Published online May 6, 2015. doi: 10.5527/wjn.v4.i2.185
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.
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.