OVERVIEW

What is acute tubular necrosis?

Acute tubular necrosis (ATN) is a common type of acute renal failure caused by renal ischemia, hypoxia, or nephrotoxicity, which induces tubular cell injury, leading to a rapid and progressive decline in renal function and resulting in a clinical syndrome. It is primarily characterized by a sudden drop in glomerular filtration rate, progressive azotemia, and water-electrolyte imbalances.

Which groups are commonly affected by acute tubular necrosis?

Acute tubular necrosis commonly occurs in individuals with kidney damage caused by exogenous drug intake or exposure to toxins, as well as those with renal injury due to ischemia or infection.

SYMPTOMS

What are the manifestations of patients with acute tubular necrosis?

Based on the presence or absence of reduced urine output, acute tubular necrosis can be divided into two types: oliguric and non-oliguric. The oliguric type can be divided into three stages:

• Oliguric stage: Daily urine output less than 400 ml is called oliguria. The duration ranges from 2–3 days to 2–4 weeks, generally not exceeding 1 month. If it exceeds 1 month, it often indicates extremely severe ATN, difficulty in renal function recovery, or more complex underlying causes of ATN. Main manifestations:

• Water retention: Generalized edema, cerebral edema, hypertension, congestive heart failure, and pulmonary edema.

• Electrolyte disturbances: Hyponatremia (serum sodium < 135 mmol/L), hyperkalemia (serum potassium > 5.5 mmol/L)—one of the major causes of death during the oliguric stage.

• Metabolic acidosis, azotemia, and related systemic damage, primarily affecting the digestive, cardiovascular, respiratory, and nervous systems.

• Polyuric stage: When urine output persistently exceeds 400 ml/day, it indicates the beginning of renal function recovery and entry into the polyuric stage.

• Early polyuric phase: Although urine output increases, due to the still low glomerular filtration rate, serum creatinine and blood urea nitrogen may remain significantly elevated, and metabolic acidosis and uremic symptoms can still be severe.

• Late polyuric phase: 24-hour urine output exceeds 2000 ml, sometimes reaching 4000–6000 ml/24 hours. At this stage, edema subsides, serum creatinine and blood urea nitrogen decrease, and metabolic acidosis and uremic symptoms gradually improve. However, due to the massive excretion of water and electrolytes, patients may experience dehydration, hyponatremia, hypokalemia, and other electrolyte imbalances. Severe hypokalemia can lead to mild paralysis, arrhythmias, and other manifestations.

• Recovery stage: Glomerular filtration rate gradually returns to normal, urine output normalizes, and serum creatinine and blood urea nitrogen decrease to normal levels. Complete renal function recovery may take 6 months to 1 year. A small number of patients may retain varying degrees of renal impairment, progressing to chronic renal failure.

The non-oliguric type does not include the oliguric stage, only the latter two stages.

What other diseases can acute tubular necrosis cause?

• Cardiovascular system: Hypertension, acute pulmonary edema, heart failure, arrhythmias, pericarditis.

• Digestive system: Markedly reduced appetite, nausea, vomiting, abdominal distension, hiccups or diarrhea, metabolic disturbances.

• Nervous system: Apathy, drowsiness, restlessness, or even coma.

• Hematologic system: Anemia, bleeding tendency, thrombocytopenia, consumptive hypocoagulability, and signs of fibrinolysis.

CAUSES

What are the causes of acute tubular necrosis?

• Acute renal ischemia and hypoxia: Massive bleeding during or after major surgery, various causes of shock and post-shock recovery, cardiopulmonary bypass resuscitation, restoration of renal blood circulation in kidney transplantation, and cardiac resuscitation are all situations involving renal ischemia-reperfusion. ATN caused by these factors tends to be more severe than other causes;

• Nephrotoxic damage:

• Medications: Contrast agents, aminoglycoside antibiotics such as gentamicin, kanamycin, and amikacin, polymyxin B, sulfonamides, amphotericin, heavy metals, chemical toxins, and biological toxins;

• Heavy metal nephrotoxins: Mercury, cadmium, arsenic, uranium, chromium, lithium, bismuth, lead, and platinum;

• Industrial toxins: Cyanide, carbon tetrachloride, methanol, toluene, and chloroform;

• Biological toxins: Fish gallbladder (e.g., grass carp), snakebites, poisonous mushrooms, bee venom, etc.;

• Infectious diseases such as epidemic hemorrhagic fever, leptospirosis, and sepsis leading to ATN;

• Crush injuries, trauma, and non-traumatic rhabdomyolysis, causing massive myoglobin deposition in the renal tubules and resulting in kidney damage.

DIAGNOSIS

Which medical histories are important for doctors to diagnose acute tubular necrosis?

