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How Do Ace Inhibitors Protect Kidneys In Diabetes

Mechanism Found That May Protect Kidneys In Early Stages Of Diabetes

Mechanism Found That May Protect Kidneys In Early Stages Of Diabetes

Follow all of ScienceDaily's latest research news and top science headlines ! Mechanism Found That May Protect Kidneys In Early Stages Of Diabetes A group of Northwestern University researchers has identified what they believe is a built-in biological mechanism that prevents kidney damage in the early stages of diabetes associated with obesity. A group of Northwestern University researchers has identified what they believe is a built-in biological mechanism that prevents kidney damage in the early stages of diabetes associated with obesity. Their study was led by Daniel Batlle, M.D., Earle, del Greco, Levin Professor of Nephrology and professor of medicine at Northwestern University Feinberg School of Medicine, and was published in the May issue of the journal Hypertension. Batlle and colleagues assessed the activity of two enzymes, ACE (for angiotensin-converting enzyme) and ACE2, which play an important role in the control of blood pressure, in the kidneys of a young mouse model of obesity and diabetes. The mouse, called db/db, develops type 2, insulin-resistant diabetes and obesity at around four to seven weeks after birth and eventually manifests some, but not all, features of human diabetic nephropathy. In eight-week old db/db mice, which were obese and had high levels of blood glucose but no evidence of diabetes-related kidney disease, the researchers found low levels of a substance known as ACE (for angiotensin-converting enzyme) and increased levels of a related enzyme, ACE2. The significance of a reduction in ACE coupled with increased ACE2 production in the kidneys needs to be clarified, said Minghao Ye, research associate in medicine at the Feinberg School and first author on the study. ACE is required for production of angiotensin II (AngII), which, among i Continue reading >>

Arbs And Your Kidneys

Arbs And Your Kidneys

I am a 66-year-old female with type 2 diabetes. My A1C was less than 6 without medication. My microalbumin is less than 3.I had a problem with my ACE inhibitor: a side effect of constant dry coughing. Recently, my blood pressure has been high, so I started taking Norvasc, which brought my blood pressure down below 110/70. I have been told Cozaar, an ARB, will protect the kidneys.Would you explain the mechanism of how ARBs affect the kidneys? Is there an added benefit to being on an ARB even though Norvasc keeps my blood pressure down? If so, what is the optimum dose of Cozaar to protect the kidneys? My cardiologist said a higher dose is better. Esther Yoo, MD, Shavano Park, Texas Craig Williams, PharmD, responds: Angiotensin receptor blockers (ARBs) and angiotensin- converting enzyme inhibitors (ACEIs) have special effects that protect the kidneys in a way other blood pressure-lowering medicines don't. ARBs and ACEIs achieve this through reducing the effects of the hormone angiotensin 2. In the kidneys, angiotensin 2 constricts the blood vessels in an especially harmful way, which results in an elevated blood pressure in the kidney that is often more severe than elevations in systemic blood pressure (what we measure with the cuff on the arm). In fact, damage to the blood vessels in the kidney and elevated kidney blood pressure can occur before any elevation in the blood pressure you typically measure. To watch for this early damage, we monitor for protein in the urine (proteinuria). You mentioned that the amount of protein in your urine (your microalbumin) is normal (anything less than 3 mg/dl or 30 g/ml is considered normal). That is very good. The numbers that you describe (blood pressure of 110/70 and normal proteinuria) are at their goals. In general, both the Nati Continue reading >>

