The term “renal failure” refers to a violation of the homeostatic functions of the kidneys. In this article we will look at the main degrees and causes of acute renal failure in children, and also talk about how emergency care is provided for acute renal failure in a child.
Degrees of renal failure
Kidney failure may be functional
(it is called transient renal ischemia) and
organic
, divided into acute renal failure (ARF) and chronic renal failure (CRF).
Functional renal failure
This is a reversible and soon passing condition. In children, it can be recorded immediately after birth due to the exclusion of the placenta as the main excretory organ for the fetus. The newborn's own kidneys begin to function as an excretory organ in the first hours of life. The first urination should occur within 48-72 hours after birth. Transient renal failure can sometimes be observed at the onset of acute glomerulonephritis or acute interstitial nephritis at the height of arterial hypertension and fluid retention (“ischemic kidney”).
Organic variants of acute renal failure and chronic renal failure are based on changes in the structure of renal tissue.
Acute renal failure
This is a nonspecific syndrome caused by hypoxia of the renal tissue with subsequent predominant damage to the tubules up to necrosis of the interstitial tissue. The syndrome is manifested by increasing azotemia, electrolyte imbalance, decompensated metabolic acidosis and impaired ability to excrete water. The manifest sign of acute renal failure is oliguria (absolute, when less than 300 ml of urine is excreted per 1 m2 of the child’s body surface per day, or relative when diuresis is less than 55-60% of the administered fluid volume without increased extrarenal losses), in combination with increasing azotemia (urea concentration in plasma exceeds 16 mmol/l), acidosis and dyselectrolythemia.
The transition from acute renal failure to chronic renal failure occurs quite rarely. The development of acute renal failure in a patient against the background of existing chronic renal failure is possible; this condition is practically uncorrectable and requires the patient to be transferred to program hemodialysis.
Chronic renal failure
This is an irreversible impairment of renal function (with a decrease in filtration capacity to 25% of the age norm and an increase in creatinine of more than 2 mg/dL) as a result of interstitial and glomerular sclerosis and tubular atrophy, which occurs as a result of severe progressive renal disease.
Causes of chronic renal failure
: glomerulonephritis, obstructive uropathy, dysplasia, tubulopathy, amyloidosis, congenital diseases, pyelonephritis, etc.
There are 4 stages of chronic renal failure:
I
- compensated (latent, reversible);
II
— hyperazotemia and anemia in combination with impaired renal functions;
III
— decompensated stage with pronounced clinical signs;
IV
- uremia (terminal stage) with oliguria and multiple organ failure.
Treatment of chronic renal failure in children:
At stage I - symptomatic.
At stage II - protein limitation to 1.5 g/kg/day.
- foods rich in potassium, carbohydrates and fats;
- vitamin therapy (B0, B1 B2, B6, E in increased doses), correction of acidosis (sodium bicarbonate), antihypertensive drugs (captopril, diazoxide, alpha-methyldopa), furosemide;
- fight against osteopathy (calcium preparations, vitamin D), antianemic therapy (erythrocyte mass).
At stages III and IV, hemodialysis is indicated.
Variants of the course of AKI and prognosis
The course of acute kidney injury can be cyclical, recurrent and irreversible. In the cyclic variant of the course of AKI, the following are distinguished:
- The initial (primary) stage - during it, kidney damage occurs. The duration of this period depends on the cause and can vary widely;
- Oliguric or anuric stage - its duration is from 2-4 days to 2-3 weeks;
- The stage of restoration of diuresis (polyuric) – from several days to 2-4 weeks.
A relapsing course is typical for chronic obstructive kidney disease (gout, nephrolithiasis, chronic necrotizing papillitis). A variety of diseases that cause total cortical or papillary necrosis (malignant hypertension, hypotension, poisoning, etc.) can lead to an irreversible course.
The prognosis is better for prerenal and postrenal acute kidney injury than for renal acute kidney injury. The mortality rate varies widely, but in renal AKI it reaches 50-70% in polytrauma, 30-40% in poisoning.
Causes of acute renal failure
Different causes of acute renal failure predominate in different age groups. In newborns, the most common causes are renal vein or artery thrombosis and disseminated intravascular coagulation syndrome (DIC). Any external influence activates blood coagulation factors, and the phagocytic and fibrinolytic system of newborns is not able to effectively eliminate fibrin degradation products from the circulation. In infancy and in children under three years of age, hemolytic-uremic syndrome (HUS) predominates as the main cause of acute renal failure. In preschoolers and schoolchildren, these are glomerulonephritis and interstitial nephritis.
All the numerous causes of acute renal failure cause renal ischemia and have a nephrotoxic effect on the tubular apparatus. Disturbances in the morphology and function of the tubules are the basis of true acute renal failure; they always prevail over lesions of the glomeruli, but oliguria is based on a drop in filtration pressure due to preglomerular and postglomerular vasoconstriction, due to an imbalance of vasoconstrictors and vasodilators. Of significant importance is the disruption of lymphatic drainage, which under physiological conditions frees the interstitium of the kidney from degradation products.
