Podocyte hypertrophy mismatch and glomerular disease
Author:
Publisher
Springer Science and Business Media LLC
Subject
Nephrology
Link
http://www.nature.com/articles/nrneph.2012.198.pdf
Reference10 articles.
1. Kriz, W., Gretz, N. & Lemley, K. V. Progression of glomerular diseases: is the podocyte the culprit? Kidney Int. 54, 687–697 (1998).
2. Kriz, W., Hähnel, B., Rösener, S. & Elger, M. Long-term treatment of rats with FGF-2 results in focal segmental glomerulosclerosis. Kidney Int. 48, 1435–1450 (1995).
3. Brenner, B. M. Nephron adaptation to renal injury or ablation. Am. J. Physiol. 249, F324–F337 (1985).
4. Vogelmann, S. U., Nelson, W. J., Myers, B. D. & Lemley, K. V. Urinary excretion of viable podocytes in health and renal disease. Am. J. Physiol. Renal Physiol. 285, F40–F48 (2003).
5. Hara, M., Yanagihara, T. & Kihara, I. Cumulative excretion of urinary podocytes reflects disease progression in IgA nephropathy and Schönlein-Henoch purpura nephritis. Clin. J. Am. Soc. Nephrol. 2, 231–238 (2007).
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