Acute renal failure is a potentially reversible, sudden onset of severe impairment or discontinuation of renal function. Characterized by a violation of all renal functions (secretory, excretory and filtration), pronounced changes in the water-electrolyte balance, rapidly increasing azotemia. The following forms of arresters are distinguished:
Prerenal OPN can develop at conditions that are accompanied by a decrease in cardiac output (with pulmonary embolism, heart failure, arrhythmia, cardiac tamponade, cardiogenic shock). Often the cause is a decrease in the amount of extracellular fluid (with diarrhea, dehydration, acute blood loss, burns, ascites caused by cirrhosis of the liver). May occur due to severe vasodilation caused by bacteriotoxic or anaphylactic shock.
It occurs when toxic effects on the renal parenchyma of fertilizers, poisonous fungi, salts of copper, cadmium, uranium and mercury. It develops with uncontrolled admission of nephrotoxic medicines (antitumor drugs, a number of antibiotics and sulfonamides). X-rays and the listed drugs prescribed in the usual dosage can cause renal argectomy in patients with impaired renal function.
In addition, this form of OPN occurs when circulating a large amount of myoglobin and hemoglobin in the blood (with severe macrogemoglobinuria, transfusion of incompatible blood, prolonged compression of tissues in trauma, drug and alcohol coma). Less often, the development of renal arrythmias is due to inflammatory kidney disease.
It develops by mechanical violation of the passage of urine with bilateral stones obstruction of the urinary tract. Less often occurs with tumors of the prostate, bladder and ureters, tuberculosis lesions, urethritis and periurethritis, dystrophic lesions of retroperitoneal tissue. In severe combined trauma and extensive surgical interventions, acute renal failure is caused by several factors (shock, sepsis, blood transfusion, treatment with nephrotoxic drugs).
There are four phases of acute renal failure:
The condition of the patient is determined by the underlying disease causing arthritis. Clinically, the initial phase is usually not detected due to the absence of characteristic symptoms. The circulatory collapse that occurs in this phase has a very short duration, so it goes unnoticed. Nonspecific symptoms of arthritis (drowsiness, nausea, lack of appetite, weakness) are masked by manifestations of the underlying disease, trauma or poisoning.
Anuria occurs rarely. The amount of urine separated is less than 500 ml per day. Characterized by pronounced proteinuria, azotemia, hyperphosphatemia, hyperkalemia, hypernatemia, metabolic acidosis. There is diarrhea, nausea, vomiting. With swelling of the lung due to hyperhydration, shortness of breath and wet wheezing appear. The patient is inhibited, sleepy, can fall into a coma. Often develops pericarditis, uremic gastroenterocolitis, complicated by bleeding. The patient is susceptible to infection due to decreased immunity. Possible pancreatitis, stomatitis, parotitis, pneumonia, sepsis.
Oligoanuric phase OPN develops within the first three days after exposure. Later, development of the oligoanuric phase is considered to be a prognostically unfavorable feature. The average duration of this stage is 10-14 days. The oliguria period can be shortened up to several hours or can be extended to 6-8 weeks. Long oliguria occurs more often in elderly patients with concomitant vascular pathology. In the oliguric stage of acute renal failure lasting more than a month, additional differential diagnostics should be performed to exclude progressive glomerulonephritis, renal vasculitis, renal artery occlusion, and diffuse necrosis of the renal cortex.
The duration of the diuretic phase is about two weeks. Daily diuresis gradually increases and reaches 2-5 liters. A gradual restoration of the water-electrolyte balance is noted. Possible gipokaliemia due to significant losses of potassium in the urine.
There is a further restoration of renal functions, taking from 6 months to 1 year.
The severity of disorders characteristic of renal failure (fluid retention, azotemia, disturbance of the water-electrolyte balance) depends on the state of catabolism and the presence of oliguria. With severe oliguria, the level of glomerular filtration is reduced, the release of electrolytes, water and nitrogen exchange products is significantly reduced, which leads to more pronounced changes in blood composition.
With oliguria, the risk of developing water and salt overload increases. Hyperkalemia in acute renal failure is caused by inadequate excretion of potassium with a persistent level of its release from the tissues. In patients who do not suffer from oliguria, the potassium level is 0.3-0.5 mmol / day. More pronounced hyperkalemia in such patients can talk about exogenous (blood transfusion, drugs, availability of foods rich in potassium in the diet) or enodgenic (hemolysis, destruction of tissues) potassium load.
