nach oben

Erschienen in:

01.02.2016 | Original Article

Urinary podocalyxin, the novel biomarker for detecting early renal change in obesity

verfasst von: Chayanut Suwanpen, Phonethipsavanh Nouanthong, Veeravich Jaruvongvanich, Krit Pongpirul, Wannarat Amornnimit Pongpirul, Asada Leelahavanichkul, Talerngsak Kanjanabuch

Erschienen in: Journal of Nephrology | Ausgabe 1/2016

Einloggen, um Zugang zu erhalten

Abstract

Background

The prevalence of obesity is increasing during the past decade along with obesity-related glomerulopathy (ORG), glomeruli injury due to the obesity. The major pathogenesis of ORG is the shedding of podocytes from the glomerular cell barrier into urine. Podocalyxin (PCX), a main surface antigen of podocyte, correlates well with glomerulosclerosis progression and glomerular injury severity, and might be a potential biomarker for early renal alteration in obesity. In addition, vascular endothelial growth factor (VEGF) and alpha-smooth muscle actin (α-SMA) also play a role in promoting glomerulosclerosis. The aim of this study was to explore whether obese subjects without other diseases excrete more PCX-positive (PCX+) cells than non-obese individuals, in comparison with urine protein-creatinine ratio (UPCR) and glomerular filtration rate (GFR) as traditional renal markers. Moreover, the effect of body mass index (BMI) on urinary VEGF, PCX or α-SMA positive cells was also investigated.

Methods

Forty-eight obese and 13 non-obese adults were included. Exfoliated cells from fresh first void morning urine were harvested, stained with PCX, VEGF, and α-SMA antibody, and quantified by flow cytometry. Correlation between interested urinary biomarkers (cells positive for PCX, VEGF plus PCX and α-SMA), UPCR and GFR with BMI and metabolic risk factors were analyzed.

Results

Obese patients had significantly higher PCX+ cells than non-obese [0.62 (0.00–13.13) vs. 0.15 (0.00–0.72) cells/ml × mg cr, p < 0.05]. There was no significant difference in GFR and UPCR between the groups. Of interest, BMI demonstrated a correlation with PCX+ cells (r = 0.343, p = 0.008) and cells positive for PCX plus VEGF (r = 0.374, p = 0.004).

Conclusion

Obese subjects without other diseases and with normal UPCR and GFR showed evidence of renal alteration through the detection of a higher number of PCX+ cells. Increasing BMI also resulted in higher number of PCX+ cells.

Drumond MC, Deen WM (1994) Structural determinants of glomerular hydraulic permeability. Am J Physiol 266:F1–F12PubMed

Kriz W (2002) Podocyte is the major culprit accounting for the progression of chronic renal disease. Microsc Res Tech 57:189–195PubMedCrossRef

Shankland SJ, Pippin JW, Duffield JS (2014) Progenitor cells and podocyte regeneration. Semin Nephrol 34:418–428PubMedPubMedCentralCrossRef

Petermann A, Floege J (2007) Podocyte damage resulting in podocyturia: a potential diagnostic marker to assess glomerular disease activity. Nephron Clin Pract 106:c61–c66PubMedCrossRef

Vogelmann SU, Nelson WJ, Myers BD, Lemley KV (2003) Urinary excretion of viable podocytes in health and renal disease. Am J Physiol Ren Physiol 285:F40–F48CrossRef

Doyonnas R, Kershaw DB, Duhme C, Merkens H, Chelliah S, Graf T et al (2001) Anuria, omphalocele, and perinatal lethality in mice lacking the CD34-related protein podocalyxin. J Exp Med 194:13–27PubMedPubMedCentralCrossRef

Skoberne A, Konieczny A, Schiffer M (2009) Glomerular epithelial cells in the urine: what has to be done to make them worthwhile? Am J Physiol Ren Physiol 296:F230–F241CrossRef

Barisoni L, Kriz W, Mundel P, D’Agati V (1999) The dysregulated podocyte phenotype: a novel concept in the pathogenesis of collapsing idiopathic focal segmental glomerulosclerosis and HIV-associated nephropathy. J Am Soc Nephrol 10:51–61PubMed

Hara M, Yanagihara T, Takada T, Itoh M, Matsuno M, Yamamoto T et al (1998) Urinary excretion of podocytes reflects disease activity in children with glomerulonephritis. Am J Nephrol 18:35–41PubMedCrossRef

10.

Hara M, Yanagihara T, Kihara I (2001) Urinary podocytes in primary focal segmental glomerulosclerosis. Nephron 89:342–347PubMedCrossRef

11.

Achenbach J, Mengel M, Tossidou I, Peters I, Park JK, Haubitz M et al (2008) Parietal epithelia cells in the urine as a marker of disease activity in glomerular diseases. Nephrol Dial Transpl 23:3138–3145CrossRef

12.

Hara M, Yanagihara T, Kihara I (2007) Cumulative excretion of urinary podocytes reflects disease progression in IgA nephropathy and Schonlein-Henoch purpura nephritis. Clin J Am Soc Nephrol 2:231–238PubMedCrossRef

13.

World Health Organization (2014) Obesity and overweight

14.

Snyder S, Turner GA, Turner A (2014) Obesity-related kidney disease. Prim Care 41:875–893PubMedCrossRef

15.