Actions when there is no immediate threat to the patient's life
Determine the possible cause and form of AKI. The most common causes of AKI are:
— Poisoning of various etiologies, most often alcohol surrogates;
- Diabetes;
— Hypovolemia of any etiology (bleeding, vomiting, diarrhea, surgical diseases of the abdominal organs, etc.);
- Sepsis;
— Various heart diseases (arterial hypertension, heart failure);
— Hypoxia of any origin;
- Prolonged hypotension of any etiology;
— Iatrogenesis (use of dextrans, intravenous radiocontrast agents, nephrotoxic antibiotics, etc.).
Attention! Anuria is more often observed with prolonged hypotension and complete obstruction of the urinary tract. If such causes cannot be detected, but there is anuria, this is most often associated with bilateral occlusion of the renal arteries (for example, dissecting aortic aneurysm) or necrosis of the renal cortical layer (poisoning).
It is easier to develop treatment tactics if you divide AKI into prerenal, renal (parenchymal) and postrenal (obstructive) forms.
Acute renal failure clinic
The clinical picture of developing acute renal failure is conventionally divided into 4 stages:
- initial or pre-nuric,
- oligoanuric,
- stage of restoration of diuresis or polyuric,
- recovery period.
1.
Clinical manifestations of the initial (preanuric) stage
acute renal failure are varied and largely determined by the causes that caused acute renal failure.
In the pre-nuric stage
it is necessary to diagnose a decrease in diuresis (an absolute decrease in the volume of urine excreted or an inadequately small diuresis in relation to the water load). It is practically important to distinguish between the functional and organic stages of renal dysfunction. In functional renal failure associated with renal ischemia, but without necrotic changes, the sodium concentration in the urine is 10-20 mmol/l less than in the blood plasma, since a compensatory increased secretion of aldosterone can cause increased sodium reabsorption. Organic changes in the tubules do not allow the corresponding receptors to respond adequately to hormonal influences. The same mechanism determines the osmolality gradient between urine and plasma: in functional renal failure, as a result of increased secretion of antidiuretic hormone, urine osmolality is at least 50 mOsm/L higher than plasma osmolality. Plasma urea concentration usually does not exceed 16 mmol/l and decreases rapidly in response to adequate therapy.
True acute renal failure is characterized by a rapid increase in plasma urea, creatinine and potassium. A pharmacological test with vasodilator drugs (iv administration of aminophylline or trental) with functional PN leads to an increase in diuresis and a decrease in azotemia and kalemia. For oliguria without signs of exicosis, fractional administration of Lasix is possible at the rate of 5-10 mg/kg of the patient’s body weight per day. The absence of a diuretic response indicates the transition of functional renal failure to true acute renal failure.
2.
Oligoanuric stage
accompanied by a deterioration in the general condition of the patient. Dysfunction of the central nervous system is manifested by depression of mental activity, decreased activity, and emotional lability. From the digestive system, anorexia, vomiting, abdominal pain, unstable stool appear, even if the cause of acute renal failure is not an intestinal infection. From the cardiovascular system, tachycardia, arterial hypertension or hypotension are noted, and collapse is possible.
Providing assistance to a patient with an immediate threat to life
Hyperkalemia (potassium > 5.5 mmol/l) is more common in oliguric (diuresis < 500 ml/day) and anuric (diuresis < 50-100 ml/day) variants of acute kidney injury. Hyperkalemia causes irregular heart rhythms and can cause cardiac arrest. ECG signs of hyperkalemia (more than 6.5 mmol/l) include: a tall, pointed T wave, and the QRS complex widens. The R wave may decrease, and sometimes various heart blocks are detected.
Blood potassium level < 7 mmol/l:
It is necessary to conduct a test with furosemide if the SBP level is more than 90-100 mm Hg. Art. and there are no signs of hypovolemia, renal obstruction. Furosemide , at the rate of 2 mg per 1 kg of patient weight (100-200 mg), is administered intravenously by dispenser for 1 hour. If the rate of diuresis increases to 60 or more ml/hour, and daily diuresis exceeds 800-1000 ml during the day, then most often the progression of hyperkalemia does not occur.
