α-酮酸在早期2型糖尿病肾病治疗中的作用

目的观察α-酮酸在早期2型糖尿病肾病治疗中的作用。方法将60例微量白蛋白尿期2型糖尿病肾病患者随机分为:(1)治疗组(n=30),予以低蛋白饮食(蛋白质0.6 g.kg-1.d-1,包括α-酮酸2.4 g,3/d);(2)对照组(n=30),予以常规蛋白饮食(蛋白质1.0 g.kg-1.d-1,不服用α-酮酸)。分别于治疗前、治疗24周后测定:(1)肾脏相关指标:血清尿素(BUN)、肌酐(Cr)、肾小球滤过率(GFR)、尿白蛋白(Alb)、尿转铁蛋白(TRF);(2)营养相关指标:血红蛋白(Hb)、血清白蛋白、体重指数(BMI);(3)代谢相关指标:空腹血糖(FPG)、餐后2h血糖(PPG)、糖化血红蛋白(HbAlc)、空腹血清胰岛素(FINS)、血清甘油三酯(TG)、血清胆固醇(TC)。计算胰岛素敏感指数(ISI)及胰岛素抵抗指数(HOMA-IR)。结果24周后治疗组尿Alb定量、尿TRF较对照组明显下降(P<0.01),血FINS及胰岛素抵抗指数也明显降低(P<0.05)、ISI提高(P<0.05),两组间血清Alb、Hb、FPG、PPG、HbA1c及血脂等无明显差异。结论α-酮酸联合低蛋白饮食(LPD)...     

复方α-酮酸片治疗慢性肾病蛋白尿50例疗效分析

目的探讨复方α-酮酸片治疗慢性肾病蛋白尿的临床疗效。方法选择94例慢性肾病蛋白尿患者,按随机数字表法分为对照组(44例)和治疗组(50例)。对照组口服氢氯噻嗪、依那普利,并给予低蛋白饮食,治疗组在对照组的基础上加服复方α-酮酸片(4~8片/次,3次/d)。两组疗程均为12周,观察治疗前后两组患者的24h尿蛋白定量、血清白蛋白、肌酐、尿素氮及临床疗效情况。结果治疗12周后,治疗组24h尿蛋白定量及尿素氮水平均明显低于对照组(P0.05),而血清白蛋白水平和治疗的总有效率均明显高于对照组,差异有统计学意义(P0.05)。结论复方α-酮酸片可以显著提高慢性肾病蛋白尿患者的血清白蛋白水平,有效控制蛋白尿。     

低蛋白饮食加复方α-酮酸片治疗慢性肾功能衰竭疗效观察

目的：探讨低蛋白饮食（LPD）加复方α-酮酸片治疗慢性肾功能衰竭（CRF）营养状态改善及生化指标的改变。方法：选择本院符合慢性肾功能衰竭诊断标准的患者68例,给予低蛋白饮食0.6 g/（kg.d）加复方α-酮酸片1片/（5 kg.d）,比较治疗前后的营养指标及生化指标的变化。结果：治疗后患者的精神状态好转,水肿减轻。尿素氮、血清磷有不同程度的下降,血清钙、血浆清蛋白有所回升。结论：低蛋白饮食加复方α-酮酸片治疗慢性肾功能衰竭为一种安全有效的方法。     

复方α-酮酸补充的极低蛋白膳食对慢性肾脏疾病患者血压的影响

目的观察复方α-酮酸补充的极低蛋白膳食(sVLPD)对慢性肾病患者血压的影响。方法53例慢性肾病患者接受标准的低蛋白膳食(LPD,0.6g·kg-1·d-1)3mo后分为2组,对照组28例继续给予LPD,试验组25例给予复方α-酮酸补充的sVLPD(0.3g·kg·d-1),均3mo。比较治疗后2组患者体重、血压、实际蛋白和钠摄入量、血生化指标等。结果治疗6mo后,试验组血压下降(13±s9)/(6±7)mmHg(P<0.05),有7例达到靶血压水平;而对照组血压无明显改变,无一例达到靶值。试验组蛋白摄入量减少(0.25±0.10)g·kg-1·d-1,钠减少(35±6)mmol·d-1,对照组没有蛋白摄入和钠摄入的改变,2组差异显著(P<0.05)。2组患者体重、血清清蛋白、血红蛋白浓度在治疗前后均无显著变化。结论复方α-酮酸补充的sVLPD有益于慢性肾病患者的降压治疗,且不影响患者的营养状态,这可能与盐摄入的减少和复方α-酮酸的补充有关。     

