Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Nephrol. May 6, 2015; 4(2): 185-195
Published online May 6, 2015. doi: 10.5527/wjn.v4.i2.185
Pathogenesis of glomerular haematuria
Claudia Yuste, Eduardo Gutierrez, Angel Manuel Sevillano, Alfonso Rubio-Navarro, Juan Manuel Amaro-Villalobos, Alberto Ortiz, Jesus Egido, Manuel Praga, Juan Antonio Moreno
Claudia Yuste, Department of Nephrology, Gregorio Marañon Hospital, 28007 Madrid, Spain
Eduardo Gutierrez, Angel Manuel Sevillano, Manuel Praga, Department of Nephrology, 12 de Octubre, 28041 Madrid, Spain
Alfonso Rubio-Navarro, Juan Manuel Amaro-Villalobos, Alberto Ortiz, Jesus Egido, Juan Antonio Moreno, Renal, Vascular and Diabetes Research Lab, IIS-Fundación Jiménez Díaz, Autonoma University (UAM), 28040 Madrid, Spain
Author contributions: All the authors contributed to this work.
Supported by Grants from FIS (Programa Miguel Servet: CP10/00479, PI13/00802 and PI14/00883) and Spanish Society of Nephrology to Moreno JA; and Institute of Research Queen Sophia, FRIAT and ISCIII fund PI10/00072 to Egido J.
Conflict-of-interest: There are no conflicts of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:
Correspondence to: Juan Antonio Moreno, PhD, Renal, Vascular and Diabetes Research Lab, IIS-Fundación Jiménez Díaz, Autonoma University (UAM), Av. Reyes Católicos 2, 28040 Madrid, Spain.
Telephone: +34-91-5504800 Fax: +34-91-5504800
Received: August 20, 2014
Peer-review started: August 21, 2014
First decision: September 28, 2014
Revised: December 19, 2014
Accepted: December 29, 2014
Article in press: December 31, 2014
Published online: May 6, 2015

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: Haematuria, Pathogenesis, Glomerular filtration barrier, Dysmorphic red blood cells, Chronic kidney disease, Microscopic haematuria

Core tip: Recent advances suggest that glomerular haematuria may be a negative prognostic factor for renal function outcome. A more fragile and easily ruptured glomerular filtration barrier (GFB) may be responsible for glomerular bleeding. Several factors have been associated to this pathogenic process, including: (1) genetic alteration of GFB components, leading to a more fragile and easily ruptured GFB structure; (2) aberrant deposition of toxic molecules in the GFB; and (3) enhanced inflammatory response, as reported in autoimmune diseases, infections, or primary glomerulonephritis. In this review we fully describe these pathological mechanisms, with special interest in haematuric diseases and their renal morphological findings.