背景:急性肾小管间质性肾炎(AIN)是一种免疫介导的疾病,可引起急性肾损伤(AKI)。我们旨在调查AIN患者的特征和治疗反应的预测因素。
方法:在本研究中,纳入了在2006年至2021年间在肾活检中诊断为AIN的31例患者。基线临床,组织病理学,和实验室发现,包括全血细胞计数(CBC),肌酐,红细胞沉降率,C反应蛋白,C3,C4,全身免疫炎症指数(SII),中性粒细胞与淋巴细胞比率(NLR),血小板与淋巴细胞比率(PLR),和尿液分析进行了评估。治疗反应,死亡率,并记录了末次随访时的肌酐水平.
结果:中位年龄为46岁,80.6%为女性。基线肌酐和蛋白尿水平中位数为4.1mg/dL和0.84g/天。中位随访期为14个月,93.5%接受免疫抑制剂治疗。5名患者(16.1%)出现终末期肾病(ESKD)。17例(54.8%)患者肾脏恢复(肌酐<1.4mg/dL)。间质纤维化程度较高,肾小管萎缩,肉芽肿形成,全球肾小球硬化,和更高的基线血红蛋白水平,除了从首发症状到免疫抑制剂开始的间隔时间较长外,还与肾脏不恢复有关,统计。此外,进展为ESKD的患者基线血红蛋白(p=0.033)和淋巴细胞(p=0.044)较高,PLR水平较低(p=0.016),以及较高程度的全球肾小球硬化(p=0.014),间质纤维化(p=0.042),和肾小管萎缩(p=0.030)。
结论:AIN的治疗反应率很低,这可能会导致ESKD。除了组织病理学标本中的慢性,较高的基线血红蛋白水平和较低的血小板/淋巴细胞比率可能是预后因素.应进一步研究AIN的新标记。
BACKGROUND: Acute tubulointerstitial nephritis (AIN) is an immune-mediated disorder that can cause acute kidney injury (AKI). We aimed to investigate the characteristics of patients with AIN and predictive factors for treatment response.
METHODS: In this
study, thirty-one patients diagnosed with AIN on kidney biopsy between 2006 and 2021 were included. Baseline clinical, histopathological, and laboratory findings, including complete blood count (CBC), creatinine, erythrocyte sedimentation rate, C‑reactive protein, C3, C4, systemic immune inflammation index (SII), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and urinalysis were evaluated. Treatment response, mortality, and creatinine levels at the time of last follow-up were also noted.
RESULTS: The median age was 46 years and 80.6% were female. Median baseline creatinine and proteinuria levels were 4.1 mg/dL and 0.84 gram/day. The median follow-up period was 14 months and 93.5% received immunosuppressives. End-stage kidney disease (ESKD) developed in five patients (16.1%). Renal recovery (creatinine < 1.4 mg/dL) was observed in 17 patients (54.8%). Higher degrees of interstitial fibrosis, tubular atrophy, granuloma formation, global glomerulosclerosis, and higher baseline hemoglobin levels, in addition to a longer interval between first symptom to initiation of immunosuppressives were associated with renal nonrecovery, statistically. Also, patients who progressed to ESKD had higher baseline hemoglobin (p = 0.033) and lymphocyte (p = 0.044) and lower PLR levels (p = 0.016), as well as higher degrees of global glomerulosclerosis (p = 0.014), interstitial fibrosis (p = 0.042), and tubular atrophy (p = 0.030).
CONCLUSIONS: Treatment response rates are low for AIN, which may lead to ESKD. Besides chronicity in histopathology specimens, higher baseline hemoglobin levels and lower platelet-to-lymphocyte ratio might be prognostic. Further studies should be conducted on new markers for AIN.