What Is Acute Tubular Necrosis?

Acute tubular necrosis (ATN) is the most common type of acute renal failure. It is caused by renal tissue ischemia and / or toxic damage caused by various causes of renal tubular epithelial cell damage / necrosis, so glomerular filtration Clinical syndromes that occur due to a sharp decrease in the rate (GFR) generally manifest as progressive azotemia, imbalances in water and electrolytes and acid-base balance, and a series of related symptoms. Patients with moderate to severe acute tubular necrosis not only have severe renal failure, And often combined with one or more complications, sometimes life-threatening, need timely and active treatment and rescue.

Basic Information

English name

acute tubual necrosis

Visiting department

Nephrology

Common causes

Acute renal ischemia, acute nephrotoxic damage, intravascular hemolysis, some infections

Common symptoms

Oliguria, polyuria, electrolyte disorders, etc.

Causes of Acute Tubular Necrosis

The causes of acute tubular necrosis are mainly acute renal ischemia, acute renal toxicity damage, intravascular hemolysis, and some infections. Sometimes renal ischemia, renal toxicity and other factors can coexist.

Acute renal ischemia is the most common type of ATN. A large amount of bleeding during or after major and medium surgery, shock and correction of various causes, cardiopulmonary resuscitation, extracorporeal kidney transplantation to restore renal blood circulation, and cardiac resuscitation are all conditions of renal ischemia and reperfusion, so generally speaking Ischemic acute renal failure is more severe than other types of ATN.

The nephrotoxic damage is mainly exogenous nephrotoxicity, such as drugs, heavy metals and chemical poisons, and biological poisons. Common drugs that cause ATN are contrast agents, aminoglycoside antibiotics such as gentamicin, kana and amikacin, polymyxin B, sulfa drugs, amphotericin and the like. Heavy metal kidney poisons such as mercury, cadmium, arsenic, uranium, chromium, lithium, bismuth, lead and platinum. Industrial poisons such as cyanide, carbon tetrachloride, methanol, toluene and chloroform. Biotoxins include herring gall, snake bites, toadstools, bee venom, etc. Infectious diseases such as epidemic hemorrhagic fever and leptospirosis cause ATN. Squeezing, trauma and non-traumatic rhabdomyolysis, causing a large amount of myoglobin to deposit in the renal tubules, causing kidney damage.

Clinical manifestations of acute tubular necrosis

Typical ATN is divided into three stages: oliguria, polyuria and renal function recovery. Non-oliguria ARF can be without obvious oliguria and polyuria. The duration of oliguria, polyuria, and recovery periods of oliguria ARF varies.

Oliguria

Daily urine output less than 400ml is called oliguria. Absolute urination rarely occurs at ATN. If there is absolute anuria, it is mostly complete urinary tract obstruction, rapid glomerulonephritis, and acute renal cortical necrosis. The duration of the oliguria is from 2 to 3 days to 2 to 4 weeks. The oliguria usually does not exceed one month; if it exceeds one month, it means that ATN is very serious, renal function is difficult to recover, or the cause of ATN is more complicated.

Water and electrolyte disorders and metabolic acidosis are prominent. Water retention is mainly due to the inability of the kidneys to excrete water and a large amount of fluid, which are manifested as generalized edema, cerebral edema, hypertension, congestive heart failure, and pulmonary edema. Congestive heart failure and pulmonary edema are one of the leading causes of death in patients with oliguria. Hyponatremia (blood sodium <135mEq / L) is more common in ARF, and is divided into dilute hyponatremia and sodium deficiency hyponatremia, mostly manifested as dilution hyponatremia; Natrium is an absolute lack of sodium in the body, mostly due to vomiting and diarrhea in patients, which may include low blood pressure, dehydration, and weight loss. Most patients with ATN can develop hyperkalemia (serum potassium> 5.5mEq / L), which is one of the important causes of oliguria death. Others such as hyperphosphatemia, hypocalcemia, and metabolic acidosis are also more common.

