阿卡波糖对尿微量白蛋白水平的影响

将32例2型糖尿病患者随机分为安慰剂组和治疗组(阿卡波糖治疗组),测定各指标.结果治疗前两组一般资料和血糖、血脂、HbA1c及24小时尿微量白蛋白水平均无明显差异.三月后,治疗组的BMI、FPG、2hPG、TG、TC、HbA1c、24小时尿微量白蛋白水平均降低,与安慰剂组、服药前比较差异具有显著性.相关分析提示24小时尿微量白蛋白水平与2hPG、HbA1c和TG呈正相关(r分别为0.64、0.72、0.60,P＜0.05).结论本研究显示,阿卡波糖可降低2型糖尿病患者的24小时尿微量白蛋白水平,对2型糖尿病肾脏病变的防治有积极作用.     

糖尿病前期尿白蛋白排泄率和微量白蛋白尿患病率的比较

目的　比较糖耐量正常 (NGT)、单纯空腹血糖受损 (I IFG)、单纯糖耐量低减 (I IGT)、糖耐量低减合并空腹血糖受损 (IGT/IFG)、新诊断的 2型糖尿病 (2型DM ) 5种不同糖代谢状态的尿白蛋白排泄率 (UAE)和微量白蛋白尿 (MAU )患病率。方法　根据 75g口服葡萄糖耐量试验 (75gOGTT)结果 ,将 2 93 4例受试者分为 :NGT组 13 3 2例、I IFG组 186例、I IGT组 470例、IGT/IFG组 2 3 6例、新诊断的 2型DM组 710例。用放射免疫法测定过夜 12h尿白蛋白。UAE在 2 0～ 2 0 0μg/min之间定义为MAU。 结果　 (1)UAE水平 [中位数 (四分位数 ) ] ,在新诊断的 2型DM组为8 50 (4 89～ 15 95) μg/min、IGT/IFG组为 6 93 (4 85～ 10 89) μg/min、I IGT组为 6 51(4 0 9～10 74) μg/min ,均高于I IFG组的 5 56(3 70～ 9 2 3 ) μg/min(P值均 <0 0 1) ;I IFG组与NGT组的 5 2 6(3 50～ 8 12 ) μg/min比较差异无显著性 (P >0 0 5) ;MAU的患病率在新诊断的 2型DM组为 2 0 7%、IGT/IFG组为 13 1%、I IGT组为 11 7%、I IFG组为 5 8%、NGT组为 5 6% ,同样呈现上述变化规律。(2 )多元逐步回归分析显示 :UAE与OGTT 2h血糖、舒张压、体重指数呈现独立正相关。logistic回归分析显示 ,导致MAU危险性增加的因素有OGTT 2h血糖、舒张     

高糖对体外培养肾小管上皮细胞增殖的影响

利用体外培养胎儿肾小管上皮细胞在不同糖浓度刺激下采用四甲基偶氮多胍(MTT)渗入法观察肾小管上皮细胞的增殖情况.结果生长在糖浓度25mmol／L中的上皮细胞24小时为0.196±0.023(吸光度),48小时为0.194±0.027;在糖浓度5.15mmol／L中,24小时为0.240±0.028,48小时为0.236±0.027;两者差异(P＜0.05).结论高糖对体外培养肾小管上皮细胞的增殖起到一定的抑制作用.     

2型糖尿病患者微量白蛋白尿缓解的相关因素

目的：评估2型糖尿病患者中微量白蛋白尿缓解的发生率以及研究可能对患者微量白蛋白尿预后产生影响的因素。     

高血压患者微量白蛋白尿的阳性率及相关因素

本文研究国内高血压患者微量白蛋白尿(MAU)的阳性率及相关因素.入选102例不伴有糖尿病及原发性肾脏疾病的原发性高血压患者.用酶联免疫法测定早晨第一次尿中微量白蛋白,并以108例健康人做对照.尿中微量白蛋白小于20μg/ml为MAU阴性,在20～200μg/ml为MAU阳性.发现MAU的阳性率为23%,显著高于正常人的5%.高血压患者中,MAU阳性者与MAU阴性者相比,体重指数大、有家族史多、收缩压和平均压较高,与空腹血浆胰岛素、胰岛素敏感性指数及脂质指标无关,而且MAU阳性患者并发中风率高.以尿微量白蛋白为应变量作多元逐步线性回归,发现收缩压、体重指数和病程可进入方程;而以中风为应变量作Logistic回归分析发现尿微量白蛋白、收缩压、体重指数和腰臀比可进入方程.说明在不伴有糖尿病的高血压患者中,MAU阳性与血压升高、肥胖和家族史相关,而与胰岛素抵抗及脂质代谢无关.MAU是中风的独立相关因素.     

