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A case of acute kidney injury with marked hyperuricemia during mizoribine administration
Tomoya Nishino1, Takeaki Shinzato, Yuuki Ohta
1Second Department of Internal Medicine, Nagasaki University of Medicine, Japan.
Abstract:
A 52-year-old woman was diagnosed with Blau syndrome and rheumatoid arthritis and was treated with prednisolone and methotrexate. Joint pain and skin ulcers were poorly controlled; therefore, mizoribine (MZ; 150 mg/day) was administered once daily from March 2011. In early July 2011, the patient was hospitalized because of acute kidney injury (AKI) and acute pancreatitis. We reasoned that AKI resulted from hyperuricemia during MZ administration because serum concentrations of uric acid (31.6 mg/dL) and MZ (trough level, 5.14 µg/mL) were markedly elevated on admission. MZ should be administered with caution because of the risk of marked hyperuricemia leading to AKI.
Insights
Mizoribine (MZ) can cause acute kidney injury due to hyperuricemia. This risk highlights the need for caution when prescribing MZ, especially in patients with pre-existing conditions.
Area of Science:
- Rheumatology
- Nephrology
- Clinical Pharmacology
Background:
- A 52-year-old woman with Blau syndrome and rheumatoid arthritis was treated with prednisolone and methotrexate.
- Poor control of joint pain and skin ulcers led to the addition of mizoribine (MZ).
Observation:
- The patient developed acute kidney injury (AKI) and acute pancreatitis after initiating MZ treatment.
- Elevated serum uric acid (31.6 mg/dL) and MZ levels (5.14 µg/mL) were noted on admission.
Findings:
- Hyperuricemia during MZ administration was identified as the likely cause of AKI.
- Markedly elevated uric acid and MZ levels correlated with the patient's adverse events.
Implications:
- Mizoribine (MZ) administration requires caution due to the risk of severe hyperuricemia.
- Hyperuricemia-induced AKI is a potential complication of MZ therapy that necessitates careful patient monitoring.
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