UMLS:C0033687 - FACTA Search

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

Although multiple antihypertensive agents are required to control blood pressure (BP) in chronic renal disease, it remains undetermined whether the combination therapy with angiotensin receptor blockers (ARB) plus calcium antagonists or angiotensin-converting enzyme inhibitors (ACEI) confers more preferable action on renal disease than the ARB monotherapy. In the present study, we compared the effect of the combination therapy with ARB plus calcium antagonists/ACEI on proteinuria with that of the ARB monotherapy in chronic nondiabetic renal disease. At 1 month of the drug treatment, the candesartan monotherapy (n=19) reduced BP from 154+/-3/93+/-2 to 146+/-3/88+/-2 mmHg (P<0.05), and a similar magnitude of BP reductions was observed with the combination therapy with candesartan plus ACEI/amlodipine (from 153+/-2/95+/-2 to 144+/-2/88+/-2 mmHg, P<0.05, n=39). The depressor action of these therapies was sustained throughout the 12-month treatment. In contrast, the reduction in proteinuria was greater with the combination therapy (-52+/-3% at 12 months, n=39) than with the candesartan monotherapy (-25+/-3%, n=19), although the baseline values of proteinuria were nearly the same in the candesartan monotherapy group (1.74+/-0.22 g/day) and the combination therapy group (2.10+/-0.19 g/day, P>0.2). Of note, the proteinuria-sparing effect did not differ between the candesartan+ACEI group and the candesartan+amlodipine group. In conclusion, the present study suggests more beneficial action of the combination therapy with ARB plus ACEI/amlodipine than the ARB monotherapy in nondiabetic renal disease. Since the reduction in BP was achieved to the same level, the distinct proteinuria-sparing action of these therapies is attributed to BP-independent mechanisms, which should vary depending on the agents used.
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PMID:Beneficial action of candesartan cilexetil plus amlodipine or ACE inhibitors in chronic nondiabetic renal disease. 1529 13

Post-transplant hypertension remains a significant risk factor for graft loss, but whether or not specific blood pressure (BP) medications affect graft outcome is still unknown. We assessed the interaction between BP control and antihypertensive drugs on graft outcome. We retrospectively examined clinic BP data for 1662 renal transplant (RTx) patients, transplanted between 1994 and 2000 at our centre. The analysis examined all patients who received central alpha-agonists and peripheral alpha-antagonists, beta-blockers, calcium channel blockers (CCBs), angiotensin-converting enzyme (ACE) inhibition (ACEI), angiotensin receptor blockers (ARBs). BP recordings during treatment were categorized for each agent. Thus, a particular BP could be categorized for multiple medications. A total of 1462 patients (pts) (88%) were Caucasian and 800 pts (46%) received cadaveric RTx. There were 10.6+/-6.8 BP measurements for each patient post-RTx. CCBs, alone among the classes of antihypertensive drugs evaluated, reduced the risk for graft loss (RR: 0.736; P=0.035) in the overall analysis. Interestingly, stratifying levels of BP control unmasked a beneficial effect on graft survival of ACEI/ARB therapy in individuals with higher levels of systolic (>152 mmHg) and diastolic blood pressure (>98 mmHg) treated with ACEI/ARBs compared to individuals treated with CCBs (P<0.01 for each). Thus, stabilizing BP is important post-RTx. CCBs are associated with improved rates of graft survival. Their role in a compromised RTx, however, deserves further study. ACEI/ARBs have clear benefits, improving graft survival in individuals with elevated systolic blood pressure and proteinuria. CCBs are not as efficacious in this setting.
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PMID:Blood pressure control in kidney transplantation: therapeutic implications. 1538 45

