Background Acute kidney injury (AKI) is a recognised complication of coronavirus disease 2019 (COVID-19), yet the reported incidence varies widely and the associated risk factors are poorly understood. Methods Data was collected on all adult patients who returned a positive COVID-19 swab while hospitalised at a large UK teaching hospital between 1st March 2020 and 3rd June 2020. Patients were stratified into community- and hospital-acquired AKI based on the timing of AKI onset. Results Out of the 448 eligible patients with COVID-19, 118 (26.3 %) recorded an AKI during their admission. Significant independent risk factors for community-acquired AKI were chronic kidney disease (CKD), diabetes, clinical frailty score and admission C-reactive protein (CRP), systolic blood pressure and respiratory rate. Similar risk factors were significant for hospital-acquired AKI including CKD and trough systolic blood pressure, peak heart rate, peak CRP and trough lymphocytes during admission. In addition, invasive mechanical ventilation was the most significant risk factor for hospital-acquired AKI (adjusted odds ratio 9.1, p < 0.0001) while atrial fibrillation conferred a protective effect (adjusted odds ratio 0.29, p < 0.0209). Mortality was significantly higher for patients who had an AKI compared to those who didn’t have an AKI (54.3 % vs. 29.4 % respectively, p < 0.0001). On Cox regression, hospital-acquired AKI was significantly associated with mortality (adjusted hazard ratio 4.64, p < 0.0001) while community-acquired AKI was not. Conclusions AKI occurred in over a quarter of our hospitalised COVID-19 patients. Community- and hospital-acquired AKI have many shared risk factors which appear to converge on a pre-renal mechanism of injury. Hospital- but not community acquired AKI was a significant risk factor for death.

Background Obesity poses significant challenges to healthcare globally, particularly through its bi‐directional relationship with co‐morbid metabolic conditions such as type 2 diabetes and hypertension. There is also emerging evidence of an association between obesity and chronic kidney disease (CKD) which is less well characterized. Methods A literature search of electronic libraries was conducted to identify and present a narrative review of the interplay between obesity and CKD. Findings Obesity may predispose to CKD directly as it is linked to the histopathological finding of obesity‐related glomerulopathy and indirectly through its widely recognized complications such as atherosclerosis, hypertension, and type 2 diabetes. The biochemical and endocrine products of adipose tissue contribute to pathophysiological processes such as inflammation, oxidative stress, endothelial dysfunction, and proteinuria. The prevention and management of obesity may prove critical in counteracting both the development and advancement of CKD. Moreover, measures of abdominal adiposity such as waist circumference, are generally associated with worse morbidity and mortality in individuals receiving maintenance hemodialysis. Conclusion Obesity is a risk factor for the onset and progression of CKD and should be recognized as a potential target for a preventative public health approach to reduce CKD rates within the general population. Future research should focus on the use of glucagon‐like peptide‐1 receptor agonists and sodium–glucose cotransporter 2 inhibitors in patients with CKD and obesity due to their multi‐faceted actions on major outcomes.

Background Atherosclerotic renovascular disease (ARVD) often follows an asymptomatic chronic course which may be undetected for many years. However, there are certain critical acute presentations associated with ARVD and these require a high index of suspicion for underlying high-grade RAS (renal artery stenosis) to improve patient outcomes. These acute presentations, which include decompensated heart failure syndromes, accelerated hypertension, rapidly declining renal function, and acute kidney injury (AKI), are usually associated with bilateral high-grade RAS (> 70% stenosis), or high-grade RAS in a solitary functioning kidney in which case the contralateral kidney is supplied by a vessel demonstrating renal artery occlusion (RAO). These presentations are typically underrepresented in large, randomized control trials which to date have been largely negative in terms of the conferred benefit of revascularization. Case presentation Here we describe 9 individual patients with 3 classical presentations including accelerated phase hypertension, heart failure syndromes, AKI and a fourth category of patients who suffered recurrent presentations. We describe their response to renal revascularization. The predominant presentation was that consistent with ischaemic nephropathy all of whom had a positive outcome with revascularization. Conclusion A high index of suspicion is required for the diagnosis of RAS in these instances so that timely revascularization can be undertaken to restore or preserve renal function and reduce the incidence of hospital admissions for heart failure syndromes.