History of nephrotoxic drug use, exposure to heavy metals or industrial toxins, history of infectious diseases, history of crush injuries or trauma, history of major or moderate surgeries, history of significant blood loss, history of shock.

What tests are needed for acute tubular necrosis?

• Complete blood count: To assess anemia and its severity, helping determine signs of hemolytic anemia and aiding in etiological diagnosis.

• Renal function tests: Serum creatinine is the best indicator for evaluating kidney function.

• Urinalysis: When renal blood flow begins to decrease, it may show reduced urinary sodium concentration and fractional excretion of sodium, along with increased urine osmolality and urine creatinine/serum creatinine ratio. Urine sediment examination may reveal characteristic findings such as renal tubular epithelial cells, epithelial cell casts, and dark brown granular casts.

• Blood gas analysis: Mainly to assess the presence, severity, and nature of acidosis.

• Liver function tests: To evaluate hepatocyte necrosis or other dysfunctions, and determine whether acute renal failure is caused by primary liver failure.

• Blood electrolyte tests: Strict monitoring of electrolyte levels is necessary during both oliguric and polyuric phases to prevent severe electrolyte imbalances.

• Renal biopsy: Generally not required for diagnosis unless primary kidney disease is suspected rather than ischemic or toxin-related conditions. It serves as a differential diagnostic tool and guides treatment.

• Renal ultrasound: In ATN, kidney size remains normal, whereas chronic renal failure typically shows reduced kidney size.

Which diseases are easily confused with acute tubular necrosis?

• Prerenal oliguria: Patients often have shock, sodium/water loss, blood loss, congestive heart failure, or severe liver disease. Simple prerenal azotemia is usually mild, and renal function normalizes after fluid resuscitation. If renal hypoperfusion persists for more than 2 hours, ATN may develop. Thus, if blood pressure has normalized but oliguria and azotemia persist, ATN should be considered.

• Postrenal urinary obstruction: Presents as sudden complete or intermittent anuria, with renal colic and flank tenderness. Urinalysis shows no significant changes. B-mode ultrasound or urinary tract X-ray can quickly differentiate the condition.

• Acute interstitial nephritis: Diagnosis relies on identifying the underlying cause. Differentiation from ATN can be challenging, and renal biopsy is often needed. Most cases require glucocorticoid therapy.

• Renovascular diseases: Conditions like acute bilateral renal vein thrombosis or renal artery occlusion can cause acute renal failure. Renal angiography, radionuclide renal scanning, or dynamic renal γ imaging can confirm the diagnosis.

TREATMENT

Which department should I visit for acute tubular necrosis?

Nephrology.

How is acute tubular necrosis treated?

Clinical treatment mainly includes supportive therapy, etiological treatment, and replacement therapy:

• Actively correct water-electrolyte imbalances and acid-base disturbances: Strictly control fluid intake. Based on arterial blood gas analysis results, promptly and appropriately administer sodium bicarbonate to correct acidosis. Closely monitor changes in blood potassium levels and actively address hyperkalemia.

• Provide timely and appropriate blood purification therapy: When conditions such as acute pulmonary edema, refractory hyperkalemia, uremic encephalopathy, or severe metabolic acidosis occur, prompt and active renal replacement therapy should be initiated.

• Actively correct anemia and strengthen nutritional therapy: Avoid nephrotoxic drugs, actively control infections, address the underlying cause, and promote renal function recovery.

Can acute tubular necrosis lead to death?

Patients with moderate to severe acute tubular necrosis not only experience significant renal failure but often also have one or more complications, which can sometimes be life-threatening. Timely and aggressive treatment and emergency care are essential.

DIET & LIFESTYLE

What should patients with acute tubular necrosis pay attention to in their diet?

• For those who can eat, try to supplement nutrition through the gastrointestinal tract, mainly giving light liquid or semi-liquid food.

• Limit water, sodium salt, and potassium salt as appropriate.

• Protein should be restricted in the early stages.

• Severe ATN patients often have obvious gastrointestinal symptoms. Supplementing part of the nutrition through the gastrointestinal tract should not be rushed. Provide rich nutrition, including sufficient calories, an adequate amount of high-quality protein, and vitamins.

PREVENTION

How to prevent acute tubular necrosis?

• Actively eliminate causative factors and treat primary diseases;

• Target key aspects of the pathogenesis: replenish blood volume, improve microcirculation; relieve tubular obstruction. For example: for surgical, traumatic, or burn patients, aggressive fluid resuscitation to prevent hypovolemia can help avoid ATN. For ATN caused by certain drugs (contrast agents, aminoglycosides, amphotericin B, cisplatin), rhabdomyolysis, hemolysis, multiple myeloma, or hypercalcemia, fluid therapy also has a preventive effect;

• Lastly, controlling infections and thoroughly removing necrotic tissue in trauma are also crucial for preventing ATN.