Background Previous attempts to improve the quality of health journalism have not led to more responsible reporting of health news. Method We reviewed the front pages of three daily tabloid and three daily broadsheet UK newspapers during a 1 month period in 2017 for medical headlines in which claims were made for diets, lifestyle behaviours or drug therapies that influence health. Results Front page medical headlines were carried by the Daily Express (11), Daily Mail (two), Daily Mirror (one) and Daily Telegraph (one). Neither the Guardian nor the Independent carried medical stories on their front pages during the period of study. Eleven headlines suggested benefits and three suggested harm. One headline accurately reflected its source material, but in this instance the source material was of doubtful clinical relevance. The remaining 13 headlines either exaggerated benefit (seven), exaggerated harm (two) or made false claims (four). Conclusions The cumulative effect of everyday misreporting of medical stories in UK newspapers may not only serve to confuse the public but also have serious consequences for public health.

Post-operative acute kidney injury (AKI) is a common complication of surgery with significant short- and long-term adverse consequences. The adoption of diagnostic criteria for AKI (RIFLE, AKIN and KDIGO) has facilitated comparison of data reported by different centres, confirming that even mild AKI is associated with excess mortality. It remains unclear whether this is caused by the kidney injury itself or whether AKI is simply a marker of underlying disease severity. There is no trial evidence to support the use of any specific therapeutic intervention in post-operative AKI. Best current treatment is, therefore, preventative by optimizing hydration and avoidance of nephrotoxins, emphasizing the importance of earlier detection and identification of individuals at high risk for AKI. In this review, we examine the latest literature on the management of post-operative AKI in adult patients, specifically the diagnosis and definition of AKI, epidemiology and pathogenesis and risk stratification in cardiac and non-cardiac surgery. We also review the latest evidence on pharmacological and non-pharmacological interventions.

The placebo-corrected incidence of rhabdomyolysis in a systematic review of 20 statin trials was 1.6/100,000 per year.It is likely to be higher than this in everyday clinical practice when statins are knowingly or inadvertently co-prescribed with drugs that interfere with their metabolism.We report a case of rhabdomyolysis causing muscle weakness and prolonging an episode of dialysisdependent acute kidney injury, which occurred when fusidic acid was co-prescribed with atorvastatin.Renal function and muscle power recovered when both drugs were withdrawn.We found four other cases of rhabdomyolysis with fusidic acid and atorvastatin and three with fusidic acid and simvastatin in the literature, a review of which suggests that the risks of rhabdomyolysis vary with the extent to which an individual statin is dependent for its metabolism on the cytochrome P450 3A4 isoenzyme and the degree to which this isoenzyme's activity is inhibited by a particular antimicrobial.Of note, the interaction between statins and fusidic acid did not feature in seven of eight recent reviews of statin toxicity.Our case report highlights the importance of close monitoring of patients on statins, especially when new drugs are started or if patients become unwell, by checking creatine kinase and liver function tests and by examining for new muscle weakness.Our review of statin-antimicrobial drug interactions suggests that fusidic acid is another CYP450 3A4 enzyme inhibitor with the potential to cause rhabdomyolysis when co-prescribed with simvastatin and atorvastatin.

BACKGROUND UK, US and European guidelines recommend the decision to initiate dialysis should be based on a combination of measurements of kidney function, nutritional status and clinical symptoms. Such recommendations assume an accurate and reproducible measure of glomerular filtration rate (GFR). METHODS Prospective study of 97 patients with chronic kidney disease (CKD) and serum creatinine >200 micromol/l (2.26 mg/dl) who between them contributed 388 24 h urine collections. Our main outcome measure was the number of patients with low residual renal function identified by different tests, using widely accepted thresholds. We calculated sensitivity, specificity, positive and negative predictive values and receiver operating characteristic curves for each comparison using a combined urea and creatinine clearance of <15 ml/min to indicate the likely presence of end stage renal disease (CKD stage 5). RESULTS Seventy five patients had a combined urea and creatinine clearance <15 ml/min during the study. Using the highest measurement of serum creatinine for each patient, the best of the prediction equations was the 4-variable modification of diet in renal disease (MDRD) equation (area under ROC curve 0.93). This was followed by Kt/V (AUC 0.91) and Cockroft Gault with and without correction for ideal body weight (AUC 0.89). Further analyses showed that the 4-variable MDRD equation had higher NPV (64%) but lower PPV (89%) than the other tests (NPV 40-49%, PPV 92-100%), for identifying patients whose combined clearance was <15 ml/min. CONCLUSION The 4-variable MDRD formula is currently the best available prediction equation for GFR, but will nevertheless over estimate residual renal function when this is significantly impaired in up to 36% cases. Collection of 24 h urine samples may still have a role in the assessment of patients with stages 4 and 5 CKD.