At least 17 million people in the United States have diabetes mellitus, and another 50 million have hypertension. These chronic diseases increasingly coexist in our aging population. Both diseases are important predisposing factors for the development of cardiovascular disease (CVD) and renal disease, and the coexistence of these risk factors is a very powerful promoter of CVD and renal disease. There is accumulating evidence that the rigorous treatment of hypertension and other risk factors such as dyslipidemia and hyperglycemia considerably lessens the burden of CVD and renal disease in patients with diabetes mellitus. There is considerable evidence that strategies addressing diet and exercise reduce the development of diabetes and are an important component of treatment in persons who have established diabetes. There are also considerable data suggesting that the treatment strategies that interrupt the renin-angiotensin system have special benefits in patients with diabetes and may prevent the development of clinical diabetes in hypertensive patients with impaired glucose tolerance. Data from a recent study indicate that the control of systolic blood pressure, using a diuretic agent as part of antihypertensive therapy, reduces the risk of stroke and other CVD end points. Recent reports indicate that angiotensin receptor-blocking agents decrease the rate of development of proteinuria and diabetic renal disease. These observations will likely have a significant impact on treatment of hypertension in patients with type 2 diabetes mellitus.
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PMID:Treatment of hypertension in patients with diabetes. 1545 59

When kidney disease of any aetiology results in substantial loss of nephrons, a common clinical syndrome, characterised by hypertension, proteinuria and a progressive decline in renal function, ensues. This observation suggests that common mechanisms may contribute to progressive renal injury and that therapeutic interventions that inhibit these common pathways may afford renal protection. Research to date has identified several mechanisms that may contribute to progressive renal injury including glomerular haemodynamic changes, multiple effects of angiotensin II and detrimental effects of excessive filtration of plasma proteins by injured glomeruli. Clinical trials over the past decade have identified several interventions that are effective in slowing the rate of progression of chronic kidney disease (CKD). The use of ACE inhibitors, angiotensin receptor antagonists or a combination of the two should be regarded as fundamental to any therapy for slowing the rate of CKD progression. Hypertension should be treated aggressively to achieve a blood pressure target of < 130/80 mm Hg. Reduction of proteinuria to < 0.5 g/day should be regarded as an independent therapeutic goal. Although inconclusive, there is some evidence to support moderate dietary protein restriction to 0.6 g/kg/day in appropriate patients. Hyperlipidaemia may contribute to CKD progression and should be treated to reduce cardiovascular risk and potentially improve renal protection. Smoking cessation should be encouraged and, where necessary, assisted. Among diabetic patients tight glycaemic control should be achieved (glycosylated haemoglobin < 7%). These interventions are simple and relatively inexpensive. If applied to all patients with CKD they will result in substantial slowing of renal function decline in many patients and thereby reduce the number who progress to end-stage renal disease and require renal replacement therapy.
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PMID:Slowing the progression of adult chronic kidney disease: therapeutic advances. 1545 27

Clinical trials have demonstrated the benefit of blood pressure (BP) reduction in reducing the risk of cardiovascular and renal complications in patients with diabetes mellitus. Incorporation of agents that inhibit the renin-angiotensin-aldosterone system (RAAS) into antihypertensive regimens has been shown to provide reductions in renal and cardiovascular events that are mediated by both BP-dependent and -independent mechanisms. Recent studies exploring these potential mechanisms have demonstrated a direct role of angiotensin II (ATII) in the pathology of the vasculature and other sites of end-organ injury. In animal models of diabetes, inhibition of the RAAS with angiotensin-converting enzyme (ACE) inhibition or angiotensin type 1 (AT(1)) receptor blockade has been shown to prevent atherosclerosis, an effect that was independent of BP reduction. In addition to its direct effects on the vasculature, ATII also has direct detrimental effects on end organs, including the kidney and the heart, which lead to the development of proteinuria and left ventricular hypertrophy (LVH), respectively. Left ventricular hypertrophy has been shown to be predictive of cardiovascular and renal events, and the benefits of RAAS inhibition with angiotensin receptor blocker therapy are accompanied by a reduction in LVH. In addition to preventing the cardiovascular and renal complications of diabetes, the RAAS blockade has also been shown, in several large randomized clinical trials, to inhibit new onset of diabetes. Recent studies have revealed that many tissues, including pancreatic islets and adipose tissue, have a local RAAS. In the diabetic rat model (Zucker diabetic fatty rats), pancreatic islets exhibit an increased intraislet expression of ACE and AT(1) as well as increased intraislet fibrosis, apoptosis, and oxidative stress. The local RAAS also appears to play a role in the function of the adipocyte. Angiotensin II inhibits adipocyte differentiation, potentially decreasing the storage capacity of adipose tissue. The reduced capacity of adipose tissue to store fatty acids may cause their accumulation in other tissues, leading to insulin resistance and development of diabetes. Collectively, these studies demonstrate that ATII has direct effects on multiple tissues, and inhibition of ATII action in these tissues may be responsible for many of the clinical benefits observed with RAAS inhibition.
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PMID:The role of the renin-angiotensin-aldosterone system in diabetes and its vascular complications. 1553 6

