OVERVIEW

What is Acute Kidney Injury?

Acute Kidney Injury (AKI) is a clinical syndrome characterized by a rapid decline in kidney function due to various causes within a short period. Common clinical manifestations include azotemia, disturbances in water-electrolyte and acid-base balance, oliguria, or anuria.

Previously referred to as acute renal failure, recent research has shown that even mild acute kidney dysfunction can significantly increase patient mortality. As a result, the term "acute kidney injury" is now preferred over "acute renal failure."

AKI is one of the common diseases in nephrology. It has a sudden onset and progresses rapidly. Without timely treatment, it can lead to functional damage in multiple organs and, in severe cases, death. Treatment includes addressing the underlying cause, maintaining internal homeostasis, providing nutritional support, actively managing complications, and renal replacement therapy.

The prognosis of AKI is polarized. Some patients may recover completely, while hospital-acquired AKI has a mortality rate as high as 50%. Others may require lifelong renal replacement therapy due to irreversible kidney damage, severely impacting their quality of life.

Is Acute Kidney Injury Common?

Yes. Studies indicate that the incidence of AKI among hospitalized patients is approximately 5%–7%, and in developed countries, this rate can reach 13%–18%.

What Are the Types of Acute Kidney Injury?

Based on the location and cause of the injury, AKI can be classified into prerenal AKI, intrinsic renal AKI, and postrenal AKI. The etiology and pathogenesis vary for each type.

SYMPTOMS

What are the common manifestations of acute kidney injury?

The early symptoms of acute kidney injury are often subtle and may be masked by the primary disease, leading to misdiagnosis or missed diagnosis. Systemic symptoms of AKI may include the following aspects:

• Digestive system: Loss of appetite, nausea, vomiting, bloating, diarrhea, etc. In severe cases, gastrointestinal bleeding may occur.

• Respiratory system: In addition to infections, acute pulmonary edema caused by fluid overload is common, presenting as difficulty breathing, coughing, and shortness of breath.

• Circulatory system: Due to oliguria and uncontrolled fluid intake, excessive body fluid may lead to hypertension and heart failure. Toxin accumulation, electrolyte imbalances, anemia, and acidosis can cause various arrhythmias and myocardial damage.

• Nervous system: Symptoms of uremic encephalopathy may occur, such as impaired consciousness, agitation, delirium, convulsions, and coma.

• Hematologic system: Bleeding tendencies and mild anemia may be observed. It should be noted that infection is a common and serious complication of AKI.

AKI has diverse causes, which can be classified into three categories based on anatomical location: prerenal, renal, and postrenal. Among renal causes, acute tubular necrosis is the most common, with relatively typical manifestations as follows:

• Oliguric phase: Daily urine output is less than 400 ml or even anuria, typically lasting 1–2 weeks. During this phase, patients may also experience symptoms related to azotemia, water-electrolyte imbalances, and acid-base disturbances, such as generalized edema, difficulty breathing, lethargy, sluggishness, seizures, arrhythmias, cardiac arrest, and generalized convulsions.

• Transitional phase: Daily urine output exceeds 400 ml, indicating the beginning of renal function recovery. Symptoms of azotemia, water-electrolyte imbalances, and acid-base disturbances may still persist.

• Polyuric phase: Daily urine output may reach over 2500 ml, with severe cases reaching 4000–6000 ml, typically lasting 1–3 weeks. Early in this phase, symptoms of azotemia, water-electrolyte imbalances, and acid-base disturbances may still be present. As urine output increases, generalized edema gradually subsides, and blood pressure, urea nitrogen, and creatinine levels tend to normalize. However, dehydration, hypotension, hyponatremia, and hypokalemia may also occur.

• Recovery phase: Renal function gradually returns to normal, though a few patients may experience incomplete recovery, resulting in permanent kidney damage.

What complications can acute kidney injury cause?

• Hyperkalemia: May cause arrhythmias, cardiac arrest, etc.

• Hyponatremia: May cause lethargy, sluggishness, etc.

• Hyperphosphatemia: May cause skin itching.

• Hypocalcemia: May cause perioral paresthesia, muscle twitching, seizures, hallucinations, and lethargy.

• Hypermagnesemia: May cause arrhythmias, etc.

