Therapy for PSGN is supportive and involves dietary sodiumrestriction, diuretics, and antihypertensive agents as needed.Although treating the streptococcal infection does not prevent PSGN, antibiotic treatment is still warranted with active streptococcal infection. Therapies for children with otherforms of GN depend on the underlying cause and severity.In some cases, anti-inflammatory therapy involving corticosteroids and/or other immunosuppressive agents may beused. Treatment with angiotensin-converting enzyme inhibitors may reduce proteinuria and glomerular hyperperfusion but should be used with caution in the setting of acutekidney injury.
PSGN usually has a benign outcome. In typical cases, the gross hematuria, proteinuria, and edema decline quickly (in 5 to 10 days). Microscopic hematuria may persist for months or even years; over 95% of children recover completely with no longterm sequelae.
Children with IgA nephropathy and other forms of chronic GN have a greater risk of progression to ESRD. The prognosis for renal recovery in chronic GN and in RPGN is variable and related to the underlying disorder and disease severity. The presence of persistent, heavy proteinuria, hypertension, decreased kidney function, and severe glomerular lesions on biopsy is associated with poor outcomes.
Children with idiopathic isolated asymptomatic microscopichematuria or suspected thin basement membrane disease typically have an excellent renal prognosis. Long-term follow-up,including yearly urinalysis (to rule out proteinuria) and bloodpressure, is required to exclude progressive forms of renal disease.
Hemolytic uremic syndrome (HUS) is characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and renal injury and is an important cause of acute kidney injury in children. HUS typically occurs in children less than 5 years of age but can occur in older children. The most common type of HUS is associated with a prodromal diarrheal illness (D+HUS). Contamination of meat, fruit, vegetables, or water with verotoxin (VT)-producing Escherichia coli (most commonly E. coli O157:H7) is responsible for many outbreaks. VT may be produced by other E. coli strains as well as other bacteria such as Shigella. VT causes hemorrhagic enterocolitis of variable severity and results in HUS in 5% to 15% of affected children.
HUS presenting without a prodrome of diarrhea (atypical HUS) may occur at any age. The clinical course is usually more severe than that of D+HUS. Atypical HUS can be secondary to infection (Streptococcus pneumonia, human immunodeficiency virus), genetic and acquired defects in complement regulation, medications, malignancy, systemic lupus erythematosus, and pregnancy.
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Classic D+HUS begins with enterocolitis, often with bloody stools, followed in 7 to 10 days by weakness, lethargy, and
Anemia Thrombocytopenia Presence of schistocytes, helmet cells, and burr cells on peripheral blood smear Increased LDH Decreased haptoglobin Increased indirect bilirubin Increased AST Elevated reticulocyte count
Elevated creatinine Presence of hematuria, proteinuria, pyuria, casts on urinalysis
Leukocytosis Positive stool culture for E. coli O157:H7 Positive stool test for shiga-toxin Elevated amylase/lipase
AST, Aspartate aminotransferase; LDH, lactate dehydrogenase.