Diabetic Kidney Disease

Diabetic Kidney Disease

What is diabetic kidney disease? Diabetic kidney disease is a type of kidney disease caused by diabetes. Diabetes is the leading cause of kidney disease. About 1 out of 4 adults with diabetes has kidney disease.1 The main job of the kidneys is to filter wastes and extra water out of your blood to make urine. Your kidneys also help control blood pressure and make hormones that your body needs to stay healthy. When your kidneys are damaged, they can’t filter blood like they should, which can cause wastes to build up in your body. Kidney damage can also cause other health problems. Kidney damage caused by diabetes usually occurs slowly, over many years. You can take steps to protect your kidneys and to prevent or delay kidney damage. What are other names for diabetic kidney disease? Diabetic kidney disease is also called DKD, chronic kidney disease, CKD, kidney disease of diabetes, or diabetic nephropathy. How does diabetes cause kidney disease? High blood glucose, also called blood sugar, can damage the blood vessels in your kidneys. When the blood vessels are damaged, they don’t work as well. Many people with diabetes also develop high blood pressure, which can also damage your kidneys. Learn more about high blood pressure and kidney disease. What increases my chances of developing diabetic kidney disease? Having diabetes for a longer time increases the chances that you will have kidney damage. If you have diabetes, you are more likely to develop kidney disease if your blood glucose is too high blood pressure is too high African Americans, American Indians, and Hispanics/Latinos develop diabetes, kidney disease, and kidney failure at a higher rate than Caucasians. You are also more likely to develop kidney disease if you have diabetes and smoke don’t follow your di Continue reading >>

Angiotensin-converting Enzyme Inhibition And Renal Protection In Nondiabetic Patients: The Data Of The Meta-analyses

Angiotensin-converting Enzyme Inhibition And Renal Protection In Nondiabetic Patients: The Data Of The Meta-analyses

Angiotensin-Converting Enzyme Inhibition and Renal Protection in Nondiabetic Patients: The Data of the Meta-Analyses *Mario Negri Institute for Pharmacological Research; and Unit of Nephrology, Azienda Ospedaliera, Ospedali Riuniti di Bergamo, Bergamo, Italy Dr. Piero Ruggenenti, Mario Negri Institute for Pharmacological Research, Negri Bergamo Laboratories, Via Gavazzeni, 11-24125 Bergamo, Italy. Phone: +39-035-319-888; Fax: +39-035-319-331; E-mail: manuelap{at}marionegri.it ESRD represents a major health problem. The number of patients who enter kidney replacement programs has increased at an average of 7% per year in the past 10 yr. A large number of experimental and clinical studies have demonstrated that chronic nephropathies share common pathogenic mechanisms that contribute to renal disease progression, even independent of the original cause. Clinical studies found a significant correlation between the extent of urinary protein excretion and the rate of GFR decline in both diabetic and nondiabetic chronic nephropathies. Randomized trials, in particular the Ramipril Efficacy In Nephropathy (REIN) study, also showed that treatments that reduce proteinuria (namely angiotensin-converting enzyme [ACE] inhibitors) are renoprotective and limit progression to ESRD. Meta-analyses of randomized clinical trials also evaluated the role of proteinuria and of ACE inhibition therapy in chronic renal disease progression. Their findings were consistent with those of the REIN study and confirmed in larger series of patients the predictive value of proteinuria and the renoprotective effect of proteinuria reduction by ACE inhibition therapy. Thus, the meta-analyses may confirm and extend previous findings generated by randomized clinical trials. Conceivably, well-designed studies i Continue reading >>

Ace Inhibitors And Protection Against Kidney Disease Progression In Patients With Type 2 Diabetes: What's The Evidence?

Ace Inhibitors And Protection Against Kidney Disease Progression In Patients With Type 2 Diabetes: What's The Evidence?

Although angiotensin-converting enzyme inhibitors are frequently used as antihypertensive agents to lower blood pressure and slow progression of nephropathy in patients with type 2 diabetes, evidence of their efficacy has been drawn primarily from small trials with surrogate end points. No adequately powered, long-term trials have tested their effects to reduce the incidence of hard end points, such as progression to end-stage renal disease or even doubling of serum creatinine in the population of patients with nephropathy from type 2 diabetes. While the results of angiotensin-converting enzyme inhibitor trials from nondiabetic causes and even type 1 diabetes may be extrapolated to the patient with nephropathy associated with type 2 diabetes, the hard evidence is not available. This review critically evaluates the limited evidence in support of angiotensin-converting enzyme inhibitors as renal-protective agents in people with type 2 diabetes. Diabetic nephropathy, a common complication in patients with type 2 diabetes, is the leading cause of end-stage renal disease (ESRD) in the United States.[ 1 ] Angiotensin-converting enzyme (ACE) inhibitors have been considered agents of choice for providing protection against the progression of kidney disease for patients with type 1 diabetes.[ 2 ] The increasing use of ACE inhibitors to treat the early stage of nephropathy (i.e., microalbuminuria) is a response to the growing emphasis on initiating early treatment with a belief that this will prevent future organ damage.[ 3 , 4 ] However, the evidence that ACE inhibitors confer renal protection in patients with type 2 diabetes is based primarily on surrogate measurements, such as reduction of proteinuria or improvement of kidney function as assessed by changes in creatinine clea Continue reading >>

