Departments of Internal Medicine and Pathology, The Ohio State University Medical Center, Columbus, Ohio 43210, USA.
Nephron Clin Pract. 2011;119(2):c145-53. doi: 10.1159/000324762. Epub 2011 Jul 8.
Relapse or worsening of nephrotic syndrome (NS) in idiopathic membranous nephropathy (IMN) is generally assumed to be due to recurrent disease. Here we document that often that may not be the case.
This is a prospective study of 7 consecutive IMN patients whose renal status improved, then worsened after completing a course of immunosuppressive therapy. Each underwent detailed testing and repeat kidney biopsy.
In 4 patients (group A), the biopsy showed recurrent IMN (fresh subepithelial deposits). Immunosuppressive therapy was begun. In the other 3 patients (group B), the biopsy showed that the deposits had been eradicated. However, the glomerular basement membrane (GBM) was thickened and vacuolated. Immunosuppressive therapy was withheld. Groups A and B were comparable except that group B had very high intakes of salt and protein, based on 24-hour urine testing. Reducing their high salt intake sharply lowered proteinuria to the subnephrotic range and serum creatinine stabilized.
This work is the first to demonstrate that relapse/worsening of NS can occur in IMN even though the GBM deposits have been eradicated. High salt and protein intake in combination with thickened and vacuolated GBM appears to be the mechanism.
特发性膜性肾病（IMN）患者的肾病综合征（NS）复发或加重通常被认为是疾病复发所致。但在此我们证明事实并非总是如此。
这是一项连续纳入 7 例 IMN 患者的前瞻性研究，这些患者在完成一疗程免疫抑制治疗后，肾脏状况先改善后恶化。每位患者均接受了详细检查和重复肾活检。
4 例患者（A 组）的活检显示为复发的 IMN（新鲜的上皮下沉积物），开始进行免疫抑制治疗。在另外 3 例患者（B 组）中，活检显示沉积物已被清除，但肾小球基底膜（GBM）增厚并出现空泡。未进行免疫抑制治疗。A 组和 B 组除了 B 组患者的 24 小时尿液检测提示高盐和高蛋白摄入量外，其他方面均相似。严格减少高盐和高蛋白的摄入量可使蛋白尿显著减少至亚肾病范围，且血清肌酐稳定。
本研究首次证明，即使 GBM 沉积物已被清除，IMN 患者的 NS 仍可能复发或加重。高盐和高蛋白摄入结合增厚和空泡化的 GBM 似乎是其发病机制。
