Pediatric emergency medicine trisk 2900 2900
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children who presented with isolated hematuria with or without
nonnephrotic range proteinuria, but 20% of those who have significant
proteinuria on initial diagnosis will go on to develop CKD.
Acute Interstitial Nephritis
Goals of Treatment
Patient care for AIN is primarily supportive. The symptomatic
consequences such as fluid and electrolyte imbalances from AKI and
associated systemic symptoms should be mitigated. The offending agent
should be identified, if possible and discontinued or treated, if not already
done so. Symptomatic relief of systemic symptoms such as fever or rash
may need to be provided.
CLINICAL PEARLS AND PITFALLS
The causative agent should be discontinued or treated promptly,
when possible.
Care is generally supportive.
Clinical Considerations
Clinical recognition. AIN is characterized by inflammatory infiltration
within the interstitium of the kidney leading to AKI. It is often the result of
a drug reaction but can be caused by infection or systemic processes, as
well. Many medications can cause AIN, and it is often difficult or
impossible to identify the potential offending agent. Nonsteroidal antiinflammatories, antibiotics (including penicillins, cephalosporins,
sulfonamides, ciprofloxacin, and rifampin), proton pump inhibitors,
allopurinol, antiretrovirals, and 5-aminosalicylates are a few of the
implicated drugs. Injury is not dose dependent and may occur in the setting
of previous tolerance of the medication. The onset of AIN may occur weeks
to months after the first exposure to the causative agent but is usually within
3 to 5 days if it is secondary to a reexposure. Numerous infections have also
been implicated including cytomegalovirus (CMV), Epstein–Barr virus
(EBV), Leptospira , Yersinia , Legionella , and Mycobacterium tuberculosis
. Autoimmune disorders including systemic lupus erythematosus (SLE) and
