الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
In recent years there has been a worldwide ’epidemic’ of renal failure in diabetic patients. The majority of these patients have type 2diabetes [1]
Along with hyperglycemia, dyslipidemia, and cigarette smoking, hypertension is a major contributor to the development and progression of macrovascular and microvascular complications in people with diabetes[2] Compared to the general population, people with diabetes face a two- to fourfold increased risk of cardiovascular disease (CVD)[3].Concomitant hypertension triples the already high risk of coronary artery disease (CAD), doubles total mortality and stroke risk, and may be responsible for up to 75% of all CVD events in people with diabetes [4] Similarly, hypertension significantly accelerates the progression of diabetic nephropathy, retinopathy, and neuropathy [2]
Follow-up observation of individuals with no proteinuria at baseline showed that the risk of developing end-stage renal disease increased with progressively higher baseline blood-pressure values. This blood-pressure-dependent risk was substantially greater in type 2 diabetics than in nondiabetic patients [5]
Parents of patients with diabetes plus diabetic nephropathy have higher blood pressures than parents of diabetic patients without diabetic nephropathy, indicates that a genetic predisposition to hypertension increases the risk of developing this form of kidney disease [6]. The same dependency of risk on family history of hypertension and pre-diabetic blood pressure has been observed in type 2diabetes [7]
A hereditary predisposition to diabetic nephropathy is also indicated by the finding that nondiabetic offspring of patients with type 2diabetes plus diabetic nephropathy have higher blood pressures and urinary albumin levels than offspring of diabetic parents without diabetic nephropathy [8].In light of the clustering of cardiovascular disease in families of diabetic patients who develop diabetic nephropathy taking the family history with particular attention to hypertension and cardiovascular events—is an important element in the management of diabetic patients. [9]
Reducing blood pressure in people with hypertension and diabetes decreases both macrovascular and microvascular complications. Clinical trials using a variety of antihypertensive agents have demonstrated that modest reductions in blood pressure of just 9–11 mmHg systolic and 2–9 mmHg diastolic decrease CVD events by 34–69% and microvascular complications (retinopathy and nephropathy) by 26–46% within just 2–5 years [10]
A diagnosis of hypertension is confirmed if carefully measured blood pressure is ≥ 130/80 mmHg on two office visits over a 1-month period. If average blood pressure is ≥ 140/90 mmHg or if there is albuminuria or TOD, simultaneous pharmacological and lifestyle modification therapy should be initiated at the second office visit. If initial blood pressure averages 130–139/80–89 mmHg and albuminuria and TOD are absent, an initial trial of lifestyle modification limited to 3 months is reasonable [11]
Clinical trials including large numbers of patients with both diabetes and hypertension have demonstrated reductions in CVD events and microvascular complications, using thiazide diuretics, ACE inhibitors, angiotensin receptor blockers (ARBs), dihydropyridine (DHP) and nondihydropyridine (nonDHP) calcium channel blockers (CCBs), and β-blockers. [12]
Most diabetic hypertensive patients with normal renal function require a combination of two to three antihypertensive agents to lower blood pressure to < 130/80 mmHg; patients with concomitant chronic kidney disease may require three or more agents [12]
ACE inhibitors and ARBs do have specific renoprotective effects independent of the level of blood pressure or the extent of blood pressure lowering, at least in some subgroups of diabetic patients [13]
A recent study of normo-albuminuric, hypertensive type 2 diabetic patients found that an ACE inhibitor delayed the development of persistent microalbuminuria compared to the CCB verapamil, despite similar levels of blood pressure lowering [14]
Another recent study demonstrated that ACE inhibitors and ARBs equivalently slow the progressive loss of glomerular filtration rate (GFR) in patients with diabetic nephropathy [15]
Combining ACE inhibitors with ARBs is theoretically attractive. Addition of an ARB to an ACE inhibitor could counteract the incomplete suppression of angiotensin II seen with ACE inhibitors; adding an ACE inhibitor to an ARB would preserve the inhibition of bradykinin degradation by the ACE inhibitor. However, clinical benefits of combination ACE inhibitor and ARB therapy have not yet been fully documented. [16].When larger doses of longer-acting ACE inhibitors have been used, for example lisinopril 40 mg/day, there is usually no additive effect from the ARB on blood pressure [16]
According to the above mentioned studies, there is an immense need to conduct the current study to review the recent advances in the diagnosis and management of diabetic nephropathy in adults having hypertension aiming eventually to minimize the consequences of such problem.