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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The renin-angiotensin system plays an important role in the regulation of blood pressure. The use of angiotensin converting enzyme inhibitors or angiotensin receptor blockers both control hypertension by interruption of the production or action of angiotensin II, the major end-product of the renin-angiotensin system. The use of angiotensin converting enzyme inhibitors in pregnant women revealed serious and deleterious effects on fetal development including renal failure, renal dysplasia, hypotension, oligohydramnios, pulmonary hypoplasia, and hypocalvaria. The fetal effects of angiotensin converting enzyme inhibitors seem to be greatest during the 2nd and 3rd trimesters of pregnancy. The fetal effect of angiotensin converting enzyme inhibitors during the 1st trimester is controversial. These effects may represent the effect of hypoperfusion in the fetus and not a teratogenic effect. The effect of angiotensin receptor blockers is similar to converting enzyme inhibitors. Angiotensin converting enzyme inhibitors and angiotensin receptor blockers should be avoided in all pregnant women. Alternative antihypertensive medications should be considered for use in women of childbearing years.
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PMID:Fetopathy associated with exposure to angiotensin converting enzyme inhibitors and angiotensin receptor antagonists. 1642 19

Blood pressure strongly predicts microalbuminuria and later progression to renal failure in people with diabetes. Ambulatory blood pressure monitoring seems to be superior to office blood pressure in predicting progression to microalbuminuria in type 1 diabetes. The associations of ambulatory blood pressure with office blood pressure and microalbuminuria in type 2 diabetes remain unclear. We studied the association of office blood pressure taken with an automated device and ambulatory blood pressure with spot urine albumin:creatinine ratio in 1180 older people with type 2 diabetes participating in the Informatics for Diabetes Education and Telemedicine Study. Office and awake systolic blood pressure were independently associated with albuminuria (P<0.001 for both) in a multivariate linear regression analysis that adjusted for age, gender, duration of diabetes, hemoglobin A1c, number of antihypertensive medications, and use of an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker. Twelve percent of participants had well-controlled office blood pressure but not ambulatory blood pressure, whereas 14% had well-controlled ambulatory but not office blood pressure. The prevalence of microalbuminuria and macroalbuminuria in these subgroups was intermediate between those with well-controlled or uncontrolled blood pressure by both methods. We found, in a multiethnic group of older subjects with type 2 diabetes, that office systolic blood pressure and awake systolic ambulatory blood pressure exhibited independent associations with degree of albuminuria.
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PMID:Office and ambulatory blood pressure are independently associated with albuminuria in older subjects with type 2 diabetes. 1658 16

The incidence of resistant hypertension, the failure to reduce blood pressure below 140/90 mm Hg, despite the use of 3 antihypertensive medications at optimal doses including a diuretic, is estimated to be less than 5% of the hypertensive population. Resistant hypertension increases the risk of stroke, myocardial infarction, congestive heart failure, and renal failure. Evaluation of the patient with resistant hypertension should include 24-hour ambulatory blood pressure monitoring or home measurements and a limited search for secondary causes. Treatment should focus on optimizing the drug regimen in a logical way, based on the patient's comorbidities and tolerability. Long-acting, well-tolerated once-daily medications are preferred, and the regimen should include in sequence a diuretic, beta-blocker, angiotensin-converting enzyme/angiotensin receptor-blocker inhibitors, and a calcium-channel blocker. This article reviews the definitions and causes and provides specific recommendations for the evaluation and management of patients with this life-threatening condition.
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PMID:Resistant hypertension: diagnosis and management. 1689 Dec 88

Anemia, defined as a hemoglobin level of less than 12 g/dL, often is seen in congestive heart failure (CHF). It is associated with an increased mortality and morbidity and increased hospitalizations. Compared with nonanemic patients the presence of anemia also is associated with worse cardiac clinical status, more severe systolic and diastolic dysfunction, a higher beta natriuretic peptide level, increased extracellular and plasma volume, a more rapid deterioration of renal function, a lower quality of life, and increased medical costs. The only way to determine if anemia is merely a marker for more severe CHF or actually is contributing to the worsening of the CHF is to correct the anemia and see if this favorably influences the CHF. In several controlled and uncontrolled studies, correction of the anemia with subcutaneous erythropoietin (EPO) or darbepoetin in conjunction with oral and intravenous iron has been associated with an improvement in clinical status, number of hospitalizations, cardiac and renal function, and quality of life. However, larger, randomized, double-blind, controlled studies still are needed to verify these initial observations. The effect of EPO may be related partly to its nonhematologic functions including neovascularization; prevention of apoptosis of endothelial, myocardial, cerebral, and renal cells; increase in endothelial progenitor cells; and anti-inflammatory and antioxidant effects. Anemia also may play a role in increasing cardiovascular morbidity in chronic kidney insufficiency, diabetes, renal transplantation, asymptomatic left ventricular dysfunction, left ventricular hypertrophy, acute coronary syndromes including myocardial infarction and chronic coronary heart disease, and in cardiac surgery. Again, controlled studies of correction of anemia are needed to assess its importance in these conditions. The anemia in CHF mainly is caused by a combination of renal failure and CHF-induced increased cytokine production, and these can both lead to reduced production of EPO, resistance of the bone marrow to EPO stimulation, and to cytokine-induced iron-deficiency anemia caused by reduced intestinal absorption of iron and reduced release of iron from iron stores. The use of angiotensin-converting enzyme inhibitor and angiotensin receptor blockers also may inhibit the bone marrow response to EPO. Hemodilution caused by CHF also may cause a low hemoglobin level. Renal failure, cardiac failure, and anemia therefore all interact to cause or worsen each other--the so-called cardio-renal-anemia syndrome. Adequate treatment of all 3 conditions will slow down the progression of both the CHF and the chronic kidney insufficiency.
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PMID:The interaction between heart failure and other heart diseases, renal failure, and anemia. 1694 68

