慢性肾脏病患者耳鸣耳聋患病率及临床特点调查

目的:探讨慢性肾脏病(CKD)患者耳鸣耳聋的患病率及其相关临床特点。方法:采用横断面的调查方法,收集CKD患者相关信息和耳鸣耳聋的性质及程度,对肾脏病患者耳鸣耳聋患病率及其临床特点进行分析。结果:(1)CKD患者中耳鸣的患病率为51.6%,耳聋患病率为44.8%。耳鸣频率以高频为主,耳聋以双耳轻度听力损害的感音神经性耳聋居多。(2)CKD患者随年龄层的增加,耳聋的患病率呈明显的上升趋势。(3)继发性肾脏病患者的耳聋患病率高于原发性肾小球疾病的患者。(4)在不同临床诊断中,糖尿病肾病及高血压肾病耳聋的患病率最高。(5)CKD患者耳聋的患病率随CKD分期的增加呈明显上升趋势。说明肾脏病患者耳聋的患病率与肾功能状态及肾小球滤过率密切相关。结论:(1)CKD患者以高频耳鸣为主,轻度听力损害的感音神经性耳聋居多。(2)CKD患者随年龄层的增加及肾功能和肾小球滤过率的下降,耳聋的患病率呈明显的上升趋势。(3)继发性肾脏病患者的耳聋患病率高于原发性患者,其中糖尿病肾病及高血压肾病耳聋的患病率最高。     

蛋白尿引起慢性肾脏病肾小管损伤的机制及治疗

越来越多的基础及临床研究表明,无论原发病如何,蛋白尿均可加速慢性肾脏病(CKD)的进展,直至发展为终末期肾病(ESRD).蛋白尿对CKD疾病预后的预测价值已经明确,对于1型糖尿病肾病(DN)患者和非糖尿病患者,蛋白尿基线水平是一个独立判断预后的指标[1,2].     

面对慢性肾病患者心血管病的严重挑战--"新"危险因素与防治对策

慢性肾病(CKD)流行病学的最新资料表明,心血管疾病(CVD)是CKD患者最主要的并发症,而且其患病率大大高于普通人群;CVD也是导致CKD患者死亡的头号杀手,至今死亡率仍居高不下.因此,CKD患者CVD问题已引起国内外学者的高度关注.     

三维圆周应变评价早期慢性肾病患者左心室心肌收缩功能变化

目的采用三维整体圆周应变(GCS)评价早期慢性肾病(CKD)患者左心室心肌收缩功能。方法选取26例CKD2期患者(CKD2期组)、20例CKD3期(CKD3期组)患者及30名健康志愿者(对照组)。对所有受检者行常规二维超声心动图和三维斑点追踪成像(3D-STE),测量并比较常规超声心动图指标,包括左心室舒张末期间间隔厚度(IVSTd)、左心室舒张末期内径(LVEDd)、左心室舒张末期后壁厚度(LVPWTd)、左心室舒张末期容积(EDV)和收缩末期容积(ESV),以及3D-STE指标,包括三维左心室射血分数(3D-LVEF)、三维左心室心肌质量指数(3D-LVMi)及左心室GCS。结果与对照组比较,CKD2期组的IVSTd增大,LVEDd、GCS减小;CKD3期组的IVSTd、LVESV、3D-LVMi增大,LVEDd、3D-LVEF、GCS减小;与CKD2期组比较,CKD3期组的IVSTd、3D-LVMi增大,LVEDd、GCS减小,以上差异均有统计学意义(P均0.05)。结论早期CKD患者左心室心肌收缩功能已减低,可通过GCS进行评价。     