Glomerular filtration rate (GFR) is accepted as the best overall measure of kidney function but measurement using reference procedures (e.g. 51Cr-EDTA) is impractical for large-scale application.Internationally there has been a recent thrust towards earlier detection of chronic kidney disease (CKD), primarily using estimated GFR (eGFR) as a tool [1].Quality requirement one of Part 2 of the Renal NSF was aimed at prevention and early detection of CKD and to satisfy this it was recommended that clinical biochemistry laboratories report eGFR alongside all requests received for serum creatinine measurement in adults [2].In April 2006, the Department of Health in England recommended universal eGFR reporting using the ID-MS standardized MDRD equation [3] with appropriate adjustment for assay differences and the Quality and Outcomes Framework (QOF) introduced a register of people in primary care with stages 3-5 CKD.Clinical practice guidelines to support these initiatives have been published [4].After years of deliberation laboratory testing of kidney function seems to have taken a step forward and the age of eGFR is truly upon us.But how good is eGFR at measuring kidney function?Problems with the laboratory measurement of serum creatinine may be masked but have not disappeared following the superimposition of eGFR.Both analytical and biological variations of serum creatinine concentration contribute to imprecision of eGFR, which must be taken into account when interpreting guidelines.Is an upper reporting limit of 90 ml/min/1.73m 2 appropriate?Should the blood sample itself be obtained under fasting conditions [5]?Does eGFR using the MDRD equation predict progression of CKD?The MDRD equation was derived in a US population of middleaged patients with CKD.A correction is applied for Black-Americans but the transferability of this to African-Caribbean (or Chinese and South Asian) populations in the UK has not been widely confirmed.Perhaps most significantly, the MDRD study did not address individuals over 75 years of age, the age group amongst which most CKD resides.This talk will review the evidence addressing some of these important issues.

The prevalence of end-stage renal disease in the UK looks set to increase for several more years. Since CKD is essentially a disease of older age, and because age is no longer seen as a contraindication for treatment, it follows that older people are now the fastest growing group of patients starting dialysis. Sadly this has not always been matched by an increase in services necessary to support them on dialysis. Expansion of dialysis facilities does not necessarily mean that all 80-year-old patients with end-stage renal disease should be offered treatment, which will often be inappropriate because of functional impairment, or will become inappropriate in the setting of severe dementia, advanced cancer or other serious co-morbid illness. Many questions about the management of older people with end-stage renal disease remain unanswered. Well designed prospective studies are required.

Hyperkalaemia is an ever present threat in dialysis units and is encountered frequently on general wards, particularly in patients with renal failure. It is important because it can cause life threatening cardiac dysrhythmia, with death by asystole or ventricular fibrillation commonly the first clinical manifestation. I Preferred therapy varies, reflecting the lack of clear evidence for an optimal regimen, but broadly speaking the choice of treatment is based upon the serum potassium level, the ECG and the likelihood that potassium will rise further. In this review we highlight the causes, sequelae and evidence for the treatment of hyperkalaemia. Our starting point is a serum potassium of 6 mmol/l. Thereafter, we suggest it may be useful to distinguish two groups of patients on the basis of their ECG: those whose ECG is normal, whom we consider to have severe hyperkalaemia, and those with ECG evidence of raised serum potassium or life threatening hyperkalaemia.

OBJECTIVE:To compare characteristics, management, and outcome of myocardial infarction (MI) in men and women. DESIGN:Prospective observational study. SETTING:District general hospital in southwest Scotland. PARTICIPANTS:966 men and 597 women admitted with first MI between 1994 and 2000 with follow up to the end of 2001. RESULTS:393 (40.7%) men and 305 (51.1%) women died during a median follow up of 3.4 years for the survivors. Univariate analysis indicated an excess mortality among women (hazard ratio (HR) 1.45, 95% confidence interval (CI) 1.25 to 1.68), which disappeared after adjustment for age, smoking, co-morbidity, previous vascular disease, diabetes, hypertension, and social deprivation (HR 1.02, 95% CI 0.87 to 1.20). There was also an excess early mortality within 30 days among women (HR 1.54, 95% CI 1.20 to 1.98), though this did not retain significance after adjustment for the same covariates (HR 1.04, 95% CI 0.79 to 1.37). Small and insignificant differences were found in the proportion of men and women receiving thrombolysis on admission and secondary prophylactic drugs at discharge, except for statins and beta blockers, which were respectively more (adjusted odds ratio 1.48, 95% CI 1.10 to 1.98) and less (adjusted odds ratio 0.78, 95% CI 0.60 to 1.00) commonly prescribed to women. CONCLUSION:Results suggest that the poorer outcome for women after MI reported in other studies may reflect sex bias in management as well as differences in age and co-morbidity and support the view that if women have access to the same quality of care as men then survival will be the same.

