Editing Podocyte (section)

==Clinical significance==
[[File:Morphologic patterns of podocyte injury.jpg|thumb|300px|Morphologic patterns of podocyte injury.<ref>{{cite journal| author=Cutrim ÉMM, Neves PDMM, Campos MAG, Wanderley DC, Teixeira-Júnior AAL, Muniz MPR | display-authors=etal| title=Collapsing Glomerulopathy: A Review by the Collapsing Brazilian Consortium. | journal=Front Med (Lausanne) | year= 2022 | volume= 9 | issue=  | pages= 846173 | pmid=35308512 | doi=10.3389/fmed.2022.846173 | pmc=8927620 | doi-access=free}}<br>- [https://creativecommons.org/licenses/by/4.0/ CC-BY 4.0] license</ref>]]

A loss of the [[foot processes]] of the podocytes (i.e., podocyte effacement) is a hallmark of [[minimal change disease]], which has therefore sometimes been called foot process disease.<ref>{{cite journal | vauthors = Vivarelli M, Massella L, Ruggiero B, Emma F | title = Minimal Change Disease | journal = Clinical Journal of the American Society of Nephrology | volume = 12 | issue = 2 | pages = 332–345 | date = February 2017 | pmid = 27940460 | pmc = 5293332 | doi = 10.2215/CJN.05000516 }}</ref>

Disruption of the filtration slits or destruction of the podocytes can lead to massive [[proteinuria]], where large amounts of protein are lost from the blood.

An example of this occurs in the congenital disorder [[Finnish-type nephrosis]], which is characterised by neonatal proteinuria leading to end-stage [[kidney failure]]. This disease has been found to be caused by a mutation in the [[nephrin]] gene.

