Chronic renal failure in children

Introduction to children with chronic renal failure Chronic renal failure (chronic renal failure) is referred to as chronic renal failure, which is reduced by the destruction of renal units, resulting in severe impairment of renal excretory regulation and endocrine and metabolic functions, resulting in a series of symptoms, signs and complications of water and electrolytes, acid-base balance disorders. disease. The cause of chronic renal failure in children is closely related to the age of children in the first detection of renal failure. Chronic renal failure below 5 years of age is often the result of anatomical abnormalities, such as renal hypoplasia, abnormal renal development, urinary tract obstruction, and other congenital malformations; chronic renal failure after age 5 is followed by glomerular disease such as glomerulonephritis, Hemolytic uremic syndrome or hereditary lesions such as Alport syndrome, mainly cystic lesions of the kidney. basic knowledge The proportion of illness: 0.03% Susceptible people: young children Mode of infection: non-infectious Complications: heart failure, pericarditis, cardiomyopathy, renal osteodystrophy

Causes of chronic renal failure in children

Regardless of the cause of kidney damage, once renal function damage reaches a dangerous level, it is difficult to avoid progress to end-stage renal failure, although progress to the incomplete understanding of renal dysfunction, but related to the following important factors, including progressive immunity Damage, hemodynamics affects the high filtration of viable glomeruli, dietary protein and phosphorus intake, persistent proteinuria and hypertension.

Continued deposition of the immune complex or anti-GBM antibody on the glomerulus can lead to glomerular inflammation leading to the formation of scars.

Regardless of the mechanism that initially causes kidney damage, high filtration damage may be a common process leading to the eventual destruction of the glomerulus. Loss of nephron caused by any cause may cause functional and structural hypertrophy of the remaining nephron, at least part of the glomerular blood flow. Increased, increased blood flow increases the strength of glomerular filtration in the nephron, and the high filtration of surviving glomeruli can be used to maintain renal function but can also impair the mechanisms of these glomeruli. The underlying mechanisms of damage include increased Hydrostatic pressure acts directly on the integrity of the capillaries, causing the protein to pass through the capillaries or both, eventually causing changes in the glomerular internuclear membrane and epithelial cells, resulting in glomerular sclerosis, as the sclerosis progresses, the remaining Increased burden of diarrhea in the nephron, increased glomerular blood flow and high filtration of the malignant circulation inhibit angiotensin-converting enzymes. High filtration may slow the progression of renal failure.

The exercise model of chronic renal failure shows that the development of high-protein diet to accelerate renal failure may be due to the expansion of the input arterioles and high filtration damage. Conversely, the low protein diet slows the rate of renal dysfunction, and human studies have confirmed that normal human kidneys are small. Ball filtration rate is directly related to protein intake and suggests that protein accountants such as restricted diets can slow the rate of renal impairment in patients with chronic renal insufficiency.

Some studies have shown that chronic renal insufficiency in animal models, such as limiting dietary phosphorus intake, protects kidney function by preventing the deposition of calcium-phosphorus salts in blood vessels and tissues or by inhibiting the secretion of hormones from the parathyroid glands. The cause of nephrotoxin is still unclear.

Sustained proteinuria or hypertension can directly damage the glomerular capillary wall, leading to glomerular sclerosis and high filtration damage.

When the renal function begins to deteriorate, the remaining nephrons play a compensatory role to maintain the normal internal environment. If the glomerular filtration rate is as low as 20%, the patient will develop clinical symptoms and biochemical changes and metabolic abnormalities of uremia, uremia. The pathophysiological manifestations are as follows:

(1) Nitrogenemia: It is caused by a decrease in glomerular filtration.

(2) low sodium or sodium storage: the kidney loses the ability to regulate sodium and water, and can cause hyponatremia in patients with long-term salt or diuretics, such as nephrotic syndrome, congestive heart failure, no urine or ingestion When the salt is out of date, there is sodium retention.