A 67 year old woman developed acute renal failure with serum potassium 9.4 mmol/l requiring emergency dialysis after seven days of diarrhoea while taking an ACE inhibitor for vascular disease. Review of the literature, the British National Formulary, and the patient information leaflets for each of the 11 ACE inhibitors currently marketed in the UK suggests that this potentially life threatening complication of ACE inhibition is not yet widely recognised.

Background— Limited data describe the cardiovascular benefit of HMG-CoA reductase inhibitors (statins) in people with moderate chronic kidney disease (CKD). The objective of this analysis was to determine whether pravastatin reduced the incidence of cardiovascular events in people with or at high risk for coronary disease and with concomitant moderate CKD. Methods and Results— We analyzed data from the Pravastatin Pooling Project (PPP), a subject-level database combining results from 3 randomized trials of pravastatin (40 mg daily) versus placebo. Of 19 700 subjects, 4491 (22.8%) had moderate CKD, defined by an estimated glomerular filtration rate of 30 to 59.99 mL/min per 1.73 m 2 body surface area. The primary outcome was time to myocardial infarction, coronary death, or percutaneous/surgical coronary revascularization. Moderate CKD was independently associated with an increased risk of the primary outcome (adjusted HR 1.26, 95% CI 1.07 to 1.49) compared with those with normal renal function. Among the 4491 subjects with moderate CKD, pravastatin significantly reduced the incidence of the primary outcome (HR 0.77, 95% CI 0.68 to 0.86), similar to the effect of pravastatin on the primary outcome in subjects with normal kidney function (HR 0.78, 95% CI 0.65 to 0.94). Pravastatin also appeared to reduce the total mortality rate in those with moderate CKD (adjusted HR 0.86, 95% CI 0.74 to 1.00, P =0.045). Conclusions— Pravastatin reduces cardiovascular event rates in people with or at risk for coronary disease and concomitant moderate CKD, many of whom have serum creatinine levels within the normal range. Given the high risk associated with CKD, the absolute benefit that resulted from use of pravastatin was greater than in those with normal renal function.

Dumfries and Galloway Royal Infirmary (Whiteley) Department of Cardivascular and Medical Sciences, Western Infirmary (Padmanabhan) Department of Medicine, Dumfries and Galloway Royal Infirmary (Isles) Dept of Public Health, University of Glasgow (Hole)

Western Infirmary (Padmanabhan) Dumfries and Galloway Royal Infirmary (Whiteley) (Isles) Western Infirmary (Connell) Dept of Public Health, University of Glasgow (Hole)

