ORCID Profile
0000-0002-1179-0023
Current Organisation
University of Oxford
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Publisher: Elsevier BV
Date: 11-2010
Publisher: American Medical Association (AMA)
Date: 06-10-2020
Publisher: Elsevier BV
Date: 10-2020
Publisher: Elsevier BV
Date: 10-2020
Publisher: Elsevier BV
Date: 07-2014
Publisher: Elsevier BV
Date: 05-2021
Publisher: Oxford University Press (OUP)
Date: 21-07-2011
DOI: 10.1093/NDT/GFR394
Abstract: Glomerulonephritis occurs in 1% of Hodgkin's lymphoma patients. In the even rarer setting of rapidly progressive glomerulonephritis, lymphoma may go unrecognized. We describe a case of necrotizing glomerulonephritis in which treatment with cyclophosphamide and steroids led to resolution of lymphadenopathy. Two years later, recrudescent lymphadenopathy was shown to be Hodgkin's lymphoma, but renal disease did not recur.
Publisher: Elsevier BV
Date: 05-2021
Publisher: Elsevier BV
Date: 2016
Publisher: American Medical Association (AMA)
Date: 23-06-2010
Abstract: Blood homocysteine levels are positively associated with cardiovascular disease, but it is uncertain whether the association is causal. To assess the effects of reducing homocysteine levels with folic acid and vitamin B(12) on vascular and nonvascular outcomes. Double-blind randomized controlled trial of 12,064 survivors of myocardial infarction in secondary care hospitals in the United Kingdom between 1998 and 2008. 2 mg folic acid plus 1 mg vitamin B(12) daily vs matching placebo. First major vascular event, defined as major coronary event (coronary death, myocardial infarction, or coronary revascularization), fatal or nonfatal stroke, or noncoronary revascularization. Allocation to the study vitamins reduced homocysteine by a mean of 3.8 micromol/L (28%). During 6.7 years of follow-up, major vascular events occurred in 1537 of 6033 participants (25.5%) allocated folic acid plus vitamin B(12) vs 1493 of 6031 participants (24.8%) allocated placebo (risk ratio [RR], 1.04 95% confidence interval [CI], 0.97-1.12 P = .28). There were no apparent effects on major coronary events (vitamins, 1229 [20.4%], vs placebo, 1185 [19.6%] RR, 1.05 95% CI, 0.97-1.13), stroke (vitamins, 269 [4.5%], vs placebo, 265 [4.4%] RR, 1.02 95% CI, 0.86-1.21), or noncoronary revascularizations (vitamins, 178 [3.0%], vs placebo, 152 [2.5%] RR, 1.18 95% CI, 0.95-1.46). Nor were there significant differences in the numbers of deaths attributed to vascular causes (vitamins, 578 [9.6%], vs placebo, 559 [9.3%]) or nonvascular causes (vitamins, 405 [6.7%], vs placebo, 392 [6.5%]) or in the incidence of any cancer (vitamins, 678 [11.2%], vs placebo, 639 [10.6%]). Substantial long-term reductions in blood homocysteine levels with folic acid and vitamin B(12) supplementation did not have beneficial effects on vascular outcomes but were also not associated with adverse effects on cancer incidence. isrctn.org Identifier: ISRCTN74348595.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 08-2014
Publisher: Elsevier BV
Date: 07-2022
Publisher: Elsevier BV
Date: 11-2010
DOI: 10.1016/J.AHJ.2010.08.012
Abstract: Lowering low-density lipoprotein (LDL) cholesterol with statin therapy has been shown to reduce the incidence of atherosclerotic events in many types of patient, but it remains uncertain whether it is of net benefit among people with chronic kidney disease (CKD). Patients with advanced CKD (blood creatinine ≥ 1.7 mg/dL [≥ 150 μmol/L] in men or ≥ 1.5 mg/dL [ ≥ 130 μmol/L] in women) with no known history of myocardial infarction or coronary revascularization were randomized in a ratio of 4:4:1 to ezetimibe 10 mg plus simvastatin 20 mg daily versus matching placebo versus simvastatin 20 mg daily (with the latter arm rerandomized at 1 year to ezetimibe 10 mg plus simvastatin 20 mg daily vs placebo). The key outcome will be major atherosclerotic events, defined as the combination of myocardial infarction, coronary death, ischemic stroke, or any revascularization procedure. A total of 9,438 CKD patients were randomized, of whom 3,056 were on dialysis. Mean age was 61 years, two thirds were male, one fifth had diabetes mellitus, and one sixth had vascular disease. Compared with either placebo or simvastatin alone, allocation to ezetimibe plus simvastatin was not associated with any excess of myopathy, hepatic toxicity, or biliary complications during the first year of follow-up. Compared with placebo, allocation to ezetimibe 10 mg plus simvastatin 20 mg daily yielded average LDL cholesterol differences of 43 mg/dL (1.10 mmol/L) at 1 year and 33 mg/dL (0.85 mmol/L) at 2.5 years. Follow-up is scheduled to continue until August 2010, when all patients will have been followed for at least 4 years. SHARP should provide evidence about the efficacy and safety of lowering LDL cholesterol with the combination of ezetimibe and simvastatin among a wide range of patients with CKD.