原发性高血压患者的糖代谢状态及其与尿白蛋白水平的关系

目的观察原发性高血压患者的糖代谢状态，并分析其与尿蛋白水平的关系，为临床原发性高血压的并发症防治提供依据。方法我院同期收治的400例原发性高血压患者（血压控制良好184例、控制不良216例），均抽取空腹静脉血，采用全自动生化分析仪测定空腹血糖（FBG）、血尿素氮、肌酐；收集24h尿液，采用自动散射比浊仪测定白蛋白含量。结果血压控制良好者糖代谢异常率（糖代谢异常＋糖尿病）显著低于血压控制不良者，Z=-49．87（P〈0．05）；伴血糖调节异常及糖尿病者的24h尿白蛋白水平显著高于糖代谢正常者（P〈0．05）；糖代谢状态不同者的血尿素氮、肌酐均无显著差异，但随血糖升高有增高趋势；随糖代谢异常加重尿白蛋白阳性率显著升高，P〈0．05（r=48．124）。结论原发性高血压患者中约半数合并糖代谢异常（尤以血压控制不良者为著），且随糖代谢异常程度加重尿白蛋白水平升高；临床应重视对此类患者的筛选和管理，在降压治疗的同时有效控制和稳定血糖，以改善肾脏功能。     

微量白蛋白尿与糖尿病足溃疡关系的临床分析

目的 探讨微量的蛋白尿与搪尿病足溃疡之间关系。方法 将252例Ⅱ型搪尿病病人分为搪尿病足(DF)病变组和无足部病变(NDF)组，测定24h尿白蛋白进行分析。结果 尿微量白蛋白与搪尿病足显著相关。结论 尿微量白蛋白是搪尿病足溃疡的危险因素之一，及早控制尿微量白蛋白有助于减少DF的发生。     

糖尿病患者尿微量白蛋白测定与病程、血糖水平的相关分析

尿微量白蛋白 (UAE)测定是目前临床上常用的诊断早期糖尿病肾病的方法。我们检测了 86例尿常规蛋白阳性的糖尿病患者的尿微量白蛋白排泄量(UAE) ,对其与糖尿病病程、血糖水平的相互关系进行了分析。1　资料与方法1 .1　临床资料　本组男 38例 ,女 48例 ;年龄 30～78岁 ,平均 55.4～ 2 4 .8岁。糖尿病 1型 5例 ,2型 81例 ,常规尿蛋白均阳性。另设正常对照组 2 6例 ,其中男 1 1例 ,女 1 5例 ;年龄 2 8～ 73岁 ,平均 52 .6± 2 1 .7岁 ;无慢性疾病及肾病史。1 .2方法　收集晨尿 5ml置 4℃待用 ,用放免法测定UAE,放免药盒由中国原子能科学研…     

Mechanisms of metabolic memory and renal hypoxia as a therapeutic target in diabetic kidney disease

Diabetic kidney disease (DKD) is a worldwide public health problem. The definition of DKD is under discussion. Although the term DKD was originally defined as ‘kidney disease specific to diabetes,’ DKD frequently means chronic kidney disease with diabetes mellitus and includes not only classical diabetic nephropathy, but also kidney dysfunction as a result of nephrosclerosis and other causes. Metabolic memory plays a crucial role in the progression of various complications of diabetes, including DKD. The mechanisms of metabolic memory in DKD are supposed to include advanced glycation end‐products, deoxyribonucleic acid methylation, histone modifications and non‐coding ribonucleic acid including micro ribonucleic acid. Regardless of the presence of diabetes mellitus, the final common pathway in chronic kidney disease is chronic kidney hypoxia, which influences epigenetic processes, including deoxyribonucleic acid methylation, histone modification, and conformational changes in micro ribonucleic acid and chromatin. Therefore, hypoxia and oxidative stress are appropriate targets of therapies against DKD. Prolyl hydroxylase domain inhibitor enhances the defensive mechanisms against hypoxia. Bardoxolone methyl protects against oxidative stress, and can even reverse impaired renal function; a phase 2 trial with considerable attention to heart complications is currently ongoing in Japan.     