Ace-inhibitor Use And The Long-term Risk Of Renal Failure In Diabetes

Ace-inhibitor Use And The Long-term Risk Of Renal Failure In Diabetes

Angiotensin-converting enzyme (ACE) inhibitors have been used for an increasing number of indications since their introduction as antihypertensive drug therapy for treatment-resistant hypertension.1., 2., 3., 4., 5., 6. One of these suggested indications, namely slowing the rate of progression of nephropathy in diabetic patients with or without hypertension,3 can potentially have a major impact on this disease. Indeed, diabetic nephropathy, occurring in 20–40% of diabetics, is currently believed to be the most important cause of morbidity and mortality among diabetic patients.7 As diabetic nephropathy accounts for nearly 45% of new patients reaching end-stage renal disease (ESRD) in the USA, the clinical impact of potential ACE-inhibitor-mediated renal effects, beyond that resulting from blood pressure reduction, should be substantial.8 However, despite the extensive use of ACE inhibitors to prevent diabetic nephropathy, the incidence of ESRD owing to diabetes in the USA has increased 266% in the decade between 1984 and 1994.9 Although increasing incidence of diabetes, longer survival, and liberalized acceptance criteria of ESRD programs may account for a part of it, other possible explanations should be entertained.10 The evidence for the effectiveness of ACE inhibitors in preventing diabetic nephropathy is surprisingly not persuasive. Although numerous studies have been conducted on the renal effects of ACE inhibitors, including a meta-analysis of more than a hundred studies that suggested that ACE inhibitors were unique in decreasing proteinuria, beyond that mediated by their hypotensive effect, and had a favorable effect on decline in glomerular filtration rate,11 studies based on major outcomes are not all as decisive. In type I diabetes, the ACE inhibitor captop Continue reading >>

The Effect Of Ace Inhibitors On Kidney Function In Patients With Type 1 Diabetes

The Effect Of Ace Inhibitors On Kidney Function In Patients With Type 1 Diabetes

The Effect of ACE Inhibitors on Kidney Function in Patients with Type 1 Diabetes Article, Author, and Disclosure Information Author, Article, and Disclosure Information The summary below is from the full report titled Should All Patients with Type 1 Diabetes Mellitus and Microalbuminuria Receive Angiotensin-Converting Enzyme Inhibitors? A Meta-Analysis of Individual Patient Data. It is in the 6 March 2001 issue of Annals of Internal Medicine (volume 134, pages 370-379). The author is the ACE Inhibitors in Diabetic Nephropathy Trialist Group. Summaries for Patients are a service provided by Annals to help patients better understand the complicated and often mystifying language of modern medicine. Summaries for Patients are presented for informational purposes only. These summaries are not a substitute for advice from your own medical provider. If you have questions about this material, or need medical advice about your own health or situation, please contact your physician. The summaries may be reproduced for not-for-profit educational purposes only. Any other uses must be approved by the American College of Physicians-American Society of Internal Medicine. Continue reading >>

Ace_inhibitor_pharmacology [tusom | Pharmwiki]

Ace_inhibitor_pharmacology [tusom | Pharmwiki]