Prevention and regression of diabetic renal disease can be obtained through the combination of strict blood pressure control, which frequently requires the combination of different antihypertensive drugs, with tight glycaemic control. Recent evidence obtained with the angiotensin receptor blockers has allowed the recognition by most guidelines that this class of agents constitutes the first choice to treat hypertension in type 2 diabetic patients presenting with diabetic renal disease at any stage of evolution, from microalbuminuria to advanced renal failure. Of course this must be accompanied by an integral coverture of the increased global cardiovascular risk that always accompanies this situation. This short review contains the most relevant evidence in favour of angiotensin receptor blockers, with particular emphasis on the capacities of candesartan for controlling blood pressure and protecting the kidney. In patients with type 2 diabetes and varying degrees of albuminuria, treatment with candesartan 8-32mg daily was shown to reduce urinary albumin excretion (UAE) by up to 60%. When given in addition to an ACE inhibitor (dual blockade), reductions in UAE of 25-35% relative to ACE inhibitor monotherapy have been found.
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PMID:Angiotensin receptor blockade in diabetic renal disease--focus on candesartan. 1733 65

In IgA nephropathy (IgAN), ACE inhibitors (ACE-I) and angiotensin receptor blockers (ARB) are beneficial against hypertension, and their anti-proteinuric effect has been clearly demonstrated. However, sub-analyses of IgAN patients enrolled in large studies failed to prove a benefit against progression to renal failure. The European Community Biomed Concerted Action - a placebo-controlled randomized controlled trial begun in 1995 - in children and adults (9-35 years old) with proteinuria > 1 < 3.5 g/day/1.73 m(2) and normal or moderately reduced renal function proved the significant benefit of ACE-I on progression of kidney disease. The combination of ACE-I and ARB in proteinuric normotensive IgAN patients showed greater antiproteinuric effect and the COOPERATE trial also reported a superior effect of combination therapy in protecting against renal function deterioration. Treating IgAN with fish oil has a good rationale for renal inflammation as well as for prevention of cardiovascular morbidity. However, the published reports gave conflicting conclusions and also very recent data did not show significant benefits. In conclusion, ACE-I and ARB have a definite role in treating IgAN, particularly the hypertensive and proteinuric forms. These patients should be treated to target BP to <130/70 mm Hg and proteinuria <0.5 g/day.
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PMID:Angiotensin antagonists and fish oil for treating IgA nephropathy. 1749 34

The renal diseases associated with monoclonal immunoglobulin deposits constitute a diverse range of clinical and pathological entities. Renal prognosis is variable, and there currently are no standard treatment regimens. We describe the effect of rituximab treatment on 3 patients with renal insufficiency and proteinuria with monoclonal immunoglobulin deposits associated with glomerulonephritis on renal biopsy. Two patients with hypertension and chronic lymphocytic leukemia had a membranoproliferative glomerulonephritis pattern on kidney biopsy associated with monoclonal immunoglobulin G deposits. Both patients experienced partial remission of their disease and 1 patient was able to come off hemodialysis therapy after treatment with 7 and 11 biweekly doses of rituximab, 375 mg/m(2), in addition to angiotensin-converting enzyme inhibitor and angiotensin receptor blocker. Both patients subsequently experienced relapse of their hematologic and renal diseases and eventually progressed to end-stage renal disease and death. A third patient had diffuse proliferative glomerulonephritis with immunoglobulin G lambda deposits on renal biopsy. She was treated with an angiotensin receptor blocker and two 1,000-mg infusions of rituximab separated by 2 weeks, with sustained partial remission at 18 months' follow-up. Rituximab therapy, in addition to corticosteroids and angiotensin blockade, may improve the clinical course of patients with renal diseases associated with dysproteinemias, delaying the onset of end-stage renal failure or other adverse outcomes. Additional clinical studies should be planned.
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PMID:Rituximab treatment of dysproteinemias affecting the kidney: a review of three cases. 1790 Apr 64

