; High; impaired glucose tolerance and insulin resistance, elevated levels of insulin and glucagon.
(2) Diuretic period: When the urine volume is >2500ml/m2, it enters the polyuria stage, and the renal function gradually recovers. The blood BUN and Cr decrease several days after the start of polyuria, and the symptoms of various systems caused by the accumulation of poison are alleviated. Dehydration and hypokalemia and hyponatremia are prone to occur during the urine.
(3) Recovery period: After the polyuria period, the urine volume gradually returned to normal, blood BUN, Cr gradually normal, renal tubular concentration function and acidification function gradually recovered, a small number of kidney function damage can be left in different degrees, manifested as chronic renal insufficiency Need to maintain dialysis treatment.
2. Non-oliguric acute renal insufficiency
(1) No oliguria, average daily urine volume >1000ml.
(2) Multiple secondary to aminoglycoside antibiotics and contrast agents cause kidney damage.
(3) The clinical manifestations are less urinary, less complication, and low mortality.
3. Highly decomposed acute renal insufficiency
(1) Causes: Multiple secondary to large-area burns, crush injuries, major infections and serious infections, sepsis.
(2) Blood biochemical changes: tissue decomposition is extremely vigorous, blood BUN, Cr and blood potassium rise rapidly, HCO3- rapidly decreases, blood BUN rises daily >14.3mmol/L, blood Cr rises daily >176mol/L, blood K daily Rise >1.0 mmol/L.
(3) High mortality: hyperkalemia and metabolic acidosis are extremely serious and the mortality rate is high.
Examine
Examination of acute renal failure in children
1.B type ultrasonic inspection
The size of the kidney can be observed, and the presence of kidney stones and hydronephrosis can be indicated. If the kidney size is normal and there is obvious hydronephrosis, it is strongly suggestive of post-renal sexual causes.
2. Abdominal x-ray film
Used to observe the size of the kidney and to find positive stones.
3. Blood routine
Common hemoglobin and red blood cells are slightly reduced. In the case of secondary infection, there are often leukocytosis and nuclear left shift, and some may have platelet decrease.
4. Blood biochemical determination
The changes in oliguria are most significant. Common urea nitrogen, creatinine increased significantly, bicarbonate decreased significantly, and many electrolyte disorders may occur. High potassium and low sodium were the most common, low calcium and high phosphorus, and polyuria. In the early stage, there are also obvious metabolic acidosis and azotemia. Blood electrolytes often have abnormal changes, especially low potassium or high sodium.
5. Urine routine
Common urine specific gravity reduction and proteinuria, sediment microscopic examination showed red blood cells, white blood cells and casts, such as those caused by prerenal factors, early urine specific gravity is often high, urine sediment microscopic examination and urine protein qualitative and no abnormal findings; kidney Sexual factors often have obvious abnormalities in proteinuria and sediment microscopy.
6. Renal puncture
Indications for acute renal failure caused by renal causes can understand the pathological type and extent of renal lesions, and help to formulate treatment plans and judge prognosis.
7. Radionuclide examination (SPECT)
It is helpful to find ARF caused by renal vascular disease (embolic) and post-renal ARF caused by obstruction; three-phase dynamic imaging of 99mTc diethylenetriamine pentaacetic acid (DTPA) in renal tubular necrosis shows good perfusion and poor absorption. 131I-o-iodosodium urate (OIH) showed unclear renal imaging and specificity.
Diagnosis
Diagnosis and diagnosis of acute renal failure in children
diagnosis
Diagnosis of ARF should first start from the clinical, to determine whether ARF is oliguria, non-oliguric, or high-decomposition, and then find out whether the cause is pre-renal, renal or post-renal, and finally clear the cause.
The Diagnostic Criteria of the Chinese Academy of Pediatrics Nephrology in 1993 to develop ARF is:
1. Diagnosis basis
(1) Significant reduction in urine output: oliguria (<250ml/m2) or no urine (<50ml/m2), and no urine loss is non-oliguric type acute renal failure.
(2) azotemia: serum creatinine (Scr)>176mol/L, BUN>15mmol/L, or daily Scr increase>4488mol/L or BUN increase>3.577.5mmol/L, kidney condition when conditional Small ball filtration rate (such as endogenous creatinine clearance rate) Ccr often <30ml / (min · 1.73m2)
(3) often have acidosis, water and electrolyte disorders and other performance.
2. Clinical staging
(1) oliguria: oliguria or no urine, with azotemia, excessive water (weight gain, edema, hypertension, cerebral edema), electrolyte imbalance (hyperkalemia, hyponatremia, hyperphosphatemia, Low blood calcium, etc.), metabolic acidosis, and the presence of multiple systems involved in the circulatory, nervous, respiratory, and blood systems.
(2) Diuretic period: the amount of urine gradually increases or increases sharply (>2500ml/m2), edema is relieved, azotemia has not disappeared, and even mildly increased, which may be accompanied by water and electrolyte imbalance.
(3) Recovery period: recovery of azotemia, improvement of anemia, and recovery of renal tubular concentrating function is slow, it takes about several months.
3. Laboratory identification of prerenal and renal renal failure.
Differential diagnosis
1. moderate to severe dehydration
Severe diarrhea, vomiting or insufficient intake can cause dehydration, urine output is often significantly reduced, severe cases can be auria, can be combined with varying degrees of acidosis, should be differentiated from acute renal failure, but this disease often has obvious fluid loss, insufficient intake History, oliguria and dehydrated signs are generally parallel with blood pressure and peripheral circulatory failure, blood urea nitrogen is normal or only slightly elevated, blood potassium is low, urine is generally no abnormal, urine specific gravity is high, positive After rehydration treatment, the condition improved rapidly and the amount of urine increased rapidly.
2. Infectious toxic shock
Found in poisoned bacterial dysentery or other serious infections, often due to insufficient circulating blood volume, oliguria, but no abnormal changes in urine, high urine specific gravity, rapid expansion of blood volume and rapid improvement after the application of vasoactive drugs, The amount of urine increased, and blood urea nitrogen and creatinine did not change significantly.
3. Urinary retention
Seen in acute myelitis or high-dose atropines, the clinical manifestations are longer (hours to more than ten hours) without urine discharge, but often the bladder can be filled and filled, the bladder area is cloudy, and the bladder is often pressed. Urine overflow, combined with the primary disease and medication history, diagnosis is not difficult, catheterization or bladder puncture can be clearly diagnosed.
