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Endogenous bradykinin and B1-B5 during angiotensin-converting enzyme inhibitor-associated angioedema.
Hubers SA, Kohm K, Wei S, Yu C, Nian H, Grabert R, Sexton DJ, Brown NJ
(2018) J Allergy Clin Immunol 142: 1636-1639.e5
MeSH Terms: Aged, Angioedema, Angiotensin-Converting Enzyme Inhibitors, Bradykinin, Enalapril, Female, Humans, Kininogen, High-Molecular-Weight, Lisinopril, Male, Middle Aged, Peptide Fragments, Quinapril
Added November 7, 2018
0 Communities
1 Members
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13 MeSH Terms
Angiotensin receptor blocker vs ACE inhibitor effects on HDL functionality in patients on maintenance hemodialysis.
Kaseda R, Tsuchida Y, Gamboa JL, Zhong J, Zhang L, Yang H, Dikalova A, Bian A, Davies S, Fogo AF, Linton MF, Brown NJ, Ikizler TA, Kon V
(2018) Nutr Metab Cardiovasc Dis 28: 582-591
MeSH Terms: Adult, Angiotensin II Type 1 Receptor Blockers, Angiotensin-Converting Enzyme Inhibitors, Biomarkers, Cholesterol, HDL, Double-Blind Method, Female, Humans, Inflammation Mediators, Kidney Failure, Chronic, Male, Middle Aged, Oxidative Stress, Ramipril, Renal Dialysis, Tennessee, Time Factors, Treatment Outcome, Valsartan
Show Abstract · Added August 3, 2018
BACKGROUND AND AIMS - Angiotensin receptor blockers (ARB) and angiotensin converting enzyme inhibitors (ACEI) reduce cardiovascular events in the general population. Maintenance hemodialysis (MHD) patients are at high cardiovascular risk but few studies have directly addressed the comparative efficacy of these drugs. MHD disrupts the normally atheroprotective actions of high density lipoprotein (HDL), therefore, we compared ACEI or ARB treatment on HDL functions in MHD.
METHODS AND RESULTS - HDL was isolated at the starting point (pre) and 3-6 months later (post) in 30 MHD randomly assigned to placebo, ramipril or valsartan. Outcomes included cholesterol efflux, inflammatory cytokine response, effects on Toll-like receptors (TLR), superoxide production, methylarginine and serum amyloid A (SAA) levels. HDL from ARB- or ACEI-treated subjects was more effective in maintaining efflux than HDL of placebo. HDL from ARB- or ACEI-treated subjects but not placebo lessened cellular superoxide production. In contrast, neither ARB nor ACEI improved HDL anti-inflammatory effect. Indeed, HDL of ACEI-treated subjects potentiated the cytokine responses in association with activation of TLR but did not alter the HDL content of methylarginines or SAA.
CONCLUSION - Both ACEI and ARB stabilized HDL cholesterol acceptor function and sustained cellular anti-oxidative effects but not anti-inflammatory effects, and ACEI-treatment instead amplified the HDL inflammatory response. The findings reveal possible utility of antagonizing angiotensin actions in MDH and suggest a possible mechanism for superiority of ARB vs ACEI in the setting of advanced kidney disease.
Copyright © 2018 The Italian Society of Diabetology, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition, and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.
1 Communities
3 Members
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19 MeSH Terms
The Vasculature in Prediabetes.
Wasserman DH, Wang TJ, Brown NJ
(2018) Circ Res 122: 1135-1150
MeSH Terms: Angiotensin-Converting Enzyme Inhibitors, Animals, Blood Vessels, Cardiovascular Diseases, Combined Modality Therapy, Diabetes Mellitus, Type 2, Diet, Reducing, Disease Progression, Endothelium, Vascular, Extracellular Matrix, Fatty Acids, Nonesterified, Fibrinolysis, Glucose, Humans, Hyperglycemia, Hypoglycemic Agents, Inflammation, Insulin Resistance, Life Style, Metabolic Syndrome, Mice, MicroRNAs, Microcirculation, Muscle, Skeletal, Obesity, Prediabetic State, Risk, Weight Loss
Show Abstract · Added March 26, 2019
The frequency of prediabetes is increasing as the prevalence of obesity rises worldwide. In prediabetes, hyperglycemia, insulin resistance, and inflammation and metabolic derangements associated with concomitant obesity cause endothelial vasodilator and fibrinolytic dysfunction, leading to increased risk of cardiovascular and renal disease. Importantly, the microvasculature affects insulin sensitivity by affecting the delivery of insulin and glucose to skeletal muscle; thus, endothelial dysfunction and extracellular matrix remodeling promote the progression from prediabetes to diabetes mellitus. Weight loss is the mainstay of treatment in prediabetes, but therapies that improved endothelial function and vasodilation may not only prevent cardiovascular disease but also slow progression to diabetes mellitus.
