UMLS:C0033687 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Target Concepts:

Query: UMLS:C0033687 (proteinuria)
24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interest in evidence-based medicine is increasing greatly, with the focus on treatment that prevents organ failure and that may prolong life. Type 1 and Type 2 diabetes are conditions associated with increased mortality, mainly as a result of renal and cardiovascular diseases, and blindness. All three complications usually occur together. In recent years, more focus has been placed on treating patients early to prevent future organ damage. Microalbuminuria is an important intermediary end-point that correlates strongly with future advanced renal disease, retinopathy and mortality. Several trials have studied patients with microalbuminuria and also patients in more advanced stages of the disease who have proteinuria (termed overt nephropathy). Recent evidence indicates that achieving optimal glycaemic control reduces the risk of an increase in urinary albumin excretion before the development of microalbuminuria. Angiotensin-converting enzyme (ACE) inhibitors are effective in reducing microalbuminuria, partly independent of their blood pressure reducing effects. In Type 1 and Type 2 diabetic patients with microalbuminuria, long-term treatment with ACE inhibitors (7-8 years) prevents the predicted decrease in glomerular filtration rate (GFR); optimal glycaemic control is also important in preventing the decline in GFR. This is important because GFR is usually well preserved in Type 1 and Type 2 diabetic patients with microalbuminuria and a predicted decline in GFR can therefore be prevented. In overt renal disease, studies that focused mostly on Type 1 diabetic patients have shown that the rate of decline in GFR can be reduced. Long-term studies in Type 1 diabetic patients have also demonstrated that mortality caused by end-stage renal disease can be postponed. Mortality associated with cardiovascular diseases, e.g. myocardial infarction, is reduced more effectively in diabetic patients treated with ACE inhibitors and beta-blockers than in non-diabetic patients treated with the same drugs. Screening for microalbuminuria, the attainment of optimal glycaemic control, and early treatment with ACE inhibitors and other antihypertensive drugs are necessary to prevent progression of diabetic complications, especially diabetic nephropathy. However, there is some controversy about the initial use of calcium channel blockers. In conclusion, early achievement of improved glycaemic control is the most important factor in the prevention of diabetic complications. Antihypertensive treatment is clearly also important.
...
PMID:Preventing end-stage renal disease. 986 93

Some antihypertensive drugs may have a renoprotective effect, that is partially independent of their ability to reduce blood pressure. ACE-inhibitors are safe and effective agents that are capable of reducing proteinuria and preventing CRF progression. The results of the AIPRI extension study suggest that they may also have a long-term renoprotective effect. ACE gene polymorphism may partially influence the response to these agents. Angiotensin II receptor 1 antagonists (AT1RA) are effective in reducing proteinuria, but their clinical impact is still a matter of study. It has been shown that non-dihydropyridine and some dihydropyridine calcium channel blockers (CCBs) reduce proteinuria and are also renoprotective, but there is a lack of large-scale prospective randomised trials. Given that the use of various drugs is usually needed to achieve good blood pressure control in patients with CRF, the possibility that a combination of ACE-inhibitors with CCBs or ATIRAs may have an additive renoprotective effect is intriguing.
...
PMID:The renoprotective effect of antihypertensive drugs. 1004

Approximately 150 million people worldwide have diabetes mellitus, of whom 90% are type II diabetics. It is therefore of no surprise that diabetic nephropathy has become the leading cause of end-stage renal disease. Opposite to what has been known previously, kidney disease is at least as common in type II as in type I diabetes. However, because the majority of type II diabetics has hypertension for many years before diabetes mellitus becomes clinically relevant, renal lesions are often heterogeneous with frequent exclusive presence of ischemic changes. For the treatment of hypertension in diabetics without nephropathy (no microalbuminuria), drugs that exert beneficial effects or are at least neutral with respect to lipid and glucose metabolism, such as ACE inhibitors, angiotensin II-receptor antagonists, non-dihydropyridine-calcium channel blockers and the thiazide-like indapamide, are to be preferred. Although metabolically neutral, dihydropyridine calcium channel blockers should be used with caution, since an increase in cardiovascular morbidity and mortality in type II diabetics treated with these compounds has most recently been described. Once that diabetic nephropathy is established, blood pressure should be lowered to 120/80 mmHg (measured in seated position). Antihypertensive treatment should primarily be based on ACE inhibitors; angiotensin II-receptor antagonists are a valuable alternative if ACE inhibitors are not tolerated. Both ACE inhibitors and angiotensin II-receptor antagonists should be used with high caution in elderly patients with severe atherosclerosis in whom acute renal failure could occur due to the presence of bilateral renal artery stenosis. Newer studies indicate that non-dihydropyridine calcium channel blockers such as verapamil and diltiazem may be as effective as ACE inhibitors in preserving renal function in diabetic nephropathy. A fix-dose combination of the ACE inhibitor trandolapril with verapamil is now available; it should be reserved for patients whose blood pressure and/or proteinuria can not be adequately controlled with ACE inhibitors. Finally, indapamide is the only antihypertensive diuretic with nephroprotective properties.
...
PMID:[Antihypertensive therapy in diabetes mellitus]. 1006 31

