Felix G. Riepe
Division of Paediatric Endocrinology
Department of Paediatrics
Christian Albrechts Universität zu Kiel
Germany
Name/email consistency: high
- Revealing a subclinical salt-losing phenotype in heterozygous carriers of the novel S562P mutation in the alpha subunit of the epithelial sodium channel. Riepe, F.G., van Bemmelen, M.X., Cachat, F., Plendl, H., Gautschi, I., Krone, N., Holterhus, P.M., Theintz, G., Schild, L. Clin. Endocrinol. (Oxf) (2009)
- Clinical and molecular features of type 1 pseudohypoaldosteronism. Riepe, F.G. Horm. Res. (2009)
- Functional and structural consequences of a novel point mutation in the CYP21A2 gene causing congenital adrenal hyperplasia: potential relevance of helix C for P450 oxidoreductase-21-hydroxylase interaction. Riepe, F.G., Hiort, O., Grötzinger, J., Sippell, W.G., Krone, N., Holterhus, P.M. J. Clin. Endocrinol. Metab. (2008)
- Recent advances in diagnosis, treatment, and outcome of congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Riepe, F.G., Sippell, W.G. Rev. Endocr. Metab. Disord (2007)
- Exclusion of serum- and glucocorticoid-induced kinase 1 (SGK1) as a candidate gene for genetically heterogeneous renal pseudohypoaldosteronism type I in eight families. Riepe, F.G., Holterhus, P.M. Am. J. Nephrol. (2007)
- Absence of exercise-induced leptin suppression associated with insufficient epinephrine reserve in patients with classic congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Riepe, F.G., Krone, N., Krüger, S.N., Sweep, F.C., Lenders, J.W., Dötsch, J., Mönig, H., Sippell, W.G., Partsch, C.J. Exp. Clin. Endocrinol. Diabetes (2006)
- Elucidating the underlying molecular pathogenesis of NR3C2 mutants causing autosomal dominant pseudohypoaldosteronism type 1. Riepe, F.G., Finkeldei, J., de Sanctis, L., Einaudi, S., Testa, A., Karges, B., Peter, M., Viemann, M., Grötzinger, J., Sippell, W.G., Fejes-Toth, G., Krone, N. J. Clin. Endocrinol. Metab. (2006)
- Autosomal-dominant pseudohypoaldosteronism type 1 in a Turkish family is associated with a novel nonsense mutation in the human mineralocorticoid receptor gene. Riepe, F.G., Krone, N., Morlot, M., Peter, M., Sippell, W.G., Partsch, C.J. J. Clin. Endocrinol. Metab. (2004)