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Oxidative Stress in Diabetic Nephropathy with Early Chronic Kidney Disease.
Miranda-Díaz, AG, Pazarín-Villaseñor, L, Yanowsky-Escatell, FG, Andrade-Sierra, J
Journal of diabetes research. 2016;:7047238
Abstract
The increase in the prevalence of diabetes mellitus (DM) and the secondary kidney damage produces diabetic nephropathy (DN). Early nephropathy is defined as the presence of microalbuminuria (30-300 mg/day), including normal glomerular filtration rate (GFR) or a mildly decreased GFR (60-89 mL/min/1.73 m(2)), with or without overt nephropathy. The earliest change caused by DN is hyperfiltration with proteinuria. The acceptable excretion rate of albumin in urine is <30 mg/day. Albuminuria represents the excretion of >300 mg/day. Chronic kidney disease (CKD) is characterized by abnormalities in renal function that persist for >3 months with health implications. Alterations in the redox state in DN are caused by the persistent state of hyperglycemia and the increase in advanced glycation end products (AGEs) with ability to affect the renin-angiotensin system and the transforming growth factor-beta (TGF-β), producing chronic inflammation and glomerular and tubular hypertrophy and favoring the appearance of oxidative stress. In DN imbalance between prooxidant/antioxidant processes exists with an increase in reactive oxygen species (ROS). The overproduction of ROS diminishes expression of the antioxidant enzymes (manganese superoxide dismutase, glutathione peroxidase, and catalase). The early detection of CKD secondary to DN and the timely identification of patients would permit decreasing its impact on health.
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Cardiovascular risk prediction in people with chronic kidney disease.
Matsushita, K, Ballew, SH, Coresh, J
Current opinion in nephrology and hypertension. 2016;(6):518-523
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Abstract
PURPOSE OF REVIEW Clinical guidelines are not consistent regarding whether or how to utilize information on measures of chronic kidney disease (CKD) for predicting the risk of cardiovascular disease (CVD). This review summarizes recent literature regarding CVD prediction in the context of CKD. RECENT FINDINGS Previous studies used different definitions of CKD measures and CVD outcomes, and applied distinct statistical approaches. A recent individual-level meta-analysis from the CKD Prognosis Consortium is of value as it has uniformly investigated creatinine-based estimated glomerular filtration rate (eGFR) and albuminuria as CKD measures and applied the same statistical approach across 24 cohorts with more than 630 000 participants. In this meta-analysis, eGFR and albuminuria improve CVD risk prediction beyond traditional CVD risk factors, particularly for CVD mortality and heart failure. Albuminuria demonstrates more evident improvement than eGFR. Moreover, several recent studies have shown that other filtration markers, for example, cystatin C and β2-microglobulin, and measures of atherosclerosis or cardiac damage (e.g., coronary artery calcium and cardiac troponins) can further improve CVD prediction in the CKD population. SUMMARY Future clinical guidelines may require updates regarding whether/how to incorporate CKD measures and other biomarkers in CVD prediction, depending on the CVD outcomes of interest, target population, and availability of those measures/biomarkers in that population.
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Angiotensin-converting enzyme (ACE) inhibitors for proteinuria and microalbuminuria in people with sickle cell disease.
Sasongko, TH, Nagalla, S, Ballas, SK
The Cochrane database of systematic reviews. 2015;(6):CD009191
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Abstract
BACKGROUND Sickle cell disease is a group of disorders characterized by deformation of erythrocytes. Renal damage is a frequent complication in sickle cell disease as a result of long-standing anemia and disturbed circulation through the renal medullary capillaries. Due to the improvement in life expectancy of people with sickle cell disease, there has been a corresponding significant increase in the incidence of renal complications. Microalbuminuria and proteinuria are noted to be a strong predictor of subsequent renal failure. There is extensive experience and evidence with angiotensin-converting enzyme (ACE) inhibitors over many years in a variety of clinical situations for patients who do not have sickle cell disease, but their effect in people with this disease is unknown. It is common practice to administer ACE inhibitors for sickle nephropathy due to their renoprotective properties; however, little is known about their effectiveness and safety in this setting. This is an update of a Cochrane Review first published in 2013. OBJECTIVES To determine the effectiveness of ACE inhibitor administration in people with sickle cell disease for decreasing intraglomerular pressure, microalbuminuria and proteinuria and to to assess the safety of ACE inhibitors as pertains to their adverse effects. SEARCH METHODS The authors searched the Cochrane Cystic Fibrosis and Genetic Disorders Group's Hameoglobinopathies Trials Register comprising references identified from comprehensive electronic database searches and handsearches of relevant journals and abstract books of conference proceedings.Date of the most recent search: 03 June 2015. SELECTION CRITERIA Randomized or quasi-randomized controlled trials of ACE inhibitors designed to reduce microalbuminuria and proteinuria in people with sickle cell disease compared to either placebo or standard treatment regimen. DATA COLLECTION AND ANALYSIS Three authors independently applied the inclusion criteria in order to select studies for inclusion in the review. Two authors assessed the risk of bias of studies and extracted data and the third author verified these assessments. MAIN RESULTS Five studies were identified through the searches, only one met our inclusion criteria. The included study randomized 22 participants (seven males and 15 females) having proteinuria or microalbuminuria with sickle cell