Another major manifestation of ATN oliguria is azotemia and related system damage. During ATN, the excretion of protein metabolites in the body occurs and accumulates in the body, leading to azotemia or uremia. Creatinine (Cr) and urea nitrogen (BUN) themselves are not the main uremic toxins, but they are the main indicators of toxin accumulation in the body. Generally speaking, their blood concentrations are consistent with the severity of uremia. In patients with high catabolism, blood urea nitrogen rises at a rate of more than 30 mg / dl / day.

When severe ATN occurs uremia, the clinical manifestations and complications of various systems of the body mainly involve the digestive system, cardiovascular system, respiratory system, and nervous system.

2. Polyuria

When the urine volume continues to increase, exceeding 400ml / day, it indicates that renal function begins to recover and enters the polyuria phase. In the early stage of polyuria, although the urine output increases, the glomerular filtration rate is still low, so serum creatinine and urea nitrogen can still be significantly increased, and metabolic acidosis and uremia symptoms can still be severe. In the later stage of polyuria, the urine volume is more than 2000ml / 24 hours, and many can reach 4000 6000ml / 24 hours. At this time, the patient's edema disappears, blood creatinine and urea nitrogen decrease, metabolic acidosis and uremia symptoms gradually decrease. However, due to the discharge of a large amount of water and electrolytes, patients may have water and electrolyte disorders such as dehydration, hyponatremia, and hypokalemia. Severe hypokalemia can manifest as paresis and arrhythmia.

3. Recovery period

The glomerular filtration rate gradually recovered, urine output was normal, and serum creatinine and urea nitrogen fell to normal ranges. It takes about six months to one year for complete recovery of renal function. A small number of patients may leave varying degrees of renal impairment and develop chronic renal failure.

Diagnosis of acute tubular necrosis

The diagnosis of ATN is mainly based on a decrease in glomerular filtration rate of more than 50% in a short period of time (hours to days), and no reduction in renal kidney volume. If the patient has underlying chronic renal failure, a reduction in GFR of more than 15% can be diagnosed. If the urine volume is <400ml / day, it is an oliguria ATN; if there is no oliguria, it is a non-oliguria ATN. For patients with an unclear history, chronic renal failure should be excluded first. When the ATN diagnosis is clear, efforts should be made to find the cause in order to treat the cause.

Acute tubular necrosis treatment

Clinical treatment includes supportive treatment, etiology treatment, alternative treatment, and drug treatment to promote renal function recovery.

1. Actively correct the water-electrolyte acid-base balance

Pulmonary edema caused by excessive water load and severe heart rhythm disturbance caused by hyperkalemia are the two main causes of death in ATN patients. Strictly control the amount of fluid, while giving large doses of diuretics (such as furosemide). According to the results of blood gas analysis, timely and reasonable supplementation of sodium bicarbonate to correct acidosis. Closely monitor changes in serum potassium levels and promptly and actively correct hyperkalemia.

2. Give dialysis treatment promptly and reasonably

When acute pulmonary edema, difficult to correct hyperkalemia, uremia encephalopathy, severe metabolic acidosis, etc. occur, renal replacement therapy should be proactive and timely, including intermittent hemodialysis, continuous arteriovenous hemofiltration, continuous kidney Replacement therapy (CRRT), peritoneal dialysis and other treatments.

3. Actively correct anemia and strengthen nutrition treatment

Avoid the use of nephrotoxic drugs, actively control the infection, remove the primary disease, and promote the recovery of renal function.

Prevention of acute tubular necrosis

Active rehydration and prevention of blood volume decrease can reduce the incidence of ATN in patients with surgery, trauma, and burns. In addition, rehydration for certain drugs (contrast agents, aminoglycosides, amphotericin B, cisplatin), rhabdomyolysis, ATN caused by hemolysis, multiple myeloma, hypercalcemia, etc. also have preventive effects. Controlling infection and thoroughly removing trauma and necrotic tissue are also important to prevent ATN.