Increased Density of Interstitial Mast Cells in Amyloid A Renal Amyloidosis

Tóth, Tibor; Tóth-Jakatics, Ria; Jimi, Shiro; Takebayashi, Shigeo

doi:10.1038/modpathol.3880184

Cited by 28 publications

(26 citation statements)

References 28 publications

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“…Unexpectedly, in the present study, 80.5% of the MCs in normal control participants were found to be MC TC subtype. The result was quite different from what had been reported by Okon and Stachura [17] and Tóth et al [33] (about 14.5% and 20.1% of MCs, respectively, in normal control participants were found to be MC TC subtype in their reports), but similar to the result of Rüger et al [11] (about 62.5% of MCs in normal controls were found to be MC TC subtype in their report). Is MC TC the major subtype of renal MCs in healthy human beings?…”

Section: Discussioncontrasting

confidence: 57%

“…The MC T MCs are believed to be T cell-dependent and the MC TC MCs are believed to be T cell-independent [38]. In human renal tissue, different results have been reported on MC subtype [11,15,17,[32][33][34]. MC subtype is believed to be disease-dependent [16].…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies suggested that MCs contributed to renal diseases mainly through promotion of tubular interstitial injury [13,[15][16][17][32][33][34]. Most investigations focused on the roles of MCs on renal fibrosis.…”

Section: Discussionmentioning

confidence: 99%

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Pathogenic role of mast cells in the development of diabetic nephropathy: a study of patients at different stages of the disease

et al. 2011

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Aims/hypothesis Increased renal mast cells have been detected in diabetic nephropathy. However, only a few patients have been examined. Evidence of the involvement of mast cells in diabetic nephropathy is still scarce, and no observation of mast cells during the development of diabetic nephropathy has yet been reported in humans. Here, we examined changes in renal mast cells in patients at different stages of diabetic nephropathy and related these to the development of the disease. Methods Eighty patients at different clinical stages of diabetic nephropathy and 16 normal kidney donors were recruited. Immunohistochemical staining for tryptase, chymase, TGF-β1, renin and TNF-α was done on renal sections from patients and control participants. Changes in mast cell number, degranulation, subtype and phenotype were examined. Correlation between mast cells and patients' clinical and pathological indices was analysed. Results With progression of diabetic nephropathy, the number and degranulation level of mast cells increased. Increase in mast cell number and degranulation level correlated significantly with tubular interstitial injury. Almost all renal mast cells in patients with diabetic nephropathy were found to produce chymase, renin, TGF-β1 and TNF-α. The level of TNF-α in mast cells increased with progression of diabetic nephropathy. Conclusions/interpretation This study suggests that mast cells are involved in development of diabetic nephropathy. Through release of bioactive substances, such as tryptase, chymase, TGF-β1, renin and TNF-α, into the tubular interstitium by degranulation, mast cells could promote renal inflammation and fibrosis, and thus contribute to diabetic nephropathy.

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Section: Discussioncontrasting

confidence: 57%

Section: Discussionmentioning

confidence: 99%

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Pathogenic role of mast cells in the development of diabetic nephropathy: a study of patients at different stages of the disease

et al. 2011

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“…It is clear that SCF and its receptor play a crucial role in migration and proliferation of haematopoietic stem cells during embryonic [13] and postnatal life [14]. Many kidney disorders with pronounced tubulointerstitial fibrosis are associated with mast cell infiltration including chronic glomerulonephritis (GN) [9, 10, 15], rapidly progressive GN [16, 17], chronic renal allograft rejection and chronic cyclosporin nephrotoxicity [18] as well as amyloidosis [19]. Upregulation of SCF has been reported in human glomerulonephritides including rapidly progressive GN [9, 16].…”