Inhibits peptidyl dipeptidase (Angiotensin Converting Enzyme or ACE). This prevents the conversion of angiotensin I to angiotensin II. ACE also inactivates bradykinin, a potent vasodilator that works in part by stimulating the release of nitric oxide and prostacyclin. ACE inhibition can thereby elevate bradykinin levels in addition to lowering Ang II levels. Ang II is one of the most potent vasoconstrictors known. Treatment of normal renin & high renin hypertension, CHF, and can reduce or prevent glomerular damage in diabetes. Ang II causes renal damage & proteinuria by several inter-related mechanisms (Schmieder et al, 2011): glomerular hypertension: resulting in increased intraglomerular pressure, decreased renal perfusion & interstitial hypoxia. This in turn results in loss of peritubular capillaries and scarring, which worsens hypoxia and establishes a vicious circle of progressive kidney damage. causes profibrotic and proinflammatory effects that contribute to kidney damage promotes endothelial dysfunction by increasing oxidative stress, reducing NO production, and loss of endothelial integrity. Chronic endothelial dysfunction results in atherosclerosis and end-organ damage. Acute renal failure can occur in patients with bilateral renal artery stenosis, heart failure or volume depletion due to diarrhea or excessive diuretic effects. Hyperkalemia due to aldosterone suppression. Dry cough develops within 1 week to 6 months in 5-20% of patients, more frequently in women, (believed to be caused by bradykinin & substance P). Angioedema (producing swelling around the mouth, nose, throat, glottis, lips and/or tongue occurs in 0.1-0.5% of patients and is also attributed to bradykinin accumulation. It can be potentially life-threatening due to airway swelling & obstruction Continue reading >>

Ace Inhibitors And The Kidney. A Risk-benefit Assessment.

Ace Inhibitors And The Kidney. A Risk-benefit Assessment.

ACE inhibitors and the kidney. A risk-benefit assessment. Groningen Institute for Drug Studies (GIDS), Department of Internal Medicine, University Hospital Groningen, The Netherlands. ACE inhibitors effectively reduce systemic vascular resistance in patients with hypertension, heart failure or chronic renal disease. This antihypertensive efficacy probably accounts for an important part of their long term renoprotective effects in patients with diabetic and non-diabetic renal disease. The renal mechanisms underlying the renal adverse effects of ACE inhibitors--intrarenal efferent vasodilation with a consequent fall in filtration pressure--are held to be involved in their renoprotective effects as well. The fall in filtration pressure presumably contributes to the antiproteinuric effect as well as to long term renoprotection. The former is suggested by the positive correlation between the fall in filtration fraction and the reduction in proteinuria found during ACE inhibition. The latter is suggested by the correlation between the (slight) reduction in glomerular filtration rate at onset of therapy and a more favourable course of renal function in the long term. Such a fall in filtration rate at the onset of ACE inhibitor treatment is reversible after withdrawal, and can be considered the trade-off for long term renal protection in patients with diabetic and nondiabetic chronic renal disease. In conditions in which glomerular filtration is critically dependent on angiotensin II-mediated efferent vascular tone (such as a post-stenotic kidney, or patients with heart failure and severe depletion of circulating volume), ACE inhibition can induce acute renal failure, which is reversible after withdrawal of the drug. Systemic and renal haemodynamic effects of ACE inhibition, b Continue reading >>

Why Do Ace Inhibitors Protect The Kidneys?

Why Do Ace Inhibitors Protect The Kidneys?

Alexs answer is correct, but its pretty heavy with jargon and could perhaps be rephrased as follows: ACE is an acronym for Angiotensin Converting Enzyme. It is an enzyme that converts an inactive form of a vasoconstrictor (raises blood pressure among other things) to its active form. Inhibiting this enzyme reduces the amount of angiotensin II (active form) in circulation, and thus reduces blood pressure generally. But blocking angiotensin production also reduces pressure directly in the kidneys, by preventing angiotensin from constricting the outgoing, or efferent, arteriole (small artery). Reducing pressure within the kidneys reduces the damage to the vessels (glomerules) of the filtration units (nephrons) that the kidney is made of. In addition, angiotensin is pro-inflammatory; it can create inflammation and damage in the kidneys directly, independent of blood pressure. The combination of reducing damage due to pressure and due to excess inflammation is why ACE inhibitors protect the kidneys. What goes wrong to necessitate their use is another discussion, but an incomplete summary is that conditions such as hypertension and diabetes exert harmful effects partly via angiotensin II and partly via overusing the kidneys to get rid of waste, both of which are lessened by ACE inhibitors. If this answer is not at the appropriate level, please elaborate on any sources of confusion or incomplete elucidation. Continue reading >>

Prevention And Treatment Of Diabetic Renal Disease In Type 2 Diabetes: The Benedict Study

