Renal disease diabetic nephropathy

Diabetic nephropathy ACE inhibitors Captopril Prevented end-stage renal disease Diabetic Collaborative Study Group >400 16... 

Patients with both type 1 and type 2 diabetes are at high risk for the development of chronic complications. Diabetes-specific microvascular pathology in tlie retina, renal glomerulus, and peripheral nerve produces retinopathy, nephropathy, and neuropathy. As a result of these microvascular complications, diabetes is the most frequent cause of new cases of bfindness in the industrialized world in persons between 25 and 74 years and the leading cause of end-stage renal disease.Diabetes is also associated with a marked increase in atherosclerotic macrovascular disease involving... 

In the treatment of hypertension, ACE inhibitors are as effective as diuretics, (3-adrenoceptor antagonists, or calcium channel blockers in lowering blood pressure. However, increased survival rates have only been demonstrated for diuretics and (3-adrenoceptor antagonists. ACE inhibitors are approved for monotherapy as well as for combinational regimes. ACE inhibitors are the dtugs of choice for the treatment of hypertension with renal diseases, particularly diabetic nephropathy, because they prevent the progression of renal failure and improve proteinuria more efficiently than the other diugs. 

Left ventricular dysfunction Post-myocardial infarction Non-diabetic nephropathy Type 1 diabetic nephropathy Type 2 diabetes mellitus Proteinuria Hyperkalaemia Bilateral renal artery stenosis disease... 

Diabetes mellitus causes about 50% of all patients being treated for End Stage Renal Disease (ESRD) in the USA and this is because the disease (type 2 disease) is pervasive. Recent studies have shown that the onset and progression of the disease can be ameliorated if treatment is instituted early on in the course of the disease. ESRD is the commonest complication of type 1 diabetes. A higher proportion of individuals with type 2 diabetes was found to have microalbuminuria and overt nephropathy shortly after the diagnosis of diabetes, because the diabetes had actually been present for many years before the diagnosis was made. There is a correlation between the degree of albuminuria and cardiovascular disease. 

Certain forms of renal disease, particularly diabetic nephropathy, are frequently associated with development of hyperkalemia at a relatively early stage of renal failure. In these cases, a thiazide or loop diuretic will enhance K+ excretion by increasing delivery of salt to the K+-secreting collecting tubule. 

Like ACE inhibitors, ARBs slow the progression of diabetic nephropathy. The antagonists are also effective in the treatment of heart failure and provide a useful alternative when ACE inhibitors are not well tolerated. Like ACE inhibitors, they are well tolerated but should not be used by patients with nondiabetic renal disease or in pregnancy. 

Vascular cells play a pivotal role in inflammatory renal disease, renal allograft rejection, hypertension, and diabetic nephropathy. However, endothelial and smooth muscle cells are relatively resistant to gene transfer. The only vector that has been reported to... 

Diabetes is the most frequent cause of end-stage renal disease. Hypertension, which is common among patients with type 2 diabetes, accelerates the development and progression of renal disease. Early and tight blood pressure control in diabetic patients, preferably with antihypertensive agents that have proven reno-protective properties, is therefore essential to minimize loss of kidney function. Several controlled clinical trials have investigated and proved the beneficial effects of ARBs on type 2 diabetic nephropathy [10-14]. 

Although ACE-inhibitor therapy can cause proteinuria, pre-existing proteinuria is not a contraindication for ACE-inhibitor treatment, as they have been found to exert nephroprotective effects in renal diseases associated with proteinuria (i.e., diabetic nephropathy). 

In type 1 diabetes, diabetic nephropathy follows a predictable course from onset of diabetes to the onset of microalbuminuria to frank nephropathy to end-stage renal disease or death. Microalbuminuria (a tiny amount of protein in the urine) develops 10-14 years after onset of diabetes. Without treatment, clinical nephropathy follows within 5 years, and severe renal impairment leading to end-stage renal failure develops approximately 5 years later. Hypertension develops in association with microalbuminuria and progresses with diabetic nephropathy, further damaging the kidneys. Once end-stage renal disease (ESRD) is reached, the toxins in the body can no longer be cleared by the kidneys and, unless treated by dialysis, can build up to fatal levels. 

The results of two trials in patients with chronic nephropathy have reinforced the benefit of ACE inhibitors in slowing the progression of chronic renal insufficiency due to renal diseases other than diabetic nephropathy (13-15) and have provided sufficient information on the safety profile of these agents in chronic renal insufficiency. This was found to be essentially the same as in patients with normal renal function. The current practice of avoiding ACE inhibitors in severe renal insufficiency, to prevent further renal impairment and hyperkalemia, is no longer justified, although careful monitoring should still be observed. 

An 84-year-old man with diabetic nephropathy and end-stage renal disease began continuous ambulatory peritoneal dialysis and over the next year had four episodes of exit-site infection and peritonitis and used mupirocin ointment. The exit-site catheter became dilated and during an episode of infection for which he used mupirocin on 6 successive days, a longitudinal rupture developed in the peritoneal catheter, which was removed. The peritoneal liquid contained Escherichia coli and Proteus mirabilis and the catheter tip contained E. coli and Enterobacter cloacae. He was treated with ciprofloxacin, without complications, and after 1 month a new peritoneal catheter was inserted. 

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