Renal failure is a common long-term complication of diabetes mellitus. Stages of diabetic nephropathy have been described that characterize its clinical course. Diabetic nephropathy develops secondary to long-standing hyperglycemia and hemodynamic changes that damage the glomerulus. Therapy that focuses on the control of glomerular pressures and systemic hypertension can slow the progression of proteinuria and deterioration of renal function. Angiotensin converting enzyme (ACE) inhibitors and calcium channel blockers have been demonstrated to be effective in the management of diabetic nephropathy. A systematic approach to the patient with diabetes with annual screening for proteinuria will help identify those individuals early in the course of disease when proper therapy may be most helpful.
...
PMID:Approach to the treatment of diabetic nephropathy. 1016 75

Type 2 (noninsulin-dependent) diabetes mellitus (DM) affects about 3% of the UK population. Diabetes often coexists with a cluster of other potent cardiovascular risk factors, including hypertension, dyslipidaemia and increased tendency for thrombosis, and increases the risk of early death from cardiovascular causes by about threefold. Microalbuminuria or proteinuria also may be present, further increasing the risk of cardiovascular mortality. Cardiovascular risk factors must be treated aggressively in patients with Type 2 diabetes and control of blood pressure at 140/85 mm Hg or lower is a priority. The management of hypertension in patients from some ethnic groups demands special consideration because they have a high incidence of diabetes and hypertensive complications. Patients must be urged to adopt appropriate lifestyle changes in the first instance but additional drug treatment for hypertension is usually required. All the major classes of antihypertensive agents lower blood pressure in Type 2 diabetic patients but have different effects on metabolic risk factors in different ways. Low-dose thiazide diuretics, beta-blockers, calcium channel blockers and angiotensin converting enzyme (ACE) inhibitors have been shown to reduce cardiovascular risk. Individually, the effects of low-dose thiazide diuretics and beta-blockers on glucose and lipid metabolism is clinically insignificant, though in combination much larger metabolic effects are seen. ACE inhibitors and calcium channel blockers have no, or small, beneficial effects on glucose and lipid metabolism, while the greater beneficial effects of alpha1-blockers on lipid profiles may render them especially useful in the Type 2 diabetic patient. Long-acting calcium-channel blockers and ACE inhibitors protect renal function and are suitable as first line therapy in patients with microalbuminuria or proteinuria. Until results from the current batch of randomized, placebo-controlled trials comparing different classes of antihypertensive agents are available, the choice of antihypertensive agent is difficult. Addressing overall cardiovascular risk factors, rather than hypertension alone, is essential in the management of the hypertensive Type 2 diabetic patient.
...
PMID:Blood pressure control, microalbuminuria and cardiovascular risk in Type 2 diabetes mellitus. 1034 35

Despite current specific therapy, progressive deterioration of renal function in patients with primary glomerulonephritis occurs. Nonspecific renoprotective interventions that have been studied include blood pressure control, antihypertensive medications, and protein-restricted diets. To prepare this article, a MEDLINE search was conducted, followed by secondary and tertiary searches. Research papers were assessed for level of evidence, and graded recommendations were formulated. Protein-restricted diets (to 0.4 to 0.6 g/kg/day) are not recommended for all patients with reduced renal function (grade A). Very low-protein diets of 0.4 g/kg/day should be considered for patients with severe renal dysfunction (serum creatinine of more than 350 micromol/liter; grade A). However, there are concerns about recommending these diets for all patients because of the potential for long-term negative outcomes such as nutritional deficiencies. Target blood pressure for persons with proteinuria of more than 1 g/day should be less than 125/75 mm Hg [mean arterial pressure (MAP) < 92 mm Hg; grade C]. For persons with proteinuria of less than 1 g/day, the target blood pressure should be approximately MAP 98 mm Hg (less than 130/80; grade C). Angiotensin-converting enzyme inhibitor (ACEI) therapy is recommended in preference to placebo, conventional, or beta-blocker therapy for renoprotection (grade A). ACEI therapy cannot be recommended above calcium channel blockers in patients with nondiabetic renal disease (grade A).
...
PMID:Conservative treatment to slow deterioration of renal function: evidence-based recommendations. 1036 91