• Hypomagnesemia: May cause muscle cramps, convulsions, and seizures.

• Metabolic acidosis: May cause deep, rapid breathing.

• Water intoxication: May cause generalized edema, cerebral edema, pulmonary edema, etc.

• Others: Such as gastrointestinal bleeding, acute respiratory distress syndrome, heart failure, anemia, nutritional and metabolic abnormalities, systemic infections, etc.

CAUSES

What are the common causes of acute kidney injury?

The common causes of acute kidney injury vary depending on the underlying mechanisms, as detailed below:

Prerenal Factors

• Reduced intravascular volume: Burns, diarrhea, vomiting, gastrointestinal bleeding, pancreatitis, trauma, malnutrition, liver failure, etc.

• Decreased cardiac output: Myocardial infarction, arrhythmias, cardiomyopathy, hypertension, severe pulmonary heart disease, etc.

• Peripheral vasodilation: Use of antihypertensive drugs, sepsis, hypoxemia, etc.

• Severe renal vasoconstriction: Sepsis, hepatorenal syndrome, etc.

• Mechanical occlusion of renal arteries: Renal artery thrombosis, renal artery embolism, etc.

Intrinsic Renal Factors

• Renal vascular diseases: Vasculitis, malignant hypertension, DIC, renal vein thrombosis, etc.

• Renal parenchymal diseases: Glomerulonephritis, interstitial nephritis, acute tubular necrosis, intratubular crystal deposition, protein deposition, etc.

• Infections: Kidney damage caused by sepsis or systemic inflammatory response syndrome.

• Others: Conditions involving kidney infiltration, such as lymphoma, leukemia, sarcoidosis, or connective tissue diseases.

Postrenal Factors

• Ureteral obstruction.

• Bladder emptying dysfunction.

• Urethral obstruction.

Who is at higher risk of acute kidney injury?

• Elderly individuals, especially those aged 80–90.
• People with pre-existing chronic kidney disease.
• Patients with hypertension or heart disease.
• Individuals with liver cirrhosis.
• Malnourished patients.
• Those taking medications such as NSAIDs or other nephrotoxic drugs.
• Patients with severe infections.
• Individuals with hematologic disorders.
• Patients with connective tissue diseases.
• Those with urinary tract stones or urologic tumors.

DIAGNOSIS

What tests are needed for patients with suspected acute kidney injury? Why are these tests performed?

• Complete blood count, blood biochemistry, blood gas analysis, blood culture: To assess kidney function, check for anemia, metabolic acidosis, or bloodstream infections.

• Autoantibody tests: To evaluate whether kidney disease or autoimmune connective tissue diseases are present.

• Urinalysis, urine biochemistry: To help determine the cause of acute kidney injury.

• Biomarker tests: To assist in early diagnosis of acute kidney injury.

• Urinary system ultrasound, abdominal X-ray, CT, renal angiography, MRI, etc.: To identify the cause of acute kidney injury.

• Kidney biopsy: To determine the cause of acute kidney injury.

What precautions should be taken when performing a kidney biopsy on a patient with acute kidney injury?

Kidney biopsy is an invasive procedure with the following precautions:

• Before the biopsy, complete blood count, coagulation tests, and other relevant examinations should be performed.

• Before the biopsy, the patient should practice urinating while lying down, as they will need bed rest for 24 hours after the procedure.

• Before the biopsy, the patient should practice holding their breath for 6–7 seconds, as they will need to cooperate by holding their breath during the procedure.

• After the biopsy, the patient must rest in bed for 24 hours.

• After the biopsy, the patient should drink plenty of water and urinate frequently to prevent blood clots from blocking the urinary tract.

• After the biopsy, the patient should eat light, easily digestible food and maintain regular bowel movements.

• If hematuria worsens or symptoms such as palpitations or shortness of breath occur, seek medical attention promptly.

How is acute kidney injury diagnosed?

According to the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines, AKI is defined as:

• An increase in serum creatinine by ≥0.3 mg/dL (≥26.5 μmol/L) within 48 hours, or

• An increase in serum creatinine to ≥1.5 times the baseline value, with this increase known or presumed to have occurred within the prior 7 days, or

• Urine output <0.5 mL/(kg·h) for 6 hours.

