Immune-mediated inflammation is the mechanism of glomerulonephritis (GN). Poststreptococcal glomerulonephritis (PSGN) is the most common form of acute GN, and IgA nephropathy is the most common chronic GN, but many other types of GN can occur. The most common identifiable lower urinary tract causes of hematuria include urinary tract infection (UTI), kidney stones, and hypercalciuria.
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Nonpathologic (urate crystals in infants, ingested foods, medications, dyes) Pathologic (hemoglobinuria from hemolytic anemia, myoglobinuria from rhabdomyolysis)
Immunologic injury (GN—e.g., PSGN, IgA nephropathy, MPGN, systemic diseases) Structural disorder (Alport syndrome, thin basement membrane disease) Toxin-mediated injury (HUS)
Inflammation (interstitial nephritis, pyelonephritis) Vascular (sickle cell trait/disease, Nutcracker syndrome) Structural (cyst rupture, Wilms tumor, urinary tract obstruction, renal trauma)
Inflammation (cystitis, hemorrhagic cystitis, urethritis) Injury (trauma, kidney stone) Hypercalciuria
GN, Glomerulonephritis; HUS, hemolytic uremic syndrome; MPGN, membranoproliferative glomerulonephritis; PSGN, poststreptococcal glomerulonephritis.
Children with acute GN commonly present with hematuria (gross or microscopic) along with other cardinal features of glomerular injury (proteinuria, hypertension, edema, oliguria, renal insufficiency). PSGN occurs most frequently in children 2 to 12 years of age and is more common in boys. Manifestations of PSGN are typical of acute GN listed previously and develop 5 to 21 days (average 10 days) after streptococcal pharyngitis infections and 4 to 6 weeks after impetigo. Acute postinfectious GN presents in the same manner as PSGN and can occur following infections with other bacterial and viral pathogens. PSGN can develop regardless of whether the child was treated with antibiotics at the time of infection. Special attention must be paid to the blood pressure because hypertension may be severe enough to lead to complications such as heart failure, seizures, and encephalopathy.
The presentation of IgA nephropathy is more variable and may take the form of acute GN, asymptomatic microscopic hematuria, or recurrent gross hematuria concurrent with an upper respiratory infection as opposed to several days later, as with PSGN. Children with hematuria secondary to systemic disorders such as Henoch-Schönlein purpura nephritis, lupus nephritis, and vasculitis-associated GN will present with other systemic features typical of the respective disease.
A special form of GN is rapidly progressive glomerulonephritis (RPGN) that presents with typical features of acute GN, but the renal insufficiency progresses more quickly and severely. Renal biopsy shows glomerular epithelial cell proliferation with crescents. RPGN may be idiopathic or secondary to any of the known types of GN. Early recognition of RPGN is crucial to prevent the progression to end-stage renal disease (ESRD) that occurs without prompt treatment.
Alport syndrome is typically caused by X-chromosome mutations in type IV collagen leading to an abnormal glomerular basement membrane (GBM) and may present with either asymptomatic microscopic or gross hematuria. Males typically