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Treatment Of Diabetic Nephropathy Pdf

Diabetic Nephropathy; Principles Of Diagnosis And Treatment Of Diabetic Kidney Disease

Diabetic Nephropathy; Principles Of Diagnosis And Treatment Of Diabetic Kidney Disease

Diabetic nephropathy; principles of diagnosis and treatment of diabetic kidney disease 1Department of Endocrinology, University of Buckingham, Royal Gwent Hospital, NHS Trust, Wales, UK *Corresponding author: Chaudhary Muhammad Junaid Nazar, [email protected] Received 2013 Sep 14; Accepted 2013 Nov 19. Published by Society of Diabetic Nephropathy Prevention. This is an open-access article distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This article has been cited by other articles in PMC. Diabetes mellitus is a leading epidemic of the present world. It is considered the leading cause of death among end-stage renal disease (ESRD) patients. The complications associated with diabetes mellitus have boosted the number of deaths in the last years. These complications are the result of long lasting effects of diabetes mellitus on the glomerular microvasculature of the kidney. Diabetic nephropathy (DN) develops in patients with several years medical history of diabetes and renal failure. However, research shows that patients with type 1 diabetes progress early to ESRD as compared to those with type 2. DN is more prevalent in ethnic minorities as compared to other groups in society. There are new and different treatment options available since medical science has progressed due to increased research efforts. Unfortunately, there is no permanent cure. The aim of this article is to explore the research of therapeutic strategies currently in use by medical practitioners in order to increase understanding of DN. Keywords: Diabetic nephropathy, End Stage renal disease, Diabetes mellitus Implication for health policy/practice/re Continue reading >>

Diabetic Nephropathy Symptoms

Diabetic Nephropathy Symptoms

Diabetic nephropathy is the damage caused to kidneys due to diabetes mellitus. Usually, the condition develops after a diabetes duration of about 10 years. Around one fourth of all people who have had diabetes for more than 10 years are at risk of diabetic nephropathy. Diabetic nephropathy is not typically characterized by symptom onset, meaning that most individuals who develop it are unaware of the condition until it has already caused considerable damage. Screening diabetic patients for kidney damage is therefore important in reducing the risk of long-term kidney damage and its associated problems. Some of the features of diabetic kidney disease that may eventually manifest include: Edema or swelling of the ankles, feet, lower legs or hands due to water retention. Urine that is foamy or frothy in appearance due to excessive protein being excreted in the urine. This is most commonly seen in the first urine of the day. Weight gain due to fluid retention and edema Stages of development of diabetic nephropathy Research provides insights into mechanisms governing healthy longevity During stage 1, the rate of kidney filtration is increased. The glomerular filtration rate (GFR) in the kidney is increased and the organ may increase in size. However, urine albumin levels and blood pressure may be only mildly raised or normal. At this early stage of nephropathy, there is no pathological damage and the condition is usually reversible. During stage 2, there is structural damage of the glomeruli and microalbuminuria starts to occur. The GFR is higher than normal. Stage 3 disease is termed early stage renal disease. The albumin excretion rate is continuously raised and may exceed 200 g/min. Blood levels of creatinine are raised and blood pressure may also be high. This stage of d Continue reading >>

