Pediatric Nephrology

, Volume 31, Issue 4, pp 523–533 | Cite as

Haematuria as a risk factor for chronic kidney disease progression in glomerular diseases: A review

  • Juan Antonio MorenoEmail author
  • Claudia Yuste
  • Eduardo Gutiérrez
  • Ángel M. Sevillano
  • Alfonso Rubio-Navarro
  • Juan Manuel Amaro-Villalobos
  • Manuel Praga
  • Jesús Egido


Haematuria has long been considered to be a benign condition associated with glomerular diseases. However, new evidences suggest that haematuria has a pathogenic role in promoting kidney disease progression. An increased risk for end-stage renal disease has been reported in adolescents and young adults with persistent microscopic haematuria. A persistent impairment of renal function has been also reported following macroscopic haematuria-associated acute kidney injury in immunoglobulin A nephropathy. Haematuria-induced renal damage has been related to oxidant, cytotoxic and inflammatory effects induced by haemoglobin or haem released from red blood cells. The pathophysiological origin of haematuria may be due to a more fragile and easily ruptured glomerular filtration barrier, as reported in several glomerular diseases. In this review we describe a number of the key issues associated with the epidemiology and pathogenesis of haematuria-associated diseases, provide an update of recent knowledge on the role of haematuria on renal function outcome and discuss specific therapeutic approaches in this setting.

Key summary points

  1. 1.

    Glomerular haematuria is a common observation in a number of renal diseases that may lead to persistent renal injury.

  2. 2.

    Haematuria in children differs from that in adults in specific aspects, particularly in the frequency of glomerular diseases and renal disease outcome.

  3. 3.

    Regular follow-up of renal function in children with isolated microhaematuria may be recommended.



Haematuria Chronic kidney disease Acute kidney injury Red blood cells Glomerulonephritis 



This study has been supported by grants from FIS (Programa Miguel Servet: CP10/00479, PI13/00802 and PI14/00883) and the Spanish Society of Nephrology to JAM, FIS 10/02668 and 13/02502, REDinREN (RD012/0021) and by Complement Research Group-CM (S2010/BMD-2316) to MP, Fundacion Conchita Rabago to ARN, and the Institute of Research Queen Sophia, FRIAT and ISCIII fund PI14/00386 to JE.


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Copyright information

© IPNA 2015

Authors and Affiliations

  • Juan Antonio Moreno
    • 1
    Email author
  • Claudia Yuste
    • 2
  • Eduardo Gutiérrez
    • 3
  • Ángel M. Sevillano
    • 3
  • Alfonso Rubio-Navarro
    • 1
  • Juan Manuel Amaro-Villalobos
    • 1
  • Manuel Praga
    • 3
  • Jesús Egido
    • 1
    • 4
  1. 1.Renal, Vascular and Diabetes Research Laboratory, IIS-Fundación Jiménez DíazAutonoma UniversityMadridSpain
  2. 2.Department of NephrologyGregorio Marañon HospitalMadridSpain
  3. 3.Department of Nephrology12 de Octubre HospitalMadridSpain
  4. 4.Spanish Biomedical Research Network in Diabetes and Associated Metabolic Disorders (CIBERDEM)MadridSpain

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