(3) Acidosis: Due to the decrease of hydrogen and ammonia ions in the kidney, sodium ions and hydrogen carbonate ions are discharged with the urine in a large amount, and the acidic metabolites are stored in the body, so acidosis occurs, but the resistance of the sick children to acidosis is better. High, so even in the case of moderate acidosis, symptoms may not appear clinically.

(4) Hyperkalemia: Causes of hyperkalemia include glomerular filtration reduction, metabolic acidosis, intake of foods high in potassium such as fruits, or application of spironolactone, ampicillin, etc. Aldosterone secretion reduces the ability of the renal tubule to secrete potassium.

(5) urinary enrichment disorder: the result of increased diuretic or medullary blood flow due to loss of nephrons.

(6) Renal osteodystrophy: 1 When the kidney is dysfunctional, phosphate can not be excreted by the kidneys and excreted by the feces. In the intestinal tract, phosphorus and calcium combine to form an insoluble complex, thus causing calcium malabsorption, resulting in low calcium, bone. Loose, deformed, 2 due to low blood phosphorus, high blood calcium, hyperparathyroidism caused by bone changes, 3 kidney function is insufficient, 1,25-(OH)2D3 synthesis disorder.

(7) anemia: 1 erythropoietin formation decreased; 2 hemolysis: 3 blood loss; 4 red blood cell life shortened; 5 iron and folic acid intake is insufficient; 6 due to accumulation of metabolites (such as erythropoietin inhibitor) can inhibit erythropoietin activity.

(8) Growth retardation: due to insufficient protein and calories, bone dystrophy, acidosis, anemia and other unexplained causes.

(9) bleeding tendency: due to thrombocytopenia and platelet dysfunction.

(10) Infection: granulocyte dysfunction and low immune function, easy to secondary infection, is the main cause of chronic renal failure.

(11) Neurological symptoms: fatigue, decreased concentration, headache, drowsiness, memory loss, unclear speech, increased neuromuscular stress, paralysis and convulsions, coma, peripheral neuropathy, due to uremia, aluminum poisoning.

(12) Gastrointestinal ulcer: It is caused by excessive secretion of gastric acid.

(13) Hypertension is due to excessive water, sodium retention and renin production.

(14) High triglyceride is caused by plasma lipoprotein lipase.

(15) Causes of pericarditis and myocardial lesions: it is not clear.

(16) Glucose intolerance: due to tissue anti-insulin.

Prevention of chronic renal failure in children

(1) Nursing care of children with chronic renal failure and hemodialysis

1. Nutrition management

The nutritional management of conservative treatment mainly adjusts the amount of food required according to the levels of serum creatinine and urea nitrogen (BUN). Nurses must record the dietary intake daily for the doctor to calculate the daily intake of protein and calories. The amount of protein intake should be able to ensure the growth of children, but should make BUN (35mmol / L, blood P20mmol / L, K <5,5mmol / L, 2.0g / kg, and hemodialysis is 1.5g / kg) Children with CRF should have a low-salt diet, eat dry and block meals, and grow up children to measure water intake.

2, limit potassium

CRF is often accompanied by hyperkalemia, requiring nurses to educate parents about fruits and vegetables with high potassium levels to avoid excessive intake.

3, strict isolation, prevention of infection

Try to avoid going to public places, hospitalized children living in a single room, the room is ventilated twice a day, UV disinfection every night, reduce dryness, soft and clean underwear.

4, psychological care

In nursing work, we should be considerate of family members and children. We must be cautious and enthusiastic in language. If necessary, we should introduce or participate in the treatment of other patients, so that children and their families can eliminate concerns and actively cooperate to make the disease get early control.

(2) Prevention

Actively prevent and cure all kinds of primary causes of CRF, such as chronic nephritis, pyelonephritis, etc., have kidney damage, need to actively prevent infection, control high blood pressure, avoid using nephrotoxic drugs, while paying attention to reasonable diet and rest, to effectively Prevent the progress of the disease and promote the recovery of the disease.