Diabetic Nephropathy: Diagnosis, Prevention, And Treatment

Diabetic Nephropathy: Diagnosis, Prevention, And Treatment

Diabetic nephropathy is the leading cause of kidney disease in patients starting renal replacement therapy and affects ∼40% of type 1 and type 2 diabetic patients. It increases the risk of death, mainly from cardiovascular causes, and is defined by increased urinary albumin excretion (UAE) in the absence of other renal diseases. Diabetic nephropathy is categorized into stages: microalbuminuria (UAE >20 μg/min and ≤199 μg/min) and macroalbuminuria (UAE ≥200 μg/min). Hyperglycemia, increased blood pressure levels, and genetic predisposition are the main risk factors for the development of diabetic nephropathy. Elevated serum lipids, smoking habits, and the amount and origin of dietary protein also seem to play a role as risk factors. Screening for microalbuminuria should be performed yearly, starting 5 years after diagnosis in type 1 diabetes or earlier in the presence of puberty or poor metabolic control. In patients with type 2 diabetes, screening should be performed at diagnosis and yearly thereafter. Patients with micro- and macroalbuminuria should undergo an evaluation regarding the presence of comorbid associations, especially retinopathy and macrovascular disease. Achieving the best metabolic control (A1c <7%), treating hypertension (<130/80 mmHg or <125/75 mmHg if proteinuria >1.0 g/24 h and increased serum creatinine), using drugs with blockade effect on the renin-angiotensin-aldosterone system, and treating dyslipidemia (LDL cholesterol <100 mg/dl) are effective strategies for preventing the development of microalbuminuria, in delaying the progression to more advanced stages of nephropathy and in reducing cardiovascular mortality in patients with type 1 and type 2 diabetes. DEFINITION AND EPIDEMIOLOGY Diabetic nephropathy is the leading cause of chronic Continue reading >>

Natural Antioxidants In The Treatment And Prevention Of Diabetic Nephropathy; A Potential Approach That Warrants Clinical Trials

Natural Antioxidants In The Treatment And Prevention Of Diabetic Nephropathy; A Potential Approach That Warrants Clinical Trials

Diabetic nephropathy is the major cause of end-stage renal disease and effective and new therapeutic approaches are needed in diabetic nephropathy and chronic kidney diseases. Oxidative stress and inflammatory process are important factors contributing to kidney damage by increasing production of oxidants. KEAP1/Nrf2/ARE pathway regulates the transcription of many antioxidant genes and modulation of the pathway up regulates antioxidants. NFB controls the expression of genes involved in the inflammatory response. Natural substances have antioxidant and anti-inflammatory activities and have an impact on NFB and KEAP1/Nrf2/ARE pathways. The preclinical studies explored the effectiveness of whole herbs, plants or seeds and their active ingredients in established diabetic nephropathy. They ameliorate oxidative stress induced kidney damage, enhance antioxidant system, and decrease inflammatory process and fibrosis; most likely by activating KEAP1/Nrf2/ARE pathway and by deactivating NFB pathway. Whole natural products contain balanced antioxidants that might work synergistically to induce beneficial therapeutic outcome. In this context, more clinical studies involving whole plants or herbal products or mixtures of different herbs and plants and their active ingredients might change our strategies for the management of diabetic nephropathy. The natural products might be useful as preventive interventions and studies are required in this field. Continue reading >>

500 Best Kidney Disease Ribbon Images On Pinterest

500 Best Kidney Disease Ribbon Images On Pinterest

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Diabetic Nephropathy Treatment & Management

Diabetic Nephropathy Treatment & Management

Approach Considerations Several issues are key in the medical care of patients with diabetic nephropathy. [20, 21] These include glycemic control, management of hypertension, and reducing dietary salt intake and phosphorus and potassium restriction in advanced cases. A meta-analysis from the Cochrane Database shows a large fall in blood pressure with salt restriction, similar to that of single-drug therapy. [22] All diabetic patients should consider reducing salt intake at least to less than 5-6 g/d, in keeping with current recommendations for the general population, and may benefit from lowering salt intake to even lower levels. Reducing dietary salt intake may help slow progression of diabetic kidney disease. Renal replacement therapy may be necessary in patients with end-stage renal disease (ESRD). A 2012 post-hoc analysis of the data merged from the Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) trial and the Irbesartan Diabetic Nephropathy Trial (IDNT) in 1177 patients demonstrated that a low-sodium diet (24-h urinary sodium/creatinine ratio (mmol/g) < 121) enhanced the renoprotective and cardioprotective effect of angiotensin receptor blockers (losartan or irbesartan) in type 2 diabetic patients with nephropathy. Compared with higher sodium intake groups, the patients in the low-sodium group had better renal (by 43%) and cardiovascular (by 37%) outcomes. These improved outcomes in the low-sodium group underscore the importance of recent calls for population-wide intervention to reduce dietary salt intake, particularly in patients with diabetes and nephropathy treated with angiotensin receptor blockers. [23] Continue reading >>