How is acute kidney injury staged? What are the criteria?

Using the KDIGO criteria, AKI is staged as follows:

• Stage 1: Serum creatinine increases to 1.5–1.9 times the baseline value, or serum creatinine rises by ≥0.3 mg/dL (≥26.5 μmol/L), or urine output decreases to <0.5 mL/(kg·h) for 6–12 hours.

• Stage 2: Serum creatinine increases to 2.0–2.9 times the baseline value, or urine output decreases to <0.5 mL/(kg·h) for 12 hours or longer.

• Stage 3: Serum creatinine increases to 3.0 times the baseline value, or serum creatinine rises to ≥4.0 mg/dL (≥353.6 μmol/L), or urine output decreases to <0.3 mL/(kg·h) for 24 hours or longer, or anuria persists for 12 hours or longer, or renal replacement therapy is initiated; or, for patients under 18 years old, eGFR declines to <35 mL/(min·1.73 m²).

TREATMENT

Which department should I visit for acute kidney injury?

Emergency department, nephrology department, or general internal medicine. Acute kidney injury requires prompt medical attention. Patients should seek diagnosis and treatment at the emergency or nephrology department of a local reputable hospital as soon as possible.

What are the treatment methods for acute kidney injury?

Treatment for acute kidney injury includes addressing the underlying cause, maintaining internal stability, providing nutritional support, actively managing complications, and renal replacement therapy (such as hemodialysis).

For life-threatening water and electrolyte abnormalities caused by AKI, immediate treatment should be initiated:

• Volume therapy: All AKI patients should undergo volume status assessment, as correcting volume depletion or overload (especially when associated with worsening cardiac output) may reverse or improve AKI.

• Volume depletion: Unless contraindicated, intravenous fluid therapy should be administered if the patient has a history of fluid loss (e.g., vomiting or diarrhea), physical signs of hypovolemia (hypotension and tachycardia), and/or oliguria. Crystalloids or colloids may be used. Crystalloid solutions (e.g., normal saline) are preferred initially, while potassium-containing solutions (e.g., lactated Ringer's) should be used cautiously. The goal is to increase cardiac output and improve tissue oxygenation in preload-dependent or volume-responsive patients. The total fluid volume depends on the degree of depletion and ongoing losses.

• Volume overload: Diuretics may be used in AKI patients to relieve fluid overload. However, diuretics are not recommended for long-term use or to delay dialysis, as dialysis and ultrafiltration are the most effective methods for volume removal in AKI, allowing clinicians to optimize nutritional support and intravenous medication. Loop diuretics (e.g., furosemide) are preferred if used temporarily.

• Hyperkalemia: For mild hyperkalemia with reversible causes (e.g., volume depletion or ACEI/ARB use), dialysis is not initially required. Treatment includes a low-potassium diet, fluid replacement, and/or discontinuation of ACEI/ARB. Close follow-up is necessary to ensure conservative treatment is effective. Potassium-binding resins may be considered for mild cases. Severe hyperkalemia (potassium > 6.5 mmol/L) or rapidly rising potassium levels require prompt hemodialysis.

• Metabolic acidosis: Common treatments include dialysis and bicarbonate administration. The choice depends on volume status, underlying cause, and severity of acidosis.

• Indications for dialysis: Generally accepted indications for dialysis in AKI include:

• Diuretic-resistant fluid overload;

• Medication-resistant hyperkalemia (serum potassium > 6.5 mmol/L) or rapidly rising potassium levels;

• Metabolic acidosis (pH < 7.1) without bicarbonate indication (e.g., volume-overloaded patients or those with lactic/ketoacidosis);

• Uremic symptoms (e.g., pericarditis, neuropathy, or unexplained altered mental status).

How is the underlying cause of acute kidney injury addressed?

Identifying the cause is essential. Patients with oliguria, anuria, or systemic edema should seek prompt diagnosis at a reputable hospital. AKI causes include prerenal, renal, and postrenal factors, each requiring different treatments. Common interventions include discontinuing nephrotoxic or allergenic drugs, controlling infections, and improving cardiac function.

What is renal replacement therapy for AKI patients?

