资深营养师出诊,为您量身定制营养处方 早期糖尿病肾病的营养治疗

糖尿病肾病是严重的微血管并发症,成为糖尿病主要死亡原因之一。系统的临床治疗能够对早期糖尿病肾病起到预防和延缓进展的目的,而饮食治疗在临床治疗中具有积极意义。下面详细介绍早期糖尿病肾病的营养治疗。     

早期糖尿病肾病的营养治疗

糖尿病肾病是严重的微血管并发症，成为糖尿病主要死亡原因之一。系统的临床治疗能够对早期糖尿病肾病起到预防和延缓进展的目的，而饮食治疗在临床治疗中具有积极意义。下面详细介绍早期糖尿病肾病的营养治疗。     

雷公藤多苷治疗糖尿病肾病的研究进展

糖尿病肾病目前已成为引起慢性肾脏病和终末期肾脏病的主要原因,减少蛋白尿、延缓肾功能恶化是其重要治疗策略.雷公藤多苷通过抗炎、抗氧化等多种机制发挥肾脏保护作用,对于延缓糖尿病肾病进展有较好疗效.本文就雷公藤多苷治疗糖尿病肾病的作用机制、临床疗效、安全性作一综述.     

糖尿病肾病治疗进展

糖尿病肾病(DN)是糖尿病的慢性并发症,已逐渐成为终末期肾病(ESRD)的主要原因。临床上通过饮食治疗、强化血糖控制、加强血压控制、降低蛋白质、抗氧化应激等综合治疗,能够有效地延缓肾病的进展、减少ESRD的发生、改善DN患者的预后。     

糖尿病肾脏疾病治疗的研究进展

糖尿病肾脏疾病是糖尿病最严重的并发症之一,是导致终末期肾病的主要病因之一。现有糖尿病肾病治疗药物较单一,疗效不尽人意,亟需基于其发病机制的崭新治疗方法来延缓疾病进展乃至改善病情,因此本文综述糖尿病肾病治疗的研究进展。     

细胞因子与糖尿病肾病

糖尿病肾病是糖尿病最常见、最严重的慢性并发症、是导致慢性肾功能衰竭的主要病因之一,但是其发病机制仍不明了。本文综述近年来细胞因子在糖尿病肾病发病中的作用的研究进展,为临床延缓糖尿病肾病进展提供依据。     

糖尿病肾病的发病机制及治疗进展

糖尿病肾病是糖尿病的主要微血管并发症之一,其发病机制仍未完全阐明,可能与糖代谢紊乱、炎症反应、遗传、血流动力学异常、氧化应激等多种因素有关,在治疗上主要通过饮食、血糖、血压、血脂的控制等方法来加以干预,以延缓病情进展和提高患者生活质量。该文就近年来关于糖尿病肾病的发病机制和治疗进展作一综述。     

糖尿病肾病的营养治疗

糖尿病肾病的饮食治疗原则 糖尿病性肾病是糖尿病的一种严重并发症,已成为糖尿病病人主要死亡原因之一。糖尿病性肾病一旦形成,治疗比较困难,越来越多的病人最终需要接受透析或肾移植治疗。饮食治疗对控制病情进展、延缓肾功能恶化和提高病人生命质量均有帮助。其饮食原则包括：     

骨髓间充质干细胞移植治疗糖尿病肾病的研究进展

糖尿病肾病（DN）是临床糖尿病最常见的微血管并发症之一,也是糖尿病终末期患者的主要死亡原因.目前的糖尿病肾病治疗方法均缺乏显著疗效,只能延缓其病情发展.因此,我们需要寻求一种安全、有效、能从根本上延缓甚至避免糖尿病肾病发生的方法.骨髓间充质干细胞（BMSCs）是目前广受学界关注的一种成体干细胞,因其具有良好的多向分化潜能和活跃的增殖特性、便于操作性等优势成为研究的重点,同时也为肾脏疾病提供了一种新的治疗途径.BMSCs在多种肾脏疾病方面的研究都已取得良好的进展,例如IgA肾病、急性肾损伤、狼疮肾病、肾病综合征等[1-2].我们对BMSCs移植治疗糖尿病肾病的研究进展作一综述.     

