Search

The annual American Heart Association (AHA) and National Institutes of Health statistical report details the most up to date statistics related to heart disease, stroke and cardiovascular risk factors, primarily within the USA. Although not a formal systematic review or meta-analysis, this 600 page report provides the most comprehensive and best summary of cardiovascular statistics for the year in question. Although data are collated from USA data registries, it serves as a critical resource for clinicians, policymakers, administrators and researchers in the northern and southern hemispheres. In this special report, we have chosen to highlight aspects of the document that are relevant to nephrologists, given the overlap of cardiovascular and renal disease. These include (i) key and emerging cardiovascular data signals in the general and chronic kidney disease (CKD) populations, (ii) ethnic and socio-economic disparity, (iii) environmental and behavioural factors that drive high levels of cardiovascular disease and which are key components of the AHA's eight components of the Life Essential cardiovascular health score, and (iv) the impact of COVID-19 both directly and indirectly on heart health. We provide some commentary and critical analysis of both the data and of the production of such data sets suggesting that similar data on CKD could also be published and linked to the AHA and other datasets. [ABSTRACT FROM AUTHOR]

The wide overlap between the syndromes of chronic kidney disease (CKD) and chronic heart failure (HF) means that familiarity with the 2021 European Society of Cardiology guidelines is of importance to nephrologists. The common risk factors for the two syndromes together with the adverse cardiac structural remodelling associated with CKD means that many kidney disease patients experience breathlessness and fall within the HF phenotypes categorized in the guidelines. The management of HF is evolving rapidly leading to significant changes in the latest guideline iteration. The 2021 guidelines have changed from the 2016 version firstly by an increased focus on identifying the three phenotypes of HF to guide appropriate evidence-based management. Secondly, a new and simplified treatment algorithm for HF with reduced ejection fraction involving the rapid sequential initiation and up-titration of four 'pillars' of drug treatment—angiotensin-converting enzyme inhibitors or angiotensin-neprilysin inhibitors, beta blockers, mineralocorticoid receptor antagonists and now, thanks to convincing trial data, sodium-glucose co-transporter 2 inhibitors. Thirdly, guidelines for device therapy have been changed with down-graded advice on indications for primary prevention implantable cardioverter defibrillator therapy for patients with non-ischaemic HF and for cardiac resynchronization therapy with left bundle branch block (LBBB) and a QRS duration <150 ms. There are updated treatment plans for HF associated with non-cardiovascular comorbidities including CKD. [ABSTRACT FROM AUTHOR]

The first successful live donor kidney transplant was performed in 1954. Receiving a kidney transplant from a live kidney donor remains the best option for increasing both life expectancy and quality of life in patients with end-stage kidney disease. However, ever since 1954, there have been multiple questions raised on the ethics of live kidney donation in terms of negative impacts on donor life expectancy. Given the close relationship between reduced kidney function in patients with chronic kidney disease (CKD) and hypertension, cardiovascular disease and cardiovascular mortality, information on the impact of kidney donation on these is particularly relevant. In this article, we review the existing evidence, focusing on the more recent studies on the impact of kidney donation on all-cause mortality, cardiovascular mortality, cardiovascular disease and hypertension, as well as markers of cardiovascular damage including arterial stiffness and uraemic cardiomyopathy. We also discuss the similarities and differences between the pathological reduction in renal function that occurs in CKD, and the reduction in renal function that occurs because of a donor nephrectomy. Kidney donors perform an altruistic act that benefits individual patients as well as the wider society. They deserve to have high-quality evidence on which to make informed decisions. [ABSTRACT FROM AUTHOR]

