Smith J D, Hayslett J P
Renal Division, Yale University School of Medicine, New Haven, CT 06510.
Am J Kidney Dis. 1992 Mar;19(3):201-13. doi: 10.1016/s0272-6386(13)80001-7.
Acute, usually reversible, renal failure has been observed in patients with normal or minimally altered glomeruli on renal biopsy. This review aims to examine the clinical features of acute renal failure in these patients and to evaluate factors that may contribute to the reduction in glomerular filtration rate (GFR). In an analysis of 79 cases affecting 75 patients reported in the English literature since 1966, with acute renal failure associated with minimal change disease or mild histopathological changes in glomeruli, the average age was 58 +/- 2 years (mean +/- 5 SEM), urine protein excretion 11.6 +/- 0.6 g/d, and serum albumin level 19 +/- 1 g/L (1.9 +/- 0.1 g/dL). Acute renal failure was documented an average of 29 +/- 5 days after onset of nephrotic syndrome, and persisted for 7 weeks in 62 episodes in the 58 patients in whom recovery of renal function occurred. Fourteen patients died of uremia or required chronic dialysis, and 3 were lost to follow-up. Although plasma volume depletion was sometimes cited as the cause of renal failure, objective signs of hypovolemia were not documented and most patients did not improve after treatment designed to correct volume deficits. In contrast, histopathological changes consistent with acute tubular necrosis (ATN) were observed in at least 60% of cases. Since the pathogenesis of acute renal failure in minimal change nephrotic syndrome is unknown, we evaluated hemodynamic determinants of GFR in patients with minimal change disease with normal or near-normal renal function, and in relevant animal models, to obtain insights into the effect of nephrotic syndrome on GFR. Although acute renal failure is uncommon, GFR is reduced concurrently with nephrotic syndrome in approximately 30% of children and adults. Absolute and effective blood volume and renal plasma flow are relatively well preserved. However, clinical and experimental observations suggest that the glomerular ultrafiltration coefficient may be reduced by as much as 50%. These findings, together with renal biopsy changes in cases with acute renal failure, suggest that severe reductions in GFR in some patients with minimal change nephrotic syndrome may result from an interaction between acute ischemic tissue injury and preexisting intrinsic renal abnormalities.
在肾活检时肾小球正常或仅有轻微改变的患者中观察到急性、通常可逆的肾衰竭。本综述旨在研究这些患者急性肾衰竭的临床特征，并评估可能导致肾小球滤过率（GFR）降低的因素。对1966年以来英文文献报道的75例患者的79例病例进行分析，这些病例的急性肾衰竭与微小病变肾病或肾小球轻微组织病理学改变相关，平均年龄为58±2岁（均值±5标准误），尿蛋白排泄量为11.6±0.6g/d，血清白蛋白水平为19±1g/L（1.9±0.1g/dL）。急性肾衰竭平均在肾病综合征发病后29±5天被记录，在58例肾功能恢复的患者中的62次发作中持续了7周。14例患者死于尿毒症或需要长期透析，3例失访。尽管有时将血浆容量减少作为肾衰竭的原因，但未记录到血容量不足的客观体征，且大多数患者在旨在纠正容量不足的治疗后并未改善。相反，至少60%的病例观察到与急性肾小管坏死（ATN）一致的组织病理学改变。由于微小病变肾病综合征急性肾衰竭的发病机制尚不清楚，我们评估了肾功能正常或接近正常的微小病变疾病患者以及相关动物模型中GFR的血流动力学决定因素，以深入了解肾病综合征对GFR的影响。尽管急性肾衰竭并不常见，但在大约30%的儿童和成人中，GFR与肾病综合征同时降低。绝对和有效血容量以及肾血浆流量相对保存良好。然而，临床和实验观察表明，肾小球超滤系数可能降低多达50%。这些发现，连同急性肾衰竭病例的肾活检变化，表明一些微小病变肾病综合征患者GFR的严重降低可能是急性缺血性组织损伤与先前存在的内在肾脏异常相互作用的结果。