Jasn | Mobile

Jasn | Mobile

University of Michigan, Ann Arbor, Michigan; Speedel Pharma Ltd., Basel, Switzerland; and King's College London School of Medicine, Guy's Hospital, London, United Kingdom Dr. Giancarlo Viberti, Unit for Metabolic Medicine, Cardiovascular Division, King's College London Medical School, 5th Floor Southwark Wing, Guy's Hospital, London SE1 9RT, UK. Phone: +44-20-7188-1910; Fax: +44-20-7188-0146; E-mail: [email protected] Received for publication December 3, 2009. In the short term, the endothelin antagonist avosentan reduces proteinuria, but whether this translates to protection from progressive loss of renal function is unknown. We examined the effects of avosentan on progression of overt diabetic nephropathy in a multicenter, multinational, double-blind, placebo-controlled trial. We randomly assigned 1392 participants with type 2 diabetes to oral avosentan (25 or 50 mg) or placebo in addition to continued angiotensin-converting enzyme inhibition and/or angiotensin receptor blockade. The composite primary outcome was the time to doubling of serum creatinine, ESRD, or death. Secondary outcomes included changes in albumin-to-creatinine ratio (ACR) and cardiovascular outcomes. We terminated the trial prematurely after a median follow-up of 4 months (maximum 16 months) because of an excess of cardiovascular events with avosentan. We did not detect a difference in the frequency of the primary outcome between groups. Avosentan significantly reduced ACR: In patients who were treated with avosentan 25 mg/d, 50 mg/d, and placebo, the median reduction in ACR was 44.3, 49.3, and 9.7%, respectively. Adverse events led to discontinuation of trial medication significantly more often for avosentan than for placebo (19.6 and 18.2 versus 11.5% for placebo), dominated by fluid o Continue reading >>

Progression Of Diabetic Nephropathy

Progression Of Diabetic Nephropathy

Diabetes Research and Clinical Practice 39 Suppl. (1998) S35 S42Progression of diabetic nephropathy A focus on arterial pressure level and methods... Diabetes Research and Clinical Practice 39 Suppl. (1998) S35 S42 Progression of diabetic nephropathy A focus on arterial pressure level and methods of reduction George L. Bakris * Rush Uni6ersity Hypertension Center, Rush Presbyterian/St. Lukes Medical Center, 1725 W. Harrison St., Suite 117, Chicago, IL, USA Abstract It is well accepted that a reduction of arterial pressure to levels of less than 140/90 mmHg will slow the decline in renal function among patients with diabetic nephropathy. More recently it is appreciated that the reduction of arterial pressure to levels much below 130/85 mmHg provides even greater levels of protection against the progression of renal disease. Given that the achievement of blood pressure reduction to such a level requires more than one medication and that the patients compliance is best with a once-daily medication, it makes sense to combine antihypertensive medications so as to maximize the benefit. In this way, fixed dose combination medications yield synergistic effects on blood pressure reduction while providing, in some cases, maximal benefit to preservation of renal function. Such a combination is the verapamil/trandolapril combination. This paper discusses in great detail the advantages of blood pressure reduction and the types of medications that may achieve both protection against diabetic nephropathy progression as well as blood pressure reduction. 1998 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Diabetes; Proteinuria; Nephropathy; Calcium antagonists; ACE inhibitors 1. Introduction Diabetic nephropathy accounts for the largest percentage of patients on dialysis Continue reading >>

