ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2022 and some content may be unavailable. To unlock all content for 2022, please visit the archives.

Abstract: TH-PO430

Study of Profile of Urinary TGF-β1 in Glomerular Diseases

Session Information

Category: Glomerular Diseases

  • 1301 Glomerular Diseases: Fibrosis and Extracellular Matrix

Authors

  • Kulkarni, Akshay Rajiv, Dr. D.Y. Patil Medical College, Hospital & Research Centre, Pimpri, Pune, Dr. D. Y. Patil Vidyapeeth, Pune, India
  • Sajgure, Atul, Dr. D.Y. Patil Medical College, Hospital & Research Centre, Pimpri, Pune, Dr. D. Y. Patil Vidyapeeth, Pune, India
  • Bale, Charan Bhadrappa, Dr. D.Y. Patil Medical College, Hospital & Research Centre, Pimpri, Pune, Dr. D. Y. Patil Vidyapeeth, Pune, India
  • Wakhare, Pavan, Dr. D.Y. Patil Medical College, Hospital & Research Centre, Pimpri, Pune, Dr. D. Y. Patil Vidyapeeth, Pune, India
  • Shinde, Nilesh, Dr. D.Y. Patil Medical College, Hospital & Research Centre, Pimpri, Pune, Dr. D. Y. Patil Vidyapeeth, Pune, India
  • Chavan, Abhijit Suresh, Dr. D.Y. Patil Medical College, Hospital & Research Centre, Pimpri, Pune, Dr. D. Y. Patil Vidyapeeth, Pune, India
  • Dighe, Tushar Anil, Dr. D.Y. Patil Medical College, Hospital & Research Centre, Pimpri, Pune, Dr. D. Y. Patil Vidyapeeth, Pune, India
Background

Transforming Growth Factor-β1(TGF-β1) is associated with fibrosis in many organ systems including the kidney, where it can be induced by angiotensin, proteinuria and hypoxia. Numerous studies have identified TGF-β1 as being upregulated during the course of progressive renal injury. Similarly, inhibition of TGF-β1 has been shown to ameliorate renal injury. TGF-β1 is not only involved in extra cellular matrix accumulation, fibrosis and progressive renal impairment, but also plays a role in changes to the glomerular filtration barrier and induction of proteinuria. Direct inhibition of TGF-β1 in models of renal disease reduces proteinuria. Our study aimed to study the profile of urinary TGF-β1 in glomerular diseases.

Methods

It was a prospective, observational study, done at a tertiary care centre in western India, over a period of 1 year. 15 subjects with biopsy proven glomerular diseases and 5 healthy controls were enrolled in the study. These particpants underwent all routine laboratory investigations and urinary TGF-β1 estimation on a 24 hour urine sample by Flowcytometry method. Cytometric array capture beads of 20 ul were mixed in 20 ul of urine in 1.5 ml tubes. After mixing, samples were incubated at room temperature for 2 hours. After incubation, 50 ul phosphate Buffered Saline was added and centrifuged at 5000 rpm for 5 mins. After centrifugation, 70 ul volume was removed. In the sample 20 ul Detection beads were added and samples were incubated for 2 hours. After incubation 160 ul buffer was added and samples were analyzed using multicolor flowcytometry. Every sample was processed thrice and average value (pg/ml) was considered for analysis of all the subjects.

Results

Of the 20 study participants, 11 were males and 9 were females. Average age in glomerular disease patients (group A) was 35.73± 14.25 years and that in control group(group B) was 30.2±5.02 years. Urinary TGF-β1 level in group A had mean value of 50.35 ±6.52(pg/ml) , while that in group B was 19.29 ±3.48 (pg/ml). The values for TGF-β1 in test samples(group A) were found significantly higher in comparison to control( group B). (p<0.0001). Mean value of UPCR was 5.50 ±5.11 in group A and 0.17±0.11 in group B.

Conclusion

Urinary TGF-β1 levels were significantly high in glomerular disease patients compared to healthy individuals.