Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011881 (diabetic nephropathy)
10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nephropathy associated with type 2 diabetes mellitus is a rising cause of end-stage renal disease and is a major public health problem. If blocking of the renin angiotensin system has a well established nephroprotective effect in type 1 diabetic nephropathy, this remained to be shown for type 2 diabetes. Two large outcome trials using angiotensin II receptor antagonists (ARA's) in proteinuric chronic renal impairment and hypertensive type 2 diabetic patients have now closed this gap: the Irbesartan Diabetic Nephropathy Trial (IDNT) and the Reduction of Endpoints in NIDDM with Angiotensin II Antagonist Losartan (RENAAL) trial. Both trials showed a significant reduction in the primary pre-specified end-point of death, or worsening of renal function (doubling of serum creatinine) or the development of end-stage renal disease. This effect goes beyond the reduction in blood pressure and makes of ARA's one of the important tools in the treatment of type 2 diabetic nephropathy.
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PMID:[Clinical study of the month. Nephroprotective role of angiotensin II receptor antagonists in type 2 diabetes: results of the IDNT and RENAAL trials]. 1176 85

Diabetic nephropathy (DN) is the most common cause of chronic renal failure (CRF), in Mexico prevalence of diabetes is higher than other countries. Genetic susceptibility, arterial hypertension, proteinuria and initial hyperfiltration are risk factors for CRF. Renal injury is mediated by protein glycation, proteinuria and hemodynamics alterations induced by arterial hypertension and impaired renal autoregulation. Angiotensin II is directly involved in renal injury through its hemodynamic effects, oxidative stress, induction of proinflammatory and profibrotic factors and cellular proliferative effect. Prospective, well controlled clinical trials in patients with type 1 and type 2 DM have shown that interrupting the renin angiotensin system with CEI or ARA effectively prevent progression of DN. Combination of both drugs may provide further nephroprotection. Antihypertensive therapy in patients with DN must include CEI or ARA and to reduce BP below 130/85 mmHg and if proteinuria is present, under 120/75.
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PMID:[Arterial hypertension and diabetic nephropathy. Evidence based therapy]. 1296 48

Considering the increasing incidence of diabetic nephropathy and its serious complications, the prevention of nephropathy evolution risk in diabetic patients is the subject of several recently initiated studies. In diabetic patients with advanced nephropathy, the lowering of proteinuria by renin angiotensin system blockers induces an evolution risk reduction, which can be further improved by increasing the dose of angiotensin II receptor antagonist (ARA II). Such a synergy can be also obtained with the association of an ARA II and an angiotensin converting enzyme (ACE) inhibitor, provided that the diuretic dose given to the patient is increased. In terms of cardiovascular risk, diabetic patients benefit from this type of treatment, as cardiovascular events increase with the level of proteinuria. In micro-albuminuria patients, sufficient doses of ARA II or ACE inhibitors are needed to avoid relapse after treatment discontinuation. In normo-albuminuria patients also, the treatment with a renin angiotensin system blocker significantly decreases the risk of development of microalbuminuria. Thus, the reduction of proteinuria or the prevention of its appearance with renin angiotensin system blockers is the main therapeutic strategy to prevent the evolution of nephropathy in diabetic patients.
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PMID:[Clinical studies on chronic diabetic nephropathy and recent data concerning prevention of risks of nephropathy and cardiovascular diseases]. 1737 Aug 50

Aliskiren (Rasilez), a direct renin inhibitor, is currently indicated for the treatment of essential hypertension, as monotherapy or in combination, especially with hydrochlorothiazide (Rasilez HCT). It may also be use to obtain a more complete blockade of the renin-angiotensin-aldosterone system (RAAS) when it is associated with an angiotensin converting enzyme inhibitor (ACEI) (or an AT1 angiotensin receptor antagonist) (ARA). There is some room for agents that may be more efficacious in reducing the progression of diabetic nephropathy than ACEI or ARA. In this context, the dual blockade of RAAS most probably offers a better efficacy than the simple blockade, but also exposes to a higher risk. Should ongoing trials confirm the preliminary favourable results, aliskiren might reach a forefront position among the armamentarium now available to optimize the RAAS blockade. The present article will summarize advances concerning the biochemical effects of the specific mode of action of aliskiren, especially the potential interferences related to increased renin/pro-renin levels, as well as results of recent clinical trials, not only in hypertension, but also in the fields of diabetes, renal insufficiency and cardiology. The objectives and design of the landmark study ALTITUDE will also be briefly presented.
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PMID:[Advances concerning aliskiren, direct renin inhibitor and aliskiren-hydrochlorothiazide]. 2006 69