Hyneck M L
Clin Pharm. 1986 Nov;5(11):892-910.
The etiology and classification, pathophysiology, diagnosis, clinical course, and drug therapy of acute renal failure (ARF) are reviewed. ARF, a rapid reduction in kidney function that results in decreased glomerular filtration rate and tubular function, is caused by many different factors and can cause multiple organ dysfunction. The major causes of ARF are classically divided into three broad categories: (1) prerenal, or hypoperfusion states, (2) intrarenal, or intrinsic renal parenchymal disease, and (3) post-renal, or urinary obstructive disorders. The underlying pathogenic abnormality is renal tubular cell damage in patients with prerenal azotemia; vascular and glomerular damage is often secondary to immunologic mechanisms. Interstitial nephritis, often drug-induced, results from an immunologically mediated inflammatory renal response. Obstructive nephropathy results from partial or complete blockade of urine flow. Diagnosis relies heavily on patient history and physical examination; laboratory data, renal imaging, and sometimes renal biopsy results can yield important clues. The clinical course of ARF consists of four phases: insult and onset, maintenance, diuresis, and recovery. Morbidity and mortality are high. Drug therapy is directed at preventing or reversing the renal lesion before ARF becomes established and supporting the patient to allow the body to correct the lesion once it occurs. Prevention of prerenal azotemia and intrarenal disease is directed at identifying patients at risk, minimizing nephrotoxicity, and maintaining adequate urine output. In patients with established renal failure, an appropriate intravascular volume and pressure must be re-established and underlying problems must be corrected. Fluid, electrolyte, and acid-base balance are critical, and other serious effects on the gastrointestinal and neurologic systems must be addressed. Even though morbidity and mortality remain unacceptably high in patients with acute renal failure, promising progress has been made during the last 20-30 years.
本文综述了急性肾衰竭（ARF）的病因及分类、病理生理学、诊断、临床病程和药物治疗。ARF是指肾功能迅速减退，导致肾小球滤过率和肾小管功能下降，由多种不同因素引起，可导致多器官功能障碍。ARF的主要病因传统上分为三大类：（1）肾前性，即低灌注状态；（2）肾内性，即肾实质疾病；（3）肾后性，即尿路梗阻性疾病。肾前性氮质血症患者的潜在致病异常是肾小管细胞损伤；血管和肾小球损伤通常继发于免疫机制。间质性肾炎常由药物引起，是由免疫介导的炎症性肾反应所致。梗阻性肾病是由尿液流动部分或完全受阻引起的。诊断很大程度上依赖于患者病史和体格检查；实验室数据、肾脏影像学检查，有时还有肾活检结果可提供重要线索。ARF的临床病程包括四个阶段：损伤与发病期、维持期、利尿期和恢复期。发病率和死亡率都很高。药物治疗旨在在ARF确立之前预防或逆转肾脏病变，并在病变发生后支持患者，使身体能够纠正病变。预防肾前性氮质血症和肾内疾病旨在识别高危患者，尽量减少肾毒性，并维持足够的尿量。对于已确诊肾衰竭的患者，必须恢复适当的血管内容量和压力，并纠正潜在问题。液体、电解质和酸碱平衡至关重要，还必须处理对胃肠道和神经系统的其他严重影响。尽管急性肾衰竭患者的发病率和死亡率仍然高得令人无法接受，但在过去20至30年中已取得了有希望的进展。