Complications of chronic renal failure in children Complications, heart failure, pericarditis, cardiomyopathy, renal osteodystrophy

Often complicated by hypertension, anemia, heart failure, pericarditis, cardiomyopathy, hydroelectric disorders and acid-base imbalance, renal osteodystrophy, fractures, infections, etc. In addition to the above systemic complications, long-term dialysis patients with chronic renal failure can also have the following complications:

1. Patients with end-stage renal disease treated with conventional dialysis for aluminum poisoning are susceptible to aluminum poisoning.

2. Dialysis-related amyloidosis dialysis-related amyloidosis (DRA) is an osteoarthrosis found in long-term dialysis patients. The clinical symptoms and incidence are closely related to the length of dialysis.

3. Trace element changes Renal failure and dialysis have a great influence on the metabolism of trace elements. They can accumulate in various parts of the body and cause toxicity.

Symptoms of chronic renal failure in children Common symptoms Fatigue edema Metabolic acidosis Gastropin hypotension Blood pressure proteinuria Nausea azotemia Chronic renal insufficiency Hyponatremia

1. Electrolytes, acid-base metabolism disorders

(1) Water metabolism: In the early stage, due to the decrease of concentration function, the amount of urine does not decrease or increase, but the amount of urine in the late stage is reduced. The end stage can be developed to have no urine. The patient's ability to regulate water metabolism is reduced. When the water intake is excessive, It is easy to stay in the body and form a dilute hyponatremia. When the intake is too small, it is easy to cause insufficient water in the body.

(2) Potassium metabolism: There is a trend of hyperkalemia. The accumulation of potassium in cells is related to the decrease of Na+-K+-ATPase activity. Hyperkalemia can be accompanied by trauma, surgery, anesthesia, blood transfusion, acidosis, sudden change of diet, etc. Intensified, elevated blood potassium in chronic renal failure is one aspect, but the overall potassium storage is still reduced, so it is still important to maintain the normal balance of potassium.

(3) Sodium metabolism: CRF can maintain the normal balance of sodium for a long time, which is related to the body fluid factors such as the kidney unit and the natriuretic hormone.

1 sodium consumption type: salt loss type nephropathy due to the reduction of extracellular fluid, hypotension, etc. have sodium loss, many diseases can cause salt loss such as pyelonephritis, renal medullary cystic disease, hydronephrosis, interstitial nephritis, etc. The collecting tubes of such patients often cannot absorb a sufficient amount of sodium salt to transport and produce low sodium.

2 sodium retention type: when excessive intake of sodium, can not be normally excreted to cause sodium retention, increased extracellular capacity in the body, high blood pressure, pulmonary congestion and heart enlargement and even heart failure.

(4) Acid-base balance: high compensatory capacity of early renal tubular synthesis of ammonia in patients with chronic renal failure is not completely lost, and other buffer systems in the body can be mobilized to compensate for metabolic acidosis, such as respiratory system, tissue compensation such as bone salt loss. Etc., when the disease progresses, the residual kidney unit is further reduced. When the GFR is less than 20 ml/min, the ability of the kidney to excrete organic acid is decreased, the ammonia excretion ability is reduced, and acidosis is caused. When the blood pH is <7.25, it is necessary to be alert to ketoacidosis.

(5) Other electrolytes: patients with chronic renal failure can not fully excrete chloride ions, hyperchloremia is proportional to sodium concentration; blood calcium concentration is often reduced, patients with chronic renal failure can often tolerate hypocalcemia without convulsions, these patients Intestinal calcium absorption capacity decreased, oral active vitamin D can increase blood calcium concentration; when GFR <20ml / min, blood magnesium can be increased, urinary excretion of magnesium is reduced, most patients are asymptomatic, no need to deal with, when blood magnesium When high (>2mmol/L) has clinical symptoms, it can be used to remove sodium diuretics, promote magnesium excretion, correct dehydration, and give dialysis therapy if necessary; when blood GFR is higher than GFR<20ml/min, the disease progresses to the kidney. Phosphorus removal is further reduced.

