Calcification and osteopontin localization in the peritoneum of patients on long-term continuous ambulatory peritoneal dialysis therapy

Yuichi Nakazato, Yasuyoshi Yamaji, Naoki Oshima, Matsuhiko Hayashi, Takao Saruta

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Background. Peritoneal calcification is an uncommon complication of continuous ambulatory peritoneal dialysis (CAPD), which is mainly observed in patients on long-term therapy. Although some asymptomatic patients must have microscopic calcification in their peritoneum, little information on this topic has been published. Recent studies have revealed active participation of adhesive/chemotactic protein osteopontin (OPN) in dystrophic calcification. Methods. Peritoneal tissue was obtained by biopsy or at autopsy from 18 CAPD patients (median duration, 122 months), 5 control haemodialysis (HD) patients, and 3 pre-CAPD patients. The distribution of calcium deposits and OPN protein was determined by von Kossa staining and immunohistochemistry, respectively. Smooth muscle cells and macrophages were identified with anti-α smooth muscle actin (α-SMA) and anti-CD68 antibodies. Results. Calcium deposits with various configurations were observed in specimens from 12 of the 18 CAPD patients. They included massive calcification facing the peritoneal cavity, scattered granular or crystalloid deposits in the submesothelial stroma, and oval-shaped deposits formed within hyalinized vasa. Most were present in highly sclerosed areas and accompanied by extracellular OPN precipitation. Cytoplasmic OPN was detected in infiltrating leukocytes, granulation tissue cells, fibroblast-like cells and mast cells. Computerized tomography examination also detected peritoneal calcification in seven of the CAPD patients. No calcium deposits or OPN staining was detected in control specimens. Conclusions. The results of our study suggest that microscopic peritoneal calcification is frequent in patients on CAPD for more than 10 years. Myofibroblast infiltration, OPN expression, calcium deposition, and associated OPN precipitation seem to be components of the peritoneal changes in such patients.

Original languageEnglish
Pages (from-to)1293-1303
Number of pages11
JournalNephrology Dialysis Transplantation
Volume17
Issue number7
Publication statusPublished - 2002

Fingerprint

Osteopontin
Continuous Ambulatory Peritoneal Dialysis
Peritoneum
Calcium
Therapeutics
Staining and Labeling
Myofibroblasts
Granulation Tissue
Peritoneal Cavity
Mast Cells
Adhesives
Smooth Muscle Myocytes
Smooth Muscle
Renal Dialysis
Actins
Anti-Idiotypic Antibodies
Autopsy
Proteins
Leukocytes
Fibroblasts

Keywords

  • Calcification
  • Continuous ambulatory peritoneal dialysis
  • Fibrosis
  • Myofibroblasts
  • Osteopontin
  • Peritoneum

ASJC Scopus subject areas

  • Nephrology
  • Transplantation

Cite this

Calcification and osteopontin localization in the peritoneum of patients on long-term continuous ambulatory peritoneal dialysis therapy. / Nakazato, Yuichi; Yamaji, Yasuyoshi; Oshima, Naoki; Hayashi, Matsuhiko; Saruta, Takao.

In: Nephrology Dialysis Transplantation, Vol. 17, No. 7, 2002, p. 1293-1303.

Research output: Contribution to journalArticle

Nakazato, Yuichi ; Yamaji, Yasuyoshi ; Oshima, Naoki ; Hayashi, Matsuhiko ; Saruta, Takao. / Calcification and osteopontin localization in the peritoneum of patients on long-term continuous ambulatory peritoneal dialysis therapy. In: Nephrology Dialysis Transplantation. 2002 ; Vol. 17, No. 7. pp. 1293-1303.
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AU - Saruta, Takao

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N2 - Background. Peritoneal calcification is an uncommon complication of continuous ambulatory peritoneal dialysis (CAPD), which is mainly observed in patients on long-term therapy. Although some asymptomatic patients must have microscopic calcification in their peritoneum, little information on this topic has been published. Recent studies have revealed active participation of adhesive/chemotactic protein osteopontin (OPN) in dystrophic calcification. Methods. Peritoneal tissue was obtained by biopsy or at autopsy from 18 CAPD patients (median duration, 122 months), 5 control haemodialysis (HD) patients, and 3 pre-CAPD patients. The distribution of calcium deposits and OPN protein was determined by von Kossa staining and immunohistochemistry, respectively. Smooth muscle cells and macrophages were identified with anti-α smooth muscle actin (α-SMA) and anti-CD68 antibodies. Results. Calcium deposits with various configurations were observed in specimens from 12 of the 18 CAPD patients. They included massive calcification facing the peritoneal cavity, scattered granular or crystalloid deposits in the submesothelial stroma, and oval-shaped deposits formed within hyalinized vasa. Most were present in highly sclerosed areas and accompanied by extracellular OPN precipitation. Cytoplasmic OPN was detected in infiltrating leukocytes, granulation tissue cells, fibroblast-like cells and mast cells. Computerized tomography examination also detected peritoneal calcification in seven of the CAPD patients. No calcium deposits or OPN staining was detected in control specimens. Conclusions. The results of our study suggest that microscopic peritoneal calcification is frequent in patients on CAPD for more than 10 years. Myofibroblast infiltration, OPN expression, calcium deposition, and associated OPN precipitation seem to be components of the peritoneal changes in such patients.

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