攀升的发病率，衰竭的肾

由于根治糖尿病肾病的方法还没有找到,所以我们目前对待糖尿病肾病最重要的是,没有肾病时积极预防,有了肾病后积极治疗,延缓糖尿病肾病向肾衰竭的进展。目前的研究显示,控制血糖和血压是延缓糖尿病肾病的重要方法,控制膳食中蛋白的过量摄人也非常重要。治疗及预防糖尿病肾病都要趁早。 需要了解的事实 1．约1／3的糖尿病患者可能患肾衰竭。     

Combating diabetic nephropathy with drug therapy

Diabetes mellitus is the leading cause of end-stage renal disease and also increases the risk of atherosclerotic vascular disease. Hypertension amplifies both problems. Detection of microalbuminuria, a common and early manifestation of diabetic nephropathy and a marker for cardiovascular risk, permits early treatment to reduce progression of nephropathy and vascular disease in diabetes. Although optimal glycemic control is essential to reduce the risk of nephropathy, aggressive blood pressure lowering to a level of 130/80 mg Hg or below in hypertensive diabetic patients is as important as glycemic control. Initial drug therapy for nephropathy should include an angiotensin-converting enzyme inhibitor (or if contraindicated, an angiotensin receptor blocker), as several large randomized double-blinded multicenter clinical trials have demonstrated an independent renoprotective effect with renin angiotensin system inhibition. The role of advanced glycation end products in the pathogenesis of renal and vascular disease in diabetes is becoming more clearly established. However, the use of therapeutic strategies directed at blocking their effect still awaits further investigation. A multifaceted intervention program that combines optimal glycemic control, lifestyle modification/cardiovascular prevention guidelines such as lipid control and smoking cessation, with appropriate antihypertensive therapy when indicated, will prevent or delay both the occurrence and progression of diabetic nephropathy.     

Clinical management of diabetic nephropathy

From the viewpoint of nephrologists dealing with diabetic patients with ESRD and the associated complications and devastating prognosis, the need to reduce the incidence, and delay the rate of progression of diabetic nephropathy is obvious. Studies published within the last year have provided support for views that seem intuitively obvious; that improved glycaemic control and reduced blood pressure are associated with delayed onset and delayed progression of diabetic nephropathy. These reports have also demonstrated the difficulty of achieving ideal blood pressure targets and glycaemic control in diabetic patients. Thus, even with available therapy it is likely that improved compliance and achieving targets will have a major impact on disease outcome. There is evidence in several subgroups that ACEi are beneficial over other agents and the favourable side-effect and efficacy profile of these agents makes it reasonable to suggest that they should be used 'first line' in all patients with diabetes unless specifically contra-indicated. However, the failure to readily achieve blood pressure targets and the need for polypharmacy suggest that novel agents are required. We believe that statin therapy will have a major impact on CVD in diabetic patients and is also likely to delay progression; studies assessing the combined affect of anti-hypertensive and statin therapy specifically on the development and progression of diabetic nephropathy will be necessary before evidence-based recommendations can be made. The role for newer agents and targeting high risk groups using genetic markers remains uncertain but we await there development with interest. The future can only get better for patients with DN.     

Education of diabetic patients with chronic kidney disease and after transplantation

Despite recent advances in the management of diabetes, diabetic nephropathy is the most frequent cause ofend-stage renal disease. Even when diabetic nephropathy is established, patient's care should be optimized to delay progression of nephropathy or other diabetic complications. Evidence exists for the effectiveness of diet intervention, blood pressure and diabetes control and treatment of metabolic syndrome. We emphasize the need for closer co-operation not only between diabetologists, primary care physicians and nephrologists, but with educated diabetic patients, too. At referral to nephrologist, many patients' care is suboptimal and referral is too late. The most important education information for patients is to stick to diet and keep adequate blood pressure and diabetes control with self-monitoring. Effectiveness of each of these recommendations is critically assessed. Patients after kidney or combined kidney and pancreas transplantation have to be educated mainly in symptoms of rejection and diabetic foot care. They are recommended to take regularly the prescribed medicines, to distinguish the adverse events of immunosuppression and keep all doctor's appointments.     

