DOI QR코드

DOI QR Code

Urine synaptopodin excretion is an important marker of glomerular disease progression

  • Kwon, Soon Kil (Renal Division, Department of Internal Medicine, Chungbuk National University College of Medicine) ;
  • Kim, Seung Jung (Renal Division, Department of Internal Medicine, Chungbuk National University College of Medicine) ;
  • Kim, Hye-Young (Renal Division, Department of Internal Medicine, Chungbuk National University College of Medicine)
  • Received : 2015.07.18
  • Accepted : 2016.06.21
  • Published : 2016.09.01

Abstract

Background/Aims: Podocytes play an important role in maintaining the glomerular filtration barrier and in formation of the slit diaphragm. Podocyte loss is associated with chronic kidney disease progression, but it is not clear whether urinary podocyte proteins in urine reflect the clinical extent of glomerular damage. We investigated the correlation between the amounts of urinary podocyte proteins and renal function and albuminuria. Methods: The study enrolled 33 patients with diabetic kidney disease or glomerular disease and measured urinary podocytes proteins using Western blotting. Urinary podocyte proteins were measured according to the density of the bands on Western blotting. We measured serum creatinine and the spot urine albumin/creatinine ratio as markers of renal damage, and compared the correlation of urinary podocyte protein in the glomerular disease patients. Results: The mean patient age was $49.3{\pm}16.5years$, the mean serum creatinine level was $2.30{\pm}1.76mg/dL$, and the mean albumin/creatinine ratio was $4.85{\pm}3.52$. Among the podocyte proteins, urine synaptopodin showed strong correlation with serum creatinine by multivariate regression analysis (p < 0.001) and showed linear correlation (r = 0.429, p < 0.01). Urine podocyte proteins were increased in patients with diabetes, and synaptopodin showed the greatest significant difference ($7.68{\pm}5.61$ vs. $2.56{\pm}3.11$, p < 0.001), but this might be associated with renal impairment. The urine albumin excretion did not differ between the diabetics and non-diabetics (p = 0.73). Conclusions: Urine synaptopodin is associated with serum creatinine elevation in the patients with glomerulonephritis including diabetic kidney disease regardless of urine albumin excretion. We suggest that the urine synaptopodin level can predict glomerular damage independently of the urine albumin excretion.

Keywords

Acknowledgement

Supported by : Chungbuk National University

References

  1. Rutherford WE, Blondin J, Miller JP, Greenwalt AS, Vavra JD. Chronic progressive renal disease: rate of change of serum creatinine concentration. Kidney Int 1977;11:62-70. https://doi.org/10.1038/ki.1977.8
  2. Fornoni A. Proteinuria, the podocyte, and insulin resistance. N Engl J Med 2010;363:2068-2069. https://doi.org/10.1056/NEJMcibr1008395
  3. Toyoda M, Najafian B, Kim Y, Caramori ML, Mauer M. Podocyte detachment and reduced glomerular capillary endothelial fenestration in human type 1 diabetic nephropathy. Diabetes 2007;56:2155-2160. https://doi.org/10.2337/db07-0019
  4. Yu D, Petermann A, Kunter U, Rong S, Shankland SJ, Floege J. Urinary podocyte loss is a more specific marker of ongoing glomerular damage than proteinuria. J Am Soc Nephrol 2005;16:1733-1741. https://doi.org/10.1681/ASN.2005020159
  5. Zheng M, Lv LL, Ni J, et al. Urinary podocyte-associated mRNA profile in various stages of diabetic nephropathy. PLoS One 2011;6:e20431. https://doi.org/10.1371/journal.pone.0020431
  6. Asanuma K, Yanagida-Asanuma E, Faul C, Tomino Y, Kim K, Mundel P. Synaptopodin orchestrates actin organization and cell motility via regulation of RhoA signalling. Nat Cell Biol 2006;8:485-491. https://doi.org/10.1038/ncb1400
  7. Faul C, Donnelly M, Merscher-Gomez S, Chang YH, Franz S, Delfgaauw J, et al. The actin cytoskeleton of kidney podocytes is a direct target of the antiproteinuric effect of cyclosporine A. Nat Med 2008;14:931-938. https://doi.org/10.1038/nm.1857
  8. Pugliese G. Updating the natural history of diabetic nephropathy. Acta Diabetol 2014;51:905-915. https://doi.org/10.1007/s00592-014-0650-7
  9. Jim B, Ghanta M, Qipo A, et al. Dysregulated nephrin in diabetic nephropathy of type 2 diabetes: a cross sectional study. PLoS One 2012;7:e36041. https://doi.org/10.1371/journal.pone.0036041
  10. Lewis EJ, Hunsicker LG, Clarke WR, et al. Renoprotective effect of the angiotensin-receptor antagonist irbesartan in patients with nephropathy due to type 2 diabetes. N Engl J Med 2001;345:851-860. https://doi.org/10.1056/NEJMoa011303
  11. Byun JM, Lee CH, Lee SR, et al. Renal outcomes and clinical course of nondiabetic renal diseases in patients with type 2 diabetes. Korean J Intern Med 2013;28:565-572. https://doi.org/10.3904/kjim.2013.28.5.565

Cited by

  1. Proteinuric Kidney Diseases: A Podocyte's Slit Diaphragm and Cytoskeleton Approach vol.5, pp.None, 2016, https://doi.org/10.3389/fmed.2018.00221
  2. Podocyturia: why it may have added value in rare diseases vol.12, pp.1, 2019, https://doi.org/10.1093/ckj/sfy081
  3. Change in Renal Glomerular Collagens and Glomerular Filtration Barrier-Related Proteins in a Dextran Sulfate Sodium-Induced Colitis Mouse Model vol.20, pp.6, 2016, https://doi.org/10.3390/ijms20061458
  4. A novel splicing variant of small nucleolar RNA host gene 4 is a podocyte-selective non-coding RNA upregulated in response to puromycin aminonucleoside-induced podocyte injury vol.165, pp.5, 2019, https://doi.org/10.1093/jb/mvy118
  5. Immunochromatographic assay to detect α‐tubulin in urine for the diagnosis of kidney injury vol.34, pp.1, 2016, https://doi.org/10.1002/jcla.23015
  6. Spatio-temporal patterning of different connexins in developing and postnatal human kidneys and in nephrotic syndrome of the Finnish type (CNF) vol.10, pp.None, 2016, https://doi.org/10.1038/s41598-020-65777-5
  7. A Review of Specific Biomarkers of Chronic Renal Injury and Their Potential Application in Nonclinical Safety Assessment Studies vol.49, pp.5, 2016, https://doi.org/10.1177/0192623320985045
  8. Urinary podocyte markers in kidney diseases vol.523, pp.None, 2021, https://doi.org/10.1016/j.cca.2021.10.017