Diabetic Nephropathy – Complications And Treatment

Diabetic Nephropathy – Complications And Treatment

Background Diabetic nephropathy (DN) or diabetic kidney disease is a syndrome characterized by the presence of pathological quantities of urine albumin excretion, diabetic glomerular lesions, and loss of glomerular filtration rate (GFR) in diabetics. Diabetes may be classified as type 1 (autoimmune β-cell destruction and absolute insulin deficiency), type 2 (relative insulin deficiency and resistance), and other types (eg, pancreatic disease). Epidemiology The prevalence of diabetes is phenomenal and the projections are staggering. When one considers the morbidity, mortality, and cost of health care, the burden of the diabetes epidemic becomes apparent. Worldwide, the prevalence of diabetes was estimated at 171 million in 2000, increasing to 382 million in 2013; and is projected to reach 592 million by 2035. This represents 8%–10% of the global population, resulting in at least 548 billion dollars in health expenditure on diabetes care. Type 2 diabetes constitutes about 85%–95% of all diabetes cases.1 In the US alone for 2011, 25.8 million children and adults have diabetes with another 79 million having a prediabetic state.2 The diabetes epidemic has resulted in DN becoming the most frequent cause of end-stage renal disease (ESRD) in most countries. In 2009–2011, diabetes was the primary cause of ESRD in about 60% of patients in Malaysia, Mexico, and Singapore. Countries with an ESRD incidence of 40%–50% include Israel, Korea, Hong Kong, Taiwan, Philippines, Japan, the US, and New Zealand.2 The incidence of ESRD due to diabetes also rises in the older age group. In 2011, the incident rates of ESRD due to diabetes in the US were 44, 266, and 584 per million for the age groups 20–44, 45–64, and 65–74 years, respectively. A similar finding was noted in the A Continue reading >>

Diabetic Nephropathy

Diabetic Nephropathy

Definition and Causes Diabetic nephropathy (DN) is typically defined by macroalbuminuria—that is, a urinary albumin excretion of more than 300 mg in a 24-hour collection—or macroalbuminuria and abnormal renal function as represented by an abnormality in serum creatinine, calculated creatinine clearance, or glomerular filtration rate (GFR). Clinically, diabetic nephropathy is characterized by a progressive increase in proteinuria and decline in GFR, hypertension, and a high risk of cardiovascular morbidity and mortality. Prevalence and Risk Factors Diabetes has become the primary cause of end-stage renal disease (ESRD) in the United States, and the incidence of type 2 diabetes mellitus continues to grow in the United States and worldwide. Approximately 44% of new patients entering dialysis in the United States are diabetics. Early diagnosis of diabetes and early intervention are critical in preventing the normal progression to renal failure seen in many type 1 and a significant percentage of type 2 diabetics. In the United States, approximately 20.8 million people, or 7.0% of the population, are estimated to have diabetes, with a growing incidence. Roughly one third of this population, 6.2 million, is estimated to be undiagnosed with type 2 diabetes. The prevalence of diabetes is higher in certain racial and ethnic groups, affecting approximately 13% of African Americans, 9.5% of Hispanics, and 15% of Native Americans, primarily with type 2 diabetes.1, 2 Approximately 20% to 30% of all diabetics will develop evidence of nephropathy, although a higher percentage of type 1 patients progress to ESRD. Pathophysiology and Natural History The common progression from microalbuminuria to overt nephropathy has led many to consider microalbuminuria to define early or incipient Continue reading >>