Prevention And Treatment Of Diabetic Renal Disease In Type 2 Diabetes: The Benedict Study

Abstract Diabetic nephropathy (DN) is the leading cause of end-stage renal failure in Western countries and carries an increased risk for cardiovascular mortality. Studies have identified a number of factors that play a part in the development of DN. Among them, hypertension and proteinuria are the most important. In the early stages of DN, when albumin is present in the urine in very low quantities (microalbuminuria) and an increase is seen in BP, there is no loss of filtrate and patients respond well to prophylactic measures. Microalbuminuria is considered an early marker of DN. Prevention of the onset of microalbuminuria, therefore, could be considered as the primary means of preventing DN. The Bergamo Nephrologic Diabetes Complication Trial (BENEDICT) was a prospective, randomized, double-blind, parallel-group study that was organized in two phases. Phase A included 1204 patients and was aimed at assessing the efficacy of the angiotensin-converting enzyme (ACE) inhibitor trandolapril, the non-dihydropyridine calcium channel blocker verapamil, and the trandolapril plus verapamil combination as compared with placebo in prevention of microalbuminuria in hypertensive patients with type 2 diabetes and normal urinary albumin excretion rate. Phase B was aimed at assessing the efficacy of the combination as compared with trandolapril alone in prevention of macroalbuminuria in patients with microalbuminuria. The BENEDICT Phase A study showed that DN can be prevented by ACE inhibitor therapy. The beneficial effect of ACE inhibition is not enhanced by combined non-dihydropyridine calcium channel blocker therapy. The apparent advantage of ACE inhibitors over other agents includes a protective effect on the kidney against the development of microalbuminuria, which is a major ris Continue reading >>

Protecting Your Kidneys

Protecting Your Kidneys

Diabetic nephropathy (kidney disease) is the leading cause of kidney failure in the United States. That’s the bad news. The good news is that the outlook for protecting your kidneys has gotten much brighter over the past decade or so. There are now a number of measures you can take that have been scientifically proven to protect your kidneys and lower the risk of developing diabetes-related kidney disease. Here’s what the research shows. When good kidneys go bad Your kidneys, which are each about the size of your fist, are located near the middle of your back, just below the rib cage. By no coincidence, they are shaped like kidney beans. One of their jobs is to filter waste products and extra water from the bloodstream. This waste and excess water, in the form of urine, flow through tubes called ureters and into the bladder. The bladder stores urine until it is full enough to create the urge to urinate. How does this filtering process work? Each kidney is made up of about one million tiny filtering units called nephrons. Tiny blood vessels called arterioles deliver blood to the nephrons. Within each nephron, the blood vessels form a complex called a glomerulus. It is within these glomeruli that the filtering activity actually takes place. The filtered blood leaves through another arteriole and is eventually carried back to the heart. Meanwhile, the material filtered from the blood passes through a tubule, where it is converted to urine, and then carried to the bladder through the ureters. (See “The Function of a Kidney” for more information about kidney anatomy.) Diabetes sets the stage for kidney damage. Chronic high blood glucose levels, often in combination with high blood pressure, damage the glomeruli and progressively diminish kidney function. (High blood Continue reading >>

About Blood Pressure Medications For Diabetic Kidney Disease

About Blood Pressure Medications For Diabetic Kidney Disease

Protecting the kidneys is very important for patients with diabetes. Most patients who have diabetic kidney disease also have high blood pressure and higher amount of protein in urine and need medication to lower the blood pressure and reduce protein in the urine. There are several classes of blood pressure pills, and usually several choices in each class. One target for some of the classes is the “renin-angiotensin system”. This is a natural hormone system in the body that is too active in patients with diabetes. At the center of the system is Angiotensin II, a hormone that makes blood vessels constrict. When small blood vessels are narrowed, it is harder for the heart to pump blood through them, so blood pressure rises. A second action of Angiotensin II is to cause chronic damage to the kidneys in diabetes. ACE Inhibitors It is no surprise then that blocking this system is important to protecting the kidneys. The most common way to block the system is by inhibiting the pathway through it. ACE inhibitors are used for this. ACE inhibitors are medicines that were first designed to treat high blood pressure, and are now used to treat chronic kidney disease especially if there is too much protein in urine. ACE inhibitors are safe for most, but not all, people. They are not safe during pregnancy or if you have higher potassium, or if you have ever had a severe allergic reaction where your tongue and lips swelled. This may put you at risk for a similar reaction to other ACE inhibitor. If you do have this kind of allergic reaction while taking the medicine, go to the emergency room promptly. ARB’s There is a related group of drugs called Angiotensin II Receptor Blockers (ARBs). ARBs block the receptors in the system, rather than the formation of angiotensin through the Continue reading >>