羟苯磺酸钙对糖尿病肾病患者肾小球滤过率下降速率的影响

目的探讨羟苯磺酸钙对糖尿病肾病患者的估算肾小球滤过率(estimated glomerular filtration rate,eGFR)下降速率的影响。方法回顾性分析2009年2月至2013年10月在我院规律随诊的糖尿病肾病患者337例,治疗组为糖尿病肾病患者144例,常规降糖药物治疗基础上加用羟苯磺酸钙胶囊口服(500 mg,每日3次),对照组为糖尿病肾病患者193例,予以常规降糖药物治疗。2组患者的初始慢性肾脏病(chronic kidney disease,CKD)分期为CKD1~3期,比较2组患者间月肾小球滤过率下降的情况。结果加用羟苯磺酸钙治疗的糖尿病肾病患者(治疗组)的月肾小球滤过率下降率(ΔeGFR)明显低于未加用羟苯磺酸钙治疗的糖尿病肾病患者(对照组)[(-0.33±2.43)ml/min比(0.19±2.24)ml/min,P0.05]。依据患者初始eGFR进行CKD分期发现,在CKD3期时,治疗组的ΔeGFR明显低于对照组[(-0.98±1.55)ml/min比(-0.17±1.32)ml/min,P0.05]。依据患者起始尿蛋白情况对治疗组进行分组比较发现,尿蛋白增多的患者ΔeGFR明显增高(P0.05)。进一步对尿蛋白定量正常组进行比较发现,治疗组的ΔeGFR明显低于对照组[(-1.29±2.32)ml/min比(0.06±1.53)ml/min,P0.01]。结论羟苯磺酸钙能改善糖尿病肾病患者肾功能,在CKD3期时更为明显,建议在尿蛋白定量正常时就开始加用羟苯磺酸钙治疗。     

慢性肾脏病合并急性冠脉综合征诊治进展

正慢性肾脏病(Chronic kidney disease,CKD)合并急性冠脉综合征(acute coronary syndrome,ACS)是指患者既往有CKD病史,并发了ACS。流行病学调查显示,1 457例冠心病造影患者的临床资料调查结果表明中重度肾病的患病率为30.96%,其中慢性肾脏病CKD3~5期所占比例分别为28.35%,2.06%,0.55%,与普通社区CKD的患病率相比明显升高,显示了CKD     

老年慢性肾脏病患者不同预后的危险因素分析及相关性研究

在我国,慢性肾脏病(CKD)的患者人数众多,已成为我国又一重要的公共卫生问题,成为继高血压、糖尿病、冠心病、脑卒中四大慢病以外的又一威胁人类健康的慢性疾病。20世纪晚期以来,随着社会老龄化进程的加快,CKD的发病率也逐渐升高。而CKD的预后终点事件包括:全因死亡、心血管事件(CVD)、急性肾损伤(AKI)、快速肾功能下降(RKFD)、终末期肾病(ESRD)。因此,CKD预后的评估以及危险因素分析对于CKD患者的早期发现、干预和管理、避免漏诊及过度诊断都尤为重要。本文着重介绍CKD患者不同预后事件的危险因素及胱抑素C在预后方面的风险评估。     

维持性血透患者高磷血症的现状与治疗进展

正慢性肾脏病(chronic kidney disease,CKD)是严重的世界公共健康问题,占全球人口8%~16%[1]。据报道,我国CKD发病率约为10.8%,终末期肾病发病率为0.04%[2]。慢性肾脏病-矿物质和骨代谢异常(CKD-MBD)是慢性肾脏病患者重要并发症之一,是累及多个系统的症候群,与CKD患者死亡率密切相关。DOPPS分析提示我国透析患者高磷血症患病率高     

干预CKD从控制清晨高血压开始

慢性肾病(CKD)逐渐成为威胁人类健康的重要疾病,我国CKD呈上升趋势,患病率达10.8%,CKD患者近1.2亿,其中50%～70%合并高血压。高血压是CKD的病因和并发症之一,《中国高血压防治指南2010》明确指出"严格控制血压是延缓肾脏病变进展,预防心血管事件发生的关键。"因此,对CKD进行干预,加强肾病高血压的管理极为重要。     

血脂异常在慢性肾脏病中的作用及机制研究进展

慢性肾脏病(chronic kidney disease,CKD)是一组慢性进展性疾病,患病率高,并发症多,预后差,已成为世界范围内的公共卫生问题。美国的调查[1]资料表明,成人CKD的患病率为14.8%;而我国的全国性调查结果提示,我国成年人CKD的患病率约为10.8%[2]。CKD患者血脂异常的患病率较高,有研究提示CKD患者血脂异常的患病率约为40%[3,4],而透析患者的血脂异常患病率则超过60%,且血脂异常对肾功能进展、心血管疾病(cardiovascular disease,CVD)等CKD并发症及患者的预后均产生重要的影响[5]。另一方面,血脂异常患者发生CKD的风险也较高,肾病进展也加快。鉴于血脂异常与CKD的相互影响,本文就血脂异常在CKD的发生、进展及预后中的作用及相关机制,对近年来国内外的相关文献报道进行综述,为CKD患者血脂异常的防治提供一定参考。     