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Anti-glomerular basement membrane (anti-GBM) disease is a rare form of small-vessel vasculitis that typically causes rapidly progressive glomerulonephritis with or without alveolar haemorrhage. Previously, there has only been one reported case of tumour necrosis factor-α (TNF-α) antagonist-induced anti-GBM disease. Here, we describe the first reported case of etanercept-induced anti-GBM disease. A 55-year-old Caucasian man was referred to our tertiary specialist renal centre with a history of painless macroscopic haematuria. The patient has been receiving weekly etanercept injections over the past 12 months for psoriatic arthropathy. The serum immunology panel results highlighted a significantly raised anti-GBM titre (370.1 U). Etanercept was stopped, and the patient was empirically commenced on pulsed methylprednisolone, cyclophosphamide, and plasma exchange. A renal biopsy showed crescentic glomerulonephritis. Few days after admission, he tested positive for coronavirus disease 2019 (COVID-19), and a decision was made to withhold cyclophosphamide. There was further decline in renal function with hyperkalaemia for which he received 2 sessions of haemodialysis. He was restarted on cyclophosphamide upon discharge. The patient was switched to rituximab treatment afterwards as he developed leucopenia 2 weeks following the commencement of cyclophosphamide. The serum creatinine level continued to improve and remained dialysis-independent. In conclusion, with the increased use of etanercept and other TNF-α antagonists, the prescribing clinician must be aware of the rare but life-threatening drug-induced vasculitis. We recommend careful monitoring of renal indices with the use of this class of medications.

