2型糖尿病合并非糖尿病肾病的临床及病理分析

目的：回顾性分析2型糖尿病合并非糖尿病肾病的临床表现及病理特征。方法：回顾性分析2004年1月～2009年12月临床疑为合并非糖尿病肾病的110例2型糖尿病患者的肾活检资料。根据肾活检结果分为单纯糖尿病肾病（DN）组和糖尿病肾病合并非糖尿病肾病（NDRD）组,并对临床和病理资料进行分析。结果：110例2型糖尿病肾病患者中,50例（45.5%）合并非糖尿病肾病。糖尿病肾病合并非糖尿病肾病组蛋白尿、血尿发生率高于单纯糖尿病肾病组,但糖尿病视网膜病变发生率低于单纯糖尿病肾病组。两组年龄、糖尿病病程、高血压、血肌酐和肾小球滤过率差异无统计学意义。所有合并的非糖尿病肾病中,IgA肾病的比率最高为34%,其他依次为膜性肾病22.0%,系膜增殖性肾小球肾炎14%,HBV相关性肾小球肾炎8.0%,微小病变型肾小球肾炎10%,高血压肾小球硬化4.0%,FSGS4.0%,新月体肾小球肾炎2.0%,狼疮性肾炎2.0%。结论：2型糖尿病肾病合并非糖尿病肾病发生率45.5%,IgA肾病最常见。血尿、蛋白尿同时缺乏糖尿病视网膜病变强烈提示合并非糖尿病肾病。对于临床表现不典型的患者,肾活检是一项排除糖尿病肾脏病变的重要手段。     

2型糖尿病合并非糖尿病性肾病1例及文献复习

目的:研究分析2型糖尿病患者合并非糖尿病性肾脏疾病(NDRD)的临床病理特点,旨在提高该病的早期诊断率.方法:报道经治疗的1例2型糖尿病合并NDRD(血管炎)的临床资料,并分析文献报道的91例患者的资料.结果:2型糖尿病可以合并多种非糖尿病性肾损害,包括各种原发性或继发性肾脏疾病,其中以IgA肾病为最多.无糖尿病视网膜病变、血尿、血糖控制满意、急性肾衰竭高度提示NDRD的存在.结论:2型糖尿病合并肾损害不一定是糖尿病肾病,可以是NDDR,早期诊断和有效治疗有助于改善预后.     

2型糖尿病合并非糖尿病肾病的临床病理特征和预测因子的分析

目的:探讨2型糖尿病(type 2 diabetes mellitus, T2DM)合并非糖尿病肾病患者的临床指标和肾活检病理特征,寻找疾病的预测因子。方法:回顾性分析2016年07月—2021年12月在我院行肾活检的76例T2DM患者病例。根据活检结果分为糖尿病肾病(diabetic nephropathy, DN)组30例,非糖尿病肾病伴/不伴糖尿病肾病(non-diabetic renal disease with/without diabetic nephropathy, NDRD±DN)组46例,对其临床指标及病理结果进行分析。结果:两组患者的年龄、性别、糖尿病病程(diabetes mellitus, DM)、糖尿病视网膜病变(diabetic retinopathy, DR)、糖化血红蛋白、血红蛋白、血肌酐、尿素氮和胱抑素C比较差异有统计学意义(P<0.05)。肾活检常见原因有活动性尿沉渣,其次为DM<5年且无大量蛋白尿和新出现的肾病综合征。NDRD±DN组最常见的病理类型是膜性肾病,IgA肾病次之。二元Logistic回归分析发现性别、年龄、DR、糖化血红蛋...     

2型糖尿病合并非糖尿病性肾脏疾病研究现状及进展

早在1936年，Kimmelestiel和Wilson等就首先报道了糖尿病患者所特有的肾脏损害，它是由于糖尿病本身的病情进展而累及肾脏微血管病变所致，故定名为糖尿病肾病（diabetic nephropathy，DN）。2007年发布的KDOQI系列临床实践指南中第一次提出了DKD（diabetic kidney disease），且指出术语“糖尿病肾病”（DN）应该被“糖尿病肾脏疾病”（DKD）取代。     

糖尿病合并非糖尿病肾病的诊断及中医药治疗

糖尿病（DM）患者出现肾损害（蛋白尿或肾功能减退）并不一定就是糖尿病肾病（ diabetic kidney disease,DKD）[1],也可能是糖尿病合并其他肾脏病,而两者的治疗方案及转归不同,本文就糖尿病合并其他肾脏病的诊断及与DKD鉴别诊断和中医治疗介绍如下.     