Update On The Protective Renal Effects Of Metformin In Diabetic Nephropathy

Update On The Protective Renal Effects Of Metformin In Diabetic Nephropathy

Update on the Protective Renal Effects of Metformin in Diabetic Nephropathy Author(s): Andreas Eisenreich* , Charite- Universitatsmedizin Berlin, Institut fur Klinische Pharmakologie und Toxikologie, Chariteplatz 1, 10117 Berlin, Germany Ulrike Leppert . Charite-Universitatsmedizin Berlin, Institut fur Physiologie, Chariteplatz 1, 10117 Berlin, Germany Journal Name: Current Medicinal Chemistry Background: Diabetic nephropathy is one of the most important complicationsin patients with diabetes mellitus. Main steps crucial for the pathogenesis of diabeticnephropathy involve amongst others the modulation of cell signaling via AMP-activatedkinase (AMPK) and mammalian target of rapamycin (mTOR), reactive oxygen generation,and endoplasmic reticulum stress under diabetic or hyperglycemic conditions. Theseprocesses mediate increased loss of renal cells, such as podocytes, which consequentiallyleads to renal damage and loss of renal functions, such as structural integrity and glomerularfiltration in diabetic nephropathy. The anti-diabetic drug metformin has been widelyused for pharmacotherapeutic treatment of patients with diabetes mellitus. Besides itsanti-diabetic actions, recent studies revealed additional nephroprotective effects of metforminin vitro and in vivo. Metformin was found to diminish apoptosis in different experimentalrenal settings. Moreover, it was shown to reduce albuminuria in diabetic ratsas well as in patients with type 2 diabetes mellitus. These effects were demonstrated to bemediated via the AMPK/mTOR signaling axis. These data indicate beneficial and renoprotectiveeffects of metformin in diabetic nephropathy. Objective: In this review, we will summarize the latest findings regarding the nephroprotectiveimpact of metformin in vitro and in vivo. Moreover, Continue reading >>

Prime Pubmed | Diabetic Nephropathy Journal Articles From Pubmed

Prime Pubmed | Diabetic Nephropathy Journal Articles From Pubmed

Podocyte hypertrophic stress and detachment precedes hyperglycemia or albuminuria in a rat model of obesity and type2 diabetes-associated nephropathy. [Journal Article] Sci Rep 2019; 9(1):18485Minakawa A, Fukuda A, Fujimoto S SR Type2 diabetes-associated nephropathy is the commonest cause of renal failure. Mechanisms responsible are controversial. Leptin-deficient hyperphagic Zucker (fa/fa) rats were modeled to test the hypothesis that glomerular enlargement drives podocyte hypertrophic stress leading to accelerated podocyte detachment, podocyte depletion, albuminuria and progression. By 6weeks, prior to development of e Type2 diabetes-associated nephropathy is the commonest cause of renal failure. Mechanisms responsible are controversial. Leptin-deficient hyperphagic Zucker (fa/fa) rats were modeled to test the hypothesis that glomerular enlargement drives podocyte hypertrophic stress leading to accelerated podocyte detachment, podocyte depletion, albuminuria and progression. By 6weeks, prior to development of either hyperglycemia or albuminuria, fa/fa rats were hyperinsulinemic with high urinary IGF1/2 excretion, gaining weight rapidly, and had 1.6-fold greater glomerular volume than controls (P < 0.01). At this time the podocyte number per glomerulus was not yet reduced although podocytes were already hypertrophically stressed as shown by high podocyte phosphor-ribosomal S6 (a marker of mTORC1 activation), high urinary pellet podocin:nephrin mRNA ratio and accelerated podocyte detachment (high urinary pellet podocin:aquaporin2 mRNA ratio). Subsequently, fa/fa rats became both hyperglycemic and albuminuric. 24 hr urine albumin excretion correlated highly with decreasing podocyte density (R2 = 0.86), as a consequence of both increasing glomerular volume (R2 = 0.70) an Continue reading >>

Proteinuria In Diabetic Nephropathy: Treatment And Evolution

Proteinuria In Diabetic Nephropathy: Treatment And Evolution

, Volume 3, Issue6 , pp 497504 | Cite as Proteinuria in diabetic nephropathy: Treatment and evolution Diabetic nephropathy is characterized by increased urinary albumin excretion and loss of renal function. Increased urinary albumin (proteinuria) is a key component of this disease. Previously, its development led to end-stage renal disease with increased mortality and morbidity for diabetic patients versus nondiabetic patients. Several treatment strategies currently exist that can prevent, slow, and even reverse diabetic nephropathy. New trials suggest that a multidisciplinary approach focused on optimizing metabolic and hypertensive control, in addition to the use of angiotensin-converting enzyme inhibitors or angiotensin 2 receptor antagonists, is effective in halting the progression of disease. Screening and implementation of these strategies is needed to reverse the epidemic of diabetic renal disease. Diabetic PatientProteinuriaDiabetic NephropathyIrbesartanEplerenone These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves. This is a preview of subscription content, log in to check access Unable to display preview. Download preview PDF. US Renal Data System: USRDS 2000 Annual Data Report. Bethesda, MD: The National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases; 2000. Google Scholar Collins A, Xue J, Ma J, Louis T: Estimating the number of patients and Medicare costs for end stage renal disease in the US to the year 2010. J Am Soc Nephrol 2000, 11:113A. Google Scholar International Diabetes Federation and International Society of Nephrology Booklet: Diabetes and Kidney Disease, "Time to Act." Brussels: International Diabetes F Continue reading >>

