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1. Correlation between the location of the index tumour and the location of positive lymph nodes in high-risk prostate cancer – a monocentric positive lymph node mapping study

Author

Decloedt, H., primary, Jacobs, B., additional, Giesen, A., additional, Matthias, V., additional, Gevaert, T., additional, Baldewijns, M., additional, Battaglia, A., additional, Laenen, A., additional, Van Den Broeck, T., additional, Moris, L., additional, Albersen, M., additional, Claessens, F., additional, Lerut, E., additional, Haustermans, K., additional, Van Poppel, H., additional, De Meerleer, G., additional, Everaerts, W., additional, and Joniau, S., additional

Published
2024
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2. E-book: Actuele thema’s in de gezondheidszorg – Uitgave 2023

Author

Lerut, E., primary, Wildemeersch, D., additional, De Schutter, I., additional, Olde Rikkert, M., additional, Jambroes, M., additional, Opstelten, W., additional, Gyselaers, W., additional, Monnier, A.A., additional, Ordies, S., additional, Averens, T., additional, Van den Broeck, K., additional, van de Veerdonk, W., additional, Franck, E., additional, De Mulder, P., additional, Desmet, P., additional, Bollaert, M., additional, Heyerick, L., additional, and Verbaeys, A., additional

Published
2023
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5. E-book: Public health - uitgave 2021

Author

Devriendt, T., primary, Shabani, M., additional, Borry, P., additional, Houf, K., additional, Van der Auwera, M., additional, Van Eygen, M., additional, Verhelst, D., additional, Lerut, E., additional, Wildemeersch, D., additional, De Schutter, I., additional, Bautmans, B., additional, Ravez, L., additional, Van den Broeck, K., additional, Werbrouck, A., additional, Annemans, L., additional, Verhaeghe, N., additional, Simoens, S., additional, Bouckaert, N., additional, Maertens de Noordhout, C., additional, Van de Voorde, C., additional, Criel, B., additional, and De Lepeleire, J., additional

Published
2022
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15. Hyperhomocysteinemia: a trigger for complement-mediated TMA?

Author

Bernards, J., Doubel, P., Meeus, G., Lerut, E., Corveleyn, A., Heuvel, L.P.W.J. van den, Meersseman, W., Kuypers, D.K., Claes, K.J., Bernards, J., Doubel, P., Meeus, G., Lerut, E., Corveleyn, A., Heuvel, L.P.W.J. van den, Meersseman, W., Kuypers, D.K., and Claes, K.J.

Abstract

Item does not contain fulltext, A 34-year-old man of North African descent was referred to the emergency department because of malignant hypertension (220/113 mmHg), acute visual disturbances and acute kidney failure (serum creatinine 14.0 mg/dL). Blood analysis was compatible with thrombotic microangiopathy (TMA). Kidney biopsy confirmed this diagnosis with histological changes including intimal edema, arteriolar thrombi, and severe tubulointerstitial damage. Fundoscopy showed hypertensive retinopathy stage IV. Subsequent biochemical screening revealed normal complement testing and a marked elevation in homocysteine concentration (161 µmol/L; normal value 7-15 µmol/L). Other secondary causes of TMA were excluded. Further genetic testing for cobalamin C (cblC) deficiency showed no pathogenic mutations in the MMACHC gene. However, a homozygous c.665C>T polymorphism (NM_005957.4) in the methylenetetrahydrofolate reductase (MTHFR) gene was found explaining the severe hyperhomocysteinemia due to reduced activity of MTHFR. Additional genetic testing for alternative complement pathway proteins showed mutations in the genes encoding factor H and factor B, both categorized as possibly pathogenic using mutation prediction software. This is the first described case of TMA in a patient with severe hyperhomocysteinemia caused by a genetic defect other than cblC. We postulate that endothelial damage due to hyperhomocysteinemia and hypertension could have triggered the TMA episode in this patient with two possible predisposing pathogenic mutations in the alternative complement pathway. Furthermore, our case demonstrates the need for complete full diagnostic testing in patients with TMA.