disease and treated the participants for six months (median length of follow up of three months) with captopril or placebo. The overall quality of the outcomes reported was high, since most aspects that may contribute to bias were regarded to be of low risk, although allocation concealment was not reported. At six months, the study reported no significant difference in urinary albumin excretion between the captopril group and the placebo group, although the mean urinary albumin excretion in the captopril group was lower by a mean difference of -49.00 (95% confidence interval -124.10 to 26.10) compared to that of placebo. However, our analysis on the absolute change score showed significant changes between the two groups by a mean difference of -63.00 (95% confidence interval -93.78 to -32.22). At six months albumin excretion in the captopril group was noted to decrease from baseline by a mean of 45 ± 23 mg/day and the placebo group was noted to increase by 18 ± 45 mg/day. Serum creatinine and potassium levels were reported constant throughout the study. The potential for inducing hypotension should be highlighted; the study reported a decrease of 8 mmHg in systolic pressure and 5 mmHg in diastolic and mean blood pressure. AUTHORS' CONCLUSIONS There is not enough evidence to show that the administration of ACE inhibitors is associated with a reduction of microalbuminuria and proteinuria in people with sickle cell disease, although a potential for this was seen. More long-term studies involving multiple centers and larger cohorts using a randomized-controlled design are warranted, especially among the pediatric age group. Detailed reporting of each outcome measure is necessary to allow a clear cut interpretation in a systematic review. One of the difficulties encountered in this review was the lack of detailed data reported in the included study.
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Diabetic Kidney Disease: A Syndrome Rather Than a Single Disease.
Piccoli, GB, Grassi, G, Cabiddu, G, Nazha, M, Roggero, S, Capizzi, I, De Pascale, A, Priola, AM, Di Vico, C, Maxia, S, et al
The review of diabetic studies : RDS. 2015;(1-2):87-109
Abstract
The term "diabetic kidney" has recently been proposed to encompass the various lesions, involving all kidney structures that characterize protean kidney damage in patients with diabetes. While glomerular diseases may follow the stepwise progression that was described several decades ago, the tenet that proteinuria identifies diabetic nephropathy is disputed today and should be limited to glomerular lesions. Improvements in glycemic control may have contributed to a decrease in the prevalence of glomerular lesions, initially described as hallmarks of diabetic nephropathy, and revealed other types of renal damage, mainly related to vasculature and interstitium, and these types usually present with little or no proteinuria. Whilst glomerular damage is the hallmark of microvascular lesions, ischemic nephropathies, renal infarction, and cholesterol emboli syndrome are the result of macrovascular involvement, and the presence of underlying renal damage sets the stage for acute infections and drug-induced kidney injuries. Impairment of the phagocytic response can cause severe and unusual forms of acute and chronic pyelonephritis. It is thus concluded that screening for albuminuria, which is useful for detecting "glomerular diabetic nephropathy", does not identify all potential nephropathies in diabetes patients. As diabetes is a risk factor for all forms of kidney disease, diagnosis in diabetic patients should include the same combination of biochemical, clinical, and imaging tests as employed in non-diabetic subjects, but with the specific consideration that chronic kidney disease (CKD) may develop more rapidly and severely in diabetic patients.
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Glomerular filtration rate and albuminuria for detection and staging of acute and chronic kidney disease in adults: a systematic review.
Levey, AS, Becker, C, Inker, LA
JAMA. 2015;(8):837-46
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Abstract
IMPORTANCE Because early-stage kidney disease is asymptomatic and is associated with both morbidity and mortality, laboratory measurements are required for its detection. OBJECTIVE To summarize evidence supporting the use of laboratory tests for glomerular filtration rate (GFR) and albuminuria to detect and stage acute kidney injury, acute kidney diseases and disorders, and chronic kidney disease in adults. EVIDENCE REVIEW We reviewed recent guidelines from various professional groups identified via the National Guideline Clearing House and author knowledge, and systematically searched MEDLINE for other sources of evidence for selected topics. FINDINGS The KDIGO (Kidney Disease Improving Global Outcomes) guidelines define and stage acute and chronic kidney diseases by GFR and albuminuria. For initial assessment of GFR, measuring serum creatinine and reporting estimated GFR based on serum creatinine (eGFRcr) using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) 2009 equation is recommended. If confirmation of GFR is required because of conditions that affect serum creatinine independent of GFR (eg, extremes of muscle mass or diet), or interference with the assay, cystatin C should be measured and estimated GFR should be calculated and reported using cystatin C (eGFRcys) and serum creatinine (eGFRcr-cys) or GFR should be measured directly using a clearance procedure. Initial assessment of albuminuria includes measuring urine albumin and creatinine in an untimed spot urine collection and reporting albumin-to-creatinine ratio. If confirmation of albuminuria is required because of diurnal variation or conditions affecting creatinine excretion, such as extremes of muscle mass or diet, the albumin excretion rate should be measured from a timed urine collection. CONCLUSIONS AND RELEVANCE Detection and staging of acute and chronic kidney diseases can be relatively simple. Because of the morbidity and mortality associated with kidney disease, early diagnosis is important and should be pursued in at-risk populations.
