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outpatient by a specialist to monitor weight, blood pressure, and response to
therapy. In children in whom infection is suspected, appropriate antibiotics
with coverage for S. pneumoniae and gram-negative bacterial infections
should be provided.
Though children with nephrotic syndrome are at risk for thromboembolic
complications, there is no clear evidence supporting prophylactic
anticoagulation. Supportive measures to reduce the risk of
thromboembolism include mobilization and avoiding intravascular volume
depletion. If thrombosis does occur, anticoagulation should be initiated.
As for long-term management of nephrotic syndrome, identification of
the underlying cause is necessary. Greater than 90% of patients with MCD
will respond to glucocorticoid therapy. Given the high frequency of MCD
as the cause of idiopathic nephrotic syndrome and the favorable response of
MCD to glucocorticoid therapy, an empiric trial of glucocorticoid therapy
without confirmatory pathology is often provided to prepubertal children
with suggestive clinical characteristics (between 1 and 10 years of age at
presentation; normal renal function, blood pressure, and complement levels;
benign urine sediment). Adolescents are also considered for empiric
therapy, though obtaining a renal biopsy prior to therapy or after a defined
period of glucocorticoid therapy without response would be reasonable
given the increased occurrence of FSGS, MPGN, and membranous
nephropathy in this age group. Patients with idiopathic nephrotic syndrome
are further classified on the basis of their response to glucocorticoid
therapy:
glucocorticoid-responsive,
glucocorticoid-dependent,
and
glucocorticoid-resistant nephrotic syndrome. Patients with responsive
disease have a favorable long-term prognosis, and those with resistant
pattern have a more guarded prognosis.

CHRONIC KIDNEY DISEASE
CLINICAL PEARLS AND PITFALLS