© 2018 American Heart Association, Inc.
1 Communities
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28 MeSH Terms
Acute kidney injury is a risk factor for subsequent proteinuria.
Parr SK, Matheny ME, Abdel-Kader K, Greevy RA, Bian A, Fly J, Chen G, Speroff T, Hung AM, Ikizler TA, Siew ED
(2018) Kidney Int 93: 460-469
MeSH Terms: Acute Kidney Injury, Aged, Angiotensin II Type 1 Receptor Blockers, Angiotensin-Converting Enzyme Inhibitors, Antihypertensive Agents, Blood Pressure, Comorbidity, Databases, Factual, Diabetes Mellitus, Diabetic Nephropathies, Disease Progression, Female, Glomerular Filtration Rate, Hospitalization, Hospitals, Veterans, Humans, Hypertension, Kidney, Male, Middle Aged, Prevalence, Prognosis, Proteinuria, Renal Insufficiency, Chronic, Retrospective Studies, Risk Factors, Severity of Illness Index, Time Factors, United States
Show Abstract · Added November 29, 2018
Acute kidney injury (AKI) is associated with subsequent chronic kidney disease (CKD), but the mechanism is unclear. To clarify this, we examined the association of AKI and new-onset or worsening proteinuria during the 12 months following hospitalization in a national retrospective cohort of United States Veterans hospitalized between 2004-2012. Patients with and without AKI were matched using baseline demographics, comorbidities, proteinuria, estimated glomerular filtration rate, blood pressure, angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker (ACEI/ARB) use, and inpatient exposures linked to AKI. The distribution of proteinuria over one year post-discharge in the matched cohort was compared using inverse probability sampling weights. Subgroup analyses were based on diabetes, pre-admission ACEI/ARB use, and AKI severity. Among the 90,614 matched AKI and non-AKI pairs, the median estimated glomerular filtration rate was 62 mL/min/1.73m. The prevalence of diabetes and hypertension were 48% and 78%, respectively. The odds of having one plus or greater dipstick proteinuria was significantly higher during each month of follow-up in patients with AKI than in patients without AKI (odds ratio range 1.20-1.39). Odds were higher in patients with Stage II or III AKI (odds ratios 1.32-1.81) than in Stage I AKI (odds ratios 1.18-1.32), using non-AKI as the reference group. Results were consistent regardless of diabetes status or baseline ACEI/ARB use. Thus, AKI is a risk factor for incident or worsening proteinuria, suggesting a possible mechanism linking AKI and future CKD. The type of proteinuria, physiology, and clinical significance warrant further study as a potentially modifiable risk factor in the pathway from AKI to CKD.
Published by Elsevier Inc.
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29 MeSH Terms
Effect of bradykinin receptor antagonism on ACE inhibitor-associated angioedema.
Straka BT, Ramirez CE, Byrd JB, Stone E, Woodard-Grice A, Nian H, Yu C, Banerji A, Brown NJ
(2017) J Allergy Clin Immunol 140: 242-248.e2
MeSH Terms: Adult, Aged, Angioedema, Angiotensin-Converting Enzyme Inhibitors, Bradykinin, Bradykinin B2 Receptor Antagonists, Double-Blind Method, Female, Humans, Male, Middle Aged, Treatment Outcome
Show Abstract · Added April 6, 2017
BACKGROUND - The B receptor antagonist icatibant is approved for treatment of attacks of hereditary angioedema. Icatibant has been reported to decrease time-to-resolution of angiotensin-converting enzyme (ACE) inhibitor-associated angioedema in 1 study of European patients.
OBJECTIVE - We sought to test the hypothesis that a bradykinin B receptor antagonist would shorten time-to-resolution from ACE inhibitor-associated angioedema.
METHODS - Patients with ACE inhibitor-associated angioedema (defined as swelling of lips, tongue, pharynx, or face during ACE inhibitor use and no swelling in the absence of ACE inhibitor use) were enrolled at Vanderbilt University Medical Center from October 2007 through September 2015 and at Massachusetts General Hospital in 2012. C1 inhibitor deficiency and patients with bowel edema only were excluded. Patients were randomized within 6 hours of presentation to subcutaneous icatibant 30 mg or placebo at 0 and 6 hours later. Patients assessed severity of swelling using a visual analog scale serially following study drug administration or until discharge.