Chronic renal dysfunction in cirrhosis: A new frontier in hepatology

Chronic kidney disease (CKD) in patients with liver cirrhosis has become a new frontier in hepatology. In recent years, a sharp increase in the diagnosis of CKD has been observed among patients with cirrhosis. The rising prevalence of risk factors, such as diabetes, hypertension and nonalcoholic fatty liver disease, appears to have contributed significantly to the high prevalence of CKD. Moreover, the diagnosis of CKD in cirrhosis is now based on a reduction in the estimated glomerular filtration rate of < 60 mL/min over more than 3 mo. This definition has resulted in a better differentiation of CKD from acute kidney injury (AKI), leading to its greater recognition. It has also been noted that a significant proportion of AKI transforms into CKD in patients with decompensated cirrhosis. CKD in cirrhosis can be structural CKD due to kidney injury or functional CKD secondary to circulatory and neurohormonal imbalances. The available literature on combined cirrhosis-CKD is extremely limited, as most attempts to assess renal dysfunction in cirrhosis have so far concentrated on AKI. Due to problems related to glomerular filtration rate estimation in cirrhosis, the absence of reliable biomarkers of CKD and technical difficulties in performing renal biopsy in advanced cirrhosis, CKD in cirrhosis can present many challenges for clinicians. With combined hepatorenal dysfunctions, fluid mobilization becomes problematic, and there may be difficulties with drug tolerance, hemodialysis and decision-making regarding the need for liver vs simultaneous liver and kidney transplantation. This paper offers a thorough overview of the increasingly known CKD in patients with cirrhosis, with clinical consequences and difficulties occurring in the diagnosis and treatment of such patients.     

Genetics of cardiovascular and renal complications in diabetes

The development of debilitating complications represents a major heathcare burden associated with the treatment of diabetes. Despite advances in new therapies for controlling hyperglycemia, the burden associated with diabetic complications remains high, especially in relation to cardiovascular and renal complications. Furthermore, an increasing proportion of patients develop type 2 diabetes at a younger age, putting them at higher risk of developing complications as a result of the increased exposure to hyperglycemia. Diabetes has become the main contributing cause to end‐stage renal disease in most countries. Although there has been important breakthroughs in our understanding of the genetics of type 1 and type 2 diabetes, bringing important insights towards the pathogenesis of diabetes, there has been comparatively less progress in our understanding of the genetic basis of diabetic complications. Genome‐wide association studies are beginning to expand our understanding of the genetic architecture relating to diabetic complications. Improved understanding of the genetic basis of diabetic cardiorenal complications might provide an opportunity for improved risk prediction, as well as the development of new therapies.     

Incidence and clinical outcomes of acute kidney injury requiring renal replacement therapy in Japan

No population-based studies have described the prevalence of acute kidney injury (AKI) treated with renal replacement therapy (RRT) in Japan. This study prospectively examined the incidence of AKI requiring RRT by surveying 16 hospitals in Shizuoka prefecture from January to October 2006. The subjects comprised 242 patients treated with RRT during the observation period. The estimated incidence of AKI requiring RRT was 13.3 cases/100,000 persons/year in this area. Major contributing factors for AKI were sepsis (34%), cardiac shock (23%), and major surgery (12%). The in-hospital mortality rate was 47.1%, paralleling the increased number of insufficient organs. Oliguria was a risk factor for in-hospital mortality. These findings suggest that the incidence of AKI treated with RRT in Japan is comparable to those in Western countries, and the prognosis of AKI patients requiring RRT is also poor in Japanese patients.     

Improvement of albuminuria after renal denervation

Objectives

The primary objective of this study was the effect of renal denervation (RDN) on elevated urinary albumin-to-creatinine ratio (UACR) in treatment-resistant hypertensive patients. In addition, patients were stratified according their UACR at baseline into micro- (30–300 mg/g, n = 37) and macroalbuminuria (≥ 300 mg/g, < 2200 mg/g, n = 22).

Background

Increased albuminuria indicates cardiovascular and renal damage in hypertension. RDN emerged as an innovative interventional approach to reduce blood pressure (BP) and may thus reduce albumin urinary excretion.

Methods

Fifty-nine treatment-resistant hypertensive patients with elevated UACR at baseline underwent catheter-based RDN using the Symplicity Flex™ catheter (Medtronic Inc., Santa Rosa, CA).

Results

In the whole and pre-specified subgroups both office and 24-h ambulatory BP were significantly reduced 6 months after RDN. In parallel, a significant reduction in UACR occurred in all patients (160 (65–496) versus 89 (29–319) mg/g creatinine, p < 0.001) and in both subgroups (microalbuminuria: 83 (49–153) versus 58 (17–113) mg/g creatinine, p = 0.001; macroalbuminuria: (536 (434–1483) versus 478 (109–1080) mg/g creatinine, p < 0.001). In accordance, the prevalence of micro- and macroalbuminuria decreased significantly. Regression analysis revealed a modest positive relationship between the decrease of UACR and the fall of systolic BP (β = 0.340, p = 0.039) independent of renal function. Renal function remained unchanged after RDN.