Recurrence of focal glomerulosclerosis (FSGS) following renal transplantation is a common cause of allograft loss and clinical morbidity. Recent attempts to control proteinuria and morbidity with plasmapheresis (PP) have met with limited success. Our experience with the use of mycophenolate mofetil (MMF) and angiotensin blockade (AB) in the management of refractory FSGS pre transplant suggested its potential benefit in post-transplant recurrence. This report presents our 25-year experience in pediatric renal transplantation of patients with FSGS divided into two treatment eras: Era 1-prior to use of daclizumab (anti-IL-2R) and Era 2-after daclizumab. A total of 179 pediatric patients were transplanted during the 25-year period. FSGS was confirmed in 27 (15%); 16 of 28 allografts (57%) had recurrence of FSGS during the post-transplant period. In Era 1, only 6 of 16 (38%) recurred in the allograft, while 10 of 12 (83%) recurred during Era 2. The odds ratio of recurrence of FSGS in the allograft after induction with anti-IL-2R was 8.3 (95% confidence interval=1.3-52, P =0.02). Only 2 patients in Era 1 received PP, while 10 in Era 2 were entered into an intensive PP protocol followed by maintenance with AB consisting of angiotensin receptor blockers alone, or in combination with angiotensin-converting enzyme inhibitor. Although proteinuria decreased an average of 80+/-16% with PP, the response was variable and severe morbid edema persisted in poor responders. Maximum benefit occurred with the addition of AB and MMF. After a follow-up of 27+/-15 months, proteinuria has shown a sustained decrease of 94+/-8% below baseline. In conclusion, our experience suggests that, with recurrent FSGS, a limited course of PP followed by maintenance therapy with AB and MMF improves symptoms and may preserve allograft function.
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PMID:Recurrent focal glomerulosclerosis in pediatric renal allografts: the Miami experience. 1560 84

Angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and diuretics may exert synergistic antiproteinuric effects. Eighteen patients with a proteinuria >1 g/24 h after 6 mo of treatment with ramipril at 5 mg/d were assigned to receive in random order ramipril at 10 mg/d, valsartan at 160 mg/d, or combined ramipril at 5 mg/d and valsartan at 80 mg/d in addition to their antihypertensive treatment. The treatment periods lasted 4 wk and were separated by a 4-wk washout with ramipril at 5 mg/d. At the end of this crossover sequence, patients received combined ramipril at 5 mg/d, valsartan at 80 mg/d, and an increased furosemide dosage for an additional 4-wk period. The primary end point was the urinary protein/creatinine ratio for two 24-h urine collections at the end of each treatment period. No significant differences were noted between the study end points of the ramipril 10, valsartan 160, and combined ramipril 5 and valsartan 80 treatment groups. However, the urinary protein/creatinine ratio was lower with combined ramipril 5 and valsartan 80-increased furosemide dosage than with valsartan 160 and combined ramipril 5 and valsartan 80, with a similar tendency compared with ramipril 10. Combined ramipril 5 and valsartan 80-increased furosemide dosage decreased systolic home BP and increased serum creatinine but did not significantly increase the number of symptomatic hypotension cases compared with the other three treatments. Thus, in patients with severe proteinuria and hypertension, a cautious increase in diuretic dosage in addition to combined angiotensin-converting enzyme inhibitors and angiotensin receptor blockers decreases proteinuria and BP but may expose the patient to prerenal failure.
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PMID:Diuretic and enhanced sodium restriction results in improved antiproteinuric response to RAS blocking agents. 1561 22