2型糖尿病合并非糖尿病肾损害12例误诊分析

随着糖尿病患者生命的延长，其慢性并发症逐渐增多，糖尿病肾病（DN）是已为人们所重视的重要并发症之一，然而，也有一些盲目诊断糖尿病肾病的现象，一旦糖尿病患者出现蛋白尿即诊断为糖尿病肾病，致使部分其他原因的肾脏疾病被误诊误治。对近年来我们诊治的2型糖尿病合并非糖尿病肾病损害进行分析皆在提高对糖尿病病人的肾小球疾病的警惕并探索其诊断治疗。     

2型糖尿病肾脏病与2型糖尿病合并非糖尿病肾损害的临床及病理比较

目的分析比较2型糖尿病。肾脏病与2型糖尿病合并非糖尿病肾损害的临床及病理特征异同点。方法回顾性分析2008年1月至2011年4月在我科住院的患者,临床诊断2型糖尿病、并有蛋白尿,行经皮肾活检穿刺术病理检查共105例患者的临床病理资料。结果（1）非糖尿病肾损害组5I例,占48．57％,一般情况如糖尿病病程、高血压病程、代谢紊乱及肾脏损害均较2型糖尿病肾脏病轻。病理类型以原发性肾小球疾病为主,病理改变包括。肾小球损伤及小管-间质改变较2型糖尿病肾脏病组轻微。（2）2型糖尿病肾脏病患者54例,占51．43％。病理损伤的严重程度与体质量指数、血肌酐、胱抑素C、视黄醇结合蛋白、尿素氮呈正相关,而与血红蛋白、白蛋白和肌酐清除率呈负相关。结论在f临床上,对于病程长、代谢紊乱及临床肾损害指标严重的患者,考虑2型糖尿病肾脏病可能性大。     

2型糖尿病患者合并非糖尿病性肾损害的临床病理分析

目的：了解2型糖尿病合并非糖尿病性肾损害的临床病理特点。方法：总结分析29例2型糖尿病合并非糖尿病肾损害的临床资料、病理改变及治疗反应。结果：2型糖尿病或糖尿病肾病可以合并多种非糖尿病肾损害,以各种类型的原发性及继发性肾小球疾病为主。原发性肾小球疾病常见病理类型有轻度系膜增生性肾小球肾炎、膜性肾病、IgA肾病和微小病变。这些患者具有以下不同于典型糖尿病肾病的特点：（1）糖尿病病程短于5年;（2）大量蛋白尿或肾功能不全时血压正常;（3）急性肾功能衰竭;（4）血尿明显。大部分肾病水平蛋白尿患者经糖皮质激素或糖皮质激素联合细胞毒类药物治疗后可完全缓解.结论：（1）2型糖尿病合并肾损害不等于糖尿病肾病;（2）2型糖尿病可以合并各种非糖尿病性肾损害;（3）当2型糖尿病伴肾脏受累者具有上述不符合糖尿病肾病特征时,应尽早行肾活检明确诊断;（4）在充分考虑患者 的临床特点、病理改变、严格控制血糖及血压的情况下,糖皮质激素或糖皮质激素联合细胞毒类药物治疗是安全有效的,可以改变患者的预后。     

2型糖尿病肾病患者骨密度的研究

目的:探讨2型糖尿病(T2DM)合并肾脏病变患者骨密度(BMD)变化的特点。方法:测定36例T2DM合并肾脏病变患者(DN组)、30例无糖尿病肾脏病变T2DM患者(NDN组)和54例健康对照组股骨颈、正位腰椎BMD,并检测糖化血红蛋白(Hb Alc)、血钙(Ca)及血肌酐(Cr)水平。结果:DN组的股骨颈BMD低于健康对照组及NDN组,差异有统计学意义(P0.05);而腰椎BMD在三组人群中差异无统计学意义(P0.05);DN组和NDN组Hb Alc均高于健康对照组(P0.05)。结论:糖尿病肾病是糖尿病骨质疏松发生发展的危险因素之一。     