Background Acute kidney injury (AKI) in hospital-admitted patients is a common complication associated with increased mortality. The diagnosis of AKI relies on the ascertainment of peak increase in serum creatinine (SCr). This study evaluated the incidence of AKI using the increase from mean 7–365 days pre-admission (AKIpre) and admission (AKIadm) SCr levels, and examined the associations of AKI and changes in SCr levels with all-cause mortality. Methods A total of 2436 patients admitted to a tertiary hospital were recruited and followed-up for a median of 47.70 (interquartile range 18.20) months. AKI incidence and severity were defined according to the Kidney Disease: Improving Global Outcomes-AKI Guidelines. Follow-up data were collected from the Hospital Episode Statistics and Office of National Statistics. Mortality was evaluated during a short- (30 days), mid- (1 year) and long-term (4 years) period. Results No difference in the AKI rates using AKIpre and AKIadm (12.5% versus 12.2%; P = 0.695) or in the AKI severity (P = 0.261) was evident. Agreement between the two definitions was modest (Kappa-statistic = 0.596, P < 0.001). Patients with AKIpre or AKIadm had increased all-cause mortality compared with those without AKI during all follow-up periods. In fully adjusted regression analysis, AKIpre [hazard ratio (HR) = 2.226, 95% confidence interval (CI) 1.140–4.347; P = 0.027] and AKIadm (HR = 2.105, 95% CI 1.090–4.064; P = 0.027) remained associated with 30-day mortality. Results for the 1- and 4-year periods were similar. Increases of >4.00 μmol/L and >6.06% from pre-admission or >6.00 μmol/L and >17.24% from admission SCr levels presented increased mortality risk during follow-up. Conclusions Use of admission or pre-admission SCr provides similar incidence rates, but they diagnose different sets of patients. Even minor increases in SCr, below those required for the classification of AKI, were associated with increased mortality. These findings can help the clinicians to identify patients at higher risk for adverse outcomes. [ABSTRACT FROM AUTHOR]

Screening for occult coronary artery disease in potential kidney transplant recipients has become entrenched in current medical practice as the standard of care and is supported by national and international clinical guidelines. However, there is increasing and robust evidence that such an approach is out-dated, scientifically and conceptually flawed, ineffective, potentially directly harmful, discriminates against ethnic minorities and patients from more deprived socioeconomic backgrounds, and unfairly denies many patients access to potentially lifesaving and life-enhancing transplantation. Herein we review the available evidence in the light of recently published randomized controlled trials and major observational studies. We propose ways of moving the field forward to the overall benefit of patients with advanced kidney disease. [ABSTRACT FROM AUTHOR]

Background In the last few years, complex techniques and advanced equipment became available to treat chronically occluded coronary arteries. Such procedures portend a series of possible complications that operators should be ready to quickly recognize and deal with. Case summary A 75-year-old lady with uncontrolled stable angina underwent percutaneous treatment of a chronically occluded right coronary artery. After balloon angioplasty and stenting, she developed a severe hypotension, refractory to fluid resuscitation and vasopressors. Computerized tomography scan demonstrated an intramural haematoma (IMH) of the right atrioventricular groove resulting in life-threatening pseudotamponade (or dry tamponade), as further confirmed by cardiac magnetic resonance imaging (MRI). The decision was for conservative management and haemodynamic support by intra-aortic balloon pump. Clinically, the patient improved and was discharged a few days later. Follow-up MRI confirmed resolution of the IMH. Discussion Severe hypotension during percutaneous treatment of chronically occluded coronary arteries may be related to various causes. Differential diagnosis is thus important in this setting and should include IMH, a rare but potentially fatal complication as it may cause compression of cardiac chambers and lead to pseudotamponade. A high index of suspicion is required to diagnose IMH but there are no clear guidelines for management of such cases. [ABSTRACT FROM AUTHOR]

View large Download slide View large Download slide [ABSTRACT FROM AUTHOR]

