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• W2100073762 abstract "Dear Editor, Polyarteritis nodosa (PN) is necrotizing arteritis of medium or small arteries without glomerulonephritis or vasculitis in the arterioles, capillaries or venules, unassociated with anti-neutrophil cytoplasmic antibodies (ANCAs).1 Here, we report the atypical survival of a patient with PN complicated with chronic interstitial nephritis for over 2 years. A 70-year-old woman with a history of subarachnoid hemorrhage, ischemic colitis and small bowel obstruction presented with aggravating persistent nocturnal fever and claudication and was admitted to our hospital. Laboratory tests revealed leukocytosis with neutrophilia (12, 200/μL) and mild normocytic anemia (9.8 g/dL) as well as elevated serum creatinine (1.0 mg/dL), C-reactive protein (CRP) (18.27 mg/dL) and immunoglobulin (Ig)G4 (191 mg/dL). Anti-nuclear antibody was positive (1 : 80), with a homogeneous and speckled appearance. ANCAs, hepatitis B antigens and hepatitis C antibody were negative. Urinalysis showed 5–9 red blood cells per high-power field and elevated urinary tubular dysfunction markers, including N-acetyl-β-d-glucosaminidase (NAG, 26.5 IU/g·creatinine) and α1-microglobulin (32.0 mg/g·creatinine). Cerebral angiography revealed a subarachnoid hemorrhage without an evident aneurysm. Moreover, self-limiting ischemic colitis and surgically treated small bowel obstruction occurred. All 3 events occurred separately within 2 years before admission. NAG and α1-microglobulin were initially elevated with normal kidney function without electrolyte disturbance; negative CRP was maintained, except during the events mentioned above. Fever, hypertension and claudication aggravation newly manifested before admission. Histopathological evidence of small intestinal vasculitis from a surgically resected specimen due to small bowel obstruction prior to this admission as well as renal and sural nerve vasculitis after admission prior to treatment initiation were observed. After prednisolone administration at a maximum dose of 75 mg/day, fever, blood pressure, CRP and urinary tubular dysfunction markers normalized on hospitalization day 28. However, on day 42, partial jejunectomy was performed, prompted by an abrupt ileal perforation. Although CRP normalized postoperatively, an additional operation was performed because of an abrupt second small bowel perforation on day 63. The patient received 1 month of antibiotics treatment from day 81 for a catheter-related infection, preventing cyclophosphamide administration. However, negative CRP was re-attained with prednisolone alone. The patient was discharged on day 224 after being administered cyclophosphamide 500 mg/body intravenously, considering minor re-elevation of CRP and history of recurrent small intestine perforation due to vasculitis, concurrent with prednisolone 16 mg/day (Fig. 1a). Regarding histopathological findings, renal biopsy showed active small-to-medium arteritis (i.e., arcuate [Fig. 1b] and interlobular artery) and severe interstitial lymphocyte infiltration without fibrosis (Fig. 1c) but no evidence of IgG4-related tubulointerstitial nephritis or glomerulonephritis. Left sural nerve biopsy showed chronic small perineurial arteritis. The first gross small intestine observation showed a large ulcer involving the whole circumference, while 2 subsequent observations showed perforations. Histopathologically, all observations showed a mixture of acute and chronic small-to-medium arteritis. Therefore, the patient was diagnosed with PN on the basis of systemic symptoms and ANCA-negative necrotizing arteritis of the small and medium arteries without glomerulonephritis or venulitis. Angiography showed a right renal artery aneurysm (Fig. 1d) and focal occlusive lesions of the superior mesenteric and bilateral renal arteries. An interstitial lesion due to chronic renal ischemia caused by arcuate and interlobular artery injury was unlikely because of the absence of renal atrophy (12 cm on the major axis on angiography), significant focal tubular necrosis (especially in the outer medulla), and interstitial fibrosis, all of which are pathological findings of chronic renal ischemia.2 Other possible causes of the vasculitis and interstitial nephritis, such as drugs and Sjögren syndrome, were excluded on the basis of history, and laboratory and histopathological findings. Although there was no angiographic evidence of intracranial aneurysm formation, the etiology of the subarachnoid hemorrhage was considered cerebral vasculitis, because the hemorrhage occurred at multiple sites simultaneously in the presence of distal dysesthesia. Although tubulointerstitial lesions are associated with ANCA-associated vasculitis,3 the relationship between PN and interstitial nephritis remains unclear. There is only 1 reported case of renal biopsy-proven PN in the literature, which was clinically suspected to be acute interstitial nephritis;4 interstitial nephritis was not confirmed histopathologically and could be classified as ANCA-associated vasculitis because of the presence of myeloperoxidase-ANCA and fibrocellular crescent. Among 18 renal biopsy cases of tubulointerstitial changes in systemic vasculitis,5 2 had necrotizing vasculitis mainly involving medium muscular arteries without glomerulonephritis; however, no information about ANCA positivity or chronicity is available for these cases. All other reported cases of interstitial nephritis are now classified as ANCA-associated vasculitis depending on the Chapel Hill definition1 or other etiologies such as drug-induced, which should not be ruled out. Thus, the present case is the first case of PN presenting with biopsy-proven chronic interstitial nephritis. Almost all PN cases require immunosuppressive treatment according to the Five-Factor Score.6 Only 2 PN cases with spontaneous recovery have been reported, including a case in a 27-year-old man7 and a child.8 Collectively considering the mixture of old and new histopathological findings and clinical courses, minor inflammation in PN, which was serologically undetectable by CRP, may have continuously existed. In summary, PN can progress insidiously in the presence of chronic interstitial nephritis. None of the authors have any conflicts of interest to declare." @default.
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• W2100073762 date "2015-05-27" @default.
• W2100073762 modified "2023-10-14" @default.
• W2100073762 title "Polyarteritis nodosa complicated with chronic interstitial nephritis" @default.
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• W2100073762 doi "https://doi.org/10.1111/1756-185x.12628" @default.
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