The progression of IgA-NP is influenced unfavourably by development and existence of hypertension. The treatment of hypertension (HTN) has an important role in these patients. Both short- and long-acting formulations of angiotensin convertase enzim inhibitors (ACEi) and calcium channel blockers (CCB) lower blood-pressure, however long-acting preparations may provide better control and may have more renoprotective effect. Verifying this hypothesis, 22 IgA-NP patients were followed for 7.25 +/- 2.36 years. The patients were on short-acting ACEi (captopril, n = 9) or dihydropyridine type CCB (nifedipin, n = 2) or both (captopril + nifedipine n = 11), after at least 3 years the medication was changed to long-acting ACEI (enalapril, n = 4; cilazapril, n = 1), or non dihydropyridine type CCB (diltiazem hydrochlorid, n = 1) or both (n = 16). Just before changing the medication these patients underwent 24 hour ambulatory blood pressure monitoring and at the same time the level of proteinuria and the creatine clearance were measured. Values of serum-creatinine were measured in every 3-4 months within a 3 years period before and after the exchange of antihypertensive drugs. The regression of 1/creatinine was a = -5.28.10(-5) +/- 1.16.10(-4) before and a = 1.03.10(-4) +/- 2.05.10(-4) after the change of medication. Using paired t-test there was a significant difference between the regressions of 1/creatine (p < 0.005). Systolic blood pressure (SBP) (128 +/- 81 Hgmm vs. 126.09 +/- 11.67 Hgmm) was not different, however, diastolic blood pressure (DBP) (84.15 +/- 7.94 Hgmm vs. 79.78 +/- 7.17 Hgmm), diastolic percent time elevation index (HTI) (43.58 +/- 23.57% vs. 25.61 +/- 20.1%) and 24-hour diastolic hyperbaric impact (114.71 +/- 81.9 vs. 51.51 +/- 51.4, p < 0.05) was lower with long-acting antihypertensive agents, as was the proteinuria (1.18 +/- 0.94 g/die vs. 0.69 +/- 1.08 g/die, p < 0.05). Diurnal variation and systolic percent time elevation index were not different. We conclude that long-acting ACEi and non dihydropyridine type CCB formulations result in better outcomes in IgA nephropathy patients compared to short-acting drugs, probably because of better and smoother blood pressure control, lowering of proteinuria and better compliance of the patients.
...
PMID:[Comparative study of the reno-protective effect of short- and long-acting antihypertensive agents in IgA nephropathy]. 1050 23

Transgenic rats (TGRs) TGR(mREN2)27 are characterized by fulminant hypertension, an inverse circadian blood pressure rhythm, and severe hypertensive target organ damage. In the present study, we evaluated cardiovascular risk factors, renal function, and urinary protein loss in transgenic rats before and after treatment with the calcium channel blocker amlodipine. Amlodipine was injected intraperitoneally in a dose of 5 mg/kg/day, either once daily at 8.00 h or twice daily in divided doses at 8.00 and 20.00 h. Untreated TGRs and Sprague-Dawley rats served as hypertensive and normotensive controls, respectively. Before and after 5 weeks of treatment, rats were placed in metabolic cages for sampling of urine. Prior to treatment, urinary excretion rates of protein, albumin, and Ca2+ were significantly higher in TGRs than in Sprague-Dawley controls. Urinary excretion of protein and albumin was reduced by 5 weeks of amlodipine treatment, whereas the excretion of Ca2+ was not affected. The reductions in renal proteinuria and albuminuria by amlodipine treatment were significantly correlated with the treatment-induced decrease in blood pressure. These findings indicate that blood pressure itself is an important contributor to albumin loss by the kidney in renin-dependent hypertension of TGRs.
...
PMID:Cardiovascular risk, renal hypertensive damage, and effects of amlodipine treatment in transgenic TGR(mREN2)27 rats. 1055 84

