His renal function have been stable, with the serum creatinine around 1

His renal function have been stable, with the serum creatinine around 1.5?mg/dL, estimated glomerular filtration rate (eGFR) 35?mL/min/1.73 m2 as calculated by a modified version of the Modification of Diet in Renal Disease formula of the Japanese Society of Nephrology [10], and no proteinuria. inflammatory cytokines [8] and promote atherosclerotic plaque regression [9]. Although these findings suggest that evolocumab might have beneficial effects on CCE, its efficacy in that regard has not yet been established. We herein statement a unique case of renal CCE induced by carotid artery stenting that was successfully treated with evolocumab. Case presentation The patient was a 77-year-old man who had been treated for hypertension, hyperlipidemia, and chronic kidney disease with valsartan 40?mg/day and pitavastatin 1?mg/day. His renal function had been stable, with the serum creatinine around 1.5?mg/dL, estimated glomerular filtration rate (eGFR) 35?mL/min/1.73 m2 as calculated by a modified version of Toreforant the Modification of Diet in Renal Disease formula of the Japanese Society of Nephrology [10], and no proteinuria. Three months before referral to our department, severe right internal carotid artery stenosis was detected by magnetic resonance angiography which was performed to explore reasons for dizziness. Dual antiplatelet therapy with aspirin 100?mg/day and clopidogrel 75?mg/day was initiated. Because right internal carotid artery stenosis of 90% had been shown by computed tomography (CT) angiography 14?weeks before referral to our department, he had undergone carotid artery stent placement 5?weeks before referral to our department. At that time, his eGFR level was 32.0?mL/min/1.73 m2. At the follow-up examination 4?weeks after carotid artery stenting, his renal function worsened Toreforant (eGFR 17.1?mL/min/1.73 m2). He was therefore referred to our department for further examination and treatment of the deteriorating renal function (Physique 1). Open in a separate window Physique 1. Clinical course of this case. The horizontal Rabbit polyclonal to ZNF96.Zinc-finger proteins contain DNA-binding domains and have a wide variety of functions, most ofwhich encompass some form of transcriptional activation or repression. The majority of zinc-fingerproteins contain a Krppel-type DNA binding domain and a KRAB domain, which is thought tointeract with KAP1, thereby recruiting histone modifying proteins. Belonging to the krueppelC2H2-type zinc-finger protein family, ZFP96 (Zinc finger protein 96 homolog), also known asZSCAN12 (Zinc finger and SCAN domain-containing protein 12) and Zinc finger protein 305, is a604 amino acid nuclear protein that contains one SCAN box domain and eleven C2H2-type zincfingers. ZFP96 is upregulated by eight-fold from day 13 of pregnancy to day 1 post-partum,suggesting that ZFP96 functions as a transcription factor by switching off pro-survival genes and/orupregulating pro-apoptotic genes of the corpus luteum axis shows the number of weeks from your initiation of evolocumab administration. The vertical axes show the eGFR and LDL-C levels. ARB: Angiotensin II receptor blocker; BP: blood pressure; Toreforant CRP: C-reactive protein; eGFR: estimated glomerular filtration rate; Eosi: eosinophils; LDL-C: low-density lipoprotein cholesterol; PCSK9: proprotein convertase subtilisin/kexin type 9. His systolic/diastolic blood pressure was 141/71?mmHg. Physical examination revealed livedo reticularis in the bilateral toes, with both dorsal pedal arteries palpable. There were no obtaining of numbness or pain in his extremities. Neither neurological symptoms, such as paralysis, dysarthria, and sensory disturbance nor gastrointestinal symptoms including abdominal pain and gastrointestinal bleeding was observed. Laboratory data showed eosinophilia (723/L), slightly elevated C-reactive protein (0.32?mg/dL), and severe renal dysfunction (eGFR 13.9?mL/min/1.73 m2). Results of serological assessments for anti-neutrophil cytoplasmic antibody, anti-glomerular basement membrane antibody, and antinuclear antibody were negative. Serum match concentrations, including C3, C4, and CH50, were within the normal range. His LDL-cholesterol level was managed at 99?mg/dL under statin administration (pitavastatin 1?mg/day) (Table 1). He had not been taking any medicines that could induce acute kidney injury (e.g., chinese herbal medicine, supplements, analgesics). Renal doppler sonography showed no accelerated blood flow in the renal arteries. Ocular fundus examination showed no evidence of CCE in the retina such as retinal cholesterol crystal emboli. Subsequent skin biopsy specimens from an affected toe revealed cholesterol clefts in the small arteries (Physique 2). Renal biopsy was not performed due to severe bleeding risk because he had been receiving dual antiplatelet therapy to prevent stent thrombosis following internal carotid artery stenting. His clinical and pathological findings pointed to a diagnosis of CCE. He was also considered to be at high risk of atherosclerotic cardiovascular events because he had hyperlipidemia with chronic kidney disease and severe carotid artery stenosis. Hence, evolocumab was administered to reduce and stabilize the aortic atherosclerotic plaque with the expectation that it might improve organ involvement in the CCE (Physique 1). One week later, his LDL-cholesterol level experienced decreased to 54?mg/dL, and his declining renal function was halted. Evolocumab administration was continued every 2?weeks. The livedo reticularis was alleviated in the bilateral toes. Finally, 20?weeks after the initiation of evolocumab administration, the patients renal function, which had gradually improved, plateaued at 18.1?mL/min/1.73 m2 (Figure 1). Open in a separate window Physique 2. Skin biopsy shows cholesterol clefts (arrows) in a small artery (hematoxylinCeosin stain, 400). Table 1. Patients laboratory results at the time of referral to our department. activation of ApoE receptor 2 [21] and down-regulation of NF- [22]. With CCE, cholesterol emboli lodge in small arteries, inducing infiltration of macrophages to the affected arteries and granuloma formation. This inflammatory reaction contributes to thrombus formation and endothelial proliferation, leading to arterial obstruction. Finally, these processes result in ischemic damage and infarction [11]. These findings suggest that evolocumab might suppress macrophage activation.