Hematuria 

  • Author: Sanjeev Gulati, MBBS, MD, DNB(Peds), DM, DNB(Neph), FIPN(Australia), FICN, FRCPC(Canada); Chief Editor: Craig B Langman, MD   more...
 
Updated: Apr 20, 2010
 

Background

Hematuria is one of the most common urinary findings that result in children presenting to pediatric nephrologists. Generally, hematuria is defined as the presence of 5 or more RBCs per high-power field in 3 of 3 consecutive centrifuged specimens obtained at least 1 week apart. In the office setting, a positive reaction on the urine dipstick test is usually the first indication of the presence of hematuria. Hematuria can be gross (ie, the urine is overtly bloody, smoky, or tea colored) or microscopic. It may be symptomatic or asymptomatic, transient or persistent, and either isolated or associated with proteinuria and other urinary abnormalities. The role of the primary care physician in the management of a child with hematuria includes the following:

  • Recognize and confirm the finding of hematuria.
  • Identify common etiologies.
  • Select patients who have significant urinary system disease that might require further expertise in either diagnosis or management and referral.
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Pathophysiology

The etiology and pathophysiology of hematuria vary. For instance, hematuria of glomerular origin may be the result of a structural disruption in the integrity of glomerular basement membrane caused by inflammatory or immunologic processes. Chemicals may cause toxic disruptions of the renal tubules, whereas calculi may cause mechanical erosion of mucosal surfaces in the genitourinary tract, resulting in hematuria.

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Epidemiology

Frequency

United States

The prevalence of gross hematuria in children is estimated to be 0.13%. In more than half of the cases (56%) this is due to an easily identifiable cause. The most common cause appears to be cystitis (20-25%). Asymptomatic microscopic hematuria is, on the average, 10-fold as prevalent as gross hematuria (1.5%, range 0.4-4.1%, depending on the criteria used to define hematuria). With repeated evaluations, the prevalence of asymptomatic microscopic hematuria decreases to less than 0.5%, supporting the notion that most cases of hematuria in children are transient. The incidence of simultaneous hematuria and proteinuria is estimated to be only 0.06%, but their coexistence signals significant renal disease.

Mortality/Morbidity

In general, children with isolated asymptomatic microscopic hematuria tend to do well, whereas those with associated findings (eg, hypertension, proteinuria, abnormal serum creatinine levels) are more likely to have serious problems. Because hematuria is the end result of various processes, the morbidity and mortality rates of the condition depend on the primary process that initiated it.

Race

The incidence of hematuria in specific racial groups is determined by the primary cause. For example, idiopathic hypercalciuria is infrequent in black and Asian children, but relatively common in whites. Conversely, hematuria caused by sickle cell disease is more common in blacks than in whites.

Sex

Sex may predispose a child to specific diseases that manifest as hematuria. For example, the sex-linked form of Alport syndrome has a male preponderance, whereas lupus nephritis is more common in adolescent girls.

Age

Prevalence of certain conditions varies with age.[1] For instance, Wilms tumors are more frequent in children of preschool age, whereas acute postinfectious glomerulonephritis is more frequent in the school-aged population. In adults, hematuria is often a sign of malignancy of the genitourinary tract (eg, renal cell carcinoma, bladder tumors, prostatic tumors). These conditions are rare in children.

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Contributor Information and Disclosures
Author

Sanjeev Gulati, MBBS, MD, DNB(Peds), DM, DNB(Neph), FIPN(Australia), FICN, FRCPC(Canada)  Associate Professor, Department of Nephrology, Sanjay Gandhi Post Graduate Institute of Medical Sciences; Senior Consultant in Pediatric Nephrology, Department of Nephrology and Transplant Medicine, Fortis Hospitals, India

Sanjeev Gulati, MBBS, MD, DNB(Peds), DM, DNB(Neph), FIPN(Australia), FICN, FRCPC(Canada) is a member of the following medical societies: American Society of Pediatric Nephrology, Indian Academy of Pediatrics, International Society of Nephrology, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Coauthor(s)

Deogracias Pena, MD  Medical Director of Dialysis, Department of Pediatrics, Cook Children's Medical Center; Clinical Associate Professor, Texas Tech University School of Medicine

Deogracias Pena, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, and American Society of Pediatric Nephrology

Disclosure: Nothing to disclose.

Specialty Editor Board

Richard Neiberger, MD, PhD  Director of Pediatric Renal Stone Disease Clinic, Associate Professor, Department of Pediatrics, Division of Nephrology, University of Florida College of Medicine and Shands Hospital

Richard Neiberger, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Federation for Medical Research, American Medical Association, American Society of Nephrology, American Society of Pediatric Nephrology, Christian Medical & Dental Society, Florida Medical Association, International Society for Peritoneal Dialysis, International Society of Nephrology, National Kidney Foundation, New York Academy of Sciences, Shock Society, Sigma Xi, Southern Medical Association, Southern Society for Pediatric Research, and Southwest Pediatric Nephrology Study Group

Disclosure: The Osler Institute Honoraria Speaking and teaching

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Adrian Spitzer, MD  Clinical Professor Emeritus, Department of Pediatrics, Albert Einstein College of Medicine

Adrian Spitzer, MD is a member of the following medical societies: American Academy of Pediatrics, American Federation for Medical Research, American Pediatric Society, American Society of Nephrology, American Society of Pediatric Nephrology, International Society of Nephrology, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Howard Trachtman, MD  Program Director, Pediatrics Research, Schneider Children's Hospital, Department of Pediatrics, Division of Nephrology, Professor, Albert Einstein College of Medicine

Howard Trachtman, MD is a member of the following medical societies: American Society of Hypertension, American Society of Nephrology, American Society of Pediatric Nephrology, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Craig B Langman, MD  The Isaac A Abt, MD, Professor of Kidney Diseases, Northwestern University, The Feinberg School of Medicine; Division Head of Kidney Diseases, Children's Memorial Hospital

Craig B Langman, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, and International Society of Nephrology

Disclosure: Merck Grant/research funds None; NIH Grant/research funds None; Raptor Pharmaceuticals, Inc Grant/research funds None; Alexion Pharmaceuticals, Inc. Grant/research funds None

References
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  2. Higashihara E, Nishiyama T, Horie S, et al. Hematuria: definition and screening test methods. Int J Urol. Apr 2008;15(4):281-4. [Medline].

