Nephroprotective Therapy Research Articles

Néphroprotection. Comment ralentir l’évolution de l’insuffisance rénale chronique ?

Most nephropathies are characterized by a progression that may result in end-stage renal failure (ESRF). Apart from the specific treatment implemented when possible, ESRF may be delayed by nephroprotective therapy. Following the definition of the risk factors likely to induce progressive renal disease, the various therapeutic strategies that may play a nephroprotective role are reviewed. The potential results are described with regard to published data, in particular randomised trials, as recommended by the evidence-based medicine principles. Blockade of the renin-angiotensin system plays a major role in terms of nephroprotection. However, this strategy should not replace lifestyle measures and pharmacological treatment of the metabolic disorders associated to nephropathies.

Néphroprotection. Comment ralentir l’évolution de l’insuffisance rénale chronique ?

Most nephropathies are characterized by a progression that may result in end-stage renal failure (ESRF). Apart from the specific treatment implemented when possible, ESRF may be delayed by nephroprotective therapy. Following the definition of the risk factors likely to induce progressive renal disease, the various therapeutic strategies that may play a nephroprotective role are reviewed. The potential results are described with regard to published data, in particular randomised trials, as recommended by the evidence-based medicine principles. Blockade of the renin-angiotensin system plays a major role in terms of nephroprotection. However, this strategy should not replace lifestyle measures and pharmacological treatment of the metabolic disorders associated to nephropathies.

Postmenopausal hormone replacement improves proteinuria and impaired creatinine clearance in type 2 diabetes mellitus and hypertension.

To determine whether hormone replacement therapy can reverse established renal microvascular damage in type 2 diabetes and hypertension. Prospective, single centre clinical trial. Outpatient clinics. Sixteen diabetic and hypertensive postmenopausal women (age 47-57 years) Administration of a cyclic combination of oestradiol and norgestrel orally for 3.5 monthly cycles. Comparing the baseline values, mean (SD) 24-hour urine protein excretion was reduced from 0.452 g (0039) to 0.370 g (0.047) (P < 0.01) and creatinine clearance was increased from 1.68 mL/sec (0.11) to 1.77 mL/sec (0.08) (P < 0.05). Fasting plasma glucose also improved from 6.92 mmol/L (0.47) to 6.51 mmol/L (0.28) (P < 0.05), as did serum total cholesterol from 7.26 mmol/L (0.28) to 6.65 mmol/L (0.14) (P < 0.05). Blood pressure did not change significantly. Univariate linear regression analysis showed no significant correlation between the individual changes in blood pressure, fasting plasma glucose or serum cholesterol and the individual changes in proteinuria or creatinine clearance. This study shows that hormone replacement therapy may reduce proteinuria, and even improve creatinine clearance, in diabetic and hypertensive postmenopausal women. These effects are additive to nephroprotective therapy, and the mechanisms appear unrelated to conventional risk factors for vascular complications, such as high blood pressure, elevated plasma glucose or serum cholesterol.

Relationships Among Diabetes, Microalbuminuria, and ACE Inhibition

Increasing worldwide rates of diabetes mellitus, combined with the significant micro- and macrovascular complications that accompany the disease, point to a heightened need to develop simple, rational strategies to protect against end-organ damage, particularly diabetic nephropathy. Although simple strategies do exist, i.e., early diagnosis of microalbuminuria (MAU) followed by nephroprotective therapy with angiotensin-converting enzyme (ACE) inhibitors, the use of these techniques should be increased. This is especially true for primary care physicians, who will continue to handle the majority of diabetic patients. To combat the underuse of this dual approach, this article reviews a stepwise approach to identifying early MAU so that therapeutic measures can be undertaken before the disorder progresses to diabetic nephropathy and, consequently, to end-stage renal disease in the majority of patients. Once a diagnosis of MAU is made, a variety of trials have demonstrated that ACE inhibitor therapy should be considered the standard therapy to retard worsening albuminuria and subsequent renal disease. ACE inhibitors can retard the progression of microalbuminuria and can lower the percentage of patients who progress to end-stage renal disease and death. Significant data indicate that ACE inhibitors should be used in MAU diabetics regardless of the level of blood pressure. In particular, the ACE inhibitor fosinopril may offer advantages because of its dual route of elimination, thus simplifying dosing in renally impaired patients. The newly developed angiotensin II receptor antagonists should be considered in patients intolerant to ACE inhibitors because of the similar effect on the interruption of the renin-angiotensin system.

Relationships among diabetes, microalbuminuria, and ACE inhibition.

Increasing worldwide rates of diabetes mellitus, combined with the significant micro- and macrovascular complications that accompany the disease, point to a heightened need to develop simple, rational strategies to protect against end-organ damage, particularly diabetic nephropathy. Although simple strategies do exist, i.e., early diagnosis of microalbuminuria (MAU) followed by nephroprotective therapy with angiotensin-converting enzyme (ACE) inhibitors, the use of these techniques should be increased. This is especially true for primary care physicians, who will continue to handle the majority of diabetic patients. To combat the underuse of this dual approach, this article reviews a stepwise approach to identifying early MAU so that therapeutic measures can be undertaken before the disorder progresses to diabetic nephropathy and, consequently, to end-stage renal disease in the majority of patients. Once a diagnosis of MAU is made, a variety of trials have demonstrated that ACE inhibitor therapy should be considered the standard therapy to retard worsening albuminuria and subsequent renal disease. ACE inhibitors can retard the progression of microalbuminuria and can lower the percentage of patients who progress to end-stage renal disease and death. Significant data indicate that ACE inhibitors should be used in MAU diabetics regardless of the level of blood pressure. In particular, the ACE inhibitor fosinopril may offer advantages because of its dual route of elimination, thus simplifying dosing in renally impaired patients. The newly developed angiotensin II receptor antagonists should be considered in patients intolerant to ACE inhibitors because of the similar effect on the interruption of the renin-angiotensin system.