Definition (Pediatr Clin North Am 2001;48:1519)
• Macroscopic hematuria is visible to the naked eye (Pediatr Clin North Am 1997;44:1191)
• Microscopic hematuria definitions vary by study, >5–10 RBCs/high-power, midstream collection (Adolesc Med Clin 2005;16:229)
Epidemiology (Pediatrics 1977;59:557; J Pediatr 1979;95:676)
• Macroscopic hematuria has an estimated incidence of 1.3 per 1,000
• Prevalence of microscopic hematuria 0.5–2% depending on population—incidence of microscopic hematuria 0.32% in girls and 0.14% of boys
Etiology (Urol Clin North Am 2004;31:559)
• In 342 children w/ asymptomatic microscopic hematuria: 81% idiopathic, 16% hyperCa, 1% PSGN; of 228 children w/ gross hematuria: 38% idiopathic, 22% hyperCa, 15% IgA nephropathy, 4% structural abnormalities (Arch Pediatr Adolesc Med 2005;159:353)
• Mimics include meds (chloroquine, iron, isoniazid, rifampin), foods (beets, blackberry),
pigments/toxins (bile, hemoglobinuria, myoglobinuria, lead, phenol, porphyria, urates)
• Glomerular dz: Recurrent gross hematuria (IgA nephropathy, benign familial
hematuria, Alport syndrome), acute postinfectious GN (PIGN), membranoproliferative GN (MPGN), SLE, membranous nephropathy (MN), rapidly progressive GN (RPGN), Henoch–Schönlein purpura, Goodpasture dz
• Interstitial and tubular Dz: Acute pyelonephritis, acute interstitial nephritis, TB, hematologic (sickle-cell dz, coagulopathies including von Willebrand dz, renal vein thrombosis, thrombocytopenia), meds (AGs, NSAID, amitriptyline, anticonvulsants, chlorpromazine, coumadin, cyclophosphamide, diuretics, PCN, thorazine)
• Urinary tract: Bacterial or viral (adenovirus) infxn related, urolithiasis and hypercalciuria, structural anomalies (including polycystic kidney disease), trauma, tumor, exercise
Evaluation (Urol Clin North Am 2004;31:559)
• Careful history and physical examination, including family history
• Macroscopic hematuria w/o significant proteinuria or RBC casts: Likely nonglomerular bleeding; requires urine cx (exclude infxn), renal & bladder U/S (exclude malig or cystic renal dz), CT (urolithiasis), &/or cystoscopy (exclude malig, other process)
• Hematuria plus any of the following is suggestive of glomerulonephritis: Edema, HTN, significant proteinuria. Initial eval: CBC (HUS), CMP, sediment, throat
cx, streptozyme panel, & complement levels (PIGN)
• See Proteinuria section for eval and Rx of disorders, for which this is a primary feature
Dx & Management of Specific Disorders (Urol Clin North Am 2004;31:559)
• Postinfectious GN: Up to 7–21 d after inciting infxn, often skin or soft tissue
• Infxn w/ Group A Strep or other infections; w/ supportive care, excellent prognosis
• Dark, tea-colored urine is common
• Pts can be asymptomatic, or have malaise, fatigue, HTN, edema, or oliguria
• C3 levels low during illness, improve over 6–8 wk
• Antistreptolysin O titers may be neg at first, streptozyme pos w/i 10 d
• Henoch–Schönlein purpura: (See Rheumatology chapter) w/ renal involvement ∼50% cases, extent variable (proteinuria, hematuria, nephrotic syndr, glomerulonephritis, AKI)
• Relapses can occur, long-term prognosis depends on degree of renal compromise
• IgA nephropathy common cause hematuria, path w/ mesangial deposition of IgA
• Poor prognostic indicators: HTN, nephrotic range proteinuria, renal insufficiency
• Controversy exists regarding utility of biopsy
• Rapidly progressive glomerulonephritis: AKI, glomerular crescents on biopsy
• EMERGENCY: Need prompt Rx w/ pulse steroids, can still progress to ESRD w/i wks. Aggressively pursue/address underlying condition