2型糖尿病肾病危险因素

在最近10年中,糖尿病终末期肾病(ESRD)的发病率和患病率逐年增长。我们通过比较及多因素分析方法,探讨了与2型糖尿病肾病发病有关的各种危险因素。一、对象和方法 1．对象:我院1999年1月1日至2002年3月31日住院患者按WHO诊断标准诊断为2型糖尿病者共692     

Prevalence of nephropathy in black patients with type 2 diabetes mellitus

The prevalence of nephropathy in black patients with type 2 diabetes mellitus is poorly defined. We performed a cross-sectional analysis of 98 unrelated and unselected black type 2 diabetic patients treated in indigent care internal medicine clinics to determine the prevalence of proteinuria and nephropathy. Serum creatinine, blood urea nitrogen, urine albumin and urine creatinine concentrations were measured. A Spearman's rank correlation was computed to test for a relationship between diabetes duration and continuous outcomes. For binary outcomes, an odds ratio and 95% confidence interval were computed for a change of 10 years diabetes duration based on logistic regression. Cases were 61% female, and had mean (+/- SD) age 59.9 +/- 12.5 years, diabetes duration 12.6 +/- 9.4 years, body mass index 32.4 +/- 9.3 kg/m(2), hemoglobin A1C (HbA1C) 9.2 +/- 2.3%, and serum creatinine concentration 1.60 +/- 1.1 mg/dl. For continuous variables, diabetes duration was positively associated with albuminuria (r = 0.31; p = 0.0017), serum creatinine (r = 0.36; p = 0.0003) and blood urea nitrogen concentration (r = 0.36; p = 0.0003). For binary variables, cases with longer diabetes duration were at increased risk for urinary albumin:creatinine >300 microg/mg (p = 0.006), elevated serum creatinine concentration (> or = 1.4 mg/dl in women or > or = 1.6 mg/dl in men; p = 0.045), elevated blood urea nitrogen concentration (> or = 20 mg/dl; p = 0.026), and clinical cerebrovascular disease (p = 0.028). HbA1C, body mass index, and blood pressure did not correlate with diabetes duration in this population. Among the cases, 33.7% had elevated serum creatinine concentration and 71.5% had abnormal levels of albuminuria (27.6% > 300 microg albumin/mg Cr and 43.9% 30-300 microg albumin/mg Cr). Abnormal proteinuria was seen in the majority of black patients with poorly controlled type 2 diabetes mellitus treated in indigent care clinics. This prevalence may be conservative, due to the widespread use of angiotensin-converting enzyme inhibitor therapy and exclusion of cases treated only by nephrologists. Approximately 70% of black patients with type 2 diabetes cared for in indigent care clinics have abnormal proteinuria and are at heightened risk for ESRD and death.     

Oxidative stress markers in type 2 diabetes patients with diabetic nephropathy

Background

Epidemiological studies show that 5–40 % of type 2 diabetes (T2DM) patients have diabetic nephropathy, and oxidative stress is one of several underlying mechanisms. We investigated associations between oxidative stress markers and severity of diabetic nephropathy.

Methods

Fifty-nine T2DM patients from the endocrinology outpatient department were included, and their levels of oxidative stress markers were measured. Three groups were determined by their urine albumin-to-creatinine ratio (UACR): group A (UACR < 30 mg/g, n = 22); group B (30 ≤ UACR < 300 mg/g, n = 22); and group C (UACR ≥ 300 mg/g, n = 15).

Results

Vitamin C levels correlated negatively and moderately with serum creatinine (γ = ?0.459, p < 0.001), urine albumin (γ _s = ?0.458, p = 0.001) and UACR (γ _s = ?0.408, p = 0.001), but only weakly with hydroxy-2-deoxyguanosine (8-OHdG) and estimated glomerular filtration rate (eGFR). Vitamin C levels decreased as 8-OHdG, serum creatinine, albumin and UACR increased. T2DM patients with more severe diabetic nephropathy had lower vitamin C levels.

