The role of C1q complement fraction in the development of diabetic nephropathy in patients with type 2 diabetes

T. S. Ryabova , I. A. Rakityanskaya , A. S. Manuilov , M. V. Zakharov

Bulletin of the Russian Military Medical Academy ›› 2019, Vol. 21 ›› Issue (1) : 18 -22.

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Bulletin of the Russian Military Medical Academy ›› 2019, Vol. 21 ›› Issue (1) : 18 -22. DOI: 10.17816/brmma13032
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The role of C1q complement fraction in the development of diabetic nephropathy in patients with type 2 diabetes

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Abstract

The role of intrarenal expression of C1q on clinical and laboratory parameters and the development of morphological changes in the renal tissue in patients with type 2 diabetes complicated by diabetic nephropathy was studied. It was noted that the presence of C1q deposits was detected in all zones of the glomerulus and interstitium of the renal tissue. The frequency of detection of C1q expression depended on the morphological class of diabetic nephropathy. With the development of nodular formations of Kimmelstil-Wilson, the frequency of detecting the expression of C1q in the area of the mesangial matrix and along the glomerulus capsule decreases to 0%. In the epithelium of the urinary tubules, C1q expression remains, regardless of class, and in the interstitial region of expression, the fraction, on the contrary, tends to increase from 8,3% in class IIa to 20% in patients with class IV diabetic nephropathy. Along the tubular basement membrane, the complement fraction was absent, regardless of the morphological class of diabetic nephropathy. Glomerular expression of the C1q-component deposits was found to contribute to the progression of chronic kidney disease, as it affects the decrease in glomerular filtration rate (F=4,533; p=0,039; β= −0,303; CI: 0,37; 13,343; p=0,039). The expression of C1q deposits in the interstitium plays a role in the development and progression of focal interstitial sclerosis (F=4,462; p=0,045; β=0,295; CI: 0,005; 0,375; p=0,045), determining the severity of tissue interstitial tubulointerstitial changes in diabetic nephropathy and is one of factors contributing to the progression of renal tissue arteriolar hyalinosis (F=4,349; p=0,05; β= −0,535 CI: −1,095; 0,001; p=0,05).

Keywords

diabetic nephropathy / type 2 diabetes / nephrobiopsy / C1q component / fibrosis and hyalinosis of arterioles / glomerular filtration rate / proteinuria / chronic kidney disease / arterial hypertension

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T. S. Ryabova, I. A. Rakityanskaya, A. S. Manuilov, M. V. Zakharov. The role of C1q complement fraction in the development of diabetic nephropathy in patients with type 2 diabetes. Bulletin of the Russian Military Medical Academy, 2019, 21(1): 18-22 DOI:10.17816/brmma13032

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References

[1]

Bossi, F. C1q induces in vivo angiogenesis, and wound healing / F. Bossi [et al.] // Mol. Immunol. – 2011. – Vol. 48. – Р. 1676.

[2]

Brooimans, R. Interleukin 2 mediates stimulation of complement C3 biosynthesis in human proximal tubular epithelial cells / R. Brooimans [et al.] // J. Clin. Invest. – 1991. – Vol. 88, № 2. – P. 379–384.

[3]

Cole, F. Tissue-specific pretranslational regulation of complement production in human mononuclear phagocytes / F. Cole [et al.] // J. Immunol. – 1985. – Vol. 134, № 4.– P. 2610–2616.

[4]

Feucht, H. Biosynthesis of complement C4 messenger RNA in normal human kidney / H. Feucht [et al.] // Nephron. – 1989. – Vol. 53. – Р. 338–342.

[5]

Flyvbjerg, A. Diabetic angiopathy, the complement system and the tumor necrosis factor superfamily / A. Flyvbjerg [et al.] // Nat. Rev. Endocrinol. – 2010. – Vol. 6, № 2.– P. 94–101.

[6]

Fraser, D. C1q Differentially Modulates Phagocytosis and Cytokine Responses during Ingestion of Apoptotic Cells by Human Monocytes, Macrophages, and Dendritic Cells / D. Fraser [et al.] // J. Immunol. – 2009. – Vol. 183, № 10. – P. 6175–6185.

[7]

Ghai, R. C1q and its growing family / R. Ghai [et al.] // Immunobiology. – 2007. – Vol. 212, № 5.– P. 253–266.

[8]

Hosszu Kinga, K. Evidence that a C1q/C1qR system regulates monocyte-derived dendritic cell differentiation at the interface of innate and acquired immunity / K. Hosszu Kinga [et al.] // Innate Immun. – 2010. – Vol. 16, № 2.– P. 115–127.

[9]

Kreutz, R. Induction of C1q expression in glomerular endothelium in a rat model with arterial hypertension and albuminuria / R. Kreutz [et al.] // J. Hypertens. – 2007. – Vol. 25, № 11. – P. 2308–2316.

[10]

Libby, P. Inflammation and atherosclerosis / P. Libby [et al.] // Circulation. – 2002. – Vol. 105, № 9. – P. 1135–1143.

[11]

Montinaro, V. Renal C3 synthesis in idiopathic membranous nephropathy: Correlation to urinary C5b-9 excretion / V. Montinaro [et al.] // Kidney Int. – 2000. – Vol. 57. – P. 137–146.

[12]

Nangaku, M. Mechanisms of tubulointerstitial injury in the kidney: final common pathways to end-stage renal failure / M. Nangaku [et al.] // Intern. Med. 2004. – Vol. 43, № 1. – P. 9–17.

[13]

Paidassi, H. C1q binds phosphatidylserine and likely acts as a multiligand-bridging molecule in apoptotic cell recognition / H. Paidassi [et al.] // J. Immunol. – 2008. – Vol. 180. – P. 2329–2338.

[14]

Paidassi, H. Investigations on the C1q-calreticulin- phosphatidylserine interactions yield new insights into apoptotic cell recognition / H. Paidassi [et al.] // J. Mol. Biol. – 2011. – Vol. 480. – P. 277–290.

[15]

Salmon, A. Endothelial glycocalyx dysfunction in disease: albuminuria and increased microvascular permeability / A. Salmon, S. Satchell // Journal of Pathology. – 2012. – Vol. 226, № 4. – P. 562–574.

[16]

Tang, S. Role of complement in tubulointerstitial injury from proteinuria / S. Tang [et al.] // Kidney Blood Press Res. – 2002. – Vol. 25, № 2. – P. 120–126.

[17]

Tervaert, T. Pathologic classification of diabetic nephropathy / T. Tervaert [et al.] // J. Am. Soc. Nephrol. 2010. – Vol. 21, № 4. – P. 556–563.

[18]

Wuding, Z. Intrarenal synthesis of complement / Z. Wuding [et al.] // Kidney International. – 2001. – Vol. 59. – P. 1227–1235.

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Ryabova T.S., Rakityanskaya I.A., Manuilov A.S., Zakharov M.V.

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