酮酸片联合卡托普利治疗糖尿病肾病临床蛋白尿的效果研究

目的 了解酮酸片联合卡托普利治疗糖尿病肾病临床蛋白尿的临床效果.方法 对2011年12月至2013年12月收治的确诊为糖尿病肾病临床蛋白尿患者进行抽样,选取100例患者随机分成两组进行对比观察,其中对照组予以胰岛素强化血糖控制,口服卡托普利,实验组在强化血糖控制的基础上加以复方α-酮酸片进行治疗,比较两组患者尿蛋白排泄量、血浆清蛋白量与临床治疗效果.结果 总有效率实验组（98％）显著优于对照组（82％）,两组比较差异具有统计学意义（P＜0.05）.实验组16例24h尿蛋白定量＜0.5 g/L,3例为0.5～1.0 g/L;对照组15例24 h尿蛋白定量＜0.5 g/L,4例为0.5 ～ 1.0 g/L;实验组1例血浆清蛋白量＜25g/L,对照组2例,两组比较差异有统计学意义（P＜0.05）.结论 针对糖尿病肾病临床蛋白尿患者而言,基于低蛋白饮食与血脂、血糖、血压控制等治疗基础上,采用复方α-酮酸片联合卡托普利进行治疗,有助于减少蛋白尿,控制糖尿病肾病进展.     

探讨低蛋白饮食配合复方α-酮酸片治疗慢性肾功能衰竭的临床疗效

目的:探讨慢性肾功能衰竭(CRF)采用低蛋白饮食(LPD)联合α-酮酸片治疗的效果.方法:选取我院2015年4月~2016年4月收治的LPD患者70例进行研究,随机分成两组,对照组35例仅给予低蛋白饮食治疗,观察组在低蛋白饮食基础上联合使用α-酮酸片治疗,对比两组治疗前后血肌酐(SCr)、血浆白蛋白(ALB)、血尿素氮(BUN)、红细胞压积(HCT),对比两组治疗有效率.结果:治疗前两组各项生化治疗差异无统计学意义,治疗后观察组改善效果优于对照组,组间数据对比差异有统计学意义(P<0.05);观察组不良反应发生率为2.86%,对照组为11.43%,X2=1.938,P>0.05.结论:在CRF的治疗中联合使用低蛋白饮食加α-酮酸片能够显著改善肾脏功能,安全性较高,值得推广.     

α-酮酸联合低蛋白饮食对老年慢性肾脏病患者肾功能与营养状态的影响

目的:探讨低蛋白饮食联合α-酮酸对延缓老年慢性肾功能衰竭(CRF)患者的病情进展、改善营养状况方面的作用。方法:150例老年CRF患者随机分为A、B、C组(各50例),A组予以常规蛋白饮食,B组予以低蛋白饮食,C组予以低蛋白饮食联合复方α-酮酸片,随访1年,监测患者的营养状况指标。结果:与B组患者相比,A、C组患者的营养状况指标升高;C组患者的肾小球滤过率下降速度明显低于A、B组患者。结论:低蛋白饮食联合α-酮酸治疗,可有效延缓老年慢性肾功能衰竭的进展,明显改善患者的营养状况,防止可能出现的营养不良。     

复方α-酮酸片联合卡托普利治疗糖尿病肾病临床蛋白尿疗效观察

目的：探讨复方α-酮酸片联合卡托普利治疗糖尿病肾病临床蛋白尿的临床效果。方法：将本科2006年3月～2008年2月门诊及住院部确诊为糖尿病肾病临床蛋白尿的患者38例随机分成对照组和治疗组,两组均给予常规控制血糖、血压、血脂、扩血管、活血化瘀等处理,口服卡托普利减少尿蛋白排出,低蛋白饮食,治疗组加服复方α-酮酸片治疗。结果：治疗组尿蛋白排泄量下降明显,与对照组比较,差异有统计学意义（P〈0.05）。结论：在低蛋白饮食、积极控制血糖、血脂、血压等治疗基础上,应用复方α-酮酸片联合卡托普利治疗糖尿病肾病临床蛋白尿,可有效减少蛋白尿,延缓糖尿病肾病的进展。     