Published
2021

16. Banff 07 Classification of Renal Allograft Pathology: Updates and Future Directions

Author

Solez, K., Colvin, R.B., Racusen, L.C., Haas, M., Sis, B., Mengel, M., Halloran, P.F., Baldwin, W., Banfi, G., Collins, A.B., Cosio, F., David, D.S.R., Drachenberg, C., Einecke, G., Fogo, A.B., Gibson, I.W., Glotz, D., Iskandar, S.S., Kraus, E., Lerut, E., Mannon, R.B., Mihatsch, M., Nankivell, B.J., Nickeleit, V., Papadimitriou, J.C., Randhawa, P., Regele, H., Renaudin, K., Roberts, I., Seron, D., Smith, R.N., and Valente, M.

Published
2008
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31. Banff ʼ05 Meeting Report: Differential Diagnosis of Chronic Allograft Injury and Elimination of Chronic Allograft Nephropathy (‘CAN’)

Author

Solez, K., Colvin, R. B., Racusen, L. C., Sis, B., Halloran, P. F., Birk, P. E., Campbell, P. M., Cascalho, M., Collins, A. B., Demetris, A. J., Drachenberg, C. B., Gibson, I. W., Grimm, P. C., Haas, M., Lerut, E., Liapis, H., Mannon, R. B., Marcus, P. B., Mengel, M., Mihatsch, M. J., Nankivell, B. J., Nickeleit, V., Papadimitriou, J. C., Platt, J. L., Randhawa, P., Roberts, I., Salinas-Madriga, L., Salomon, D. R., Seron, D., Sheaff, M., and Weening, J. J.

Published
2007

39. Correlation between the location of the index tumour and the location of positive lymph nodes in high-risk prostate cancer. A monocentric positive lymph node mapping study

Author

Jacobs, B., primary, Vanneste, M., additional, Gevaert, T., additional, Laenen, A., additional, Van Den Broeck, T., additional, Moris, L., additional, Battaglia, A., additional, Albersen, M., additional, Claessens, F., additional, Lerut, E., additional, Haustermans, K., additional, Van Poppel, H., additional, De Meerleer, G., additional, Everaerts, W., additional, and Joniau, S., additional

Published
2018
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40. Tumor molecular characteristics in patients (pts) with international metastatic renal cell carcinoma database consortium (IMDC) good (G) and intermediate/poor (I/P) risk

Author

Beuselinck, B., primary, Verbiest, A., additional, Couchy, G., additional, Job, S., additional, de Reyniès, A., additional, Caruso, S., additional, Verkarre, V., additional, Rioux-Leclercq, N., additional, Schöffski, P., additional, Vano, Y., additional, Elaidi, R.-T., additional, Lerut, E., additional, Albersen, M., additional, Oudard, S., additional, and Zucman-Rossi, J., additional

Published
2018
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42. Hyperhomocysteinemia: a trigger for complement-mediated TMA?

Author

Bernards, J, Doubel, P, Meeus, G, Lerut, E, Corveleyn, A, Van Den Heuvel, L P, Meersseman, W, Kuypers, D K, and Claes, KJ

Abstract

ABSTRACTA 34-year-old man of North African descent was referred to the emergency department because of malignant hypertension (220/113 mmHg), acute visual disturbances and acute kidney failure (serum creatinine 14.0 mg/dL). Blood analysis was compatible with thrombotic microangiopathy (TMA). Kidney biopsy confirmed this diagnosis with histological changes including intimal edema, arteriolar thrombi, and severe tubulointerstitial damage. Fundoscopy showed hypertensive retinopathy stage IV. Subsequent biochemical screening revealed normal complement testing and a marked elevation in homocysteine concentration (161 µmol/L; normal value 7–15 µmol/L). Other secondary causes of TMA were excluded. Further genetic testing for cobalamin C (cblC) deficiency showed no pathogenic mutations in the MMACHC gene. However, a homozygous c.665C>Tpolymorphism (NM_005957.4) in the methylenetetrahydrofolate reductase (MTHFR) gene was found explaining the severe hyperhomocysteinemia due to reduced activity of MTHFR. Additional genetic testing for alternative complement pathway proteins showed mutations in the genes encoding factor H and factor B, both categorized as possibly pathogenic using mutation prediction software. This is the first described case of TMA in a patient with severe hyperhomocysteinemia caused by a genetic defect other than cblC. We postulate that endothelial damage due to hyperhomocysteinemia and hypertension could have triggered the TMA episode in this patient with two possible predisposing pathogenic mutations in the alternative complement pathway. Furthermore, our case demonstrates the need for complete full diagnostic testing in patients with TMA.