Background. Arteriosclerosis is an independent predictor of increased cardiovascular mortality in chronic kidney disease (CKD). Histologically it is characterized by hypertrophy and fibrosis of the arterial media wall leading to increased arterial stiffness and end-organ damage. Caveolin-1 acts as an intracellular signalling pathway chaperone in human fibrotic and vascular diseases. The purpose of this study was to assess the association between caveolin-1 (CAV1) single-nucleotide polymorphism (SNP) rs4730751 and arterial stiffness as measured by arterial pulse wave velocity (PWV) in an early-stage CKD cohort and in a cohort with more severe CKD. Methods. Two prospectively maintained patient cohorts with non-dialysis CKD were studied: 144 patients in the Chronic Renal Impairment in Birmingham (CRIB) cohort and 147 patients in the Renal Impairment in Secondary Care (RIISC) cohort, with matched exclusion criteria and DNA sampling availability. At entry to each cohort database, each patient's initial arterial PWV was measured, as well as their anthropomorphic and biochemical data. CAV1 rs4730751 SNP genotyping was performed using Taqman technology. Results. The CAV1 rs4730751 SNP CC genotype was associated with lower arterial PWV in both CRIB early stage CKD patients [8.1 versus 8.6 m/s; coefficient -0.780 (-1.412, -0.149); P = 0.016] and RIISC more advanced stage CKD patients [8.7 versus 9.4 m/s; coefficient -0.695 (-1.288, -0.102); P = 0.022]; these relationships held following adjustment for other important confounders. Conclusions. This replicated study suggests potential utility of the studied CAV1 SNP as a genetic biomarker in CKD and a role for CAV1 in the development of arteriosclerosis in this setting. Further studies are warranted to further explore the basic science driving these clinical observations. [ABSTRACT FROM AUTHOR]

Phosphorus is an essential element for life but is a rare element in the universe. On Earth, it occurs mostly in the form of phosphates that are widespread but predominantly at very low concentration. This relative rarity has resulted in a survival advantage, in evolutionary terms, to organisms that conserve phosphate. When phosphate is made available in excess it becomes a cause for disease, perhaps best recognized as a potential cardiovascular and renal risk factor. As a reaction to the emerging public health issue caused by phosphate additives to food items, there have been calls for a public education programme and regulation to bring about a reduction of phosphate additives to food. During the Paleoproterzoic era, an increase in the bioavailability of phosphate is thought to have contributed significantly to the oxygenation of our atmosphere and a dramatic increase in the evolution of new species. Currently, phosphate is used poorly and often wasted with phosphate fertilizers washing this scarce commodity into water bodies causing eutrophication and algal blooms. Ironically, this is leading to the extinction of hundreds of species. The unchecked exploitation of phosphate rock, which is an increasingly rare natural resource, and our dependence on it for agriculture may lead to a strange situation in which phosphate might become a commodity to be fought over whilst at the same time, health and environmental experts are likely to recommend reductions in its use. [ABSTRACT FROM AUTHOR]

Background. The rate of decline in kidney function is a powerful predictor of cardiovascular risk in patients with chronic kidney disease (CKD). Serum phosphate and increased arterial stiffness are associated with elevated cardiovascular risk in CKD and the general population. We sought to determine whether serum phosphate and markers of arterial stiffness predict progression of renal dysfunction in patients with early CKD.Methods. Two hundred and twenty-five patients with Stage II–IV CKD were prospectively followed up at University Hospital Birmingham. Serum phosphate was measured at baseline and arterial stiffness was determined through measurement of aortic pulse wave velocity (PWV) and augmentation index (AIx). Progression of renal dysfunction was defined as the slope of estimated glomerular filtration rate (eGFR) against time. We determined the associations between possible predictors and rate of progression and also examined a combined end point of start of dialysis or ≥25% decline in eGFR.Results. Mean baseline eGFR was 43 ± 19 mL/min/1.73 m2 and serum phosphate 1.22 ± 0.27 mmol/L. Median follow-up was 924 days. Serum phosphate independently predicted a greater decline in eGFR; a 1 mmol/L increment in serum phosphate was associated with a 0.34 mL/min/month steeper decline (P = 0.02). Brachial and aortic systolic pressure independently predicted the rate of renal function decline but aortic PWV and AIx had no significant influence. Forty-one patients (18%) reached the combined end point; serum phosphate was significantly higher in this group (1.32 ± 0.36 versus 1.19 ± 0.24 mmol/L, P = 0.04) and was an independent predictor for the combined end point.Conclusions. Serum phosphate independently predicts decline in renal function in early CKD. Further studies are required to determine the mechanisms involved and to investigate the potential benefits of phosphate lowering on preserving kidney function. [ABSTRACT FROM AUTHOR]

Aims: The aim of this study was to assess the haemodynamic effects of tri-iodothyronine (T3) and methylprednisolone in potential heart donors. [ABSTRACT FROM PUBLISHER]