低蛋白饮食联合复方α酮酸对糖尿病肾病患者肾脏保护作用评价

目的评价低蛋白饮食联合复方α酮酸在2型糖尿病肾病(临床蛋白尿期)治疗中对肾功能及尿蛋白的影响。方法糖尿病肾病患者40例,年龄40～72岁,男21例,女19例。分为治疗组20例和对照组20例。两组均为2型糖尿病肾病Ⅳ期(临床蛋白尿期)。对照组为常规治疗组,治疗组在常规治疗基础上服用复方α酮酸(开同[1],费森尤斯卡比公司)进餐时整片服下,每次5片,3次/d。比较组间及组内治疗前后内生肌酐清除率、白蛋白排泄率。结果治疗组尿白蛋白排泄率下降明显、内生肌酐清除率有所升高。结论复方α酮酸治疗对糖尿病肾病患者有减少尿蛋白和保护肾功能的作用。     

α-酮酸联合低蛋白饮食对老年慢性肾脏病患者肾功能与营养状态的影响研究

目的:探究老年慢性肾脏病患者接受α-酮酸联合低蛋白饮食医治干预对其肾功能与营养状态的影响。方法:选取在我院接受医治的老年慢性肾脏病患者120例,选取时间为2016年5月-2017年6月,根据其就诊顺序的差异将患者分成2组。对照组患者接受低蛋白饮食医治;实验组患者接受α-酮酸联合低蛋白饮食医治干预。对比2组患者经医治干预后的肾功能与营养状态的改善程度。结果:实验组患者的BIM、Alb、SCr以及eGFR水平改善程度均优于对照组(P0.05)。结论:老年慢性肾脏病患者接受α-酮酸联合低蛋白饮食医治干预,可有效改善患者肾功能水平以及营养状态,临床效果明显。     

Influence of dietary protein levels on the fate of methylmercury and glutathione metabolism in mice.

We investigated the influence of dietary protein levels on the fate of methylmercury (MeHg), the tissue glutathione (GSH) levels and the efflux rates of GSH in C57BL/6N male mice. One group of mice was fed a 7.5% protein diet (low protein diet, LPD) and the other was fed a 24.8% protein diet (normal protein diet, NPD). The cumulative amount of Hg in urine in LPD-fed mice was approximately 3.7-times lower than in NPD group during the 7 days after oral administration of MeHg (20 mumol/kg), although the fecal Hg levels were identical in the two groups. Hg concentration in kidney, liver and blood decreased time-dependently for 7 days after the administration in both groups of mice, whereas the brain levels continued to increase during this period. Tissue Hg levels in the LPD group were significantly higher than in the NPD group except for the liver. Although the hepatic GSH level in LPD-fed mice was significantly lower than in NPD-fed mice, the levels in the kidney, brain, blood and plasma were not different between the two groups. The efflux rate (mumol/g body weight per day) of hepatic GSH in LPD-fed mice was significantly lower than in the NPD group, whereas the efflux rates of renal GSH were identical in both groups. When MeHg (20 mumol/kg)-pretreated mice were injected with acivicin, a specific inhibitor of gamma-glutamyltranspeptidase, the urinary Hg levels increased by 60- and 36-fold in groups fed LPD and NPD, respectively. As a result, the difference in urinary Hg levels between the two groups disappeared with acivicin treatment. This result indicated that LPD feeding might decrease urinary Hg excretion by increasing the retention of MeHg metabolite(s) in renal cells. Thus, our present study suggested that the dietary protein status, which could modulate the metabolism of thiol compounds, played an important role in determining the fate of MeHg.     

贝那普利与缬沙坦治疗慢性肾病蛋白尿及高血压

目的:观察贝那普利与缬沙坦单用及联用治疗慢性肾脏病患者蛋白尿及高血压的临床疗效和安全性.方法:75例慢性肾病合并高血压患者随机分为贝那普利组(n=28)、缬沙坦组(n=26)、贝那普利与缬沙坦联用组(n=21),观察治疗前、治疗第4周和第8周的血压、24 h蛋白尿定量、血尿素氮(BUN)、血清肌酐(SCr)和血尿素(SUA)等指标.结果:三组患者治疗后血压和24 h蛋白尿定量较治疗前明显下降(P<0.01),且联用组较缬沙坦组和贝那普利组降蛋白尿作用更显著(P<0.05).三组患者治疗前后BUN,Scr无明显变化,但缬沙坦组及联用组治疗后SUA较治疗前明显下降(P<0.05).结论:贝那普利与缬沙坦联用对慢性肾脏病合并高血压患者具有良好的降蛋白尿和降压作用.     

