acute kidney injury Acute kidney injury (AKI), formerly known as acute renal failure, refers to the clinical syndrome characterized by a rapid decline in renal function within a short period due to various causes. It is manifested by a decrease in glomerular filtration rate, retention of nitrogenous waste products such as creatinine and blood urea nitrogen, as well as disturbances in water, electrolyte, and acid-base balance. In severe cases, multiple organ dysfunction syndrome may occur. Recent clinical studies have confirmed that even mild renal impairment can significantly increase patient mortality. Therefore, the current trend is to rename acute renal failure as acute kidney injury, with the hope of early identification and effective intervention during the course of the disease.

Acute kidney injury (AKI) refers to a clinical syndrome in which various causes lead to a rapid decline in kidney function over a short period of time. This is characterized by a decrease in glomerular filtration rate, accompanied by retention of nitrogenous waste products such as creatinine and urea, as well as disturbances in water, electrolyte, and acid-base balance. In severe cases, it can lead to multiple organ dysfunction syndrome. Previously known as acute renal failure, recent clinical research has demonstrated that even mild impairment of kidney function can significantly increase mortality rates in patients. Therefore, there is a current trend to replace the term acute renal failure with acute kidney injury, with the hope of early recognition and effective intervention during the course of the disease.

Acute kidney injury is specifically defined as a rapid decline in kidney function due to various reasons, resulting in an increase in serum creatinine concentration or a decrease in urine output over hours to days or weeks, leading to a series of symptoms such as oliguria, anuria, and water and electrolyte imbalances. AKI can occur in patients with no prior kidney disease as well as in those with pre-existing chronic kidney disease, making it a common critical condition in clinical practice.

Traditionally, the causes of acute kidney injury have been classified based on the most severely affected anatomical parts of the kidneys. Therefore, the clinical causes of acute kidney injury have traditionally been divided into the following categories:

Prerenal - Reduced Renal Perfusion Pressure

Prerenal injury refers to a decrease in the usual blood flow to the kidneys. Acute prerenal injury results from inadequate perfusion and is often associated with hypovolemic states such as acute hemorrhage, diarrhea, or insufficient fluid replacement leading to reduced effective blood volume, decreased renal blood flow, and reduced tubular filtration rate.

Renal - Vascular Disorders

Renal vascular disorders refer to pathological changes in the renal blood vessels. Renal vascular diseases can directly affect the small and large blood vessels within the kidneys. Acute renal vascular diseases primarily affecting small vessels include small vessel vasculitis and thrombotic thrombocytopenic purpura-hemolytic uremic syndrome, scleroderma, atherosclerotic embolic disease, and malignant hypertension.

Diseases affecting larger vessels and leading to acute kidney injury include renal infarction, which can result from aortic dissection, systemic thromboembolism, renal artery anomalies (such as aneurysms), and acute renal vein thrombosis.

Renal - Glomerular or Tubulointerstitial Disorders

Renal glomerular or tubulointerstitial disorders refer to damage to the renal parenchyma. Acute kidney injury can be caused by renal ischemia, nephrotoxic substances, incompatible blood transfusions, infections, drug allergies, hypercalcemia, glomerulonephritis, tubular necrosis, vasculitis, acute systemic lupus erythematosus, and more. Nephrotoxic substances include drugs (such as antibiotics, certain chemotherapeutic agents, etc.), contrast agents, heavy metals, snake venom, and others.

Postrenal - Urinary Tract Obstruction

Postrenal injury refers to obstruction of the urinary outflow. Acute urinary tract obstruction can be caused by various factors, including stones, tumors, blood clots, and benign prostatic hyperplasia, among others.

Reduced or complete absence of urine output;

Presence of blood in the urine, resulting in red or brown-colored urine;

Swelling, especially in the legs or feet;

Nausea or loss of appetite;

Feeling weak or easily fatigued.

Specifically, the progression of the clinical disease may lead to different symptoms:

Initial phase

Patients may exhibit symptoms of ischemia, infection, but without significant renal parenchymal damage. The duration of the initial phase depends on the underlying cause, such as the amount of toxin intake or the duration and severity of hypotension.