RESULTS - Thirty-three patients were randomized and 31 received treatment, with 13 receiving icatibant and 18 receiving placebo. One patient randomized to icatibant did not complete the visual analog scale and was excluded from analyses. Two-thirds of patients were black and two-thirds were women. Time-to-resolution of symptoms was similar in placebo and icatibant treatment groups (P = .19 for the primary symptom and P > .16 for individual symptoms of face, lip, tongue, or eyelid swelling). Frequency of administration of H1 and H2 blockers, corticosteroids, and epinephrine was similar in the 2 treatment groups. Time-to-resolution of symptoms was similar in black and white patients.
CONCLUSIONS - This study does not support clinical efficacy of a bradykinin B receptor antagonist in ACE inhibitor-associated angioedema.
Copyright © 2016 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
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12 MeSH Terms
Examining EXAMINE for an Interaction With Angiotensin-Converting Enzyme Inhibition.
Wilson JR, Brown NJ
(2016) Hypertension 68: 549-51
MeSH Terms: Angiotensin-Converting Enzyme Inhibitors, Humans, Peptidyl-Dipeptidase A
Added April 6, 2017
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1 Members
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3 MeSH Terms
Response by Hubers and Brown to Letter Regarding Article, "Combined Angiotensin Receptor Antagonism and Neprilysin Inhibition".
Hubers SA, Brown NJ
(2016) Circulation 134: e11-2
MeSH Terms: Aminobutyrates, Angiotensin Receptor Antagonists, Angiotensin-Converting Enzyme Inhibitors, Heart Failure, Humans, Neprilysin, Receptors, Angiotensin, Tetrazoles
Added April 6, 2017
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1 Members
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8 MeSH Terms
Angiotensin converting enzyme inhibition increases ADMA concentration in patients on maintenance hemodialysis--a randomized cross-over study.
Gamboa JL, Pretorius M, Sprinkel KC, Brown NJ, Ikizler TA
(2015) BMC Nephrol 16: 167
MeSH Terms: Angiotensin II Type 1 Receptor Blockers, Angiotensin-Converting Enzyme Inhibitors, Arginine, Bradykinin, Cell Line, Cross-Over Studies, Double-Blind Method, Endothelium, Vascular, Female, Humans, Kidney Failure, Chronic, Male, Middle Aged, Ramipril, Renal Dialysis, Valsartan
Show Abstract · Added November 5, 2015
BACKGROUND - Endothelial dysfunction occurs in patients with end-stage renal disease (ESRD) and is associated with increased cardiovascular morbidity and mortality. Asymmetric dimethylarginine (ADMA) contributes to endothelial dysfunction in ESRD. In the general population, angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) decrease ADMA levels, but no study has compared the effect of these drugs in patients with ESRD on maintenance hemodialysis (MHD).
METHODS - We evaluated the effect of 1-week treatment with ramipril (5 mg/d), valsartan (160 mg/d), and placebo on ADMA levels in 15 patients on MHD in a double-blind, placebo-controlled, three x three cross-over study.
RESULTS - We found that ADMA levels were increased at baseline and throughout the dialysis session during ramipril treatment (p < 0.001 compared to both, placebo and valsartan). Ramipril did not increase ADMA levels in a study of patients without ESRD, suggesting that factors related to ESRD or hemodialysis contribute to the ACE inhibitor-induced increase in ADMA. We have previously shown that ACE inhibition increases bradykinin (BK) levels during hemodialysis. We therefore evaluated the effect of bradykinin on ADMA production in A549 cells; a cell line that expresses BK receptors. Incubation with BK increased intracellular ADMA concentration through BK B2-receptor stimulation.
CONCLUSION - These data indicate that short-term ACE inhibition increases ADMA in patients on MHD whereas ARBs do not. In vitro studies further suggest that this may occur through BK-mediated increase in ADMA production during ACE inhibition.
TRIAL REGISTRATION - Clinicaltrials.gov NCT00732069 August 6 2008 and NCT00607672 February 4 2008.
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3 Members
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16 MeSH Terms
A genome-wide association study identifies variants in KCNIP4 associated with ACE inhibitor-induced cough.