Kambham N, Markowitz GS, Valeri AM, Lin J, D’Agati VD (2001) Obesity-related glomerulopathy: an emerging epidemic. Kidney Int 59:1498–1509PubMedCrossRef

16.

Darouich S, Goucha R, Jaafoura MH, Zekri S, Ben Maiz H, Kheder A (2011) Clinicopathological characteristics of obesity-associated focal segmental glomerulosclerosis. Ultrastruct Pathol 35:176–182PubMedCrossRef

17.

Ziyadeh FN, Wolf G (2008) Pathogenesis of the podocytopathy and proteinuria in diabetic glomerulopathy. Curr Diabetes Rev 4:39–45PubMedCrossRef

18.

Tomasek JJ, Gabbiani G, Hinz B, Chaponnier C, Brown RA (2002) Myofibroblasts and mechano-regulation of connective tissue remodelling. Nat Rev Mol Cell Biol 3:349–363PubMedCrossRef

19.

Muchaneta-Kubara EC, el Nahas AM (1997) Myofibroblast phenotypes expression in experimental renal scarring. Nephrol Dial Transpl 12:904–915CrossRef

20.

Weisell RC (2002) Body mass index as an indicator of obesity. Asia Pacific J Clin Nutr 11(Suppl 8):S681–S684CrossRef

21.

Levey AS, Coresh J, Greene T, Marsh J, Stevens LA, Kusek JW et al (2007) Expressing the modification of diet in renal disease study equation for estimating glomerular filtration rate with standardized serum creatinine values. Clin Chem 53:766–772PubMedCrossRef

22.

Schwab SJ, Christensen RL, Dougherty K, Klahr S (1987) Quantitation of proteinuria by the use of protein-to-creatinine ratios in single urine samples. Arch Intern Med 147:943–944PubMedCrossRef

23.

Kanno K, Kawachi H, Uchida Y, Hara M, Shimizu F, Uchiyama M (2003) Urinary sediment podocalyxin in children with glomerular diseases. Nephron Clin Pract 95:c91–c99PubMedCrossRef

24.

Ye H, Bai X, Gao H, Li L, Wu C, Sun X et al (2014) Urinary podocalyxin positive-element occurs in the early stage of diabetic nephropathy and is correlated with a clinical diagnosis of diabetic nephropathy. J Diabetes Complicat 28:96–100PubMedCrossRef

25.

Akakabe Y, Koide M, Kitamura Y, Matsuo K, Ueyama T, Matoba S et al (2013) Ecscr regulates insulin sensitivity and predisposition to obesity by modulating endothelial cell functions. Nat Commun 4:2389PubMedCrossRef

26.

Barton M, Baretella O, Meyer MR (2012) Obesity and risk of vascular disease: importance of endothelium-dependent vasoconstriction. Br J Pharmacol 165:591–602PubMedPubMedCentralCrossRef

27.

Ritz E, Koleganova N, Piecha G (2011) Is there an obesity-metabolic syndrome related glomerulopathy? Curr Opin Nephrol Hypertens 20:44–49PubMedCrossRef

28.

Ritz E (2008) Metabolic syndrome and kidney disease. Blood Purif 26:59–62PubMedCrossRef

29.

Shen WW, Chen HM, Chen H, Xu F, Li LS, Liu ZH (2010) Obesity-related glomerulopathy: body mass index and proteinuria. Clin J Am Soc Nephrol 5:1401–1409PubMedPubMedCentralCrossRef

30.

Camici M (2008) Urinary biomarkers of podocyte injury. Biomark Med 2:613–616PubMedCrossRef

31.

Zhu B, Li XF, Zhu XL, Lin Y, Zhong S, Zhu CF et al (2014) ELISA analysis of urinary nephrin and podocalyxin standardized by aquaporin-2 in adult patients with nephrotic syndrome. J Nephrol 27:411–417PubMedCrossRef

32.

Habara P, Mareckova H, Sopkova Z, Malickova K, Zivorova D, Zima T et al (2008) A novel method for the estimation of podocyte injury: podocalyxin-positive elements in urine. Folia Biol 54:162–167

33.

Habara P, Mareckova H, Malickova K, Potysova Z, Hruskova Z, Zima T et al (2012) Novel flow cytometric method for the detection of podocalyxin-positive elements in urine of patients with glomerulonephritides—first promising results. Folia Biol 58:57–63

Titel: Urinary podocalyxin, the novel biomarker for detecting early renal change in obesity
verfasst von: Chayanut Suwanpen
Phonethipsavanh Nouanthong
Veeravich Jaruvongvanich
Krit Pongpirul
Wannarat Amornnimit Pongpirul
Asada Leelahavanichkul
Talerngsak Kanjanabuch
Publikationsdatum: 01.02.2016
Verlag: Springer International Publishing
Erschienen in: Journal of Nephrology / Ausgabe 1/2016
Print ISSN: 1121-8428
Elektronische ISSN: 1724-6059
DOI: https://doi.org/10.1007/s40620-015-0199-8

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

^{Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag}

Kostenlos registrieren

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.

Newsletter bestellen

Live-Webinar "Urologie und Sexualmedizin in der Praxis"

Springer Medizin

Urinary podocalyxin, the novel biomarker for detecting early renal change in obesity