Conclusion

Our results identified several oxidative stress markers that may be clinically important in diabetic nephropathy. Studies with larger sample sizes should be undertaken to confirm these findings.

     

Evolution of incipient nephropathy in type 2 diabetes mellitus

BACKGROUND: We examined the course of glomerular injury in 12 Pima Indians with long-standing (>8 years) type 2 diabetes mellitus, normal serum creatinine, and microalbuminuria. They were compared with a group of 10 Pima Indians in Arizona with new-onset (<5 years) type 2 diabetes, normal renal function, and normoalbuminuria (<30 mg albumin/g creatinine on random urine specimens). METHODS: A combination of physiological and morphological techniques was used to evaluate glomerular function and structure serially on two occasions separated by a 48-month interval. Clearances of iothalamate and p-aminohippuric acid were used to determine glomerular filtration rate (GFR) and renal plasma flow, respectively. Afferent oncotic pressure was determined by membrane osmometry. The single nephron ultrafiltration coefficient (Kf) was determined by morphometric analysis of glomeruli and mathematical modeling. RESULTS: The urinary albumin-to-creatinine ratio (median + range) increased from 84 (28 to 415) to 260 (31 to 2232) mg/g between the two examinations (P = 0.01), and 6 of 12 patients advanced from incipient (ratio = 30 to 299 mg/g) to overt nephropathy (>/=300 mg/g). A 17% decline in GFR between the two examinations from 186 +/- 41 to 155 +/- 50 mL/min (mean +/- SD; P = 0.06) was accompanied by a 17% decline in renal plasma flow (P = 0.003) and a 6% increase in plasma oncotic pressure (P = 0.02). Computed glomerular hydraulic permeability was depressed by 13% below control values at both examinations, a result of a widened basement membrane and a reduction in frequency of epithelial filtration slits. The filtration surface area declined significantly, however, from 6.96 +/- 2.53 to 5.51 +/- 1.62 x 105 mm2 (P = 0.01), a change that was accompanied by a significant decline in the number of mesangial cells (P = 0.001), endothelial cells (P = 0.038), and podocytes (P = 0.0005). These changes lowered single nephron Kf by 20% from 16.5 +/- 6.0 to 13.2 +/- 3.6 nL/(minutes + mm Hg) between the two examinations (P = 0.02). Multiple linear regression analysis revealed that among the determinants of GFR, only the change in single nephron Kf was related to the corresponding change in GFR. CONCLUSION: We conclude that a reduction in Kf is the major determinant of a decline in GFR from an elevated toward a normal range as nephropathy in type 2 diabetes advances from an incipient to an overt stage.     

