Skip to main content

Advertisement

SpringerLink
Log in

Glomerular diseases

Podocyte hypertrophy mismatch and glomerular disease

  • News & Views
  • Published:

From Nature Reviews Nephrology

View current issue Sign up to alerts

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, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

References

  1. Kriz, W., Gretz, N. & Lemley, K. V. Progression of glomerular diseases: is the podocyte the culprit? Kidney Int. 54, 687–697 (1998).

    Article  CAS  Google Scholar 

  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).

    Article  CAS  Google Scholar 

  3. Brenner, B. M. Nephron adaptation to renal injury or ablation. Am. J. Physiol. 249, F324–F337 (1985).

    CAS  PubMed  Google Scholar 

  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).

    Article  CAS  Google Scholar 

  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).

    Article  CAS  Google Scholar 

  6. Fukuda, A. et al. Growth-dependent podocyte failure causes glomerulosclerosis. J. Am. Soc. Nephrol. 23, 1351–1363 (2012).

    Article  CAS  Google Scholar 

  7. Kriz, W. & LeHir, M. Pathways to nephron loss starting from glomerular diseases—insights from animal models. Kidney Int. 67, 404–419 (2005).

    Article  Google Scholar 

  8. 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).

    Article  CAS  Google Scholar 

  9. Eremina, V. & Quaggin, S. E. The role of VEGF-A in glomerular development and function. Curr. Opin. Nephrol. Hypertens. 13, 9–15 (2004).

    Article  CAS  Google Scholar 

  10. 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).

    Article  Google Scholar 

Download references

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

  1. Department of Anatomy and Developmental Biology, Medical Faculty Mannheim, University of Heidelberg, Ludolf-Krehl-Strasse 13–17, Tridomus C/6, Mannheim, D-68167, Germany

    Wilhelm Kriz

Authors
  1. Wilhelm Kriz
    View author publications

    You can also search for this author in PubMed Google Scholar

Ethics declarations

Competing interests

The author declares no competing financial interests.

Rights and permissions

Reprints 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

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/nrneph.2012.198

  • Springer Nature Limited

Search

Navigation