The kidney in diabetes: dynamic pathways of injury and repair. The Camillo Golgi Lecture 2007

Diabetic nephropathy is the most common cause of end-stage renal disease (ESRD). The natural history of diabetic nephropathy has changed over the last decades, as a consequence of better metabolic and blood pressure management. Thus, it may now be possible to delay or halt the progression towards ESRD in patients with overt diabetic nephropathy, and the decline of renal function is not always inexorable and unavoidable. Also, the rate of progression from microalbuminuria to overt nephropathy is much lower than originally estimated in the early 80s. Furthermore, there is now evidence that it is possible, in humans, to obtain reversal of the established lesions of diabetic nephropathy. This review focuses on the contribution of kidney biopsy studies to the understanding of the pathogenesis and natural history of diabetic nephropathy and the identification of patients at high risk of progression to ESRD. The classic lesions of diabetic nephropathy and the well-established structural-functional relationships in type 1 diabetes will be briefly summarised and the renal lesions leading to renal dysfunction in type 2 diabetes will be described. The relevance of these biopsy studies to diabetic nephropathy pathogenesis will be outlined. Finally, the evidence and the possible significance of reversibility of diabetic renal lesions will be discussed, as well as future directions for research in this field.     

Preventing renal complications in diabetic patients: the Diabetics Exposed to Telmisartan And enalaprIL (DETAIL) study

Diabetic nephropathy is characterised by hypertension and persistent proteinuria. If ineffectively controlled, a progressive decline in renal function can result in end-stage renal disease. Patients with diabetic nephropathy are also at greatly increased risk of cardiovascular disease. Angiotensin-converting enzyme (ACE) inhibitors display additional renoprotective effects beyond systemic blood pressure lowering, perhaps due to reduction in intraglomerular pressure by inhibition of angiotensin II activity. In type 2 diabetics, ACE inhibitors have variable effects, with some studies showing a reduction in microalbuminuria, prevention of the progression to macroalbuminuria and maintenance of renal function. Randomised studies have demonstrated that angiotensin II receptor blockers (ARBs), as well as controlling systemic blood pressure, delay progression of proteinuria in patients with diabetic nephropathy. Telmisartan has a number of features that may make it particularly suitable for the treatment of diabetic nephropathy. In addition to its long duration of action and almost exclusive faecal excretion, its high lipophilicity should assist in tissue penetration. The Diabetics Exposed to Telmisartan And enalaprIL (DETAIL) study was designed to compare the long-term renal outcome of treatment with telmisartan 40.80 mg versus enalapril 10.20 mg (with titration to the higher dose after 4 weeks) in patients with type 2 diabetes, mild-to-moderate hypertension and albuminuria. The primary endpoint is the change in glomerular filtration rate after 5 years' randomised treatment. Secondary endpoints are annual changes in glomerular filtration rate, serum creatinine and urinary albumin excretion, as well as incidences of end-stage renal disease, cardiovascular events, all-cause mortality and adverse events. The groundbreaking DETAIL study revealed that telmisartan conferred comparable renoprotection to enalapril and was associated with a low incidence of mortality.     

Promotion,prediction and prevention of progression of nephropathy in Type 1 diabetes mellitus

The scope of the present review is to discuss the prognosis of diabetic renal disease, putative progression promoters and the possibilities for treatment and prediction of treatment efficacy. The recent changes in the incidence of diabetic nephropathy in Type 1 diabetes mellitus are discussed. Promoters of progression in diabetic nephropathy are evaluated, in particular arterial blood pressure, glycaemic control, albuminuria and cholesterol levels. Potential treatment modalities are discussed, with special focus on antihypertensive therapy, including a discussion of a specific renoprotective action of certain antihypertensive agents. Furthermore putative predictors of treatment efficacy are evaluated, demonstrating that the ability to lower the urinary albumin excretion rate after onset of treatment heralds a slow progression of the renal disease. The prognosis in diabetic renal disease has improved with an increase in median survival after onset of nephropathy from 6 to 15 years. This has exposed the importance of cardiovascular morbidity and mortality. The identification and treatment of cardiovascular risk factors has become essential. Although the prognosis has improved remarkably, the primary goal should be prevention of diabetic nephropathy, as it is unlikely that the increased risks associated with this complication can be eliminated. © 1998 John Wiley & Sons, Ltd.     