Oliguric phase

The typical oliguric phase lasts 7-14 days, with some patients experiencing it for only a few hours, while others may endure it for 4-6 weeks. Prolonged oliguric periods indicate widespread renal cortical necrosis.

Patients in the oliguric phase may have a decreased glomerular filtration rate, resulting in oliguria (<400ml/day) or anuria (<100ml/day). However, some patients may not experience oliguria and instead have non-oliguric AKI, which generally signifies a milder condition and a better prognosis.

Regardless of urine output, as renal function declines, patients may experience a range of uremic manifestations, including decreased appetite, nausea, vomiting, and generalized pruritus. Patients with volume overload (common in oliguric AKI) may exhibit weight gain, edema, and progressive azotemia, electrolyte, and acid-base imbalances, with serum creatinine increasing by 88.4-176.8umol/L and blood urea nitrogen by 7.14-8.93mmol/L.

Complications of the oliguric phase include volume overload, hyperkalemia, metabolic acidosis, as well as hypocalcemia and hyperphosphatemia.

Diuretic phase

The diuretic phase begins when urine output exceeds 400ml/day, indicating the beginning of renal function recovery.

Polyuric phase

During this phase, renal glomerular function gradually returns to normal, leading to polyuria (up to 4000-6000ml/day) lasting 1-3 weeks. Blood urea nitrogen levels may continue to rise, and renal function gradually normalizes. Reabsorption of solutes and water by renal tubular epithelial cells recovers relatively late and may take several months.

The polyuric phase is prone to hypovolemia, hyponatremia, and hypokalemia. A few patients may die during this phase due to infections and electrolyte imbalances.

Recovery phase

Complete recovery of renal function may take 6 months to 1 year. In some cases, renal function may not fully recover, leaving varying degrees of renal structural and functional defects, potentially requiring long-term dialysis to sustain life.

For life-threatening water and electrolyte abnormalities caused by AKI, immediate medical intervention is necessary:

Volume overload;

Hyperkalemia (serum potassium >5.5mmol/L) or rapid elevation of serum potassium;

Uremic symptoms, such as pericarditis or unexplained mental status decline;

Severe metabolic acidosis that cannot be corrected with medication (pH <7.1).

Patients with the above conditions, despite appropriate internal medicine treatment, may typically require early dialysis.

In daily life, patients need to pay attention to medication contraindications and seek advice from a professional medical doctor when necessary. They should actively treat underlying diseases such as hypertension and diabetes, and maintain a positive attitude towards their illness and life.

At the same time, family members should pay attention to changes in the patient's emotions and communicate in a timely manner. For elderly patients, family members should observe any physical changes and seek medical attention promptly if the patient experiences discomfort.

Avoid nephrotoxic drugs, contrast agents, and certain Chinese herbal medicines (such as Aristolochia, Caulis Akebiae, Radix Stephaniae Tetrandrae, and Houpo): High-risk groups such as the elderly, diabetics, and those with pre-existing chronic kidney disease should avoid taking nephrotoxic drugs (such as aminoglycoside antibiotics, amphotericin B, and contrast agents).

Follow the guidance of a professional medical doctor to ensure adequate calorie intake.

Low-sodium diet: Patients with poor kidney function should pay attention to a low-sodium diet and limit the consumption of high-sodium pickled vegetables (such as pickled mustard tuber, salted vegetables, etc.).

Control protein intake: Limit protein intake to 0.8g/(kg·day).

Reduce potassium and phosphorus intake: Avoid or reduce the consumption of high-potassium foods and fruits (such as yams, potatoes, and bananas). Do not consume vegetable soup, and soak vegetables for a period before processing. Avoid or reduce the consumption of high-phosphorus foods such as animal offal, nuts, and dried vegetables.

Improve lifestyle: Quit smoking and alcohol, engage in physical activity, and control weight.

Acute kidney injury has diverse causes, and there are no specific preventive measures. The main focus is on rest, a healthy diet, and paying attention to one's own physical condition. Additionally, for individuals with chronic kidney disease, diabetes, hypertension, heart failure, and other conditions that may affect the kidneys, seeking medical treatment actively can help reduce the likelihood of developing acute kidney injury.