目的 探讨糖尿病肾病(DN)合并糖尿病周围神经病变(DPN)患者血清C肽水平及其与肾功能、神经传导速度的相关性.方法 选取121例DN患者,根据其是否合并DPN将其分为合并DPN组56例和单纯DN组65例,另选取同期40例健康体检者作为健康组.比较3组研究对象的空腹C肽(FCP)水平、餐后2 h C肽(2hPCP)水平、肾功能指标[血清尿素氮、血清肌酐、24 h尿蛋白]水平、右腓总神经运动神经传导速度(MNCV)和感觉神经传导速度(SNCV).分析合并DPN组患者血清C肽水平与肾功能指标水平、神经传导速度的关系.结果 合并DPN组的FCP、2hPCP水平均低于单纯DN组与健康组,单纯DN组的2hPCP水平低于健康组(均P<0.05),而健康组与单纯DN组的FCP水平差异无统计学意义(P>0.05).合并DPN组的24 h尿蛋白、血清尿素氮、血清肌酐水平均高于单纯DN组与健康组,单纯DN组的上述指标均高于健康组(均P<0.05).合并DPN组的MNCV、SNCV均慢于单纯DN组与健康组(均P<0.05),而健康组与单纯DN组的MNCV、SNCV差异均无统计学意义(均P>0.05).合并DPN组患者的FCP、2hPCP水平与24 h尿蛋白、血清尿素氮、血清肌酐水平均呈负相关,与MNCV、SNCV均呈正相关(均P<0.05).结论 相比于单纯DN患者,合并DPN的DN患者的血清C肽水平降低、肾功能障碍程度更明显,且存在周围神经传导功能障碍.DN合并DPN患者的血清C肽水平与肾功能及周围神经传导障碍程度相关.

越来越多的证据表明,疼痛可普遍发生于慢性心力衰竭患者中,发生率随着心功能恶化而上升.疼痛可以在多方面影响患者生活质量和预后,为慢性心力衰竭治疗加大了难度,但在临床上往往没有引起足够重视.本文就慢性心力衰竭患者疼痛的发生率、常见部位、疼痛的来源、影响因素、疼痛对慢性心力衰竭患者的影响及疼痛的药物治疗进行综述,希望提高临床对慢性心力衰竭患者疼痛的认识和重视,为慢性心力衰竭患者疼痛治疗提供参考.

目的 检测老年射血分数中间值心力衰竭(HFmrEF)患者血清可溶性CD146(sCD146)的水平,探讨其对老年HFmrEF患者的临床诊断价值.方法 选取2020年9月至2021年10月间牡丹江医学院附属红旗医院老年病科和心血管内科就诊射血分数(LVEF:40％～49％)、纽约心功能分级(NYHA分级)Ⅱ级～Ⅳ级的老年心衰患者34例(老年HFmrEF组),非老年心衰患者34例(非老年HFmrEF组),同期健康体检老年者31例(健康老年组)作为研究对象.收集所有患者的年龄、性别、血压、心率、总胆红素、血肌酐、胆固醇等数据,所有患者均常规行超声心动图检查,检测血清N末端前体脑利钠肽(NT-proBNP)、sCD146水平.比较各组患者的一般资料、NT-proBNP、超声心动图相关指标、sCD146水平的差异,分析相关性,受试者工作特征曲线(ROC)评价sCD146对HFmrEF的诊断价值.结果 三组患者收缩压、舒张压、血浆白蛋白、胆固醇、低密度脂蛋白无显著性差异(P>0.05),而心率、总胆红素、同型半胱氨酸、血肌酐有明显差异(P<0.05);三组研究对象左室后壁厚度、每搏输出量无统计学意义(P>0.05),而左心室室间隔厚度、左室舒张末期前后径、左室收缩末期前后径、左室舒张末期容积中有显著差异(P<0.05);三组患者的血清NT-proBNP、sCD146水平有显著性差异(P<0.05),且HFmrEF患者的NT-proBNP、sCD146浓度均显著高于健康老年组患者;老年HFmrEF组与非老年HFmrEF组,sCD146与NT-proBNP、心功能分级呈正相关;sCD146诊断HFmr EF的曲线下面积为:0.945(95％CI:0.894,0.996),最佳截断值:68.459 ng/mL,灵敏度、特异度分别为:85.3％、93.5％.结论 血清sCD146浓度在老年HFmrEF、非老年HfmrEF显著升高,sCD146对老年HFmrEF的诊断和病情评估有意义;老年HFmrEF患者血清sCD146与NT-proBNP、心功能分级具有相关性.

Acute kidney injury (AKI) is a prevalent and serious illness in all clinical departments, with a high morbidity and death rate, particularly in intensive care units, where prevention and treatment are crucial. As a result, active prevention, early detection, and timely intervention for acute kidney injury are critical. The current diagnostic criteria for acute kidney injury are an increase in serum creatinine concentration and/or a decrease in urine output, although creatinine and urine output merely reflect changes in kidney function, and AKI suggests injury or damage, but not necessarily dysfunction. The human kidney plays a crucial functional reserve role, and dysfunction is only visible when more than half of the renal mass is impaired. Tubular damage markers can be used to detect AKI before filtration function is lost, and new biomarkers have shown a new subset of AKI patients known as "subclinical AKI." Furthermore, creatinine and urine volume are only marginally effective for detecting subclinical AKI. As a result, the search for new biomarkers not only identifies deterioration of renal function but also allows for the early detection of structural kidney damage. Several biomarkers have been identified and validated. This study discusses some of the most promising novel biomarkers of AKI, including CysC, NGAL, KIM-1, lL-18, L-FABP, IGFBP7, TIMP-2, Clusterin, and Penkid. We examine their performance in the diagnosis of subclinical AKI, limitations, and future clinical practice directions.