前列地尔联合左卡尼丁及还原型谷胱甘肽治疗中晚期慢性肾脏病临床观察

目的观察前列地尔联合左卡尼丁及还原型谷胱甘肽(GSH)治疗中晚期慢性肾脏病(CKD)的临床效果。方法将56例慢性CKD患者随机分为A组和B组各28例。A组予前列地尔治疗,B组在A组基础上予左卡尼丁及还原型GSH治疗。治疗前后观察2组血清肌酐、尿素氮(BUN)、尿白蛋白/肌酐比率(ACR)、胱抑素、超敏C反应蛋白(hsCRP)、总胆固醇(TG)、低密度脂蛋白(LDL)、甲状旁腺素(iPTH)、表皮生长因子(eGFR)水平。结果治疗后,2组胱抑素、iPTH、ACR水平均低于治疗前,且B组低于A组,差异均有统计学意义(P<0.05);治疗后B组血红蛋白、hsCRP水平低于治疗前,且B组hsCPR水平低于A组,差异均有统计学意义(P<0.05);2组治疗前后血肌酐、TG、BUN、LDL及eGFR水平差异无统计学意义(P>0.05)。结论前列地尔联合左卡尼丁及还原型GSH治疗中晚期慢性CKD可有效改善CKD进展危险因素,但其长期疗效有待观察。     

Ezetimibe decreases serum levels of asymmetric dimethylarginine (ADMA) and ameliorates renal injury in non-diabetic chronic kidney disease patients in a cholesterol-independent manner

Synthesis of nitric oxide (NO) can be blocked by inhibition of nitric oxide synthase (NOS) active site with guanidino-substituted analogues of l-arginine such as asymmetric dimethylarginine (ADMA). There is growing evidence that elevation of serum ADMA levels play a role in the progression of atherosclerosis and chronic kidney disease (CKD) in high-risk patients. Further, dyslipidemia contributes to cardiorenal disease as well. However, effects of ezetimibe, a specific inhibitor of cholesterol absorption and widely used drug for the treatment of dyslipidemia, on serum ADMA levels and renal injury remain unknown. In this study, we examined whether ezetimibe treatment decreased serum levels of ADMA, proteinuria and urinary excretion levels of 8-hydroxydeoxyguanosine (8-OHdG) and l-fatty acid binding protein (l-FABP), markers of oxidative stress and tubular injury, respectively and investigated their relationships in 10 non-diabetic CKD patients with dyslipidemia. Ezetimibe treatment (10 mg/day) for 6 months significantly decreased circulating levels of LDL-cholesterol, triglycerides and ADMA, while it increased HDL-cholesterol levels. Further, ezetimibe treatment significantly reduced urinary excretion levels of protein, l-FABP and 8-OHdG. In univariate analyses, serum ADMA levels were correlated with urinary protein, l-FABP and 8-OHdG levels. In multiple stepwise regression analysis, proteinuria was independently correlated with ADMA. Our present study demonstrated for the first time that ezetimibe decreased serum ADMA levels and improved renal injury in non-diabetic CKD patients with dyslipidemia in a cholesterol-independent manner. Ezetimibe may have pleiotropic actions, that is, ADMA-lowering and anti-oxidative effects, that could contribute to renoprotective properties of this lipid-lowering agent.     

慢性汞染毒大鼠尿汞排泄与蛋白尿的关系

大鼠慢性汞染毒时尿汞排出先呈现“快速相”,继而“缓慢相”,最后转入“稳定相”。停止染毒后2wk,尿汞可下降80-90％,提示尿汞只宜作为汞的近期接触指标。尿蛋白排出量与尿汞水平有明显相关,但并不能根据尿汞水平直接判断有无发生蛋白尿的可能。研究发现,低分子量(MW<10 000)汞复合物(LM-Hg)可能是生理状态下肾脏主要排汞形式;随染毒增加,LM-Hg反渐减少,可能是肾脏对汞解毒能力减退的反应,是蛋白尿的预兆。     

