Items in AFP with MESH term: Diabetic Nephropathies
Using ACE Inhibitors Appropriately - Article
ABSTRACT: When first introduced in 1981, angiotensin-converting enzyme (ACE) inhibitors were indicated only for treatment of refractory hypertension. Since then, they have been shown to reduce morbidity or mortality in congestive heart failure, myocardial infarction, diabetes mellitus, chronic renal insufficiency, and atherosclerotic cardiovascular disease. Pathologies underlying these conditions are, in part, attributable to the renin-angiotensin-aldosterone system. Angiotensin II contributes to endothelial dysfunction. altered renal hemodynamics, and vascular and cardiac hypertrophy. ACE inhibitors attenuate these effects. Clinical outcomes of ACE inhibition include decreases in myocardial infarction (fatal and nonfatal), reinfarction, angina, stroke, end-stage renal disease, and morbidity and mortality associated with heart failure. ACE inhibitors are generally well tolerated and have few contraindications. (Am Fam Physician 2002;66:473.)
Diabetic Nephropathy: Common Questions - Article
ABSTRACT: Diabetic nephropathy, or diabetic kidney disease, affects 20 to 30 percent of patients with diabetes. It is a common cause of kidney failure. Diabetic nephropathy presents in its earliest stage with low levels of albumin (microalbuminuria) in the urine. The most practical method of screening for microalbuminuria is to assess the albumin-to-creatinine ratio with a spot urine test. Results of two of three tests for microalbuminuria should be more than 30 mg per day or 20 mcg per minute in a three- to six-month period to diagnose a patient with diabetic nephropathy. Slowing the progression of diabetic nephropathy can be achieved by optimizing blood pressure (130/80 mm Hg or less) and glycemic control, and by prescribing an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker. Patients with diabetes and isolated microalbuminuria or hypertension benefit from angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. In the event that these medications cannot be prescribed, a nondihydropyridine calcium channel blocker may be considered. Serum creatinine and potassium levels should be monitored carefully for patients receiving angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. These medications should be stopped if hyperkalemia is pronounced.
Progressive Skin Fibrosis - Photo Quiz
Antihypertensive Agents for Prevention of Diabetic Nephropathy - Cochrane for Clinicians
ACE Inhibitors vs. ARBs for Patients with Diabetic Kidney Disease - Cochrane for Clinicians
Angiotensin Blockade in Patients with Diabetic Nephropathy - FPIN's Clinical Inquiries
ABSTRACT: Tight glucose control with intensive therapy in patients with type 1 diabetes (formerly known as juvenile-onset or insulin-dependent diabetes) can delay the onset and slow the progression of retinopathy, nephropathy and neuropathy. Optimal blood glucose control is defined by a target glycosylated hemoglobin level of less than 7 percent, a preprandial glucose level of 80 to 120 mg per dL (4.4 to 6.7 mmol per L) and a bedtime glucose level of 100 to 140 mg per dL (5.6 to 7.8 mmol per L). This article provides guidelines to help family physicians teach patients with type 1 diabetes how to achieve tight glucose control to help minimize complications. Guidelines include maintaining blood glucose levels at near normal by taking doses of short-acting insulin throughout the day supplemented by a nighttime dose of intermediate-acting insulin, monitoring blood glucose levels frequently, following a prudent diet, exercising regularly and effectively managing hypoglycemia, as well as empowering patients to lead their control efforts and rigorously controlling other risk factors for cardiovascular disease. Support from physicians, family members and friends is crucial to the success of a regimen of tight glucose control.
ABSTRACT: Nearly one-half of persons with chronic kidney disease have diabetes mellitus. Diabetes accounted for 44 percent of new cases of kidney failure in 2008. Diabetic nephropathy, also called diabetic kidney disease, is associated with significant macrovascular risk, and is the leading cause of kidney failure in the United States. Diabetic nephropathy usually manifests after 10 years’ duration of type 1 diabetes, but may be present at diagnosis of type 2 diabetes. Screening for microalbuminuria should be initiated five years after diagnosis of type 1 diabetes and at diagnosis of type 2 diabetes. Screening for microalbuminuria with a spot urine albumin/creatinine ratio identifies the early stages of nephropathy. Positive results on two of three tests (30 to 300 mg of albumin per g of creatinine) in a six-month period meet the diagnostic criteria for diabetic nephropathy. Because diabetic nephropathy may also manifest as a decreased glomerular filtration rate or an increased serum creatinine level, these tests should be included in annual monitoring. Preventive measures include using an angiotensin- converting enzyme inhibitor or angiotensin II receptor blocker in normotensive persons. Optimizing glycemic control and using an angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker to control blood pressure slow the progression of diabetic nephropathy, but implementing intensive glycemic and blood pressure control is associated with more adverse outcomes. Low-protein diets may also decrease adverse renal outcomes and mortality in persons with diabetic nephropathy.