Conclusions

In summary, following RDN, the magnitude of albuminuria as well as the prevalence of micro- and macroalbuminuria decreased in treatment-resistant hypertensive patients. Since albuminuria is an independent renal and cardiovascular risk factor, our findings suggest a reduction of renal and cardiovascular risk in these patients.     

Fracaso renal agudo en pacientes hospitalizados por COVID-19

Background and aimIn December 2019, a coronavirus 2019 (COVID-19) outbreak, caused by SARS-CoV-2, took place in Wuhan, China, and was declared a global pandemic in March 2020 by the World Health Organization. It is a prominently respiratory infection, with potential cardiological, hematological, gastrointestinal and renal complications. Acute kidney injury (AKI) is found in 0.5-25% of hospitalized COVID-19 patients and constitutes a negative prognostic factor. Renal damage mechanisms are not completely clear. We report the clinical evolution of hospitalized COVID-19 patients who presented with AKI requiring attention from the Nephrology team in a tertiary hospital in Madrid, Spain.MethodsThis is an observational prospective study including all COVID-19 cases that required hospitalization and Nephrology management from March 6th to May 12th 2020. We collected clinical and analytical data of baseline characteristics, COVID-19 and AKI evolutions.ResultsWe analyzed 41 patients with a mean age of 66.8 years (SD 2.1), 90.2% males, and with a history of chronic kidney disease in 36.6%. A percentage of 56.1 presented with severe pneumonia or acute respiratory distress syndrome, and 31.7% required intensive care. AKI etiology was prerenal in 61%, acute tubular necrosis in the context of sepsis in 24.4%, glomerular in 7.3% and tubular toxicity in 7.3% of the cases. We reported proteinuria in 88.9% and hematuria in 79.4% of patients. A percentage of 48.8 required renal replacement therapy. Median length of stay was 12 days (IQR 9-23) and 22% of the population died. Patients who developed AKI during hospital stay presented with higher C-reactive protein, LDH and D-dimer values, more severe pulmonary damage, more frequent ICU admission, treatment with lopinavir/ritonavir and biological drugs and renal replacement therapy requirement.ConclusionsHypovolemia and dehydration are a frequent cause of AKI among COVID-19 patients. Those who develop AKI during hospitalization display worse prognostic factors in terms of pulmonary damage, renal damage, and analytical findings. We believe that monitorization of renal markers, as well as individualized fluid management, can play a key role in AKI prevention.     

Comparison of spironolactone and trichlormethiazide as add‐on therapy to renin–angiotensin blockade for reduction of albuminuria in diabetic patients

To compare the efficacy of spironolactone and trichlormethiazide, as add‐on therapy to renin–angiotensin system (RAS) blockade, for reduction of albuminuria in diabetic patients with chronic kidney disease (CKD), we conducted this randomized, open‐labeled, parallel‐group, active‐controlled, per‐protocol‐design study. Type 2 diabetic patients receiving an angiotensin‐converting enzyme inhibitor or angiotensin II receptor blocker, with persistent albuminuria (≥100 mg/g creatinine) were randomly assigned to either spironolactone (25 mg/day) or trichlormethiazide (2 mg/day). The primary outcome was the change in albuminuria at 24 weeks of treatment. In patients who completed 24 weeks of treatment with spironolactone (n = 18) and trichlormethiazide (n = 15), albuminuria decreased significantly by −57.6 ± 21.3% (SD) (P < 0.001) and −48.4 ± 27.1% (P < 0.001), respectively. There was no significant difference in the change in albuminuria between groups (P = 0.270). This pilot study suggests add‐on therapy with spironolactone or trichlormethiazide to RAS blockade may be comparably beneficial to reducing albuminuria in type 2 diabetic patients. This trial was registered with UMIN‐CTR (no. UMIN000008914).     

Review of the renal endpoints used in cardiovascular safety clinical trials in type 2 diabetes mellitus patients and their importance in primary care

Chronic kidney disease (CKD) is one of the most common complications of type 2 diabetes mellitus (T2DM). Furthermore, CKD confers a considerable increase in the risk of cardiovascular (CV) morbidity and mortality. In line with the need to improve knowledge in this field, this article aims to describe the renal endpoints used in the different cardiovascular outcome trials (CVOTs). The objective is to better know the renal variables used in the different CVOTs in order to optimize the implementation of advances in the prevention of progressive diabetic kidney disease in patients with T2DM in clinical practice.