活性维生素D_3治疗慢性肾脏病(Ⅰ～Ⅲ)的临床观察

目的观察活性维生素D3治疗慢性肾脏病(chronic kidney disease,CKD)(Ⅰ～Ⅲ期)的疗效及安全性,旨在探讨治疗CKD(Ⅰ～Ⅲ期)安全、有效的新方法。方法将符合CKD(Ⅰ～Ⅲ期)的100例住院患者随机分为活性维生素D3治疗组(n=50)和对照组(n=50)根据不同的病因,尿蛋白定量、肾功能情况、病理类型及血压等情况给予相应的常规治疗。治疗组在对照组的基础上给予活性维生素D3(骨化三醇)1.0mg/d口服,观察12周,主要观察尿蛋白量下降程度、肾功能变化情况及血清钙、磷水平。结果治疗组尿蛋白显著下降[(3.99±1.25)g vs(1.05±0.33)g/24h,P<0.01],血尿素氧(BUN)、血肌酐(Scr)亦明显下降。[(6.8±3.1)mmol/L vs(4.2±1.1)μmol/L,P<0.05]、[(128.5±60.5)μmol/L vs(98±40.1)μmol/L,P<0.05]。对照组尿蛋白亦明显下降[(3.73±1.32g)vs(2.11±0.98)g/24h,P<0.05],BUN,Scr无明显变化,[(7.0±2.8)mmol/L vs(6.8±1.4)mmol/L,P>0.05],[(130.1±61.8)μmol/L VS(129±50.3)μmol/L,P>0.05],两组血清钙均略有升高,但无统计学差异。结论活性维生素D3能明显减少CKD(Ⅰ～Ⅲ期)患者尿蛋白,延缓肾功能进展,疗效优于对照组,且无明显副作用,是治疗CKD(Ⅰ～Ⅲ期)安全,有效的药物。     

慢性肾脏病患者血清脂肪细胞因子水平及其作用的研究

目的检测慢性肾脏病（CKD）患者血清脂联素（ADPN）、抵抗素（Res）、肿瘤坏死因子-α（TNF-α）、超敏C反应蛋白（hs-CRP）水平,探讨CKD患者血清脂肪细胞因子水平的变化及其作用。方法选择CKD患者104例,分为肾病组、肾炎组、肾衰非透析组、腹膜透析组和血液透析组。另设健康对照组。用ELISA方法检测上述各项指标,比较各组间的差别。结果①CKD患者血清ADPN水平在肾病组[（22.40±6.02）mg/L]、肾炎组[（12.41±4.01）mg/L]、肾衰非透析组[（15.88±4.94）mg/L]、腹膜透析组[（14.55±3.51）mg/L]和血液透析组[（14.26±4.54）mg/L]均显著升高（与对照组[（4.95±2.19）mg/L]相比,P＆lt;0.01）,并以肾病组升高为著;②患者的血清Res水平在肾衰非透析组[（9.95±2.65）μg/L]、腹膜透析组[（10.9±2.55）μg/L]和血液透析组[（10.52±4.77）μg/L]均显著升高（与对照组[（4.60±1.47）μg/L]和肾病组[（5.80±2.16）μg/L]、肾炎组[（5.57±1.24）μg/L]患者相比,P〈0．01）;③cKD患者的血清ADPN水平与Res、尿蛋白量呈正相关（P〈0．05）,与血白蛋白水平呈负相关（P〈O．01）;血清Res水平与TNF一α、hs-CRP、血肌酐呈正相关（P〈0．01）,与肾小球滤过率呈负相关（P〈0．01）。结论CKD患者的血清ADPN、Res水平显著升高,并与尿蛋白量、炎性因子和肾小球滤过率等因素有关。ADPN和Res在CKD患者动脉粥样硬化的启动和发展中可能起一定作用。     

Effect of Type 2 Diabetes Mellitus and Diabetic Nephropathy on IgG Pharmacokinetics and Subcutaneous Bioavailability in the Rat