Telmisartan in the management of diabetic nephropathy: a contemporary view

Diabetic nephropathy, a complex disorder with heterogeneous etiologies, remains one of the most threatening diseases worldwide. There were around 177 million people with diabetes mellitus worldwide, and it has been estimated to be increased to 360 million by 2030. Given that about 20-30% of these people develop diabetic nephropathy, the present treatment protocols primarily aim for an efficient glucose and blood pressure control to arrest the initiation and progression of diabetic nephropathy. The treatment of diabetic nephropathy near the beginning at microalbuminuria stage with angiotensin-II-AT1 receptor blockers (ARBs) improves blood pressure control and halts disease progression of diabetic nephropathy. In fact, ARBs exert renoprotective effects independently of their blood pressure lowering effect, as they have direct defensive action on the diabetic kidney. Indubitably, it would be better if an ARB has both glucose-lowering and blood pressure controlling potentials efficiently. Intriguingly, telmisartan has such possessions considering its dual role of AT1 receptor blocking action and peroxisome proliferator-activated receptor gamma (PPARγ) partial agonistic property. The additional PPARγ agonistic potential of telmisartan could make it a distinctive intervention in the ARB class to prevent the progression of diabetic nephropathy through activation of PPARγ-mediated insulin sensitization, and renal anti-inflammatory and anti-oxidant actions. Indeed, telmisartan reduced insulin resistance and glucose intolerance, and halted the progressive renal dysfunction associated with diabetic nephropathy by inhibiting the incidence of albuminuria, and preventing the progression of glomerulosclerosis, renal interstitial inflammation and fibrosis. This review will discuss the current status of therapeutic potentials of telmisartan in treating diabetic nephropathy.     

The case for combining angiotensinconverting enzyme inhibitors and calcium-channel blockers

Tight blood pressure control among diabetic and nondiabetic patients with hypertension is perhaps the single most effective intervention used to delay progression to end-stage renal disease (ESRD). The renoprotective actions of angiotensin-converting enzyme (ACE) inhibitors in patients with diabetic and hypertensive nephropathy is well established. Drugs of this class fairly uniformly reduce glomerulosclerosis, delay the deterioration in renal function, and improve proteinuria, a predictive surrogate marker for renal injury. Calcium-channel blockers (CCBs) in the phenylalkylamine (verapamil) and benzothiazepine (diltiazem) classes also improve proteinuria and delay the progression of renal disease in diabetic and nondiabetic hypertensive nephropathy beyond that attributable to blood pressure control. The short-acting dihydropyridine CCBs worsen proteinuria and accelerate renal injury in both animal models and humans with hypertension or diabetes. A very limited number of studies in animals or humans with hypertension or diabetes have demonstrated at least an additive renoprotective effect when the combination of ACE inhibitors and nondihydropyridine CCBs has been compared with each agent administered as monotherapy. Because patients with impaired renal function and either hypertension or diabetes appear to benefit from aggressive blood pressure reduction, many of these patients will require two or more drugs to achieve the currently recommended blood pressure goals. Combinations of ACE inhibitor and CCB are attractive because they may provide better blood pressure control, appear to be better tolerated with fewer side effects than either drug alone, and may exert a greater renoprotective effect in patients at risk for renal failure than either an ACE inhibitor or a CCB.     

Antihypertensive drugs and diabetic nephropathy

Diabetic nephropathy is the most common cause of endstage renal disease in the United States. Hypertension is a major risk factor that predisposes individuals with diabetes to the development of renal disease and is very common in patients with diabetes. The benefit of blood pressure control on the rate of progression of diabetic nephropathy is being increasingly demonstrated in both type 1 and type 2 diabetic patients. Angiotensin converting enzyme inhibitors have proven renoprotective benefits in human studies, but the results of studies with calcium channel blockers are somewhat inconclusive. The other classes of antihypertensives also may have certain indications in the population of patients with diabetic nephropathy. In this paper we will critically review current strategies for the treatment of hypertension in patients with established diabetic nephropathy.     

Diabetic nephropathy.

Diabetic nephropathy remains a leading cause of end-stage renal disease (ESRD) in western societies, accounting for over one-third of all patients beginning renal replacement therapy. Patients with Type 2 diabetes comprise the largest and fastest-growing single disease group requiring renal support therapy. In addition to the high risk of progression to ESRD, diabetic nephropathy is associated with a very high risk of cardiovascular morbidity and mortality, which is not abolished by dialysis and renal transplantation. While the prognosis of patients with diabetic nephropathy has considerably improved, a greater focus has recently been placed on treating diabetic patients early in order to prevent future organ failure. Microalbuminuria is an important intermediary end-point that correlates strongly with future advanced renal disease and cardiovascular mortality. Recent evidence indicates that optimum glycaemic control, tight blood pressure control, and the regular screening for and early treatment of microalbuminuria are necessary to prevent the development and progression of diabetic renal disease. By utilizing such strategies, the challenge is to reduce the cumulative incidence of overt nephropathy, with its associated increase in cardiovascular mortality, and the requirement for renal support therapy. Over the next 5-10 years, the patient with Type 2 diabetes will need to be the specific focus of such preventive treatment modalities.