The causes of ARF development may be different, but at all exposures the renal function is abruptly expressed. First of all, it can be a shock as a result of injuries and massive tissue damage, blood loss or burns. Other causes of acute renal failure are severe surgery, liver and pancreas damage, myocardial infarction, frostbites, abortions, or transfusion of incompatible blood.

Children can often have manifestations of arthritis with poisoning with drugs, poisons, with insect bites, snakes, eating mushrooms. Often, OPN is the result of severe infections - hemorrhagic fevers and leptospirosis, the result of dehydration with infectious diarrhea, endotoxin shock.

Also, OPN develops with damage to the urinary tract with their obstruction in tumors, ureteral compression, thrombosis of the renal arteries, with acute pyelonephritis or glomerulonephritis.

Pathogenesis.

For the development of acute renal failure, it is necessary to defeat at least 90% of all nephrons with a decrease in their glomerular filtration. It is possible to distinguish three forms of development of arresters depending on the level of damage. With prerenal or hemodynamic form, failure occurs as a result of acute kidney ischemia due to a violation of the flow of blood to the renal artery. With a renal or parenchymal form, the glomeruli are damaged by toxins or a sharp inflammatory process in the parenchyma, which is most common in children. The postural or obstructive form will develop as a result of the acute emergence of urinary efflux from the kidneys.

Signs of arresters.

During the OPN four main stages are distinguished:.

initial,.

oligo-anuric,.

polyurethane,.

stage of recovery.

At the initial stage, the symptoms are usually caused by the underlying disease that causes acute renal failure. One of the nonspecific symptoms of this stage may be nausea, weakness, drowsiness, poor appetite and malaise. Usually they remain unnoticed due to the fact that the person is sick initially.

In the oligoanuric stage, there is a sharp and progressive decrease in the amount of urine released by the patient to 500 ml or less. In urine a lot of protein, expressed azotemia, increased levels of phosphate, potassium and sodium in the blood, there may be metabolic acidosis. Expressed diarrhea, nausea and vomiting, there may be pulmonary edema with dyspnea and damp rales, the patient is sharply hardened, an uremic coma is possible. There can be pericarditis, gastroenterocolitis with bleeding. Drastically reduced immunity with a propensity to form septic complications. Typically, oligoanuria begins by the third day of kidney damage, lasts up to one to two weeks, with late development of oligoanuria, the forecast is unfavorable.

Symptoms of the polyuric stage occur at the end of the first or second week of the disease, there is an increase in the daily urine separation to 2-3 or more liters. Gradually stops the water-salt exchange. There may be a loss of large amounts of potassium in the urine.

In the stage of recovery, the symptoms of disturbances in the functioning of the kidneys finally disappear and the patient recovers. This stage lasts for up to a year.

Diagnostics of arresters.

The basis of diagnosis - laboratory and instrumental data, leading is precisely the laboratory diagnosis.

The main signs of OPN are an increase in the level of potassium and nitrogenous substances in the blood and urine, a sharp decrease in daily diuresis up to anuria. Conduct a general analysis of blood and urine, blood and urine biochemistry, Zimnichkoi urine, daily urine samples, blood for coagulation.

From instrumental methods, ultrasound of the kidneys and bladder, radiography, urography, kidney catheterization, kidney kidney scanning, kidney biopsy.

dr20. en.

Keywords:.