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Akt2 relaxes podocytes in chronic kidney disease

Nature Medicine volume 19, pages 1212–1213 (2013)Cite this article

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A signaling cascade is activated in podocytes to induce survival and cope with stress during advanced glomerular disease, a new study shows. The findings may also explain why the immunosuppressor sirolimus, an inhibitor of this pathway, can cause proteinuria in a subset of patients with chronic kidney disease (pages 1288–1296).

The loss of proteins into the urine, or proteinuria, often occurs at early stages of chronic kidney disease (CKD), a condition that affects about 500 million people worldwide, and this loss is a driver of both morbidity and mortality. Kidney podocytes are the gatekeepers in renal ultrafiltration, ensuring that proteins larger than albumin are essentially kept in the circulation and solutes and other aqueous products are being routed for excretion in the urine. Proteinuria occurs upon damage to podocytes that results in simplification of their foot processes, a term called effacement, which, if not reversed, can lead to loss of podocytes through detachment, necrosis and apoptosis1. After loss of a critical number of podocytes, progression of renal disease ensues with an increase in serum creatinine and loss of functional nephrons, which poses an additional overload in the remaining kidney cells, causing metabolic and mechanical stress and finally leading to their death. To date, effective therapies that completely halt or reverse the pathological changes resulting from advanced proteinuria and podocyte injury are still lacking.

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Figure 1: Podocyte function under conditions of nephron reduction.

Marina Corral Spence

References

  1. Reiser, J. & Sever, S. Annu. Rev. Med. 64, 357–366 (2013).

    Article  CAS  Google Scholar 

  2. Canaud, G. et al. Nat. Med. 19, 1288–1296 (2013).

    Article  CAS  Google Scholar 

  3. Wei, C. et al. Nat. Med. 14, 55–63 (2008).

    Article  CAS  Google Scholar 

  4. Nagase, M. & Fujita, T. Nat. Rev. Nephrol. 9, 86–98 (2013).

    Article  CAS  Google Scholar 

  5. Sarbassov, D.D. et al. Mol. Cell 22, 159–168 (2006).

    Article  CAS  Google Scholar 

  6. Laplante, M. & Sabatini, D.M. Cell 149, 274–293 (2012).

    Article  CAS  Google Scholar 

  7. Huber, T.B. et al. Mol. Cell Biol. 23, 4917–4928 (2003).

    Article  CAS  Google Scholar 

  8. Nozaki, S. et al. Cell Signal. 25, 1361–1371 (2013).

    Article  CAS  Google Scholar 

  9. Diekmann, F. et al. Transplant. Rev. (Orlando) 26, 27–29 (2012).

    Article  Google Scholar 

  10. Gödel, M. et al. J. Clin. Invest. 121, 2197–2209 (2011).

    Article  Google Scholar 

  11. Kistler, A.D. et al. Kidney Int. 81, 1053–1055 (2012).

    Article  CAS  Google Scholar 

  12. Yaddanapudi, S. et al. J. Clin. Invest. 121, 3965–3980 (2011).

    Article  CAS  Google Scholar 

Download references

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  1. Jochen Reiser is at the Department of Medicine, Rush University, Chicago, Illinois, USA.,

    Jochen Reiser

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  1. Jochen Reiser
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Correspondence to Jochen Reiser.

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Competing interests

J.R. is an inventor on issued and pending patents on new mechanisms and technologies for proteinuric kidney diseases. He stands to gain royalties from the commercialization of these technologies.

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Reiser, J. Akt2 relaxes podocytes in chronic kidney disease. Nat Med 19, 1212–1213 (2013). https://doi.org/10.1038/nm.3357

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