With persistent oliguria, blood potassium levels > 7 mmol/l , the patient needs hemodialysis or hemofiltration. If this is not possible, use the following to reduce hyperkalemia or its consequences:
- Intravenous administration of 60 ml of 40% glucose and 10 IU of simple insulin;
- Calcium chloride 10% – 10-20 ml intravenously slowly (preferably with a dispenser) over 5-10 minutes;
- Inhalation with a metered dose inhaler of 3-4 doses (300-400 mcg) of salbutamol , or another short-acting inhaled beta-2 agonist, which quite reliably reduces potassium concentrations. If necessary, inhalation at the same dose can be repeated after 2-3 hours;
- Sodium hydroxybutyrate at a dose of 60-100 mg/kg intravenously rapidly reduces serum potassium levels. It is convenient to use if the patient is undergoing mechanical ventilation;
- In case of decompensated acidosis (pH < 7.2), 1 mmol/kg sodium bicarbonate should be administered. In this case, experts recommend caution, since the introduction of additional sodium leads to an increase in blood volume. In addition, excess bases reduce the concentration of ionized calcium, which can cause tetany;
- Typically, these measures allow you to reduce the level of potassium in the blood for 2-4 hours;
- It is necessary to re-monitor the level of electrolytes in the blood after 2-4 hours.
Attention. If it is suspected that the patient has an elevated level of potassium in the blood, but it is not possible to determine its concentration, doctors use intravenous administration of 40% glucose with insulin and prescribe furosemide.
Forms of acute renal failure
In both adults and children, three forms of acute renal failure are conventionally distinguished: prerenal, renal and postrenal.
Prerenal acute renal failure:
- a sharp drop in blood pressure (shock, large blood loss),
- hemolysis and myolysis (crush syndrome, burn disease, transfusion of incompatible blood),
- large losses of electrolytes in a short time and dehydration (severe acute intestinal infections, inadequate intake of diuretics and laxatives),
- endogenous intoxications.
In practice, these factors are often combined.
Renal acute renal failure:
- kidney damage by exogenous nephrotoxins (heavy metal salts, mercury, poisonous mushrooms),
- toxic-allergic lesions (reactions to taking antibiotics, sulfonamides and other drugs),
- secondary kidney damage as a result of infectious diseases (anaerobic sepsis, leptospirosis, pseudotuberculosis),
- complications of diffuse renal diseases, glomerulonephritis, secondary glomerulonephritis against the background of vasculitis, systemic lupus erythematosus).
Postrenal acute renal failure:
As a rule, these are obstructive uropathy.
Infectious complications
Infectious complications develop frequently and are one of the main causes of death in AKI. The most common manifestations are urinary tract infections and pneumonia. For the purposes of prevention, you should, as far as possible, avoid using any catheters (urinary, intravenous, etc.).
The choice of antibacterial therapy depends on the nature of the infectious disease. For initial antibiotic therapy, 3rd generation cephalosporins are usually used. They try to exclude antibiotics with nephrotoxic effects (vancomycin, aminoglycosides, 1st generation cephalosporins, etc.). If hemodialysis is not performed, doctors should adjust the dose of most drugs depending on the severity of kidney damage.
Gastrointestinal bleeding
Gastrointestinal bleeding complicates the course of acute kidney injury in 15-30% of patients. Uremia leads to erosive lesions of the mucous membranes and impaired platelet function. As with many other critical conditions, in AKI, as a result of hemodynamic disturbances and hypoxia, many people develop stress damage to the gastrointestinal mucosa. And first of all - the stomach.
For prevention, you can use a proton pump inhibitor, for example omeprazole - IV drip at a dose of 40 mg 2 r. per day. In the absence of proton pump inhibitors, H2-histamine receptor blockers are prescribed: ranitidine 50 mg intravenously every 6 hours, or famotidine 20 mg intravenously every 8 hours. If the patient's condition allows, these medications can be administered enterally. H2 receptor blockers, and to a lesser extent proton pump inhibitors, can change the patient's mental status and cause thrombocytopenia. They should be prescribed with extreme caution to patients with encephalopathy and thrombocytopenia.
Anemia
Anemia in AKI occurs in frequent cases. It is usually caused by suppression of hematopoiesis and blood loss. For symptoms characteristic of severe anemia, a decrease in hemoglobin levels <70-80 g/l, blood transfusion is prescribed.
Uremia
The fatality rate decreases if urea can be maintained below 30 mmol/L. Once the blood urea level reaches this level, dialysis is usually started. Uremia often leads to neurological disorders (for example: epileptiform seizures, drowsiness, clonic convulsions, flapping tremor, polyneuritis), which serve as an indication for dialysis.
Uremic pericarditis often manifests as nothing more than a pericardial friction rub. The only way to treat this complication is dialysis, and in such cases the dose of heparin is tried to be kept to a minimum.
Feeding the patient
If the patient is not undergoing hemodialysis, protein intake is limited to approximately 0.5-1 g/kg/day, which reduces the formation of nitrogenous waste. Ensuring the energy value of food is achieved by increasing the amount of fats and carbohydrates. To prevent an increase in catabolism, the total calorie content of food should be 35-40 kcal/kg per day.
With a high intensity of catabolic processes, or in malnourished patients, a diet with a higher protein content is prescribed, and dialysis begins at an earlier date. Limiting table salt in the diet to 2-4 g/day helps reduce fluid retention. Potassium intake should not be higher than 40 mmol/day. Foods and medications containing magnesium should be avoided.