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Angiotensin-converting enzyme (ACE) inhibitors for proteinuria and microalbuminuria in people with sickle cell disease.
Sasongko, TH, Nagalla, S, Ballas, SK
The Cochrane database of systematic reviews. 2013;(3):CD009191
Abstract
BACKGROUND Sickle cell disease is a group of disorders characterized by deformation of erythrocytes. Renal damage is a frequent complication in sickle cell disease as a result of long-standing anemia and disturbed circulation through the renal medullary capillaries. Due to the improvement in life expectancy of people with sickle cell disease, there has been a corresponding significant increase in the incidence of renal complications. Microalbuminuria and proteinuria are noted to be a strong predictor of subsequent renal failure. There is extensive experience and evidence with angiotensin-converting enzyme (ACE) inhibitors over many years in a variety of clinical situations for patients who do not have sickle cell disease, but their effect in patients with this disease is unknown. It is common practice to administer ACE inhibitors for sickle nephropathy due to their renoprotective properties; however, little is known about their effectiveness and safety in this setting. OBJECTIVES To determine the effectiveness of ACE inhibitor administration in people with sickle cell disease for decreasing intraglomerular pressure, microalbuminuria and proteinuria and to to assess the safety of ACE inhibitors as pertains to their adverse effects. SEARCH METHODS The authors searched the Cochrane Cystic Fibrosis and Genetic Disorders Group's Hameoglobinopathies Trials Register comprising references identified from comprehensive electronic database searches and handsearches of relevant journals and abstract books of conference proceedings.Date of the most recent search: 05 July 2012. SELECTION CRITERIA Randomized or quasi-randomized controlled trials of ACE inhibitors designed to reduce microalbuminuria and proteinuria in people with sickle cell disease compared to either placebo or standard treatment regimen. DATA COLLECTION AND ANALYSIS Three authors independently applied the inclusion criteria in order to select studies for inclusion in the review. Two authors assessed the risk of bias of studies and extracted data and the third author verified these assessments. MAIN RESULTS Five studies were identified through the searches, only one met our inclusion criteria. The included study randomized 22 participants (7 males and 15 females) having proteinuria or microalbuminuria with sickle cell disease and treated the participants for six months (median length of follow-up of three months) with captopril or placebo. At six months, the study reported no significant difference in urinary albumin excretion between the captopril group and the placebo group, although the mean urinary albumin excretion in the captopril group was lower by a mean difference of -49.00 (95% confidence interval -124.10 to 26.10) compared to that of placebo. However, our analysis on the absolute change score showed significant changes between the two groups by a mean difference of -63.00 (95% confidence interval -93.78 to -32.22). At six months albumin excretion in the captopril group was noted to decrease from baseline by a mean of 45 ± 23 mg/day and the placebo group was noted to increase by 18 ± 45 mg/day. Serum creatinine and potassium levels were reported constant throughout the study. The potential for inducing hypotension should be highlighted; the study reported a decrease of 8 mmHg in systolic pressure and 5 mmHg in diastolic and mean blood pressure. AUTHORS' CONCLUSIONS There is not enough evidence to show that the administration of ACE inhibitors is associated with a reduction of microalbuminuria and proteinuria in people with sickle cell disease, although a potential for this was seen. More long-term studies involving multiple centers and larger cohorts using a randomized-controlled design are warranted, especially among the pediatric age group. Detailed reporting of each outcome measure is necessary to allow a clear cut interpretation in a systematic review. One of the difficulties encountered in this review was the lack of detailed data reported in the included study.
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Non-invasive methods of glucose measurement: current status and future perspectives.