In 2002 Professor Moin Saleem at the University of Bristol made the first conditionally immortalised human podocyte cell line.<ref>{{Cite journal |last1=Saleem |first1=Moin A. |last2=O'Hare |first2=Michael J. |last3=Reiser |first3=Jochen |last4=Coward |first4=Richard J. |last5=Inward |first5=Carol D. |last6=Farren |first6=Timothy |last7=Xing |first7=Chang Ying |last8=Ni |first8=Lan |last9=Mathieson |first9=Peter W. |last10=Mundel |first10=Peter |date=March 2002 |title=A conditionally immortalized human podocyte cell line demonstrating nephrin and podocin expression |journal=Journal of the American Society of Nephrology |volume=13 |issue=3 |pages=630–638 |doi=10.1681/ASN.V133630 |issn=1046-6673 |pmid=11856766|doi-access=free }}</ref>{{Explain|date=January 2024}} This meant that podocytes could be grown and studied in the lab. Since then many discoveries have been made. Nephrotic syndrome occurs when there is a breakdown of the glomerular filtration barrier. The podocytes form one layer of the filtration barrier. Genetic mutations can cause podocyte dysfunction leading to an inability of the filtration barrier to restrict urinary protein loss. There are currently 53 genes known to play a role in genetic nephrotic syndrome.<ref>{{Cite journal |last1=Bierzynska |first1=Agnieszka |last2=McCarthy |first2=Hugh J. |last3=Soderquest |first3=Katrina |last4=Sen |first4=Ethan S. |last5=Colby |first5=Elizabeth |last6=Ding |first6=Wen Y. |last7=Nabhan |first7=Marwa M. |last8=Kerecuk |first8=Larissa |last9=Hegde |first9=Shivram |last10=Hughes |first10=David |last11=Marks |first11=Stephen |last12=Feather |first12=Sally |last13=Jones |first13=Caroline |last14=Webb |first14=Nicholas J. A. |last15=Ognjanovic |first15=Milos |date=April 2017 |title=Genomic and clinical profiling of a national nephrotic syndrome cohort advocates a precision medicine approach to disease management |url=https://pubmed.ncbi.nlm.nih.gov/28117080/ |journal=Kidney International |volume=91 |issue=4 |pages=937–947 |doi=10.1016/j.kint.2016.10.013 |issn=1523-1755 |pmid=28117080|s2cid=4768411 |hdl=1983/c730c0d6-5527-435a-8c27-a99fd990a0e8 |hdl-access=free }}</ref> In idiopathic nephrotic syndrome, there is no known genetic mutation. It is thought to be caused by a hitherto unknown circulating permeability factor.<ref>{{Cite journal |journal=Nephrology Dialysis Transplantation |url=https://academic.oup.com/ndt/article/29/12/2207/1853198 |title= Permeability factors in idiopathic nephrotic syndrome: historical perspectives and lessons for the future |date=2014 |doi=10.1093/ndt/gfu355 |doi-access=free |access-date=2023-04-26 |publisher=academic.oup.com |last1=Maas |first1=Rutger J. |last2=Deegens |first2=Jeroen K. |last3=Wetzels |first3=Jack F. |volume=29 |issue=12 |pages=2207–2216 |pmid=25416821 }}</ref> Recent evidence suggests that the factor could be released by T-cells or B-cells,<ref>{{Cite journal |last1=Hackl |first1=Agnes |last2=Zed |first2=Seif El Din Abo |last3=Diefenhardt |first3=Paul |last4=Binz-Lotter |first4=Julia |last5=Ehren |first5=Rasmus |last6=Weber |first6=Lutz Thorsten |date=2021-11-18 |title=The role of the immune system in idiopathic nephrotic syndrome |journal=Molecular and Cellular Pediatrics |volume=8 |issue=1 |pages=18 |doi=10.1186/s40348-021-00128-6 |issn=2194-7791 |pmc=8600105 |pmid=34792685 |doi-access=free }}</ref><ref>{{Cite journal |last1=May |first1=Carl J. |last2=Welsh |first2=Gavin I. |last3=Chesor |first3=Musleeha |last4=Lait |first4=Phillipa J. |last5=Schewitz-Bowers |first5=Lauren P. |last6=Lee |first6=Richard W. J. |last7=Saleem |first7=Moin A. |date=2019-10-01 |title=Human Th17 cells produce a soluble mediator that increases podocyte motility via signaling pathways that mimic PAR-1 activation |journal=American Journal of Physiology. Renal Physiology |volume=317 |issue=4 |pages=F913–F921 |doi=10.1152/ajprenal.00093.2019 |issn=1522-1466 |pmc=6843047 |pmid=31339775}}</ref> podocyte cell lines can be treated with plasma from patients with nephrotic syndrome to understand the specific responses of the podocyte to the circulating factor. There is growing evidence that the circulating factor could be signalling to the podocyte via the [[Proteinase-activated receptor 1|PAR-1 receptor]].<ref>{{Cite journal |last1=May |first1=Carl J. |last2=Chesor |first2=Musleeha |last3=Hunter |first3=Sarah E. |last4=Hayes |first4=Bryony |last5=Barr |first5=Rachel |last6=Roberts |first6=Tim |last7=Barrington |first7=Fern A. |last8=Farmer |first8=Louise |last9=Ni |first9=Lan |last10=Jackson |first10=Maisie |last11=Snethen |first11=Heidi |last12=Tavakolidakhrabadi |first12=Nadia |last13=Goldstone |first13=Max |last14=Gilbert |first14=Rodney |last15=Beesley |first15=Matt |date=March 2023 |title=Podocyte protease activated receptor 1 stimulation in mice produces focal segmental glomerulosclerosis mirroring human disease signaling events |journal=Kidney International |volume=104 |issue=2 |pages=265–278 |doi=10.1016/j.kint.2023.02.031 |pmid=36940798 |s2cid=257639270 |issn=0085-2538|doi-access=free |pmc=7616342 }}</ref>{{Explain|date=January 2024}}

Presence of podocytes in urine has been proposed as an early diagnostic marker for [[preeclampsia]].<ref>{{cite journal | vauthors = Konieczny A, Ryba M, Wartacz J, Czyżewska-Buczyńska A, Hruby Z, Witkiewicz W | title = Podocytes in urine, a novel biomarker of preeclampsia? | journal = Advances in Clinical and Experimental Medicine | volume = 22 | issue = 2 | pages = 145–149 | year = 2013 | pmid = 23709369 | url = http://www.advances.am.wroc.pl/pdf/2013/22/2/145.pdf }}</ref>