Yan Wang1, Feng Yu2, Di Song1, Su-Xia Wang1, Ming-Hui Zhao3. 1. Renal Division, Department of Medicine, Peking University First Hospital, Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China and Peking-Tsinghua Center for Life Sciences, Beijing, P.R. China.Renal Division, Department of Medicine, Peking University First Hospital, Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China and Peking-Tsinghua Center for Life Sciences, Beijing, P.R. China.Renal Division, Department of Medicine, Peking University First Hospital, Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China and Peking-Tsinghua Center for Life Sciences, Beijing, P.R. China.Renal Division, Department of Medicine, Peking University First Hospital, Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China and Peking-Tsinghua Center for Life Sciences, Beijing, P.R. China. 2. Renal Division, Department of Medicine, Peking University First Hospital, Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China and Peking-Tsinghua Center for Life Sciences, Beijing, P.R. China.Renal Division, Department of Medicine, Peking University First Hospital, Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China and Peking-Tsinghua Center for Life Sciences, Beijing, P.R. China.Renal Division, Department of Medicine, Peking University First Hospital, Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China and Peking-Tsinghua Center for Life Sciences, Beijing, P.R. China.Renal Division, Department of Medicine, Peking University First Hospital, Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China and Peking-Tsinghua Center for Life Sciences, Beijing, P.R. China. yufengevert1@sina.com. 3. Renal Division, Department of Medicine, Peking University First Hospital, Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China and Peking-Tsinghua Center for Life Sciences, Beijing, P.R. China.Renal Division, Department of Medicine, Peking University First Hospital, Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China and Peking-Tsinghua Center for Life Sciences, Beijing, P.R. China.Renal Division, Department of Medicine, Peking University First Hospital, Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China and Peking-Tsinghua Center for Life Sciences, Beijing, P.R. China.Renal Division, Department of Medicine, Peking University First Hospital, Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China and Peking-Tsinghua Center for Life Sciences, Beijing, P.R. China.Renal Division, Department of Medicine, Peking University First Hospital, Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China and Peking-Tsinghua Center for Life Sciences, Beijing, P.R. China.
Abstract
OBJECTIVE: The podocyte lesion in LN is still an intriguing controversy. We assess the associations between podocyte lesions and clinico-pathological features in a large cohort of LN patients. METHODS: The clinico-pathological data of 202 patients with renal biopsy-proven LN were retrospectively studied. The degree of podocyte lesions was assessed morphologically and its correlations with clinico-pathological parameters were further analysed. RESULTS: The podocyte foot processes of most LN patients significantly effaced, reflected by the median foot process width (FPW) of 1397.39 nm, and 13 patients met the histological criteria of lupus podocytopathy. The FPW was correlated with proteinuria (r = 0.509, P < 0.001) and the cut-off value of FPW, >1240 nm, could differentiate nephrotic proteinuria from non-nephrotic proteinuria with sensitivity 81.5% and specificity 62.7%. The FPW varied significantly with different types of LN, and the patients with combined LN presented with the most severe lesions. The complete remission rate was significantly higher and the long-term renal outcome was better in the group with calcineurin inhibitors than that with other regimens in patients with FPW >1240 nm. CONCLUSION: Podocyte damage was common in LN. Pure lupus podocytopathy might act as an extreme form of lupus podocyte lesion, and more patients might present with severe podocyte effacement concealed in different types of LN, which needs further investigation.
OBJECTIVE: The podocyte lesion in LN is still an intriguing controversy. We assess the associations between podocyte lesions and clinico-pathological features in a large cohort of LN patients. METHODS: The clinico-pathological data of 202 patients with renal biopsy-proven LN were retrospectively studied. The degree of podocyte lesions was assessed morphologically and its correlations with clinico-pathological parameters were further analysed. RESULTS: The podocyte foot processes of most LN patients significantly effaced, reflected by the median foot process width (FPW) of 1397.39 nm, and 13 patients met the histological criteria of lupus podocytopathy. The FPW was correlated with proteinuria (r = 0.509, P < 0.001) and the cut-off value of FPW, >1240 nm, could differentiate nephrotic proteinuria from non-nephrotic proteinuria with sensitivity 81.5% and specificity 62.7%. The FPW varied significantly with different types of LN, and the patients with combined LN presented with the most severe lesions. The complete remission rate was significantly higher and the long-term renal outcome was better in the group with calcineurin inhibitors than that with other regimens in patients with FPW >1240 nm. CONCLUSION: Podocyte damage was common in LN. Pure lupus podocytopathy might act as an extreme form of lupus podocyte lesion, and more patients might present with severe podocyte effacement concealed in different types of LN, which needs further investigation.
Authors: Taro Iwamoto; Jessica M Dorschner; Shanmugapriya Selvaraj; Valeria Mezzano; Mark A Jensen; Danielle Vsetecka; Shreyasee Amin; Ashima Makol; Thomas Osborn; Kevin Moder; Vaidehi R Chowdhary; Peter Izmirly; H Michael Belmont; Robert M Clancy; Jill P Buyon; Ming Wu; Cynthia A Loomis; Timothy B Niewold Journal: J Rheumatol Date: 2021-11-15 Impact factor: 4.666
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