In the Ramipril Efficacy in Nephropathy study, ramipril decreased the rate of GFR decline (deltaGFR) and progression to end-stage renal disease (ESRD) in 352 patients with proteinuric chronic nephropathies. This study investigated whether in these patients disease outcome and response to treatment were affected by gender or insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene. deltaGFR (0.43 +/- 0.05 versus 0.48 +/- 0.08 ml/min per 1.73 m2) and incidence of ESRD (23 and 22%, respectively) were comparable in male and female patients. However, compared to conventional treatment, ramipril decreased deltaGFR (-52% versus -19%) and progression to ESRD (-74% versus -40%) more effectively in women than in men. Thus, the relative risk (95% confidence interval [CI]) of events (ESRD) between conventional and ramipril treatment was 5.52 (1.59 to 19.17, P = 0.003) in women, but only 1.80 (1.08 to 2.97, P = 0.02) in men. This gender-related effect of ramipril was associated with more reduction in proteinuria (-7.8 +/- 4.2% versus -21.9 +/- 5.7%, P = 0.05) and was still evident even after correction for potentially confounding factors such as baseline GFR, daily sodium intake, ramipril dose, BP control, and concomitant treatment with diuretics or dihydropyridinic calcium channel blockers (adjusted RR [95% CI]: women, 5.07 [1.26 to 20.38], P = 0.02; men, 1.44 [0.85 to 2.44], P = 0.17). Ramipril uniformly decreased deltaGFR and incidence of ESRD in women with either DD (-39% and - 100%) or II + ID (-71% and -82%) genotype, and in men (-25% and -50%) with the DD genotype, but had no beneficial effect in men with the II + ID genotype (+18% and +34%). Thus, the relative risk of events (ESRD) between conventional and ramipril-treated men was higher in subjects with the DD genotype (1.85; 0.69 to 4.94) and lower in those with the II +/- ID genotype (0.71; 0.28 to 1.80). Again, in parallel with deltaGFR and events, proteinuria decreased in women with DD (-23.3 +/-8.0%) or II + ID (-16.0 +/- 9.5%) genotype and in men with the DD genotype (-14.8 +/- 7.0%), but did not change in men with II + ID genotype (+ 1.0 +/- 7.8%). Of note, the ACE genotype-related effect of ramipril was still evident even after correction for the above potentially confounding factors (adjusted RR [95% CI]: DD, 2.52 [0.83 to 7.63], P = 0.10; II + ID, 0.35 [0.12 to 1.01], P = 0.05). Thus, among patients with chronic proteinuric nephropathies, men are at increased risk of progression due to their lower response to ACE inhibitor treatment. ACE inhibition is uniformly renoprotective in women regardless of the ACE polymorphism, and in men with the DD genotype, but is virtually devoid of beneficial effects in men with the II or ID genotype. This information may help to guide therapeutic interventions in clinical practice and to interpret the results of prospective trials in chronic renal disease.
...
PMID:Chronic proteinuric nephropathies. II. Outcomes and response to treatment in a prospective cohort of 352 patients: differences between women and men in relation to the ACE gene polymorphism. Gruppo Italiano di Studi Epidemologici in Nefrologia (Gisen) 1061 44

Hypertension in renal allograft recipients is a common problem arising from multiple factors, including peripheral vascular damage caused by pretransplant hypertension, side effects of immunosuppressive medications, allograft dysfunction, renal artery stenosis, recurrent glomerulonephritis, synthesis of vasoconstrictive hormones by the native kidneys, and excessive dietary salt intake. Identification of modifiable factors causing hypertension and concurrent medical conditions, and measurement of glomerular filtration rate, cyclosporine/tacrolimus blood levels, and magnitude of proteinuria are essential to tailor treatment for an individual patient. Lifestyles that exacerbate hypertension should be modified. For pharmacological therapy, diuretics and calcium channel blockers are first-line agents in patients on cyclosporine shortly after transplant. Angiotensin-converting enzyme inhibitors are good choices for patients with significant proteinuria. Reduction of immunosuppression will improve hypertension in some patients, but entails a potential risk of rejection or graft loss. Angioplasty is necessary in patients with a functionally significant stenosis of the allograft renal artery. Other patients on maximal medical therapy may benefit from native nephrectomy.
...
PMID:The best way to manage hypertension after renal transplantation. 1067 27

<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>