Vascular system

(1) Hypertension: Common causes are:

1GFR decreased, and nitric oxide secretion decreased: the myeloid lipid decreased in VDML vasculature, causing an increase in extracellular volume, an increase in cardiac output, and then an increase in peripheral resistance and thickening of the vessel wall.

2 renin, angiotensin, aldosterone system active, excessive secretion of renin.

(2) pericarditis: urinary pericarditis seems to be caused by unknown biochemical substances, uric acid deposition and abnormal metabolism, is a fibrous pericarditis, there is exudation, hemorrhage, audible and pericardial friction sound, occasionally pericardial tamponade.

(3) Cardiomyopathy: It can occur in the late stage, with varying degrees of cardiac hypertrophy, interstitial fibrosis, myocardial calcification, oxalate deposition, clinical manifestation of heart enlargement, decreased cardiac output, and various arrhythmias.

3. Gastrointestinal system of gastric dysfunction, common vomiting, nausea and other symptoms, increased water, salt metabolism and acid-base balance disorders, negative nitrogen balance increased, calcium absorption decreased, and gastrointestinal bleeding is also more common, due to mucosa There are diffuse small bleeding points, inflammation, and ulcers.

4. Mental and mental symptoms are weak, insomnia, irritability, depression, memory loss, or resistance to psychological behavior. When uremia is accompanied by secondary hyperparathyroidism, the calcium concentration of brain cells can be increased, and abnormal brain electricity appears. Figure, clinical can be paralyzed, stupor, and even coma, peripheral neurological symptoms such as painful limb paralysis, deep sputum reflexes disappeared, muscle weakness, paralysis and even feeling disappeared, is believed to be related to the accumulation of molecular substances in the body.

5. Blood system

(1) anemia: positive hemoglobin, positive cell anemia, increased with renal dysfunction, mainly due to the reduction of erythropoietin production in the kidney; followed by shortened red blood cell life, iron in the diet, insufficient folic acid intake also participate in certain factors, Neutrophil chemotaxis changes, lymphocyte function is inhibited, and immune function is reduced.

(2) bleeding tendency: there may be nose bleeding, bleeding after injury, gastrointestinal bleeding and bleeding time prolonged, platelet dysfunction, adhesion and aggregation ability decreased, and the release of the third factor is related.

6. Sugar, protein, fat metabolism disorder CRF when the kidneys clear insulin ability, blood insulin increased, chronic renal failure patients generally have negative nitrogen balance, abnormal plasma and intracellular free amino acid spectrum and hypoalbuminemia, blood Increased triglycerides, increased low-density lipoprotein, and decreased high-density lipoprotein may be associated with decreased lipoprotein esterase and hepatic esterase activity.

7. When other GFR drops to a certain extent, there may be hyperurememia, hyperuricemia, pruritus with pigmentation, and a uremia odor in the body, which is related to increased urea secretion and reduced discharge. CRF patients are due to nutrition. Poor, immune function is low, easy to suffer from a variety of infections, children due to inadequate intake and endocrine disorders and other factors may have growth retardation, or renal rickets.

Examination of children with chronic renal failure

1. Urine examination of urine routine protein is generally (ten) one (++), late renal damage is obvious when the urine protein is reduced, urine sediment microscopic examination has different degrees of hematuria, tubular urine, thick and broad wax The cast type has diagnostic value for chronic renal failure, the urine specific gravity is reduced to below 1.018, or fixed at about 1.010, and the urine osmotic pressure is below 450 mOsm/kg.

2. Blood routine examination of hemoglobin reduction, generally below 80g / L, severe <50g / L, is normal form of positive pigment anemia, white blood cells are normal or decreased, white blood cells can be elevated during infection or severe acidosis, platelets are normal or reduced The erythrocyte sedimentation rate increases.