免疫法粪便隐血试验预测慢性肾脏病患者预后的意义

目的 探讨免疫法粪便隐血试验(IFOBT)在慢性肾脏病患者发生结直肠病变的预测意义及作为慢性肾脏病患者预后指标的临床价值.方法 前瞻性纳入176例慢性肾脏病(CKD)患者和180例健康人作为对照.使用免疫法粪便隐血试验进行检测,比较两组粪便隐血阳性发生率.同时对CKD患者随访4.5年,分析各项临床、生化指标,并以患者接受肾脏替代治疗或死亡为终点事件.采用Logistic回归进行危险因素分析,采用Kaplan-Meier分析和COX回归模型进行生存分析.结果 176例CKD患者IFOBT阳性率17％,高于健康对照组5.3％(x2=13.236,P＜ 0.01).与IFOBT阴性的CKD患者相比,IFOBT阳性的CKD患者年龄较大[(62.030±15.544)岁比(48.660±19.018)岁,P＜0.01]、红细胞沉降率明显升高[(71.800±31.657) mm/h比(57.210±32.712) mm/h,P＜0.05]、C反应蛋白明显升高[6.230 (3.000～14.148) mg/L比3.000(3.000 ～6.833)mg/L,P＜0.05]、Scr明显升高[419.100(103.200～546.625) μmol/L比175.100 (68.150～462.950) μmol/L,P＜0.05],而血红蛋白[(97.970±20.590 )g/L比(107.170±27.988)g/L,P＜0.05]及肾小球滤过率(eGFR)[11.400 (8.671～53.544) ml· min-1· (1.73 m2)-1比35.274(10.961～82.145)ml·min-1.(1.73 m2)-1,P＜0.01]显著降低.相关法分析显示CKD患者IFOBT检测值与eGFR(r=-0.20,P＜0.01)呈负相关;与Scr呈正相关(r=0.171,P＜0.05);与年龄呈正相关(r=0.175,P＜0.05).Logistic回归和COX回归分析结果显示IFOBT检测值、eGFR和红细胞沉降率是CKD患者预后的重要影响因素.Kaplan-Meier分析显示IFOBT检测值＞100 μg/L是影响CKD患者生存率的重要因素.结论 慢性肾脏病患者易发生结直肠出血性疾病,粪便隐血阳性是影响CKD患者预后的重要危险因素,而免疫法粪便隐血试验是可行有效的检测方法,对于CKD患者结直肠病变的预测具有重要的临床意义.     

Effects of correction of metabolic acidosis on blood urea and bone metabolism in patients with mild to moderate chronic kidney disease: a prospective randomized single blind controlled trial

BACKGROUND: There are no controlled trials on the efficacy of oral bicarbonate therapy in patients with mild to moderate chronic kidney disease (CKD). This prospective randomized controlled study was done to evaluate the effects of correction of metabolic acidosis on renal functions and bone metabolism in this group of patients. PATIENTS AND METHODS: Forty patients were randomized to treatment with oral bicarbonate or placebo for a period of 3 months. Investigations at baseline included venous pH, bicarbonate, renal functions, serum iPTH, and bone radiology. The treatment group (Group B) received daily oral sodium bicarbonate therapy at a dose of 1.2 mEq/kg of body weight. Their venous blood pH and bicarbonate levels were estimated weekly to keep blood pH near 7.36 and bicarbonate at 22-26 mEq/L by adjusting the dose of sodium bicarbonate. At the end of 3 months, all the tests were repeated in both groups. RESULTS: After oral bicarbonate therapy (OBT), there was a significant decline in the rise of blood urea level in Group B associated with a sense of well-being in 50% patients. The rise in parathormone (PTH) was six times the baseline value in Group A and only 1.5 times baseline value in Group B, although not statistically significant. There was no significant change in total calcium, phosphorus, alkaline phosphatase, creatinine, total protein, or albumin levels. CONCLUSION: Correction of metabolic acidosis in patients with moderate CKD attenuates the rise in blood urea and PTH, which might prevent the deleterious long-term consequences of secondary hyperparathyroidism.     