Ciudin, A, Hernandez, C, Simo, R
Current diabetes reviews. 2012;(1):48-54
Abstract
Diabetes mellitus (DM) is a very common disease which, if a good glycemic control is not achieved, can lead to serious chronic complications such as cardiovascular disease, retinopathy, nephropathy and neuropathy. Selfmonitoring of blood glucose is a fundamental tool for the proper adjustment of the treatment of diabetes and, at present, it is based mainly on capillary blood obtained by finger-prick (the classical glucometers). Since this method is painful and the strips are expensive, investigators have been attracted by the idea of using a non-invasive device for determining blood glucose which would permit more frequent testing and a tighter control of diabetes. The non-invasive measurement of blood glucose is based on the ability of the glucose molecule to interact with various chemical or physical methods. Nevetheless, in spite of some encouraging results and the efforts made over the past 30-40 years, there is no device available at present for use in clinical practice. A possible explanation might be the combination between the specific features of each method and the specific characteristics of diabetic patients, which make them respond differently to physical and chemical methods when compared to their healthy counterparts. In this paper we will give an overview of the noninvasive devices tested so far and their implications for the clinical management of the diabetic patient.
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Vascular and metabolic properties of manidipine.
Buset Ríos, N, Rodríguez Esparragón, F, Fernández-Andrade Rodríguez, C, Rodríguez Pérez, JC
Nefrologia : publicacion oficial de la Sociedad Espanola Nefrologia. 2011;(3):268-74
Abstract
The combination of renin-angiotensin system blockers with calcium channel blockers appears to be one of the most effective options for treating hypertension and diabetes.Nevertheless, not all calcium blockers behave in the same manner. Manidipine, unlike other third-generation dihydropyridine derived drugs, blocks T-type calcium channels present in the efferent glomerular arterioles, reducing intraglomerular pressure and microalbuminuria. In addition,T-type channels are related to proliferation, inflammation,fibrosis, vasoconstriction and activation of the renin-angiotensin system. The inhibition of these factors could explain the non-haemodynamic effects of manidipine as compared to other blockers.
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Therapeutic approaches in lowering albuminuria: travels along the renin-angiotensin-aldosterone-system pathway.
Heerspink, HJ
Advances in chronic kidney disease. 2011;(4):290-9
Abstract
Achieving optimal blood pressure and albuminuria control is a major therapeutic treatment goal in patients with renal insufficiency. Angiotensin-converting enzyme-inhibitors (ACEIs) and angiotensin-receptor blockers (ARB) are the mainstay of therapy in these patients. However, despite these therapies many patients remain at high risk of renal or cardiovascular disease that shows a relationship with albuminuria. Various approaches have been tested to maximize the efficacy of ACEI and ARB. Increasing the dose of an ACEI or ARB beyond the maximal registered antihypertensive dose causes a distinct decrease in albuminuria without additional effects on blood pressure. The combination of an ACEI and ARB is another possibility to further reduce albuminuria. However, the alleged beneficial effects on hard renal and cardiovascular outcome are not unambiguously demonstrated. Adding a direct renin inhibitor to an ACEI or ARB has been shown to lower albuminuria in patients with and without diabetes. Long-term trials are currently under way to determine the effects of direct renin inhibition on clinical outcomes. Volume excess has been shown to blunt the blood pressure and albuminuria response to ACEI or ARB therapy. Intervening in volume status by means of restricting dietary sodium intake or diuretic therapy has convincingly been shown to lower blood pressure and albuminuria. Whether this strategy translates into a reduction in the risk of renal or cardiovascular events has not (yet) been investigated in prospective randomized trials. Various options are at hand which have been shown to maximize the blood pressure and albuminuria response to ACEI and ARB treatment. However, long-term studies supporting the benefits of these strategies on hard renal and cardiovascular outcomes are warranted.
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Influence of microalbuminuria in achieving blood pressure goals.
Duka, I, Bakris, G
Current opinion in nephrology and hypertension. 2008;(5):457-63
Abstract
PURPOSE OF REVIEW In all individuals with hypertension regardless of diabetes status, microalbuminuria is an independent risk marker for cardiovascular events including myocardial infarction, stroke and other conditions. While blood pressure reduction is important in reducing this marker in individuals with hypertension other factors such as salt intake play an important role in reducing oxidant stress and other factors related to the genesis of microalbuminuria. RECENT FINDINGS Clinical trials demonstrate that drugs interfering with the renin-angiotensin system--angiotensin-converting enzyme inhibitors and angiotensin receptor blockers--should be used as first-line antihypertensive therapy in patients with microalbuminuria because they seem to have a blood pressure-independent antiproteinuric effect. A combination of an angiotensin-converting enzyme inhibitor with an angiotensin receptor blocker or other classes of medications shown to decrease protein excretion, such as nondihydropyridine calcium antagonists or aldosterone receptor blockers, should be considered to decrease albuminuria further; beta-blockers with alpha-blocking properties such as carvedilol have also been shown to reduce microalbuminuria probably secondary to its antioxidant properties. SUMMARY This review provides a summary of current evidence regarding the associations of blood pressure with microalbuminuria, the rationale for currently recommended blood pressure goals, and the use of various classes of antihypertensive agents in proteinuric patients.