A common cause of death in end-stage renal disease (ESRD) patients on dialysis is sudden cardiac death (SCD). Compared to the general population, the percentage of cardiovascular deaths that are attributed to SCD is higher in patients treated by dialysis. While coronary artery disease (CAD) is the predominant cause of SCD in dialysis patients, reduced heart rate variability (HRV) may play a role in the higher risk of SCD among other risk factors. HRV refers to beat-to-beat alterations in heart rate as measured by periodic variation in the R-R interval. HRV provides a non-invasive method for investigating autonomic input into the heart. It quantifies the amount by which the R-R interval or heart rate changes from one cardiac cycle to the next. The autonomic nervous system transmits impulses from the central nervous system to peripheral organs and is responsible for controlling the heart rate, blood pressure and respiratory activity. In normal individuals, without cardiac disease, the heart rate has a high degree of beat-to-beat variability. HRV fluctuates with respiration: it increases with inspiration and decreases with expiration and is primarily mediated by parasympathetic activity. HRV has been used to evaluate and quantify the cardiac risk associated with a variety of conditions including cardiac disorders, stroke, multiple sclerosis and diabetes. In this narrative review, we will examine the association between HRV and SCD. This report explains the measurement of HRV and the consequences of reduced HRV in the general population and dialysis patients. Lastly, this review will outline the possible use of HRV as a clinical predictor for SCD in the dialysis population. The current understanding of SCD based on HRV findings among the ESRD population support the use of more aggressive treatment of CAD; greater use of angiotensin converting enzyme inhibitor (ACE-i)/angiotensin receptor blockers (ARBs) and beta-blockers and more frequent and/or nocturnal haemodialysis to improve the survival of a patient with kidney failure.
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PMID:Heart rate variability (HRV) in kidney failure: measurement and consequences of reduced HRV. 1872 54

An important endpoint in treating chronic kidney disease, a prevalent disease that can lead to kidney failure and cardiovascular disease, is reducing proteinuria. Proteinuria is an independent risk factor for disease progression and the development of cardiovascular disease and is a key factor that can be used to guide therapy designed to maximize kidney protection. Proteinuria is targeted by using pharmacologic agents that suppress the renin-angiotensin-aldosterone system (RAAS), a regulator of intravascular volume and blood pressure; this has been shown to decrease proteinuria, slow disease progression, and improve coronary disease outcome, independent of effects on blood pressure. The efficacy of RAAS blockers, including angiotensin receptor blockers and angiotensin-converting enzyme inhibitors, may be limited by currently recommended doses, which are based on treatment of hypertension. Data are now emerging from clinical trials demonstrating that use of 'supratherapeutic doses' (doses greater than those approved for lowering blood pressure), compared with standard doses, has favorable safety, tolerability, and efficacy in reducing proteinuria in both diabetic and nondiabetic patients with chronic kidney disease. Supratherapeutic dosing may be a valuable approach for optimizing RAAS blockade and providing renoprotection.
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PMID:Supratherapeutic doses of angiotensin receptor blockers to decrease proteinuria in patients with chronic kidney disease. 1806 56

Diabetes is currently one of the leading causes of end-stage renal failure requiring renal replacement therapy in the Western World. About 15% to 20% of type 1 diabetic patients and 30% to 40% of type 2 diabetic patients will eventually develop end-stage renal failure. To prevent the development or progression of diabetic kidney disease, good glycaemic control remains the cornerstone in the management of diabetic patients. Beyond glycaemic control, other metabolic factors have been shown to be involved in the development of diabetic kidney disease, i.e. advanced glycation endproducts (AGEs) and the aldose reductase pathway. Furthermore, an adequate control of high blood pressure and treatment of microalbuminuria are major therapeutic targes. To achieve adequate blood pressure control, a combination therapy with different classes of antihypertensive agents is often necessary, especially including angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. Other vasoactive factors involved in diabetic nephropathy such as endothelin and nitric oxide will be covered briefly. Besides hyperglycaemia and high blood pressure, other risk factors have been identified in the development or progression of diabetic kidney disease: smoking, hyperlipidaemia, obesity and high protein intake. Their impact on renal function will be highlighted. Finally, recent research has also identified intracellular pathways such as the diacylglycerol-protein kinase C pathway and several growth factors, such as growth hormone, insulin-like growth factor, transforming growth factor-beta, vascular endothelial growth factor, and platelet derived growth factor as players in diabetic kidney disease.
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PMID:Novel insights in the treatment of diabetic nephropathy. 1822 60


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