| disease | Acute Renal Failure |
Acute kidney failure is a syndrome characterized by rapid deterioration of kidney function, retention of metabolic waste products, and disturbances in water, electrolyte, and acid-base balance, caused by various factors, including prerenal azotemia, renal, and postrenal causes. This chapter focuses on acute kidney failure represented by acute tubular necrosis (ATN).
bubble_chart Diagnosis
1. Medical History and Symptoms
Most patients have no prior history of kidney disease, but the cause of the disease is clear, such as severe trauma, post-surgical complications, grade III infections, sepsis, obstetric complications, severe vomiting or diarrhea, poor circulatory function, or nephrotoxic drugs leading to insufficient renal blood flow or nephrotoxic damage. Apart from the clinical manifestations of the primary disease, the majority present with oliguric ATN, often developing oliguria or anuria 1–2 days after the onset of the primary disease. Urine output does not increase after fluid resuscitation. Early symptoms include loss of appetite, nausea, vomiting, diarrhea, and other gastrointestinal symptoms. Persistent oliguria may lead to hypertension, acute pulmonary edema, and in some cases, arrhythmias and pericardial effusion. With hyperkalemia, symptoms like nausea and vomiting worsen, accompanied by arrhythmias. In advanced stages, patients may exhibit apathy, drowsiness, dysphoria, restlessness, or even unconsciousness. Gastrointestinal bleeding and various infections, particularly respiratory and urinary tract infections, are common complications. After 1–2 weeks, urine output increases (>400ml/day), marking the onset of the polyuric phase. Blood creatinine and urea nitrogen levels begin to decline after about a week, and symptoms gradually improve. However, persistent polyuria with water-electrolyte imbalances may cause nausea, weakness, muscle laxity, limb numbness, abdominal distension, and fullness. If uncorrected, dehydration and electrolyte imbalances can be fatal. If kidney function and electrolytes return to normal and clinical symptoms improve, the patient enters the convalescent stage, though some may still have urine output exceeding 2500ml/day. Some ATN cases lack an oliguric phase, with urine output consistently above 500ml, classified as non-oliguric ATN, which generally has a milder course and better prognosis.
2. Physical Examination Findings The patient appears acutely ill. In addition to signs of the primary disease, grade I anemia may be present. During the oliguric phase, hypertension and
edema are common. Severe cases may exhibit impaired consciousness, deep and rapid breathing, enlarged heart borders, or arrhythmias.
3. Auxiliary Examinations
(1) Urine specific gravity ranges between 1.010–1.020, with proteinuria (+ to ++). Red and white blood cells,
renal tubular epithelial cells, cellular casts, and granular casts may be observed, with coarse epithelial cell casts being the most significant.
(2) In the absence of massive blood loss or hemolysis, severe anemia is uncommon, with hemoglobin levels typically not falling below 80g/L.
(3) Renal function tests: Ccr decreases by more than 50% of the normal value, potentially dropping to 1–2ml/min. Blood creatinine and urea nitrogen rise rapidly. Urinary N-acetyl-β-D-glucosaminidase, lysozyme, and β2-microglobulin levels are often elevated.
(4) Blood gas analysis often reveals electrolyte imbalances such as hyperkalemia and decreased CO2 combining power, indicating metabolic acidosis.
(5) Ultrasound shows normal or significantly enlarged kidneys, with enhanced cortical echogenicity or swollen renal pyramids.
(6) Renal biopsy is definitive for diagnosing ATN.
4. Differential Diagnosis
First, ATN should be distinguished from rapidly worsening chronic kidney failure. It must also be differentiated from prerenal azotemia, postrenal acute kidney failure, and acute kidney failure caused by severe glomerulonephritis.
bubble_chart Treatment Measures
1. Actively treat the primary disease or predisposing factors, correct hypovolemia, combat shock, and implement effective anti-infection measures to prevent the occurrence of ATN.
2. Within 24–48 hours after oliguria, perform a fluid challenge or add diuretics, such as 10% glucose, low-molecular-weight dextran, and furosemide, or concurrently use vasodilators like calcium antagonists, low-dose dopamine, and prostaglandin E1. If prerenal azotemia is ruled out, fluid intake should be controlled under the principle of "output-based intake, preferring less to more," while correcting electrolyte and acid-base imbalances. Provide high-quality protein at 0.6 g/kg/day and calories at 30–35 kcal/kg/day. Mild cases may delay or avoid dialysis with aggressive and effective drug therapy. However, immediate dialysis is required if acute left heart failure, hyperkalemia, or severe acidosis occurs. (Refer to the hemodialysis section.)
4. During the convalescence stage, no special treatment is needed. Avoid nephrotoxic drugs, prevent high-protein intake, and gradually increase physical activity.
5. Other management: If other complications occur, such as bleeding, infection, hypertension, or metabolic acidosis, corresponding treatments should be administered. (Refer to the relevant sections.)
