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Review
. 2015 May 6;4(2):185-95.
doi: 10.5527/wjn.v4.i2.185.

Pathogenesis of glomerular haematuria

Claudia Yuste  1 , Eduardo Gutierrez  1 , Angel Manuel Sevillano  1 , Alfonso Rubio-Navarro  1 , Juan Manuel Amaro-Villalobos  1 , Alberto Ortiz  1 , Jesus Egido  1 , Manuel Praga  1 , Juan Antonio Moreno  1
Affiliations
Review

Pathogenesis of glomerular haematuria

Claudia Yuste et al. World J Nephrol. .

Abstract

Haematuria was known as a benign hallmark of some glomerular diseases, but over the last decade, new evidences pointed its negative implications on kidney disease progression. Cytotoxic effects of oxidative stress induced by hemoglobin, heme, or iron released from red blood cells may account for the tubular injury observed in human biopsy specimens. However, the precise mechanisms responsible for haematuria remain unclear. The presence of red blood cells (RBCs) with irregular contours and shape in the urine indicates RBCs egression from the glomerular capillary into the urinary space. Therefore glomerular haematuria may be a marker of glomerular filtration barrier dysfunction or damage. In this review we describe some key issues regarding epidemiology and pathogenesis of haematuric diseases as well as their renal morphological findings.

Keywords: Chronic kidney disease; Dysmorphic red blood cells; Glomerular filtration barrier; Haematuria; Microscopic haematuria; Pathogenesis.

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Figures

Figure 1
Figure 1
Haematuria-induced kidney injury in tubular cells. Hb: Haemoglobin; Bb: Bilirubin; Bv-red: Biliverdin reductase; CO: Carbon monoxide; Fe: Iron; HO-1: Heme oxygenase 1; MCP: Monocyte chemoattractant protein; NF-κb: Nuclear factor kappa b; TGF-β: Transforming growth factor beta; TNF-α: Tumour necrosis factor alpha.
Figure 2
Figure 2
Glomerular filtration barrier structure and red blood cell egression leading to haematuria. CL: Capillary lumen; BC: Bowman’s capsule; E: Endothelial cell; GBM: Glomerular basement membrane; Gly: Glycosaminoglicans; M: Mesangium; P: Podocyte; RBC: Red blood cell; SD: Slit diaphragm; SP: Subpodocyte space; TC: Tubular cell; US: Urinary space.
See this image and copyright information in PMC

References

    1. Kelly JD, Fawcett DP, Goldberg LC. Assessment and management of non-visible haematuria in primary care. BMJ. 2009;338:a3021. - PubMed
    1. Cohen RA, Brown RS. Clinical practice. Microscopic hematuria. N Engl J Med. 2003;348:2330–2338. - PubMed
    1. Clarkson AR, Seymour AE, Thompson AJ, Haynes WD, Chan YL, Jackson B. IgA nephropathy: a syndrome of uniform morphology, diverse clinical features and uncertain prognosis. Clin Nephrol. 1977;8:459–471. - PubMed
    1. Vivante A, Afek A, Frenkel-Nir Y, Tzur D, Farfel A, Golan E, Chaiter Y, Shohat T, Skorecki K, Calderon-Margalit R. Persistent asymptomatic isolated microscopic hematuria in Israeli adolescents and young adults and risk for end-stage renal disease. JAMA. 2011;306:729–736. - PubMed
    1. Gutiérrez E, González E, Hernández E, Morales E, Martínez MA, Usera G, Praga M. Factors that determine an incomplete recovery of renal function in macrohematuria-induced acute renal failure of IgA nephropathy. Clin J Am Soc Nephrol. 2007;2:51–57. - PubMed

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