Renal replacement therapy (dialysis) includes four options based on severity: continuous renal replacement therapy, hemodialysis, peritoneal dialysis, or sustained low-efficiency dialysis. It is critical for maintaining fluid/electrolyte balance, preventing further kidney damage, promoting recovery, and enabling other treatments.

What should AKI patients pay attention to during hospitalization?

• Oliguric phase: Strict bed rest to reduce kidney burden.

• Encourage a light, low-salt, low-fat, low-phosphorus, high-calcium, low-protein diet (e.g., milk, fish). Avoid organ meats and allergenic foods; limit water, sodium, and potassium intake as needed.

• Accurately record 24-hour intake/output and daily weight.

• Maintain personal hygiene.

• Polyuric phase: Gradually increase activity without fatigue.

• Provide high-carbohydrate, high-vitamin, high-calorie foods. For urine output > 3000 ml/day, increase potassium-rich foods (e.g., oranges, bananas).

• Monitor intake/output and supplement fluids to maintain balance.

• Boost immunity to prevent infections.

Do AKI patients need follow-up after discharge? How?

Yes. Typically, patients should return for blood tests, urinalysis, biochemistry, and cause-specific evaluations one month post-discharge. Results determine further follow-up timing to assess recovery and adjust treatment.

Is AKI prone to recurrence?

Yes, if the cause persists or new triggers emerge.

Can AKI be cured?

Prognosis depends on the cause. Acute tubular necrosis may resolve with supportive care, while untreated vasculitis can lead to permanent kidney failure. Early diagnosis and cause-specific treatment are crucial.

DIET & LIFESTYLE

What should patients with acute kidney injury pay attention to in their diet?

• During the oliguric phase, encourage eating. The diet should be light, low in salt, low in fat, low in phosphorus, high in calcium, and consist of high-quality low-protein foods such as milk and fish.

• Avoid animal offal and allergenic foods, and limit the intake of water, sodium salt, and potassium-rich foods as appropriate.

• During the polyuric phase, provide high-sugar, high-vitamin, and high-calorie foods. When daily urine output exceeds 3000 ml, increase potassium-rich foods such as oranges and bananas.

• Replenish fluids appropriately based on intake and output to maintain fluid balance.

• After discharge, avoid nephrotoxic foods and medications in daily life. Maintain a balanced diet with moderate salt intake, and quit smoking and alcohol.

What should patients with acute kidney injury pay attention to in daily life?

• Strictly follow the doctor's instructions, take medications on time and in the prescribed dosage, and do not stop medication without authorization. Schedule regular follow-ups to monitor kidney function, blood pressure, etc.

• Learn about acute kidney injury. If similar symptoms recur, seek medical attention promptly.

• In case of abnormal conditions such as cold, fever, headache, vomiting, or diarrhea, avoid self-medication or seeking unprofessional treatment. Instead, visit a local reputable hospital for proper medical guidance.

• If a medication causes a significant decrease in urine output or symptoms like rash, fever, itching, or red urine, discontinue use immediately and seek medical attention.

• When using potentially nephrotoxic medications (e.g., vancomycin) for treatment, monitor kidney function and urine output regularly.

Does acute kidney injury affect fertility?

Generally, no.

PREVENTION

Can Acute Kidney Injury Be Prevented? How to Prevent It?

Yes, it can be prevented.

• Learn about acute kidney injury and its related causes.

• Avoid taking medications indiscriminately, especially antipyretics, antibiotics, and traditional Chinese medicines with unknown ingredients.

• Avoid consuming foods with nephrotoxic effects.

• Hospitalized patients should undergo frequent kidney function monitoring to prevent acute kidney injury.

• Get regular health check-ups.

How Can Acute Kidney Injury Be Detected Early?

Acute kidney injury has no specific clinical manifestations in its early stages, making early diagnosis difficult and prone to misdiagnosis or oversight. However, early diagnosis and prompt treatment are crucial for improving prognosis. Therefore, seek medical attention immediately if the following abnormalities occur to rule out acute kidney injury.

• If urine output significantly decreases after taking a certain medication, or if symptoms such as widespread rash, fever, skin itching, or reddish urine appear.

• Sudden unexplained decrease in urine output or generalized edema.