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Acute renal failure due to intratubular crystal precipitation can be seen in a variety of clinical settings, the most common being acute uric acid nephropathy and the administration of intravenous acyclovir [1,2]. (See "Uric acid renal diseases".)
In addition, a similar problem can be induced by sulfonamide antibiotics, ethylene glycol, megadose vitamin C, methotrexate, and indinavir. Patients with any of these disorders can present with acute renal failure that may be asymptomatic or associated with symptoms and signs that may include flank pain, hematuria, pyuria, and crystalluria [3].
Acyclovir, which is usually given in an intravenous dose of 500 mg/m2, is rapidly excreted in the urine (being both filtered and secreted) and has a relatively low solubility [3]. Thus, bolus intravenous therapy, especially if the patient is not well hydrated, may lead to the deposition of acyclovir crystals in the tubules, resulting in intratubular obstruction and foci of interstitial inflammation [3,4]. Ganciclovir, another antiviral agent that is structurally related to acyclovir and is also excreted in the urine, appears to be associated with little or perhaps no risk of crystal-induced acute renal failure [3,5].
Renal function in affected patients typically begins to deteriorate soon after therapy with acyclovir is initiated. Patients may complain of nausea and flank or abdominal pain at this time, presumably induced by the urinary tract obstruction [3]. In some cases, birefringent needle-shaped acyclovir crystals can be seen in the urine, particularly under polarized light.
The decline in renal function may be severe, with the plasma creatinine concentration exceeding 8 mg/dL (704 µmol/L) in some cases. However, complete recovery typically occurs within four to nine days after acyclovir is discontinued. Therapy of established renal failure is supportive and consists of hydration and an attempt to wash out the obstructing crystals via the administration of a loop diuretic. Fluid loss induced by the diuretic must be replaced to prevent volume depletion and a late slowing of flow within the tubules.
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