Higher preoperative eGFR is a predictor of worse renal function decline after robotic assisted radical cystectomy: Implications for postoperative management

IntroductionIn patients with muscle invasive bladder cancer or high risk noninvasive bladder cancer, renal function decline is a concern after radical cystectomy with urinary diversion. The pathophysiology of this decline is multifactorial, with subclinical acidosis and metabolic derangements from the diversion thought to contribute. It is unknown whether patients with baseline chronic kidney disease (CKD) are at increased risk of further decline in renal function.MethodsWe performed a retrospective review of two high volume robotic assisted radical cystectomy (RARC) centers between 2016 and 2020. Preoperative demographics and comorbidities were collected. Postoperative estimated glomerular filtration rate (eGFR) was calculated at 12 and 24 months to determine short-term rate in decline of eGFR. Absolute and percent changes in eGFR were calculated.ResultsThere were a total of 555 patients who underwent RARC. Men comprised 76.2% of the cohort. Neoadjuvant chemotherapy was given in 31% of patients and adjuvant chemotherapy was given in 4.81% of patients. Higher preoperative eGFR (B -0.549, 95% CI -0.708 to -0.391, P < 0.001) and presence of diabetes mellitus (B -15.414, 95% CI -24.820 to -6.008, P = 0.001) were significant predictors of eGFR decline at 12 months. At 24 months, presence of diabetes mellitus (B -11.799, 95% CI -21.816 to -1.782, P = 0.021) and higher preoperative eGFR (B -0.621, 95% CI -0.796 to -0.446, P < 0.001) were correlated with a steeper decline in eGFR. Higher preoperative eGFR was also predictive of upstaging to CKD3 or higher post operatively (OR 1.019, 95% CI 1.004–1.034, P = 0.015). Intracorporeal diversion was protective, whereas presence of hypertension, diabetes mellitus, and higher preoperative eGFR predicted greater decline in eGFR.ConclusionPatients with higher preoperative eGFR and diabetes are at increased risk of renal function decline post RARC at 12 and 24 months. This suggests that patients with risk factors for renal function decline, but otherwise normal renal function at baseline, are a particularly vulnerable population for progression to CKD after RARC and should be counseled and closely followed postoperatively for renal function deterioration.     

糖尿病肾病患者血清C1q/肿瘤坏死因子相关蛋白3的表达及临床意义

目的:探讨血清C1q/肿瘤坏死因子相关蛋白3(CTRP3)的表达水平与糖尿病肾病不同程度肾脏损害的关系。方法:选取2019年1月至2019年5月本院就诊的患者,符合NKF-KDOQI标准的2型糖尿病肾病患者为糖尿病肾病组(DN组,41例),再依据肾小球滤过率估计值(eGFR)将其分为两个亚组{EDN组[21例,肾小球滤...     

Effects of Correction of Metabolic Acidosis on Blood Urea and Bone Metabolism in Patients with Mild to Moderate Chronic Kidney Disease: A Prospective Randomized Single Blind Controlled Trial

Background. There are no controlled trials on the efficacy of oral bicarbonate therapy in patients with mild to moderate chronic kidney disease (CKD). This prospective randomized controlled study was done to evaluate the effects of correction of metabolic acidosis on renal functions and bone metabolism in this group of patients. Patients and Methods. Forty patients were randomized to treatment with oral bicarbonate or placebo for a period of 3 months. Investigations at baseline included venous pH, bicarbonate, renal functions, serum iPTH, and bone radiology. The treatment group (Group B) received daily oral sodium bicarbonate therapy at a dose of 1.2 mEq/kg of body weight. Their venous blood pH and bicarbonate levels were estimated weekly to keep blood pH near 7.36 and bicarbonate at 22–26 mEq/L by adjusting the dose of sodium bicarbonate. At the end of 3 months, all the tests were repeated in both groups.Results. After oral bicarbonate therapy (OBT), there was a significant decline in the rise of blood urea level in Group B associated with a sense of well-being in 50% patients. The rise in parathormone (PTH) was six times the baseline value in Group A and only 1.5 times baseline value in Group B, although not statistically significant. There was no significant change in total calcium, phosphorus, alkaline phosphatase, creatinine, total protein, or albumin levels. Conclusion. Correction of metabolic acidosis in patients with moderate CKD attenuates the rise in blood urea and PTH, which might prevent the deleterious long-term consequences of secondary hyperparathyroidism.     