  3. Quigley R. Evaluation of hematuria and proteinuria: how should a pediatrician proceed?. Curr Opin Pediatr. Apr 2008;20(2):140-4. [Medline].

  4. Diven SC, Travis LB. A practical primary care approach to hematuria in children. Pediatr Nephrol. Jan 2000;14(1):65-72. [Medline].

  5. Dodge WF, West EF, Smith EH, Bruce Harvey 3rd. Proteinuria and hematuria in schoolchildren: epidemiology and early natural history. J Pediatr. Feb 1976;88(2):327-47. [Medline].

  6. Crompton CH, Ward PB, Hewitt IK. The use of urinary red cell morphology to determine the source of hematuria in children. Clin Nephrol. Jan 1993;39(1):44-9. [Medline].

  7. Cruz CC, Spitzer A. When you find protein or blood in the urine. Contemp Pediatr. 1998;15:89-109.

  8. D'Amico G. The commonest glomerulonephritis in the world: IgA nephropathy. Q J Med. Sep 1987;64(245):709-27. [Medline].

  9. Emancipator SN, Gallo GR, Lamm ME. IgA nephropathy: perspectives on pathogenesis and classification. Clin Nephrol. Oct 1985;24(4):161-79. [Medline].

  10. Feld LG, Stapleton FB, Duffy L. Renal biopsy in children with asymptomatic hematuria or proteinuria: survey of pediatric nephrologists. Pediatr Nephrol. Aug 1993;7(4):441-3. [Medline].

  11. Feld LG, Waz WR, Perez LM, Joseph DB. Hematuria. An integrated medical and surgical approach. Pediatr Clin North Am. Oct 1997;44(5):1191-210. [Medline].

  12. Kalia A, Travis LB, Brouhard BH. The association of idiopathic hypercalciuria and asymptomatic gross hematuria in children. J Pediatr. Nov 1981;99(5):716-9. [Medline].

  13. Kincaid-Smith P, Fairley K. The investigation of hematuria. Semin Nephrol. May 2005;25(3):127-35. [Medline].

  14. Krieger I, Sargent DA. A postural sign in the sensory deprivation syndrome in infants. J Pediatr. Mar 1967;70(3):332-9. [Medline].

  15. Meyers KE. Evaluation of hematuria in children. Urol Clin North Am. Aug 2004;31(3):559-73, x. [Medline].

  16. Roy S 3rd. Hematuria. Pediatr Rev. Jun 1998;19(6):209-12; quiz 213. [Medline].

  17. Sargent JD, Stukel TA, Kresel J, Klein RZ. Normal values for random urinary calcium to creatinine ratios in infancy. J Pediatr. Sep 1993;123(3):393-7. [Medline].

  18. Seigel M, Lee ML. Hematuria. Semin Arthritis Rheum. 1974;3:1.

  19. Ward JF, Kaplan GW, Mevorach R, et al. Refined microscopic urinalysis for red blood cell morphology in the evaluation of asymptomatic microscopic hematuria in a pediatric population. J Urol. Oct 1998;160(4):1492-5. [Medline].

  20. Yadin O. Hematuria in children. Pediatr Ann. Sep 1994;23(9):474-8, 481-5. [Medline].

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Approach to hematuria.
Nonglomerular hematuria.
Glomerular hematuria.
Microscopy of urinary sediment. Typical appearance in non-glomerular hematuria: RBCs are uniform in size and shape but show two populations of cells because a small number have lost their hemoglobin pigment.
Microscopy of urinary sediment. Typical appearance of RBCs in glomerular hematuria: RBCs are small and vary in size, shape, and hemoglobin content.
Microscopy of urinary sediment. A cast containing numerous erythrocytes, indicating glomerulonephritis.
Table. Histologic Findings
Condition Histology History Laboratory Data
Systemic lupus erythematosusMild glomerulitis, proliferative changes, immune complex deposition, crescents, immunoglobulin depositionHematuria, proteinuria, hypertension, joint pains, rashesAbnormal C3, C4, ANA, and dsDNA levels; anemia; thrombocytopenia
IgA nephropathyIgA deposition in the mesangium, glomerular sclerosis, proliferative changes, crescents in severe casesGross, intermittent, painless hematuriaNo specific changes, although increased serum



IgA levels observed in some patients



Henoch-Schönlein purpuraSame as IgA nephropathyPurpura, joint pains, abdominal pain, hematuriaNo specific laboratory data
Alport syndromeSome thinning of basement membranes, "basket weave" changes in the glomerular basement



membrane on electron microscopy



Sensorineural hearing loss, corneal abnormalities, hematuria, renal failureNo specific changes
Thin basement membrane diseaseAverage glomerular basement membranes reported to be 100-200 nm in children in this conditionPersistent microscopic or gross hematuria, significant family historyNo specific changes
Mesangiocapillary glomerulonephritisGlomerular lobulations, thickening of the mesangial matrix and glomerular basement membranes, crescentsHematuria, proteinuria, hypertensionC3 levels possibly abnormal
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