The first symptoms of hyperkalemia occur when the potassium level exceeds 6.0-6.5 mmol / l. Patients complain of muscle weakness. In some cases, flaccid tetraparesis develops. There are changes in the ECG. The amplitude of the P teeth decreases, the P-R interval increases, bradycardia develops. A significant increase in potassium concentration can cause cardiac arrest.
In the first two stages of OPN, hypocalcemia, hyperphosphataemia, and mild hypermagnesia are observed.
The consequence of pronounced azotemia is the inhibition of erythropoiesis. Reduces the life span of red blood cells. Normocytic normochromic anemia develops.
Inhibition of immunity contributes to the occurrence of infectious diseases in 30-70% of patients with acute renal failure. Attachment of infection increases the course of the disease and often causes the death of the patient. Inflammation develops in the field of postoperative wounds, the oral cavity, the respiratory system, and the urinary tract suffer. A frequent complication of acute renal failure is sepsis, which can be caused by both gram-positive and gram-negative flora.
There is drowsiness, confusion, disorientation, inhibition, alternating with periods of excitement. Peripheral neuropathy often occurs in elderly patients.
With OPN, congestive heart failure, arrhythmia, pericarditis, arterial hypertension can develop.
Patients are disturbed by a feeling of discomfort in the abdominal cavity, nausea, vomiting, loss of appetite. In severe cases, uremic gastroenterocolitis develops, often complicated by bleeding.
The main marker of acute renal failure is an increase in potassium and nitrogen compounds in the blood on the background of a significant decrease in the amount of urine released by the body up to the state of anuria. The amount of 24-hour urine and the concentration ability of the kidneys are evaluated by the results of Zimnitsky's trial. It is important to monitor such indicators of blood biochemistry, as urea, creatinine and electrolytes. It is these indicators that make it possible to judge the severity of acute renal failure and the effectiveness of therapeutic measures.
The main task in the diagnosis of acute renal failure is to determine its shape. To do this, ultrasound of the kidneys and the bladder, which allows you to identify or exclude obstruction of the urinary tract. In some cases, bilateral catheterization of pelvis is performed. If both of the catheters are freely passed into the pelvis, but urinary excretion is not observed, it is safe to exclude the postrenal form of acute renal failure. If necessary, renal blood flow is performed by UZDG kidney vessels. Suspicion of tubular necrosis, acute glomerulonephritis or systemic disease is an indication for kidney biopsy.
Therapy is aimed, first of all, at eliminating the cause, which caused the violation of kidney function. In case of shock, it is necessary to replenish the volume of circulating blood and normalize blood pressure. When poisoning with nephrotoxins, patients are washed with the stomach and intestines. The use of such modern methods in urology as extracorporal hemocorrection allows you to quickly cleanse the body of toxins that caused the development of acute renal failure. For this purpose, hemosorption and plasmapheresis are carried out. If there is obstruction, restore the normal passage of urine. To do this, remove the stones from the kidneys and ureters, prompt removal of ureteric strictures and removal of tumors.
To stimulate diuresis, the patient is prescribed furosemide and osmotic diuretics. To reduce the vasoconstriction of the kidney vessels, dopamine is administered. Determining the volume of the injected fluid, in addition to losses during urination, vomiting and emptying of the intestine, it is necessary to take into account the loss of sweating and breathing. The patient is transferred to a protein-free diet, limiting the intake of potassium from food. Drainage of wounds, removal of necrosis sites is carried out. When choosing a dose of antibiotics should take into account the severity of kidney damage.
Hemodialysis is carried out with an increase in the level of urea to 24 mmol / l, potassium - up to 7 mmol / l. Indications for hemodialysis are symptoms of uremia, acidosis and hyperhydration. At present, to prevent complications arising from metabolic disorders, nephrologists are increasingly conducting early and preventive hemodialysis.
Lethality primarily depends on the severity of the pathological condition that has caused the development of acute renal failure. The outcome of the disease affects the age of the patient, the degree of impaired renal function, the presence of complications. In surviving patients, renal function is completely restored in 35-40% of cases, in part - in 10-15% of cases. 1-3% of patients need constant hemodialysis.