Sarcoid tubulo-interstitial nephritis: long-term outcome and response to corticosteroid therapy

Sarcoidosis is a chronic relapsing multi-systemic disorder characterized by the development of non-caseating granulomas. Granulomatous tubulo-interstitial nephritis is an uncommon manifestation of this condition. We identified 39 patients with sarcoidosis and renal disease from a single center of whom 17 patients had biopsy-proven tubulo-interstitial nephritis. They were analyzed with respect to demographic and clinical features, including response to corticosteroids and length of follow-up. They all presented with significant renal impairment. At presentation the mean+/-s.d. estimated glomerular filtration rate (eGFR) was 26.8+/-14 ml/min by modification of diet in renal disease (MDRD) equation 7. With treatment there was a significant improvement in renal function with eGFR 49.6+/-5.2 ml/min (P<0.01) at 1 year, and 47.9+/-6.8 ml/min (P<0.05) at the last review. The median follow-up was 84 months (range 6-284 months). Patients with chronic kidney disease (CKD) 3, the mean eGFR was 38.30+/-2.4 ml/min at presentation and 60.2+/-7.4 ml/min at 1 year (P=0.02) and in CKD 4 it improved from 19+/-2 to 38+/-6.6 ml/min at 1 year (P<0.05). After the 1st year, the change in eGFR was +0.8 ml/min/year for CKD 3 and -2 ml/min/year for CKD 4 (P<0.05). Three patients ceased their therapy either due to complications or poor compliance and experienced a worsening of renal function which was then reversed on re-commencing corticosteroids. Corticosteroids are effective in advanced tubulo-interstitial nephritis due to sarcoidosis. Long-term treatment is necessary to preserve renal function and to delay the onset of end-stage renal disease.     

Effect of urate-lowering therapy on renal function in chronic kidney disease stages 2-5

Objective To investigate the effect of urate-lowering therapy on renal function in chronic kidney disease (CKD) stages 2-5 patients with hyperuricemia (HUA). Methods A total of 132 patients of CKD stages 2-5 with HUA between July 2016 and December 2017 in Department of Nephrology of the Second Affiliated Hospital of Anhui Medical University were prospectively and self-controlled analyzed. Serum uric acid (SUA), estimated glomerular filtration rate (eGFR) and other clinical parameters were measured at baseline and after 1-6 months treatment. The patients were divided into group A (CKD stages 2-3a) and group B (CKD stages 3b-5) on the baseline value of eGFR. The changes of SUA and eGFR before and after treatment were compared. According to the level of SUA after 6 months treatment, patients were divided into attainment group (SUA＜360 μmol/L) and nonattainment group (SUA≥360 μmol/L). The difference of renal function in pre-treatment and post-treatment was compared. Multiple stepwise linear regression was used to analyze the relationship among the change of eGFR after receiving 6 months' treatment (deGFR) and SUA level, baseline eGFR and other indexes. Results After 1, 3, 6 months treatment, the average levels of SUA, Scr and urea nitrogen of all patients were decreased significantly while eGFR value was increased significantly (all P＜0.050) than those in pre-treatment period. After six-month-therapy, proteinuria and hematuria were improved significantly in all patients (P＜0.001, P=0.001). Compared with pre-treatment period, both the SUA levels of group A and group B were declined significantly while eGFR had a significant rise after treatment (P＜0.001). The change of eGFR post-treatment in group A was significantly higher than that of group B [(13.64±15.35) vs (8.97±9.79) ml?min-1?(1.73 m2)-1, P=0.044]. At 6 months after treatment, the eGFR value increased markedly in both attainment group and nonattainment group compared with pre-treatment period (P＜0.001). After six-month-therapy, the eGFR value in attainment group was increased more obviously than that of nonattainment group [(13.96±14.64) vs (8.03±9.69) ml?min-1?(1.73 m2)-1, P=0.021]. Multiple stepwise linear regression analysis showed that the baseline eGFR value was an influencing factor of deGFR (b=0.161, P=0.020). Conclusions The renal function of CKD stages 2-5 patients with HUA can be significantly improved by urate-lowering therapy, which can effectively reduce proteinuria and hematuria.     