Payperview: Clinical Manifestation And Natural History Of Diabetic Nephropathy - Karger Publishers

Payperview: Clinical Manifestation And Natural History Of Diabetic Nephropathy - Karger Publishers

Clinical Manifestation and Natural History of Diabetic Nephropathy I have read the Karger Terms and Conditions and agree. The prevalence of diabetes, predominantly of type 2, and the incidence of diabetic nephropathy have dramatically increased worldwide. Diabetic patients constitute the largest proportion of patients with end-stage renal disease (ESRD) requiring dialysis or transplantation; in developed countries, this accounts for up to 50% of ESRD patients, but this proportion has stabilized and possibly somewhat decreased in recent years. Chronic kidney disease in diabetic patients is more heterogeneous than previously thought. The largest proportion suffers from proteinuric diabetic nephropathy with Kimmelstiel-Wilson lesions as the underlying pathology, but reduced glomerular filtration rate in the absence of albuminuria/proteinuria is recognized in an increasing proportion of type 2 diabetic patients. Of particular interest is the recent recognition of vascular lesions in the brain and retina as predictors of nonproteinuric nephropathy with reduced GFR; although currently unproven, such lesions may also be of potential relevance for target blood pressure. Because of the high prevalence of type 2 diabetes in the population, coexisting primary kidney disease and diabetic nephropathy occur in a sizable proportion of type 2 diabetic patients with ESRD. The optimal point to start treatment differs according to target organs. There is no doubt that in proteinuric diabetic patients the earlier the treatment (blood pressure lowering, renin-angiotensin system blockade) is started, the greater is the benefit at least in patients with proteinuric disease and no major cardiovascular damage. In our opinion, there is no one target blood pressure that fits all patients. Surviv Continue reading >>

Diabetic Nephropathy

Diabetic Nephropathy

Diabetic nephropathy (diabetic kidney disease) (DN)[1] is the chronic loss of kidney function occurring in those with diabetes mellitus. It is a serious complication, affecting around one-quarter of adult diabetics in the United States. It usually is slowly progressive over years. [2] Pathophysiologic abnormalities in DN begin with long-standing poorly controlled blood glucose levels. This is followed by multiple changes in the filtration units of the kidneys, the nephrons. (There are normally about 3/4-1 1/2 million nephrons in each adult kidney).[3] Initially, there is constriction of the efferent arterioles and dilation of afferent arterioles, with resulting glomerular capillary hypertension and hyperfiltration; this gradually changes to hypofiltration over time.[4] Concurrently, there are changes within the glomerulus itself: these include a thickening of the basement membrane, a widening of the slit membranes of the podocytes, an increase in the number of mesangial cells, and an increase in mesangial matrix. This matrix invades the glomerular capillaries and produces deposits called Kimmelstiel-Wilson nodules. The mesangial cells and matrix can progressively expand and consume the entire glomerulus, shutting off filtration.[5] The status of DN may be monitored by measuring two values: the amount of protein in the urine - proteinuria; and a blood test called the serum creatinine. The amount of the proteinuria is a reflection of the degree of damage to any still-functioning glomeruli. The value of the serum creatinine can be used to calculate the estimated glomerular filtration rate (eGFR), which reflects the percentage of glomeruli which are no longer filtering the blood.[citation needed] Treatment with an angiotensin converting enzyme inhibitor (ACEI) or angiotensi Continue reading >>

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