Cilostazol-induced acute tubulointerstitial nephritis accompanied by IgA nephropathy: a case report

Abstract

BackgroundCilostazol is an antiplatelet drug that is widely prescribed for the prevention of secondary stroke. Adverse reactions to cilostazol include headaches, palpitations, and diarrhea. Little is known about the nephrotoxicity of cilostazol, such as acute kidney injury. We report a biopsy-proven case of diffuse tubulointerstitial nephritis induced by cilostazol.Case presentationA 69-year-old woman prescribed cilostazol was hospitalized for acute kidney injury. On admission, her renal function deteriorated, with an increased serum creatinine level. Urinalysis showed hematuria, proteinuria, and hyper-beta2-microglobulinuria. A renal biopsy revealed diffuse tubulointerstitial nephritis associated with IgA nephropathy, and gallium-67 scintigraphy showed uptake in the bilateral kidneys. A drug lymphocyte stimulation test for cilostazol was positive, and the patient was diagnosed with cilostazol-induced acute tubulointerstitial nephritis. Despite discontinuation of cilostazol, her renal function rapidly worsened and steroid pulse therapy was initiated, followed by oral high-dose glucocorticoid therapy. After steroid treatment, her serum creatinine level normalized in parallel with urine beta2-microglobulin.ConclusionCilostazol can induce acute tubulointerstitial nephritis.

Alogliptin-Induced Minimal Change Nephrotic Syndrome and Interstitial Nephritis

“…7 The administration period before the occurrence of AIN varies depending on the drug (ranging from 7 days to 18 months). 8,9 In this case, AIN might have developed at 14 months after beginning alogliptin treatment. AIN is reported to have classic symptoms, such as fever, arthralgia, and rash.…”

IgA Vasculitis Developed as an Adverse Effect of Tofacitinib Taken for Rheumatoid Arthritis

“…In the present case, IgA vasculitis developed 6 months after the patient started taking tofacitinib, and complete remission was achieved after 9 months and 11 days through termination of the drug, which suggests a clinical course similar to that reported for drug-induced glomerulonephritis. Secondary IgA vasculitis has been reported in patients with malignancies or infections and in those taking nivolumab, cilostazol, vancomycin, carbamazepine, ceftriaxone, cyclosporine, or metronidazole (12)(13)(14). However, our patient had no malignancy or infection and was not taking any of the aforementioned drugs.…”