The suggestion that ‘feeling bad’ may contribute to the risk of stroke is not something with which most readers of this journal are likely to feel comfortable or even familiar, but this is exactly the conclusion drawn by a group of public health researchers from Sweden in a study of a large number of subjects who had participated in a health survey [1], as reported in this issue of the journal. Four hundred and seventy-three individuals had a definite first ever stroke between 1985 and 2000. Each was matched with two controls for age, sex and residence. The measure of self-rated health in this and other studies was the response to the question ‘In general, would you say that your health is excellent, very good, good, fair or poor'. The main exclusions were individuals who had a diagnosis of myocardial infarction or cancer in the 5 years preceding their stroke, which makes it unlikely that poor self-rated health was a consequence of these particular comorbidities. The main findings of the survey by Emmelin et al. [1] were that individuals with two or more biological risk factors who rated their own health as ‘not good’ were much more likely to have a stroke. The authors went on to suggest that their findings were gender specific and education sensitive. Men appeared to be at greater risk of stroke than women, as were well-educated people of both sexes, if they rated their health as ‘not good'. They concluded that self-rated health may have a causal role in 20% of stroke cases in Northern Sweden, an impact similar to that of hypertension and smoking [1]. A previous study by the same group explored the relation between biomedical risk factors, perceived health and the development of myocardial infarction in a series of 78 myocardial infarction patients drawn from the same population survey and showed that perceived ill health amplified the risk of myocardial infarction by a factor of 5 when three biomedical risk factors were present [2]. Similar findings have been reported by others, both for stroke [3] and for coronary heart disease (CHD) [4]. We also know from a limited number of longitudinal studies that both stroke and CHD lead to loss of self-rated health [5,6] and that self-rated health predicts outcome in patients with these conditions [7,8]. These studies raise a number of interesting questions regarding the meaning and implication of self-rated health, particularly for those of us who feel more at ease with the biomedical model of stroke risk and outcome. If, as seems likely, self-rated health is a global measure of both physical and psychological health then what exactly is it measuring? Illness related variables such as chronic disease, disability and pain, together with lifestyle factors including smoking, alcohol intake and physical inactivity, may all contribute to the physical component of self-rated health [9], while mastery, chronic distress, self-esteem, social support [9] and depression [10] have been shown to be important psychological factors. The next question is whether self-rated health is an independent predictor of risk or a proxy for one of its determinants. There is good evidence, as summarized in a review by Goldstein [11], that lifestyle factors such as smoking, alcohol intake and physical inactivity, all of which may cause ill health, can increase the risk of stroke. We also know that depression is significantly associated with stroke incidence [12] and that negative attitudes to health predict worse long-term survival in stroke patients [13]. Both depression and negative attitudes to health appear likely to determine whether a person feels good or not good, and might therefore be the drivers of the association between self-rated health, stroke incidence and outcome. None of these issues were explored fully in the study by Emmelin et al. [1], although a survey of 2885 individuals who had angiographically proven CHD may provide some answers [8]. Those who rated their health as poor had a significantly greater risk of CHD-related mortality than those who rated their health as very good (odds ratio 3.6) after adjusting for all available mortality risk factors. These included socio-demographic variables, physical comorbidities, CHD disease severity, health-related quality of life, measures of social support and indices of depression. Thus in patients with pre-existing CHD, self-rated health would appear to be an independent risk factor [8]. The possibility that the response to a question as simple as ‘Would you say your health is excellent, very good, good, fair or poor’ may predict stroke risk and provide information over and above that obtained by conventional risk factors is at the very least intriguing. The fact that this risk appears to be amplified in those individuals with the most conventional risk factors is certainly worthy of further attention. Clearly, there is much to be done here [14]. In particular, we need to establish the determinants of self-rated health and confirm that its predictive power is independent of other risk factors. We also need to investigate whether self-rated health is a stable characteristic or whether it changes, and we need to know whether we can alter it and, consequently, whether this improves outcome. Meanwhile what, if any, advice can be given to patients as a result of the study by Emmelin et al. [1] and others like it? In a recent review of the determinants of successful ageing, the definition of which included the absence of death or disability before age 80 years, seven protective factors were found that were under at least some personal control. These were an absence of alcohol abuse, not smoking, being physically active, an acceptable body mass index, marital stability, coping mechanisms and a good education [15]. It is likely that each of these could contribute to an estimate of self-rated health, suggesting avenues of intervention for patients whose self-rated health is described as poor. Consequently, when we review our hypertensive patients, we might ask them to rate their own health while we are checking their blood pressure and take more notice if they say they are ‘feeling bad'. Acknowledgements I should like to thank Lesley Howells, Lorna McArthur, Bob Lewin and Martin Dennis for their helpful comments.

Background-The National Cholesterol Education Program (NCEP) recently proposed a simple definition for metabolic syndrome. Information on the prospective association of this definition for coronary heart disease (CHD) and type 2 diabetes is currently limited.Methods and Results-We used a modified NCEP definition with body mass index in place of waist circumference. Baseline assessments in the West of Scotland Coronary Prevention Study were available for 6447 men to predict CHD risk and for 5974 men to predict incident diabetes over 4.9 years of follow-up. Mean LDL cholesterol was similar but C-reactive protein was higher (P<0.0001) in the 26% of men with the syndrome compared with those without. Metabolic syndrome increased the risk for a CHD event [univariate hazard ratio (HR) = 1.76 (95% CI, 1.44 to 2.15)] and for diabetes [univariate HR = 3.50 (95% CI 2.51 to 4.90)]. Metabolic syndrome continued to predict CHD events (HR = 1.30, 95% CI, 1.00 to 1.67, P = 0.045) in a multivariate model incorporating conventional risk factors. Men with 4 or 5 features of the syndrome had a 3.7-fold increase in risk for CHD and a 24.5-fold increase for diabetes compared with men with none (both P<0.0001). C-reactive protein enhanced prognostic information for both outcomes. With pravastatin, men with the syndrome had similar risk reduction for CHD as compared with those without (HR, 0.73 and 0.69; pravastatin versus placebo).Conclusions-A modified NCEP metabolic syndrome definition predicts CHD events, and, more strikingly, new-onset diabetes, and thus helps identify individuals who may receive particular benefit from lifestyle measures to prevent these diseases.