African Americans represent a population with the highest prevalence of hypertension in the world, associated with earlier onset, more severity, poorer control rates, and more cardiovascular and renal complications than White Americans. The high prevalence of type 2 diabetes mellitus in African Americans, compared with Whites, compounds the excessive burden of cardiovascular and kidney disease. The Hypertension in African American Working Group of the International Society of Hypertension in Blacks recently developed a consensus document that presented a practical, evidence-based approach aimed at achieving better blood pressure control. It was thought that a new approach, targeted at US Blacks, was needed to achieve better blood pressure control and enhanced target tissue protection. Key elements of the document include (i) emphasis on the importance of therapeutic lifestyle modification such as weight loss, decreased sodium ingestion, increased potassium intake, exercise, and weight loss, to name a few; (ii) recommendation of combination antihypertensive agents because of the high prevalence of individuals with >15 mm Hg above SBP goal and/or 10 mmHg above DBP goal (140/90 unless there is also diabetes and/or kidney disease with >1 g proteinuria daily). Effective combinations include beta-adrenoceptor antagonist/diuretic, ACE inhibitor/diuretic, ACE inhibitor/calcium channel antagonist, and angiotensin receptor antagonist/diuretic; and (iii) the recommendations do not differ from other racial/ethnic groups where specific or compelling indications for the use of specific classes of antihypertensive agents exist.
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PMID:Clinical guidelines for the treatment of hypertension in African Americans. 1563 32

The dose-response relationship between pharmacological blockade of the renin-angiotensin system (RAS) and angiotensin II concentration in the circulation, on the one hand, and decrease of blood pressure, on the other hand, has been well established. In contrast it is currently unclear which dose of ACE inhibitors and/or angiotensin receptor blockers is optimal for nephroprotection. Clinical studies are rendered quite complex by an early decrease of glomerular filtration after RAS blockade and by side effects at higher doses such as renal sodium loss, hyperkalemia, anemia, etc. Animal experiments and recent clinical studies suggest that the doses of ACE inhibitors or angiotensin receptor blockers required for maximal reduction of proteinuria (as a surrogate marker) and for optimal nephroprotection (retardation of the loss of glomerular filtration) exceed those required for maximal lowering of blood pressure. Ongoing studies try to define the relative merits of high dose monotherapy (ACE inhibitors or angiotensin receptor blockers) versus a combination therapy of the two.
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PMID:Renal failure and ACE inhibition: how much is too much? 1567 37

Renal fibrosis is a common consequence of chronic kidney diseases (CKD). Standard therapy to prevent progression of CKD in western medicine includes dietary protein restriction, blood pressure control, angiotensin-converting enzyme inhibition and angiotensin receptor blockade. However, little is known about the renoprotective effects of Chinese herbal medicine. Cumulative evidence suggests that some Chinese herbal medicines, including Astragalus and a mixture of Astragalus plus Angelica, Ligusticum, Triptolide and Rhubarb, have a beneficial role in slowing the progression of CKD. This effect is multi-functional and multi-targeted, and is often associated with a reduction in proteinuria and the amelioration of dyslipidaemia, but not with changes in systemic blood pressure. These mechanisms include anti-inflammation and inhibition of TGF-b overproduction. On the other hand, some Chinese herbal medicines may be hazardous to patients with renal diseases. In this review, we discuss recent advances in the research of some Chinese herbs for pharmacological intervention of progressive renal diseases and kidney-related injuries.
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PMID:Herbal treatment for renal diseases. 1572 19

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