Detection of early nephropathy in Mexican patients with type 2 diabetes mellitus

BACKGROUND: The aims of this study were to determine the prevalence of early nephropathy in patients with type 2 diabetes mellitus (DM2) attending primary care medical units and to identify risk factors for nephropathy in this population. METHOD: Seven hundred fifty-six patients with DM2 attending 3 primary care medical units were randomly selected. In a first interview, an albuminuria dipstick and a detailed clinical examination were performed, and a blood sample was obtained. If the albuminuria dipstick was positive, then a 24-hour urine collection was obtained within the next 2 weeks to quantify the albuminuria. In the blood sample, glucose, creatinine, and lipids were determined. Glomerular filtration rate was calculated using the Modification of Diet in Renal Disease Study equation. Demographics and medical history were recorded from clinical examination and medical charts. RESULTS: Prevalence of early nephropathy (EN) was 40%, normal function (NF) was found in 31%, and overt nephropathy (ON) in 29%. Patients with more severe kidney damage were older (NF: 54 +/- 10; EN: 60 +/- 11; ON: 63 +/- 10 years, P < 0.05) and had a higher proportion of illiteracy (NF: 11%, EN: 17%; ON: 25%, P < 0.05). The more severe the nephropathy, the longer the median duration of DM2 (NF: 6.0; EN: 7.0; ON: 11.0 years; P < 0.05); the higher the frequency of hypertension (NF: 38%; EN: 52%; ON: 68%; P < 0.05); and the higher the systolic blood pressure (NF: 126 +/- 21; EN: 130 +/- 19; ON: 135 +/- 23 mm Hg; P < 0.05). Both nephropathy groups had a significantly higher proportion of family history of nephropathy (NF: 4%; EN: 9%; ON: 13%) and a higher frequency of cardiovascular disease (NF: 5%; EN: 12%; ON: 25%), whereas only patients with ON had peripheral neuropathy (NF: 21%; EN: 22%; ON: 43%) and retinopathy (NF: 12%; EN: 18%; ON: 42%) more frequently than others. Fasting glucose was poorly controlled in all groups (NF: 186 +/- 70; EN: 173 +/- 62; ON: 183 +/- 73 mg/dL). Large body mass index (NF: 29.3 +/- 5.3; EN: 29.7 +/- 5.6; ON: 29.6 +/- 5.5 kg/m(2)), smoking (NF: 45%; EN: 43%; ON: 44%), and alcoholism (NF: 29%, EN: 29%; ON: 26%) were frequently found in this population, although there were no significant differences. In the multivariate analysis, only age, duration of DM2, and presence of retinopathy, hypertension, and cardiovascular disease were significantly associated with nephropathy. CONCLUSIONS: Two thirds of Mexican patients with DM2 attending primary health care medical units had nephropathy, 40% of whom were at an early stage of the disease. Many modifiable and nonmodifiable risk factors were present in these patients, but the most significant predictors for nephropathy are older age, longer duration of diabetes, and the presence of retinopathy, hypertension, and cardiovascular disease.     

Development and validation of a predictive model for the differential diagnosis of diabetic nephropathy and non-diabetic renal disease in patients with type 2 diabetes mellitus

Objective To develop and validate a predictive model for the differential diagnosis of diabetic nephropathy (DN) and non-diabetic renal disease (NDRD) in patients with type 2 diabetes mellitus. Methods A retrospective study with patients with type 2 diabetes who underwent renal biopsy in the First Affiliated Hospital of Zhengzhou University from February 2012 to January 2015 was conducted. The dataset was randomly split into development (70.0%) and validation (30.0%) cohorts. Baseline predictors for model development was selected by using univariable and multivariable logistic regression. The model's performance in the two cohorts, including discrimination and calibration, was evaluated by the C-statistic, calibration curve and the P value of the Hosmer-Lemeshow test. Results Among the 931 patients with type 2 diabetes, 478 cases (51.3%) diagnosed as DN alone, 214 cases (23.0%) as NDRD alone and 239 cases (25.7%) as DN plus superimposed NDRD (MIX). Among NDRD and MIX patients, membranous nephropathy was the most common pathological type, followed by IgA nephropathy. The variables selected in the final predictive model were age, duration of diabetes, diabetic retinopathy, systolic blood pressure, hemoglobin, fasting blood glucose, glycosylated hemoglobin, cystatin C. The model performed well with good discrimination and calibration. The C-statistics were 0.913(95%CI 0.892-0.935) in the derivation cohort and 0.897(95%CI 0.876-0.919) in the validation cohort. The model had the best P value of 0.934 of the Hosmer-Lemeshow test. Conclusions A simple predictive model with high accuracy is constructed for predicting the presence of NDRD and MIX for type 2 diabetic patients. The nomogram can be used as a decision support tool to provide a non-invasive method for differential diagnosis of DN and NDRD, which may help clinicians assess the risk-benefit ratio of kidney biopsy for type 2 diabetic patients with renal impairment.     