The urate-lowering efficacy of febuxostat and its effect on renal function in hyperuricemic patients with chronic kidney disease stages 3-5

Objective To investigate the urate-lowering efficacy and renal effect of febuxostat in hyperuricemic patients with chronic kidney disease (CKD) stages 3-5. Methods A prospective, randomized, controlled trial of CKD stages 3-5 patients with hyperuricemia was conducted from June 2015 to June 2016. Patients were randomly assigned to either febuxostat group (treatment group) or allopurinol group (control group). Patients in treatment group received febuxostat 40 mg/d after study initiation, and the dosage was changed to 20 mg/d if serum uric acid (sUA)＜360 μmol/L. Patients in control group were administered a dose of 100 mg/d of allopurinol. Serum uric acid, serum creatinine and other clinical parameters were measured at baseline and 1-6 months after treatment. The rate of achieving target sUA level and the change of eGFR in two groups were performed using SPSS 21.0. Results A total of 98 patients met the inclusion criteria and completed the trial. The treatment group and the control group had 51 cases and 47 cases, respectively. There was no significant difference between the two groups in age, sex, body mass index (BMI), blood pressure, serum creatinine, eGFR, sUA and renal diseases (P＞0.05). At month 1-6, there were significant differences between treatment group and control group in the rate of achieving target sUA level (P＜0.01). At month 1 and month 3, no statistical difference was observed in the change of eGFR between the two groups (P=0.624, P=0.319). At month 6, the changes in eGFR were +2.23 ml?min-1?(1.73 m2)-1 and -4.36 ml?min-1?(1.73 m2)-1 in the treatment and control group, respectively, and the difference between the two groups was significant (P=0.037). In patients with CKD stages 3-5, generalized estimating equation showed that after adjusting for confounding variables, the eGFR increased 1.149 ml?min-1?(1.73 m2)-1 (P=0.003) and 24-hour urinary protein decreased 0.019 g/d (P=0.037) when per 60 μmol/L decreased in sUA. Febuxostat 20 mg/d was able to keep target sUA levels in 90.2% patients with CKD stages 3-5 within half a year and no serious adverse effects appeared. Conclusions Febuxostat performs better than allopurinol in lowering urate and delaying progression of renal function in patients with CKD stages 3-5 and HUA. Febuxostat 20 mg/d may be the effective and safe maintenance dose to maintain target sUA level in patients with CKD stages 3-5, but whether it can be used as the best long-term maintenance dose needs to be further studied.     

165例特发性膜性肾病临床及病理特征与肾功能的相关性分析

目的 研究特发性膜性肾病（IMN）患者肾功能水平与临床及病理特征之间的相关性。方法 对2010年1月至2016年12月于深圳大学附属第一医院确诊的165例IMN患者的临床及病理资料进行回顾性分析；按照基线肾功能水平eGFR（估算肾小球滤过率）分为CKD1期组、CKD2期组、CKD3+4+5期组,比较患者人口学、临床生化指标及病理指标等的差异。采用相关性方程分析肾功能与年龄、24 h尿蛋白量、血压、临床生化指标及病理指标的相关性。采用二元logistic回归方程分析影响肾功能下降的危险因素。结果 ①患者年龄14～84（45.33±15.19）岁，临床表现为肾病综合征82例（49.6%）,伴高血压76例（46.1%）,合并水肿129例（78.1%）；②与CKD1期的患者相比，CKD2期以上的患者临床及病理具有男性比例高、高龄、高血压及肾病综合征发生率高的特点,且CKD分期越高（即eGFR水平越低）的患者，肾小球节段硬化、肾间质炎症细胞浸润及肾小动脉壁增厚的比例越高；③相关性分析结果提示，肾功能与年龄、高血压、24 h尿蛋白、血清尿酸水平、肾间质炎症细胞浸润、肾小管萎缩、肾小动脉壁增厚呈负相关（P<0.05）；④logistic多因素回归分析显示性别、24 h尿蛋白定量、高尿酸血症、肾间质炎症细胞浸润为IMN患者肾功能损害的独立危险因素。结论 IMN患者初诊时年龄、是否合并肾病综合征及高血压是eGFR下降的相关因素；男性、大量蛋白尿、高尿酸血症、肾间质炎症细胞浸润是影响IMN患者肾功能重要的预测因子。