Published
2021
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43. Molecular subtypes of metastatic clear-cell renal cell carcinoma are associated with outcome after metastasectomy with curative intent

Author

Verbiest, A., primary, Couchy, G., additional, Job, S., additional, Zucman-Rossi, J., additional, Caruana, L., additional, Lerut, E., additional, Oyen, R., additional, De Reyniès, A., additional, Tosco, L., additional, Joniau, S., additional, Van Poppel, H., additional, Wozniak, A., additional, and Beuselinck, B., additional

Published
2017
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44. [OP.1B.01] VITAMIN K DEPENDENT PROTECTION OF RENAL FUNCTION IN MULTI-ETHNIC POPULATION STUDIES

Author

WEI, F., primary, Drummen, N.E.A., additional, Schutte, A.E., additional, Thijs, L., additional, Jacobs, L., additional, Petit, T., additional, Yang, W.Y., additional, Smith, W., additional, Zhang, Z.Y., additional, Gu, Y.M., additional, Kuznetsova, T., additional, Verhamme, P., additional, Allegaert, K., additional, Schutte, R., additional, Lerut, E., additional, Evenepoel, P., additional, Vermeer, C., additional, and Staessen, J.A., additional

Published
2016
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46. De novo INF2 mutations expand the genetic spectrum of hereditary neuropathy with glomerulopathy

Author

Mademan, I. Deconinck, T. Dinopoulos, A. Voit, T. Schara, U. Devriendt, K. Meijers, B. Lerut, E. Jonghe, P.D. Baets, J.

Subjects
congenital, hereditary, and neonatal diseases and abnormalities
Abstract

Objective: Identification of mutations in the inverted formin-2 (INF2) gene in patients with Charcot-Marie-Tooth (CMT) disease combined with focal segmental glomerulosclerosis (FSGS) in order to expand the genetic and phenotypic spectrum. Methods: We sequenced INF2 in 5 patients with CMT disease and FSGS. Mutations were subsequently screened in family members of the index patient and 264 control individuals. Results: In 3 patients, we detected 2 novel de novo INF2mutations (p.Leu77Arg and p.Leu69-Ser72-del) and a third, most likely de novo mutation (p.Gly114Asp). One of our patients displayed intellectual disability, a phenotypic characteristic not previously associated with INF2. The same patient also showed a more pronounced sensorineural hearing loss than described before. Conclusions: In exon 2 of INF2, we identified 3 novel mutations that likely affect the protein structure and function. Our findings expand the genetic spectrum of INF2-associated disorders and broaden the associated phenotype with the co-occurrence of intellectual disability and more severe hearing loss than previously reported. De novo INF2 mutations may be more common in patients with CMT disease and FSGS in comparison to FSGS alone. Furthermore, renal dysfunction is more severe and starts earlier in life when associated with CMT disease. Our study confirms that INF2 mutations are a major cause of disease in patients with CMT disease and early signs of nephropathy. Diagnostic screening of INF2 is strongly recommended in isolated patients presenting with CMT disease and FSGS. © 2013 American Academy of Neurology.

Published
2013

47. RANK/OPG ratio of expression in primary clear-cell renal cell carcinoma is associated with bone metastasis and prognosis in patients treated with anti-VEGFR-TKIs

Author

Beuselinck, B, primary, Jean-Baptiste, J, additional, Couchy, G, additional, Job, S, additional, De Reynies, A, additional, Wolter, P, additional, Théodore, C, additional, Gravis, G, additional, Rousseau, B, additional, Albiges, L, additional, Joniau, S, additional, Verkarre, V, additional, Lerut, E, additional, Patard, J J, additional, Schöffski, P, additional, Méjean, A, additional, Elaidi, R, additional, Oudard, S, additional, and Zucman-Rossi, J, additional

Published
2015
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