The objective of this research was to assess the effects of type 2 diabetes mellitus (T2DM) and diabetic nephropathy (DN) on the pharmacokinetics of human IgG (hIgG), an antibody isotype, in Zucker diabetic fatty (ZDF) rats. Furthermore, the specific role of T2DM in the altered disposition of hIgG was evaluated by treating diabetic rats with pioglitazone, while the role of chronic kidney disease (CKD) was assessed using 5/6 nephrectomized Sprague Dawley rats. ZDF male (lean non-diabetic control and obese diabetic) and pioglitazone-treated ZDF rats were studied at ages 12–13 weeks (only DM was present), and at ages 29–30 weeks (progression to DN). All animals were dosed with 1 mg/kg of hIgG intravenously (IV) or subcutaneously (SC). ZDF rats had significantly higher blood glucose concentrations and urinary albumin excretion compared to control rats. Significant increases in total clearance (2.5-fold) and renal clearance (100-fold) of hIgG were observed; however the major increase in total clearance was due to increased non-renal clearance. Greater changes in urinary albumin excretion and total and renal clearances of IgG (3.5-fold and 300-fold, respectively) were observed with progression to DN. SC bioavailability of hIgG in all animal groups was similar (>84%). With pioglitazone-treatment, diabetic animals remained euglycemic and treatment was able to reverse the clearance changes, although incompletely. In the CKD group, no difference in hIgG clearance was observed when compared with controls. In conclusion, the increased clearance of hIgG in ZDF diabetic animals, reversal by pioglitazone treatment and lack of effect of CKD, demonstrate the influence of T2DM on hIgG pharmacokinetics.KEY WORDS: antibody, chronic kidney disease, renal clearance, urinary albumin excretion, Zucker diabetic fatty rat     

大剂量贝那普利治疗慢性肾病蛋白尿的临床研究

目的观察大剂量贝那普利治疗慢性肾病蛋白尿的，临床疗效及安全性。方法79例慢性肾病患者采用完全随机单盲法分成2组，贝那普利组完成观察35例，对照组完成观察32例，2组患者均给予激素或激素加环磷酰胺，或仅用潘生丁、保肾康等一般治疗。贝那普利组在上述治疗基础上加用贝那普利，开始以10mg／d，1周后加至20mg／d，2周后加至30～40mg／d，分2次口服，疗程24周。结果贝那普利组完全缓解19例，部分缓解10例，部分有效4例，无效2例，总有效率94．3％；对照组完全缓解14例，部分缓解9例，部分有效5例，无效4例，总有效率87．5％，2组有统计学意义（P〈0．05）。贝那普利组治疗前24h尿蛋白定量（2．67±1．32）g，治疗后为（0．67±0．58）g，差异有统计学意义（P〈0．01）；对照组治疗前24h尿蛋白定量（2．74±1．29）g，治疗后为（0．94±0．73）g，差异有统计学意义（P〈0．01）；2组治疗后尿蛋白定量比较差异有统计学意义（P〈0．05）。贝那普利组与对照组血压、血肌酐差异无统计学意义。结论大剂量贝那普利治疗慢性肾病有降低尿蛋白的作用，安全有效。     

Comparison of sorbinil and ponalrestat (Statil) diminution of proteinuria in the BB rat.

Diabetic nephropathy leading to kidney failure is a major complication of type I (insulin-dependent) diabetes mellitus and is associated with progressive proteinuria. In the present 6-month study, effects of two structurally dissimilar aldose reductase inhibitors (sorbinil and ponalrestat or Statil) were examined on prevention of proteinuria in insulin-dependent spontaneously diabetic BB rats and compared with age-matched BB resistant controls. Prior to aldose reductase inhibitor treatment, all diabetic BB rats exhibited hyperglycemia (> 300 mg/dl), glycosuria (> 2,000 mg/dl) and 24-hour urinary protein excretion ranging from 5.01 to 11.23 mg/day. After daily administration of ponalrestat (20 mg/kg) for 3 months, 24-hour urinary protein excretion was 11.53 +/- 1.76 mg/day in ponalrestat-treated rats, despite persistence of hyperglycemia (444 +/- 31 mg/dl) and glycosuria (> 2,000 mg/dl); by contrast, urinary protein excretion was 17.76 +/- 2.59 mg/day in the control group of untreated BB diabetic rats. Ponalrestat initially protected against excretion of an array of urinary proteins having molecular weights between 30,000 and 100,000 daltons. These effects sustained throughout the 4th month of treatment, tended to change toward valves in control rats by the 5th month. At the end of 6 months, ponalrestat-treated diabetic rats excreted 18.73 +/- 3.20 mg/day of protein, similar to valves in untreated BB diabetic rats; both demonstrated a 4-fold increase in urinary protein excretion when compared to age-matched BB resistant controls. Proteinuria was attributed to an increase in albumin and an array of proteins having molecular weights between 30,000 and 100,000 daltons.(ABSTRACT TRUNCATED AT 250 WORDS)