3. Blood biochemical examination of total plasma protein <60g / L, albumin <30 g / L, blood calcium is often lower than 2mmoL / L blood phosphorus > 1,6mmoL / L, serum potassium, sodium, chlorine, CO2CP, anion gap with The condition changes.

4. Renal function test BUN, Scr level determination, Ccr measurement, urine concentration-dilution function determination.

5. Other examination X-ray abdominal plain film, B-mode ultrasound, radionuclide kidney scan, CT and magnetic resonance examination to determine the shape and size of the kidney and the presence or absence of urinary tract obstruction, stagnant water, stones, cysts and tumors, etc. It is very helpful, and the kidney volume is reduced in the late stage of chronic renal failure (except polycystic kidney disease and renal tumor).

Diagnosis and diagnosis of chronic renal failure in children

Chronic renal failure is easy to diagnose when various symptoms are obvious in the late stage. It is important to recognize early chronic renal failure and try to delay the progressive deterioration of renal function.

1. Staged diagnosis of chronic renal failure

(1) Compensatory period of renal insufficiency: serum creatinine is 110 ~ 177mol / L (1.2 ~ 2mg / dl), GFR remaining 50% ~ 80%, no clinical symptoms.

(2) Decompensated renal insufficiency (nitrogenemia): serum creatinine is 178-445mol/L (25mg/dl), GFR remains 25%50%, may have mild anemia, acidosis , nocturia, fatigue.

(3) Renal failure period (uremic period): Cr is 446-707 mol/L (5-8 mg/dl), and GFR remains 10% to 25%. It has obvious gastrointestinal symptoms and anemia signs, and may have metabolic acid. Poisoning and abnormalities in calcium and phosphorus metabolism.

(4) End-stage renal disease: Cr is greater than or equal to 708 mol/L (8 mg/dl), and GFR remains less than 10%. There are various symptoms of uremia, including digestive, neurological, and cardiovascular dysfunction, water and salt metabolism disorders. Acid, alkali imbalance, severe anemia and so on.

2. To determine the cause of CRF caused by the diagnosis of primary disease, such as edema caused by glomerular disease, abnormal urine is easier to diagnose, but some patients have hidden symptoms, no history of kidney disease, some symptoms such as Poor, do not love activities, nocturnal or enuresis and other symptoms are not specific, but also due to anemia to be investigated, refractory rickets, growth retardation, polydipsia, polyuria came to see a doctor, you need to undergo a careful physical examination, urine Check (including specific gravity), blood biochemical and renal function, and detect CRF, and try to find the cause, such as renal dysplasia caused by congenital malformation of urinary system, polycystic kidney disease, genetic disease such as renal failure caused by Alport syndrome The age of onset is earlier, symptoms appear at 1 to 2 years old, often edema, short stature, renal osteopathy is more common, CRF caused by glomerular disease is more common in older children, often >5 years old, may be accompanied Anemia, high blood pressure, edema, moderate proteinuria, hematuria, low specific gravity urine, or secondary urinary tract infection, the acute onset of renal failure needs to be differentiated from acute renal failure, the clinical manifestations of the two are similar. Causes and incentives The same, but most patients with acute renal failure have a good prognosis. A small number of patients can gradually develop to CRF after recovery. Chronic renal insufficiency due to congenital or hereditary kidney disease, children are significantly more than adults, and children with congenital urinary There are many dysplasias, and adult congenital or hereditary kidney diseases are mainly found in congenital polycystic kidney disease.

In the differential diagnosis, it should be excluded from the presence of pyelonephritis, or chronic kidney disease, due to certain incentives (such as dehydration, infection, urinary tract obstruction, the application of certain nephrotoxic drugs), temporary renal dysfunction After removal of such incentives, renal function can often return to the original level.

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