Cell hypertrophy is the only mechanism by which podocytes can cope with increased functional demands, whereas other glomerular cells can adapt by cell proliferation. In the setting of systemically stimulated glomerular growth, a 'mismatch' of inadequate podocyte hypertrophy and overall glomerular growth may lead to podocyte loss and development of focal segmental glomerulosclerosis.
This is a preview of subscription content, access via your institution
Relevant articles
Open Access articles citing this article.
-
Sex- and age-related differences in renal and cardiac injury and senescence in stroke-prone spontaneously hypertensive rats
Biology of Sex Differences Open Access 22 May 2023
-
Podocyte number and density changes during early human life
Pediatric Nephrology Open Access 27 December 2016
-
Regenerative medicine for the kidney: stem cell prospects & challenges
Clinical and Translational Medicine Open Access 21 May 2013
Access options
Subscribe to this journal
Receive 12 print issues and online access
$209.00 per year
only $17.42 per issue
Buy this article
- Purchase on Springer Link
- Instant access to full article PDF
Prices may be subject to local taxes which are calculated during checkout
References
Kriz, W., Gretz, N. & Lemley, K. V. Progression of glomerular diseases: is the podocyte the culprit? Kidney Int. 54, 687–697 (1998).
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).
Brenner, B. M. Nephron adaptation to renal injury or ablation. Am. J. Physiol. 249, F324–F337 (1985).
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).
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).
Fukuda, A. et al. Growth-dependent podocyte failure causes glomerulosclerosis. J. Am. Soc. Nephrol. 23, 1351–1363 (2012).
Kriz, W. & LeHir, M. Pathways to nephron loss starting from glomerular diseases—insights from animal models. Kidney Int. 67, 404–419 (2005).
Nagata, M. & Kriz, W. Glomerular damage after uninephrectomy in young rats. II. Mechanical stress on podocytes as a pathway to sclerosis. Kidney Int. 42, 148–160 (1992).
Eremina, V. & Quaggin, S. E. The role of VEGF-A in glomerular development and function. Curr. Opin. Nephrol. Hypertens. 13, 9–15 (2004).
Hughson, M. D., Hoy, W. E., Douglas-Denton, R. N., Zimanyi, M. A. & Bertram, J. F. Towards a definition of glomerulomegaly: clinical-pathological and methodological considerations. Nephrol. Dial. Transplant. 26, 2202–2208 (2011).
Acknowledgements
The author wishes to thank K. Lemley for critical reading of the text. The author's work cited in this commentary was supported by Deutsche Forschungsgemeinschaft and Prof. Dr Karl and Gerhard Schiller-Stiftung.
Author information
Authors and Affiliations
Ethics declarations
Competing interests
The author declares no competing financial interests.
Rights and permissions
About this article
Cite this article
Kriz, W. Podocyte hypertrophy mismatch and glomerular disease. Nat Rev Nephrol 8, 618–619 (2012). https://doi.org/10.1038/nrneph.2012.198
Published:
Issue Date:
DOI: https://doi.org/10.1038/nrneph.2012.198
This article is cited by
-
Sex- and age-related differences in renal and cardiac injury and senescence in stroke-prone spontaneously hypertensive rats
Biology of Sex Differences (2023)
-
Podocyte number and density changes during early human life
Pediatric Nephrology (2017)
-
Quantifying podocyte depletion: theoretical and practical considerations
Cell and Tissue Research (2017)
-
Putting the glomerulus back together: per aspera ad astra (“a rough road leads to the stars”)
Kidney International (2014)
-
Oxidative Stress and Organ Damages
Current Hypertension Reports (2014)
