Ai-Bo Qin1,2,3,4,5, Xiao-Juan Yu1,2,3,4,5, Su-Xia Wang1,2,3,4,5,6, Fu-de Zhou1,2,3,4,5, Ming-Hui Zhao1,2,3,4,5,7. 1. Renal Division, Department of Medicine, Peking University First Hospital, Beijing, China. 2. Institute of Nephrology, Peking University, Beijing, China. 3. Key Laboratory of Renal Disease, Ministry of Health of China, Beijing, China. 4. Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China, Beijing, China. 5. Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases, Chinese Academy of Medical Sciences, Beijing, China. 6. Electron Microscopy Laboratory, Pathological Center, Peking University First Hospital, Beijing, China. 7. Peking-Tsinghua Center for Life Sciences, Beijing, China.
Abstract
INTRODUCTION: Long-term exposure to mercury can cause minimal change disease. However, the current understanding of mercury-associated minimal change disease (M-MCD) is inadequate. To improve the understanding of M-MCD, this study retrospectively analyzed the clinicopathological, ultrastructural, and prognostic features of M-MCD, in comparison with primary minimal change disease (P-MCD). METHODS: We retrospectively analyzed the clinicopathological data of 21 M-MCD patients and 21 P-MCD patients. Electron micrographs of glomerular capillaries were taken, and the foot process width (FPW) was measured. A receiver operating characteristics (ROC) curve analysis was performed to determine the optimum cutoff value of FPW that can differentiate the M-MCD from P-MCD. RESULTS: M-MCD patients presented similar clinical and routine pathological characteristics with P-MCD patients but had lower levels of FPW (935.0 [interquartile range (IQR) 853.7-1,176.7] nm vs. 1,403.2 [IQR 1,089.2-1,841.8] nm, p = 0.002). ROC curve analysis showed that FPW value below 1,385 nm might help to differentiate M-MCD from P-MCD (area under the curve of 0.787, sensitivity of 94.7%, and specificity of 52.4%). For patients with M-MCD, 77.8% achieved complete remission after mercury detoxification monotherapy. Patients with M-MCD had a lower relapse rate than patients with P-MCD (0 vs. 47.1%, p = 0.003). In addition, there was no significant difference in remission time between M-MCD patients treated with mercury detoxification monotherapy and those initially treated with immunosuppressive therapy (2.0 [IQR 1.0-6.0] months vs. 2.0 [IQR 1.5-2.5] months, p = 0.606). CONCLUSIONS: M-MCD patients showed similar clinicopathological features with P-MCD patients, but with less severe foot process effacement, suggesting different pathogenesis of these 2 disease entities. The treatment of mercury detoxification was highly effective for patients with M-MCD and can be considered as a primary choice in clinical practice.
INTRODUCTION: Long-term exposure to mercury can cause minimal change disease. However, the current understanding of mercury-associated minimal change disease (M-MCD) is inadequate. To improve the understanding of M-MCD, this study retrospectively analyzed the clinicopathological, ultrastructural, and prognostic features of M-MCD, in comparison with primary minimal change disease (P-MCD). METHODS: We retrospectively analyzed the clinicopathological data of 21 M-MCD patients and 21 P-MCD patients. Electron micrographs of glomerular capillaries were taken, and the foot process width (FPW) was measured. A receiver operating characteristics (ROC) curve analysis was performed to determine the optimum cutoff value of FPW that can differentiate the M-MCD from P-MCD. RESULTS: M-MCD patients presented similar clinical and routine pathological characteristics with P-MCD patients but had lower levels of FPW (935.0 [interquartile range (IQR) 853.7-1,176.7] nm vs. 1,403.2 [IQR 1,089.2-1,841.8] nm, p = 0.002). ROC curve analysis showed that FPW value below 1,385 nm might help to differentiate M-MCD from P-MCD (area under the curve of 0.787, sensitivity of 94.7%, and specificity of 52.4%). For patients with M-MCD, 77.8% achieved complete remission after mercury detoxification monotherapy. Patients with M-MCD had a lower relapse rate than patients with P-MCD (0 vs. 47.1%, p = 0.003). In addition, there was no significant difference in remission time between M-MCD patients treated with mercury detoxification monotherapy and those initially treated with immunosuppressive therapy (2.0 [IQR 1.0-6.0] months vs. 2.0 [IQR 1.5-2.5] months, p = 0.606). CONCLUSIONS: M-MCD patients showed similar clinicopathological features with P-MCD patients, but with less severe foot process effacement, suggesting different pathogenesis of these 2 disease entities. The treatment of mercury detoxification was highly effective for patients with M-MCD and can be considered as a primary choice in clinical practice.
Authors: Jeroen K J Deegens; Henry B P M Dijkman; George F Borm; Eric J Steenbergen; José G van den Berg; Jan J Weening; Jack F M Wetzels Journal: Kidney Int Date: 2008-08-27 Impact factor: 10.612
Authors: José G van den Berg; Marius A van den Bergh Weerman; Karel J M Assmann; Jan J Weening; Sandrine Florquin Journal: Kidney Int Date: 2004-11 Impact factor: 10.612
Authors: L C Racusen; K Solez; R B Colvin; S M Bonsib; M C Castro; T Cavallo; B P Croker; A J Demetris; C B Drachenberg; A B Fogo; P Furness; L W Gaber; I W Gibson; D Glotz; J C Goldberg; J Grande; P F Halloran; H E Hansen; B Hartley; P J Hayry; C M Hill; E O Hoffman; L G Hunsicker; A S Lindblad; Y Yamaguchi Journal: Kidney Int Date: 1999-02 Impact factor: 10.612