Total plasma homocysteine and arteriosclerotic outcomes in type 2 diabetes with nephropathy

Total serum homocysteine (tHcy) has been shown to predict de novo and recurrent cardiovascular events in many studies. However, results in diabetic populations with minimal nephropathy are mixed. The independent relationship between tHcy and arteriosclerotic outcomes and congestive heart failure (CHF) events in a population with high cardiovascular risk and diabetic nephropathy was examined. A total of 1575 individuals were enrolled in the international Irbesartan Diabetic Nephropathy Trial (IDNT) and followed for 2.6 yr. All participants had baseline diabetic nephropathy, overt proteinuria, and hypertension and were recruited between 1996 and 1999. A total of 492 total arteriosclerotic outcomes (primary outcome) and 317 CHF events (secondary outcome) were tallied. Established cardiovascular risk factors were highly prevalent, as were high tHcy levels (quintiles [microM]: first 4.5 to 11; second >11 to 13; third >13 to 15; fourth >15 to 19; fifth >19). No association between tHcy and arteriosclerotic outcomes was observed in a univariate model or after adjustment for study randomization and established cardiovascular risk factors. The strongest outcome predictor was the presence of baseline cardiovascular disease, followed by an inverse relationship to diastolic BP. The significant univariate association between tHcy and CHF events disappeared when serum creatinine alone was added to the model. These findings question the utility of tHcy in predicting de novo or recurrent cardiovascular events in individuals with diabetic nephropathy. Further studies are needed to confirm whether these negative results apply to other populations with heavy cardiovascular risk burdens. Previous positive findings can potentially be explained through tHcy's role as a sensitive surrogate marker for kidney disease, itself a recognized cardiovascular risk factor.     

Genetic susceptibility to nephropathy in Pima Indians with type 2 diabetes mellitus

Summary: In Pima Indians, the incidence of end-stage renal disease, nearly all of which is attributable to type 2 diabetes mellitus, is more than 20 times that in the general United States population. Studies in the Pimas indicate that factors other than diabetes per se enhance susceptibility to the development of diabetic nephropathy. Aggregation of renal disease in families, a relationship between parental blood pressure and diabetic nephropathy in the offspring, and an association between higher prediabetic blood pressure and the occurrence of renal disease after the onset of diabetes all point to individual differences in susceptibility. Although clustering of environmental exposures may be responsible for these findings, they may also represent genetic transmission of susceptibility to renal disease. Recently, linkage analyses were performed in 98 diabetic sib-pairs, both affected by diabetic nephropathy. Two adjacent markers on chromosome 7 met the criteria for suggestive linkage with two-point analysis. Positioned between these markers is the gene coding for aldose reductase. Polymorphisms of this locus are associated with diabetic microvascular complications in other populations. Linkage studies provide evidence that familial aggregation of diabetic renal disease reflects, in part, genetic transmission of susceptibility that appears to be independent of the transmission of diabetes.     

Anemia and end-stage renal disease in patients with type 2 diabetes and nephropathy

BACKGROUND: Diabetic nephropathy is the leading cause of end-stage renal disease (ESRD). Anemia is common in diabetics with nephropathy; however, the impact of anemia on progression to ESRD has not been carefully examined. METHODS: We studied the relationship between baseline hemoglobin concentration (Hb) and progression of diabetic nephropathy to ESRD in 1513 participants enrolled in Reduction in Endpoints in NIDDM with the Angiotensin II Antagonist Losartan study and followed for an average of 3.4 years. Multivariate Cox proportional hazards models were used to analyze the relationship between Hb and ESRD, after adjusting for predictors for ESRD. Analyses were performed with Hb stratified by quartile: first quartile <11.3 g/dL, second quartile 11.3 to 12.5 g/dL, third quartile 12.6 to 13.8 g/dL, and fourth quartile >/=13.8 g/dL (reference) and as a continuous variable. RESULTS: Baseline hemoglobin concentration was correlated with subsequent development of ESRD. After adjustment for predictors of ESRD, the hazard ratios for the first, second, and third Hb quartiles were 1.99 (95% CI, 1.34-2.95), 1.61 (95% CI 1.08-2.41), and 1.87 (95% CI 1.25-2.80). With hemoglobin as a continuous variable, the adjusted hazard ratio was 0.90 (95% CI 0.84-0.96, P= 0.0013). The average increase in adjusted relative risk was 11% for each 1 g/dL decrease in hemoglobin concentration. CONCLUSION: Our data suggest that even mild anemia, Hb <13.8 g/dL increases risk for progression to ESRD. Hemoglobin is an independent risk factor for progression of nephropathy to ESRD in type 2 diabetes.