Section: Introductionmentioning

confidence: 99%

Stem Cell Factor in a Rat Model of Serum Nephrotoxic Nephritis

Kossi

Haylor

Johnson

et al. 2007

Nephron Exp Nephrol

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Background: Stem cell factor (SCF) has been implicated in many disease processes characterized by tissue remodelling and fibrosis. The growth factor (SCF) was evaluated in a rat model of nephrotoxic serum nephritis (NTN), characterized by early inflammation followed by later tissue fibrosis. Methods: NTN was induced in male Wistar Kyoto rats using rabbit anti-rat glomerular basement membrane antibodies. Animals were sacrificed at days 7, 15, 30 and 45 (n = 4–10 per group). Rats’ kidneys were immunostained for ED1 as marker of inflammation, CD34, SCF, c-kit, mast cell tryptase and markers of fibrosis; collagens III and IV and α-SMA. Changes in SCF protein and mRNA content were evaluated by Western blotting and Northern blotting, respectively. Results: In the NTN kidney, levels of immunoreactive SCF and SCF receptor (c-kit) were significantly higher in glomerular, tubular and interstitial compartments. Mast cells were barely detectable in NTN and control rat sections. Double immunostaining showed the co-localization of SCF with α-SMA and of the SCF receptor with CD34 and ED1 positive cells. Immunostainable SCF protein in each of the 3 compartments, glomerular, tubular and interstitial, showed a positive linear correlation with serum creatinine, proteinuria, glomerulosclerosis score and interstitial fibrosis scores. Using multivariate analysis, immunostainable tubular SCF was a predictor of glomerular sclerosis and immunostainable glomerular SCF predicted tubular atrophy. Increased SCF immunostain was not a consequence of altered transcription as there was a fall in SCF mRNA determined by Northern blotting. Western blotting of NTN kidney homogenates revealed two bands for SCF, a 43-kDa band which decreased, and a 19-kDa band which increased throughout the study. Conclusion: These results highlight the potential role of SCF and its receptor in the remodelling process of the NTN kidney. Upregulation of SCF may involve a translational mechanism, with the soluble SCF protein KL-S1 (19 kDa) being derived from the transmembrane SCF protein KL-1 (43 kD) by proteolytic cleavage. The immunohistochemical staining of few CD34+ cells in NTN kidneys warrants further evaluation of the nature of these cells in the context of the inflammatory as well as the fibrotic processes.

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“…A chronic inflammatory reaction is occasionally present [8]. An increased number of mast cells has also been described [17,111]. Heterotopic ossifications and calcifications may be present occasionally [98].…”

Section: Histologymentioning

confidence: 90%

Amyloid in surgical pathology

Röcken

Sletten

2003

Virchows Archiv

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Amyloid is defined as a proteinaceous tissue deposit that shows a typical green birefringence in polarized light after staining with Congo red, the presence of non-branching linear fibrils of indefinite length with a mean diameter of 10 nm, and a distinct X-ray diffraction pattern consistent with Pauling's model of a cross beta-fibril. Amyloid may deposit locally or may present as a systemic disease. The origin of amyloid is diverse: 25 different fibril proteins have been described so far. The precursor proteins differ from each other in their primary structures and functions. The only common denominator is the propensity to form anti-parallel cross beta-fibrils under certain circumstances. Early diagnosis of amyloid is still a major challenge in surgical pathology. Histological proof can be obtained using Congo-red staining and polarization microscopy. However, small deposits may be difficult to discern, and sensitivity can be improved using fluorescence microscopy. Classification of amyloid is mandatory, since amyloid is treatable and different treatment regimens are applied to different amyloid diseases. This review focuses on the epidemiology, clinical features, pathology and diagnosis of amyloid in surgical pathology.

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Increased Density of Interstitial Mast Cells in Amyloid A Renal Amyloidosis

Cited by 28 publications

References 28 publications

Pathogenic role of mast cells in the development of diabetic nephropathy: a study of patients at different stages of the disease

Pathogenic role of mast cells in the development of diabetic nephropathy: a study of patients at different stages of the disease

Stem Cell Factor in a Rat Model of Serum Nephrotoxic Nephritis

Amyloid in surgical pathology

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