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.
Highlights
Cilostazol is an antiplatelet drug that is widely prescribed for the prevention of secondary stroke
We report a case of cilostazol-induced Acute tubulointerstitial nephritis (ATIN) accompanied by immunoglobulin A (IgA) nephropathy
A renal biopsy was performed after stopping oral cilostazol and revealed diffuse lymphocyte infiltration in the interstitium accompanied by mild interstitial fibrosis and tubular atrophy (Fig. 3a, b and c)
Summary
Cilostazol is a phosphodiesterase type III inhibitor and an antiplatelet drug for recurrent stroke prevention [1]. We report a case of cilostazol-induced ATIN accompanied by immunoglobulin A (IgA) nephropathy. Case presentation A 69-year-old woman (height, 148.7 cm; weight, 59.3 kg) was admitted to our hospital because of acute kidney injury She had a history of right corona radiata infarct and had been taking cilostazol (50 mg) twice daily for to prevent recurrent cerebral infarction; cilostazol had been prescribed at another hospital 13 months before admission. The serum IgE level was normal (80 U/mL) She had not had signs of headaches, palpitations, diarrhea, rash, flank pain, arthralgia, eosinophilia, or macroscopic hematuria. A renal biopsy was performed after stopping oral cilostazol and revealed diffuse lymphocyte infiltration in the interstitium accompanied by mild interstitial fibrosis and tubular atrophy (Fig. 3a, b and c). After two courses of this regimen, we reduced the dose
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