Publisher: Elsevier BV
Date: 04-2016
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 30-10-2020
Abstract: Conventional epidemiology associates increased body mass index (BMI) with higher risk of CKD. Diabetes and high BP explain half of the association. However, residual confounding factors preclude causal inferences and impede mediation assessments. A genetic approach (Mendelian randomization) may overcome these limitations. Analyses of 281,228 genotyped UK Biobank participants identified positive independent genetic associations between central and general adiposity with CKD, suggesting both are causal risk factors. Conventional approaches underestimate the role of known mediators. Diabetes and BP (and correlates) explain % of genetic associations between waist-to-hip ratio and CKD and two-thirds between BMI and CKD. In people without diabetes, obesity appeared to cause CKD. BP accounted for about half of the BMI-CKD associations. The size of any causal contribution of central and general adiposity to CKD risk and the underlying mechanism of mediation are unknown. Data from 281,228 UK Biobank participants were used to estimate the relevance of waist-to-hip ratio and body mass index (BMI) to CKD prevalence. Conventional approaches used logistic regression. Genetic analyses used Mendelian randomization (MR) and data from 394 waist-to-hip ratio and 773 BMI-associated loci. Models assessed the role of known mediators (diabetes mellitus and BP) by adjusting for measured values (conventional analyses) or genetic associations of the selected loci (multivariable MR). Evidence of CKD was found in 18,034 (6.4%) participants. Each 0.06 higher measured waist-to-hip ratio and each 5-kg/m 2 increase in BMI were associated with 69% (odds ratio, 1.69 95% CI, 1.64 to 1.74) and 58% (1.58 1.55 to 1.62) higher odds of CKD, respectively. In analogous MR analyses, each 0.06–genetically-predicted higher waist-to-hip ratio was associated with a 29% (1.29 1.20 to 1.38) increased odds of CKD, and each 5-kg/m 2 genetically-predicted higher BMI was associated with a 49% (1.49 1.39 to 1.59) increased odds. After adjusting for diabetes and measured BP, chi-squared values for associations for waist-to-hip ratio and BMI fell by 56%. In contrast, mediator adjustment using multivariable MR found 83% and 69% reductions in chi-squared values for genetically-predicted waist-to-hip ratio and BMI models, respectively. Genetic analyses suggest that conventional associations between central and general adiposity with CKD are largely causal. However, conventional approaches underestimate mediating roles of diabetes, BP, and their correlates. Genetic approaches suggest these mediators explain most of adiposity-CKD–associated risk.
Publisher: Elsevier BV
Date: 03-2020
Publisher: Massachusetts Medical Society
Date: 19-07-2100
Publisher: Elsevier BV
Date: 02-2022
Publisher: Oxford University Press (OUP)
Date: 26-02-2013
Publisher: Springer Science and Business Media LLC
Date: 05-2017
Publisher: Elsevier BV
Date: 07-2019
Publisher: Elsevier BV
Date: 02-2021
Publisher: Massachusetts Medical Society
Date: 21-08-2008
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 05-2014
DOI: 10.2215/CJN.10371013
Publisher: Springer Science and Business Media LLC
Date: 16-07-2020
DOI: 10.1038/S41366-020-0642-3
Abstract: Whether measures of central adiposity are more or less strongly associated with risk of albuminuria than body mass index (BMI), and by how much diabetes/levels of glycosylated haemoglobin (HbA1c) explain or modify these associations, is uncertain. Ordinal logistic regression was used to estimate associations between values of central adiposity (waist-to-hip ratio) and, separately, general adiposity (BMI) with categories of urinary albumin-to-creatinine ratio (uACR) in 408,527 UK Biobank participants. Separate central and general adiposity-based models were initially adjusted for potential confounders and measurement error, then sequentially, models were mutually adjusted (e.g. waist-to-hip ratio adjusted for BMI, and vice versa), and finally they were adjusted for potential mediators. Levels of albuminuria were generally low: 20,425 (5%) had a uACR ≥3 mg/mmol. After adjustment for confounders and measurement error, each 0.06 higher waist-to-hip ratio was associated with a 55% (95%CI 53–57%) increase in the odds of being in a higher uACR category. After adjustment for baseline BMI, this association was reduced to 32% (30–34%). Each 5 kg/m 2 higher BMI was associated with a 47% (46–49%) increase in the odds of being in a higher uACR category. Adjustment for baseline waist-to-hip ratio reduced this association to 35% (33–37%). Those with higher HbA1c were at progressively higher odds of albuminuria, but positive associations between both waist-to-hip ratio and BMI were apparent irrespective of HbA1c. Altogether, about 40% of central adiposity associations appeared to be mediated by diabetes, vascular disease and blood pressure. Conventional epidemiological approaches suggest that higher waist-to-hip ratio and BMI are independently positively associated with albuminuria. Adiposity–albuminuria associations appear strong among people with normal HbA1c, as well as people with pre-diabetes or diabetes.
Publisher: Springer Science and Business Media LLC
Date: 29-04-2015
Publisher: Elsevier BV
Date: 04-2018
Publisher: Massachusetts Medical Society
Date: 28-09-2017
Publisher: Massachusetts Medical Society
Date: 25-02-2021
Publisher: Elsevier BV
Date: 09-2016
Publisher: Elsevier BV
Date: 2022
Publisher: American Medical Association (AMA)
Date: 10-08-2021
Publisher: Elsevier BV
Date: 08-2017
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Richard Haynes.