Mosley JD, Shaffer CM, Van Driest SL, Weeke PE, Wells QS, Karnes JH, Velez Edwards DR, Wei WQ, Teixeira PL, Bastarache L, Crawford DC, Li R, Manolio TA, Bottinger EP, McCarty CA, Linneman JG, Brilliant MH, Pacheco JA, Thompson W, Chisholm RL, Jarvik GP, Crosslin DR, Carrell DS, Baldwin E, Ralston J, Larson EB, Grafton J, Scrol A, Jouni H, Kullo IJ, Tromp G, Borthwick KM, Kuivaniemi H, Carey DJ, Ritchie MD, Bradford Y, Verma SS, Chute CG, Veluchamy A, Siddiqui MK, Palmer CN, Doney A, MahmoudPour SH, Maitland-van der Zee AH, Morris AD, Denny JC, Roden DM
(2016) Pharmacogenomics J 16: 231-7
MeSH Terms: Angiotensin-Converting Enzyme Inhibitors, Case-Control Studies, Computational Biology, Cough, Databases, Genetic, Electronic Health Records, Female, Gene Frequency, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Kv Channel-Interacting Proteins, Logistic Models, Male, Multivariate Analysis, Odds Ratio, Phenotype, Polymorphism, Single Nucleotide, Risk Assessment, Risk Factors, Scotland, United States
Show Abstract · Added February 22, 2016
The most common side effect of angiotensin-converting enzyme inhibitor (ACEi) drugs is cough. We conducted a genome-wide association study (GWAS) of ACEi-induced cough among 7080 subjects of diverse ancestries in the Electronic Medical Records and Genomics (eMERGE) network. Cases were subjects diagnosed with ACEi-induced cough. Controls were subjects with at least 6 months of ACEi use and no cough. A GWAS (1595 cases and 5485 controls) identified associations on chromosome 4 in an intron of KCNIP4. The strongest association was at rs145489027 (minor allele frequency=0.33, odds ratio (OR)=1.3 (95% confidence interval (CI): 1.2-1.4), P=1.0 × 10(-8)). Replication for six single-nucleotide polymorphisms (SNPs) in KCNIP4 was tested in a second eMERGE population (n=926) and in the Genetics of Diabetes Audit and Research in Tayside, Scotland (GoDARTS) cohort (n=4309). Replication was observed at rs7675300 (OR=1.32 (1.01-1.70), P=0.04) in eMERGE and at rs16870989 and rs1495509 (OR=1.15 (1.01-1.30), P=0.03 for both) in GoDARTS. The combined association at rs1495509 was significant (OR=1.23 (1.15-1.32), P=1.9 × 10(-9)). These results indicate that SNPs in KCNIP4 may modulate ACEi-induced cough risk.
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4 Members
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22 MeSH Terms
Pyridoxamine dihydrochloride in diabetic nephropathy (PIONEER-CSG-17): lessons learned from a pilot study.
Dwyer JP, Greco BA, Umanath K, Packham D, Fox JW, Peterson R, Broome BR, Greene LE, Sika M, Lewis JB
(2015) Nephron 129: 22-8
MeSH Terms: Aged, Angiotensin-Converting Enzyme Inhibitors, Antihypertensive Agents, Antioxidants, Creatinine, Diabetes Mellitus, Type 2, Diabetic Nephropathies, Diuretics, Double-Blind Method, Drug Therapy, Combination, Female, Humans, Male, Pilot Projects, Pyridoxamine
Show Abstract · Added January 30, 2015
BACKGROUND/AIMS - Pyridoxamine dihydrochloride (Pyridorin™) blocks pathogenic oxidative pathways in the progression of diabetic nephropathy. The pyridoxamine pilot study was designed to test entry criteria and outcomes. Subjects had SCr 1.3-3.5 mg/dl, protein-to-creatinine ≥1,200 mg/g and used a surrogate outcome of ΔSCr over 52 weeks. Subjects had to be on a maximally tolerated dose of ACE/ARB for 3 months; stable other antihypertensive doses for 2 months; stable diuretic dose for 2 weeks, and BP ≤160/90 mm Hg; or enter a Pharmaco-Stabilization Phase (PSP). This pilot failed to detect an effect on ΔSCr in intent-to-treat analysis.
METHODS - We queried the locked clinical trial database for subgroups in which there was a treatment effect.
RESULTS - Subjects not requiring PSP and those with entry SCr <2.0 mg/dl had a treatment effect. Subjects entering PSP required more changes in antihypertensive medications and experienced larger ΔSCr over 52 weeks. PSP subjects with BP >140/90 mm Hg had no treatment effect, but those ≤140/90 mm Hg did.
CONCLUSION - Time required for acute effects of ACE/ARB to stabilize is unknown, but these data suggest >3 months. Thus, subjects in the pivotal trial must be on ACE/ARB for 6 months. Frequent antihypertensive adjustment could engender SCr changes unrelated to CKD progression. Thus, we will require subjects to have BP ≤150/90 mm Hg and on stable antihypertensives for 26 weeks, or ≤140/90 mm Hg and on stable antihypertensives for 13 weeks. Since ΔSCr over 52 weeks is limited as a surrogate outcome, the pivotal trial uses a time-to-event analysis of baseline SCr to at least a 50% increase in SCr or ESRD as the primary outcome. This substantial ΔSCr is protected from noise and is clinically relevant. The pyridoxamine pilot provided critical information to inform the design of PIONEER-CSG-17, which we conducted under the SPA agreement with FDA.
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15 MeSH Terms