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Increased chymase-positive mast cells in children with crescentic glomerulonephritis

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Abstract

Mast cell-derived chymase is an angiotensin II-forming enzyme that appears to be involved in tubulointerstitial fibrosis in the kidneys. Previous studies have shown that the level of chymase increases in grafted kidneys after rejection and in adult patients with diabetic nephropathy. However, the significance of chymase in children with renal diseases has not been investigated. Using immunohistochemistry, we have investigated chymase expression in biopsy samples of renal tissue from 104 children with kidney diseases, including rapidly progressive crescentic glomerulonephritis (n = 3), diabetic nephropathy (n = 2), allografted kidney (n = 3), membranoproliferative glomerulonephritis (n = 6), immunoglobulin A nephropathy (n = 33) and Henoch–Schönlein purpura nephritis (n = 23). Increased numbers of chymase-positive mast cells were observed in the renal cortex of all three patients with crescentic glomerulonephritis (mean 26.0/mm2; range 19.3–36.8/mm2). Chymase-positive cells were also observed in the renal biopsy of an allografted kidney and in those from children with diabetic nephropathy. The mean number of chymase-positive cells in renal tissue samples characterized by each renal disease was significantly correlated with the mean intensity of the interstitial fibrosis in that same tissue sample (Spearman’s rank correlation test p = 0.0013; rank correlation coefficient  0.84). These findings suggest that mast cell-derived chymase plays an important role in juvenile crescentic glomerulonephritis.

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References

  1. Yamada M, Ueda M, Naruko T, Tanabe S, Han YS, Ikura Y, Ogami M, Takai S, Miyazaki M (2001) Mast cell chymase expression and mast cell phenotypes in human rejected kidneys. Kidney Int 59:1374–1381

    Article  CAS  Google Scholar 

  2. Ritz E (2003) Chymase: a potential culprit in diabetic nephropathy? J Am Soc Nephrol 14:1738–1747

    Article  Google Scholar 

  3. Huang XR, Chen WY, Truong LD, Lan HY (2003) Chymase is upregulated in diabetic nephropathy: implications for an alternative pathway of angiotensin II-mediated diabetic renal and vascular disease. J Am Soc Nephrol 14:1738–1747

    Article  CAS  Google Scholar 

  4. Miyake-Ogawa C, Miyazaki M, Abe K, Harada T, Ozono Y, Sakai H, Koji T, Kohno S (2005) Tissue-specific expression of renin-angiotensin system components in IgA nephropathy. Am J Nephrol 25:1–12

    Article  CAS  Google Scholar 

  5. Racusen LC, Solez K, Colvin RB, Bonsib SM, Castro MC, Cavallo T, Croker BP, Demetris AJ, Drachenberg CB, Fogo AB, Furness P, Gaber LW, Gibson IW, Glotz D, Goldberg JC, Grande J, Halloran PF, Hansen HE, Hartley B, Hayry PJ, Hill CM, Hoffman EO, Hunsicker LG, Lindblad AS, Marcussen N, Mihatsch MJ, Nadasdy T, Nickerson P, Olsen ST, Papadimitriou JC, Randhawa PS, Rayner DC, Roberts I, Rose S, Rush D, Salinas-Madrigal L, Salomon DR, Sund S, Taskinen E, Trpkiv K, Yamaguchi Y (1999) The Banff 97 working classification of renal allograft pathology. Kidney Int 55:713–723

    Article  CAS  Google Scholar 

  6. Churg J, Bernstein J, Glassock RJ (1995) Renal disease: classification and atlas of glomerular diseases, 2nd edn. Igaku-shoin Medical Publishers Tokyo

  7. Yoshikawa N, Nakanishi K, Iijima K (2001) Henoch-Schönlein purpura. In: Neilson EG, Couser WG (eds) Immunologic renal diseases, 2nd edn. Lippincott Williams & Wilkins, Philadelphia, pp 1127–1140

    Google Scholar 

  8. Tóth T, Tóth-Jakatics R, Jimi S, Ihara M, Urata H, Takebayashi S (1999) Mast cells in rapidly progressive glomerulonephritis. J Am Soc Nephrol 10:1498–1505

    PubMed  Google Scholar 

  9. Ehara T, Shigematsu H (1998) Contribution of mast cells to the tubulointerstitial lesions in IgA nephritis. Kidney Int 54:1675–1683

    Article  CAS  Google Scholar 

  10. Ikezumi Y, Suzuki T, Imai N, Ueno M, Narita I, Kawachi H, Shimizu F, Nikolic-Paterson DJ, Uchiyama M (2006) Histological differences in new-onset IgA nephropathy between children and adults. Nephrol Dial Transplant 21:3466–3474

    Article  Google Scholar 

  11. Blank U, Essig M, Scandiuzzi L, Benhamou M, Kanamaru Y (2007) Mast cells and inflammatory kidney disease. Immunol Rev 217:79–95

    Article  CAS  Google Scholar 

  12. Tchougounova E, Lundequist A, Fajardo I, Winberg JO, Abrink M, Pejler G (2005) A key role for mast cell chymase in the activation of pro-matrix metalloprotease-9 and pro-matrix metalloprotease-2. J Biol Chem 280:9291–9296

    Article  CAS  Google Scholar 

  13. Hollenberg NK, Fisher ND, Price DA (1998) Pathways for angiotensin II generation in intact human tissue: evidence from comparative pharmacological interruption of the renin system. Hypertension 32:387–392

    Article  CAS  Google Scholar 

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Acknowledgments

This study was presented at the 51st Annual Meeting of Japanese Society of Nephrology, Fukuoka, Japan, 2008.

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Correspondence to Koichi Nakanishi.

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Togawa, H., Nakanishi, K., Shima, Y. et al. Increased chymase-positive mast cells in children with crescentic glomerulonephritis. Pediatr Nephrol 24, 1071–1075 (2009). https://doi.org/10.1007/s00467-008-1044-2

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  • DOI: https://doi.org/10.1007/s00467-008-1044-2

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