Diabetische Retinopathie

Diabetic retinopathy is a microvascular complication of diabetes, which can be found in almost all diabetic patients in the course of the disease. It is the most common cause of blindness in the western world in working age patients. The main reasons for loss of diabetic macular edema, which can occur at any stage of the disease and proliferative diabetic retinopathy. Risk factors are the duration of disease and poorly controlled arterial hypertension and blood glucose levels. Regular ophthalmologic surveillance is essential even in asymptomatic patients in order to prevent long-term consequences. The therapeutic options are laser photocoagulation, vitrectomy and the newly available intravitreal application of drugs.     

Diabetische Nephropathie

Diabetic nephropathy is a renal injury and late diabetic complication which is characterized by the appearance of albuminuria, the development or worsening of arterial hypertension and a continual reduction in glomerular filtration rate. In many countries it is now the most frequent reason for dialysis due to its increasing incidence. Once having achieved this stage, the prognosis is poor, although even with microalbuminuria cardiovascular complications occur frequently. The basis for therapy consists of good diabetic control and treatment of arterial hypertension by the preferred use of ACE or AT1 receptor inhibitors.     

Diabetische Neuropathie

Ohne Zusammenfassung     

Diabetische Nephropathie

Diabetic nephropathy is a main microvascular complication in type 1 and type 2 diabetes and at present the leading cause of renal failure. The test for microalbuminuria 30–300 mg/24 h) is an important screening parameter to early establish the diagnosis of diabetic nephropathy. Furthermore, microalbuminuria is a predictor for cardiovascular complications in diabetics. Therapeutic goals are reduction of proteinuria and inhibition of progressive renal insufficiency. A strict blood pressure control is most important (therapeutic objective <130/80 mmHg in normalbuminuric diabetics, <125/75 mmHg in patients with proteinuria >1 g/24 h). Blockade of the renin-angiotensin system with AT1-receptor antagonists and ACE-inhibitors has nephroprotective beneficial effects which may be independent of blood pressure lowering. To reduce cardiovascular complications, a multimodal therapeutic concept with blood pressure and glucose control, optimising the lipid profile and platelet aggregation inhibition is needed.     

Diabetische Gastroparese

Symptoms of gastroparesis include nausea and vomiting, early satiety, post-prandial fullness, bloating and abdominal pain, but it is also frequently be asymptomatic. Patients with difficult metabolic control should be considered to have a disordered gastric emptying. Nuclear scintigraphy is the gold standard for quantifying delayed gastric emptying, but noninvasive methods, such as 13C-octanoic acid breath tests, exhibit a highly significant positive correlation to scintigraphy. The main goal of treatment is to minimize the symptoms and accelerate gastric emptying. The basic measures for achieving this are improved glucose control and low fat/low fibre diets that are easy to digest. The prokinetic agents metoclopramide, domperidone and erythromycin are successful in controlling symptoms in the majority of patients with gastroparesis due to diabetes. Patients with persistent symptoms or intermittent but severe symptoms may require surgical techniques such as the gastrostomy and jejunostomy. The significance of gastric pacing devices on gastric emptying and specific symptom controls have to be elucidated in further studies.     

Diabetische Nephropathie

Diabetic nephropathy is the most common cause of end-stage renal disease. Since the disease progresses very slowly and usually takes more than 20 years before terminal renal failure occurs, early intervention is of great importance in order to prevent this disabling complication. A good control of diabetes with HbA(1c) levels around 7% is desirable. At least as important is the treatment of elevated blood pressure values. The target value for patients with diabetes has been adjusted in the last year and is now 130-139/80-85 mmHg. Should (micro-)albuminuria or renal insufficiency be present the blood pressure target is <130/80 mmHg. For the control of hypertension the use of ACE inhibitors or angiotensin receptor blockers is recommended. In addition, the control of other risk factors and appropriate therapeutic intervention is required. A multifactorial intervention leads to the best results and can avoid the occurrence or progression of diabetic kidney disease and other micro- and/or macrovascular complications.     

Diabetische Retinopathie

Diabetic retinopathy and maculopathy frequently affect patients with chronic hyperglycemia. Apart from achieving near normoglycemia, tight blood pressure control is an essential part of the treatment. Regular screening intervals are recommended for every patient with diabetes because of the paucity of retinopathy-related symptoms. Early manifestation of retinopathy in diabetic patients is a prognostic marker for cardiovascular morbidity and mortality.     

Diabetische Kardiomyopathie

Diabetic cardiomyopathy is a myocardial disease caused by diabetes mellitus unrelated to vascular and valvular pathology or systemic arterial hypertension. Clinical and experimental studies have shown that diabetes mellitus causes myocardial hypertrophy, apoptosis and necrosis, and increases interstitial tissue. The pathophysiology of diabetic cardiomyopathy is incompletely understood and several mechanistical approaches are under debate. Metabolic impairments like hyperglycemia, hyperlipidemia, hyperinsulinemia, and alterations in the cardiac metabolism lead to structural and functional changes which show cellular effects leading to increased oxidative stress, interstitial fibrosis, myocyte death, and disturbances in ion transport and homeostasis. Diastolic dysfunction which consecutively results in systolic dysfunction with increased left ventricular volume and reduced ejection fraction is an early diagnostic parameter. Treatment of diabetic cardiomyopathy does not differ from myocardiopathies of other etiologies and therefore has to follow the appropriate guidelines. Early intervention to reverse metabolic toxicity is the most effective method of prevention.     

Diabetische Nephropathie

Diabetic nephropathy is characterized by enhanced extracellular matrix accumulation in the glomerular and tubulointerstitial compartments and thickening of basal membranes resulting in glomerulosclerosis and tubulointerstitial fibrosis as well as tubular atrophy. These processes are closely connected to hemodynamic and metabolic disorders including excessive channeling of glucose intermediaries into various pathways with increased oxidative stress and generation of advanced glycation end products (AGEs), increase of proinflammatory and profibrotic cytokines, activation of the renin-angiotensin-aldosterone system (RAAS) and stimulation of certain signal transduction pathways, such as protein kinase C (PKC), JAK/STAT- and rho-kinase signaling. Therefore, influencing activation of the receptor for advanced glycation end products or modifications in signal transduction might lead to novel therapeutic strategies. In initial clinical studies some limited evidence has been found that with selective vitamin D receptor activation therapy there is inhibition of progression of diabetic nephropathy in addition to the established blockade of the RAAS.     

Diabetische Retinopathie und Makulopathie

Diabetic retinopathy is the most frequent microvascular complication in diabetes. Its early development indicates an increased cardiovascular risk. Since the early stages lack symptoms, yearly screening intervals are mandatory. Each retinopathy level determines evidence-based treatment with mutual interactive contributions from diabetology and ophthalmology. Intravitreal injection of inhibitors of the vascular endothelial growth factor may improve the so far only modestly successful therapy of diabetic macular edema.