Ace Inhibitors

Ace Inhibitors

A class of medicine usually used to treat high blood pressure. Angiotensin-converting enzyme (ACE) inhibitors also appear to protect people with diabetes from diabetic nephropathy (kidney disease). People with diabetes are especially prone to hypertension (defined as a blood pressure level of 140/90 mm Hg or greater). Some 20% to 60% of individuals with diabetes have high blood pressure. Hypertension increases their risk not only of heart disease and stroke, but also of peripheral vascular disease, diabetic retinopathy, diabetic nephropathy, and possibly diabetic neuropathy. The American Diabetes Association (ADA) currently recommends a target blood pressure level of under 130/80 mm Hg in people with diabetes. The ADA recommends a number of different measures for lowering blood pressure, including weight loss, sodium restriction, and exercise. When these measures aren’t enough, the addition of one or more medicines is warranted. There are several different classes of blood pressure drugs, including angiotensin-receptor blockers (ARBs), diuretics, beta blockers, and ACE inhibitors. Overall, drug therapy has been shown to substantially decrease the risk of cardiovascular disease, diabetic retinopathy, and diabetic nephropathy. ACE inhibitors may have a special advantage in terms of slowing the progression of diabetic nephropathy. Research findings show that ACE inhibitors can slow the progression of kidney disease to a greater degree than other antihypertensive drugs that lower blood pressure by a similar amount and that they may be able to protect the kidneys even in people with diabetes whose blood pressure levels are in the normal range. This suggests that ACE inhibitors protect the kidneys by mechanisms other than just blood pressure control. Currently, the ADA reco Continue reading >>

Cochrane For Clinicians: Ace Inhibitors Vs. Arbs For Patients With Diabetic Kidney Disease - American Family Physician

Cochrane For Clinicians: Ace Inhibitors Vs. Arbs For Patients With Diabetic Kidney Disease - American Family Physician

ACE Inhibitors vs. ARBs for Patients with Diabetic Kidney Disease JUSTIN BAILEY, CAPT, USAF, MC, David Grant Medical Center Family Practice Residency Program, Travis Air Force Base, California Am Fam Physician.2007Jul1;76(1):68-69. A 57-year-old man presents with hypertension, diabetes, and early-stage diabetic kidney disease. His serum creatinine level is 1.6 mg per dL (140 mol per L), and his blood pressure is in the 140s/80s mm Hg. An antihypertensive needs to be selected for this patient. Are angiotensin-converting enzyme (ACE) inhibitors or angiotensin-II receptor blockers (ARBs) better for all-cause mortality reduction and renal protection in patients with diabetic kidney disease? Studies comparing ACE inhibitors or ARBs with placebo found no mortality benefit in patients with diabetic kidney disease. A subgroup analysis of five studies (2,034 total patients) found that, when given at full or maximally tolerated doses, ACE inhibitors reduce all-cause mortality (relative risk = 0.78, 95% confidence interval, 0.61 to 0.98). Both classes of drugs are similarly effective at preventing the progression of diabetic kidney disease. However, there were too few trials comparing ACE inhibitors with ARBs to draw clear conclusions. 1 Within two to three decades of diagnosis, roughly one third of patients with diabetes will have some degree of diabetic kidney disease. 2 Patients with diabetic nephropathy are at a higher risk of mortality, mostly from cardiovascular complications, than other patients with diabetes. 3 Drugs used to delay the progression of diabetic kidney disease include beta blockers, calcium channel blockers, diuretics, ACE inhibitors, and ARBs. Studies have shown that after a patient develops diabetic kidney disease, ACE inhibitors and ARBs are superior to th Continue reading >>

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