Background and Aims Obesity is a major issue with an estimated prevalence of 1.9 billion adults worldwide. Obesity is an important risk factor for premature death and the development of non-communicable diseases such as diabetes mellitus (DM), heart diseases, and chronic kidney disease (CKD). However, mounting evidence in the literature describes a reverse association whereby obesity may have a protective effect on mortality; this is sometimes referred to as the “obesity paradox”. Several reports question the concept of obesity paradox claiming methodology flaws such as collider stratification bias. In this study, we aimed to examine the effects of obesity on the combined outcomes of all-cause mortality (ACM) and renal replacement therapy (RRT) incidence in a cohort of patients with non-dialysis dependent CKD (NDD-CKD) by correcting for major risk factors to reduce the risk of bias. Method This retrospective study was undertaken on all patients with a documented body mass index (BMI) in the Salford Kidney Study database from October 2002 until December 2016. Patients were grouped according to their BMI into normal weight [BMI 18.5-24.9 kg/m2], overweight [BMI 25–29.9 kg/m2 and obese [BMI&gt; 30 kg/m2]. Patients were also grouped according to their level of co-morbidity into 4 groups: group 1 had CKD only; group 2 had CKD and heart failure (HF); group 3 had CKD and DM; and group 4 had CKD, DM, and HF. Univariate Cox regression as well as three stepwise models of multivariate analysis were performed to study the strength of association between BMI categories and combined outcomes (incidence of RRT and ACM) across the 4 groups of different clusters of co-morbidity. Results A total of 2416 patients were included in the analysis. The median age of the cohort was 67.3 years [IQR 55.9-75.6], 61.8% were male, and 96.4% were of white ethnicity. The median BMI was 28.1 kg/m2 [IQR 24.7-32.6] and the median estimated glomerular filtration rate (eGFR) was 30.7 ml/min/1.73m2 [IQR 20.4-43.5]. At baseline, patients with increasing level of co-morbidity tended to be older with higher prevalence of hypertension (HTN), angina, myocardial infarction (MI), and stroke with lower baseline eGFR. The risk of combined outcomes followed the same trend in the three BMI groups, risk is higher with higher index of co-morbidity (p &lt;0.001). Further analysis of four subgroups of co-morbidity was undertaken. A univariate Cox regression analysis for group 1 [CKD only, n = 1351], and group 2 [CKD and HF, n = 227] showed that patients with obesity had significant lower rates of combined outcomes compared to patients with normal BMI (HR 0.75; 95%CI = 0.63-0.89; p = 0.001 and HR 0.56; 95%CI = 0.38-0.82; p = 0.003 for group 1 and group 2 respectively). In multivariate models, obesity consistently proved to be a strong protective factor against combined outcomes (HR 0.77; 95%CI = 0.65-0.92; p = 0.005 for group 1 and HR 0.53; 95%CI = 0.34-0.83; p = 0.005 for group 2). This was independent of age, gender, HTN, angina, stroke, MI, and prescription of statins and angiotensin converting enzyme inhibitors. For group 3 [CKD and DM, n = 614], and group 4 [CKD, DM, and HF, n = 190], there was no significant difference in the combined outcomes between the different BMI groups when using univariate Cox regression analysis (for patients with obesity: HR 0.78; 95%CI = 0.61-1.01; p = 0.060 and HR 0.70; 95%CI = 0.43-1.16; p = 0.166 for both groups respectively). There was no significant difference in the incidence of RRT in any of the four groups. Conclusion In our largely white NDD-CKD cohort of patients, there was evidence of increasing risk of RRT or ACM as comorbidity increased irrespective of BMI. This is not surprising as ACM would be expected to increase as the burden of disease increases. However, when comparing the effect of BMI within groups, obesity was protective against combined outcomes in group 1 (CKD only) and group 2 (CKD+HF). This ‘protective’ effect was not seen in patients who had concomitant diabetes. These data suggest that diabetes is a potent predictor of outcomes irrespective of BMI, however, in patients without diabetes, obesity may play a protective role.

Background and Aims Infective endocarditis (IE) is a serious infective complication that usually results in prolonged hospitalisation and is associated with high morbidity and mortality. It is sometimes difficult to promptly diagnose infective endocarditis when a patient receiving hemodialysis presents with signs and symptoms of bacteremia, a delay which can lead to worse outcomes. In this study, we aimed to identify the risk factors that can predict infective endocarditis in haemodialysis patients with bacteremia. Method This retrospective observational study was conducted on all patients diagnosed with infective endocarditis (IE) and receiving maintenance hemodialysis between 2005 and 2018 in Salford Royal Hospital and its satellite dialysis units (catchment population of 1.5 million). The IE patients were propensity score matched in a 1:2 ratio with similar hemodialysis patients without IE but with bacteremia between 2011 and 2015. Propensity scores were generated by using binary logistic regression analysis incorporating age, gender, diabetes status, and dialysis vintage as variables. Logistic regression analysis was used to predict the risk factors associated with developing IE. Statistics were performed using SPSS version-24. Results We had a sample of 105 patients (35 IE vs 70 bacteremia). The median age of the patients was 65 years with a predominance of males (60%). 43% were diabetic, 11.5% were receiving immunosuppression and 72% had a catheter for dialysis access. IE patients had higher peak C-reactive protein (CRP) during admission compared to patients with bacteremia and no IE (253 mg/l vs 152 mg/l, p=0.001). Patients who developed IE had a longer duration of dialysis catheter use than the bacteremia group (150 vs 19 days; p&lt;0.001) (table 1). There was no significant difference between causative microorganisms in both groups. Staphylococcus aureus caused most cases (54% in IE and 47% in bacteremia). Our study showed clearly that patients who had IE had longer hospital stay (45 vs 18 days, p=0.001) with a far higher 30-day mortality rate (54.3% vs 17.1%, p&lt;0.001). Logistic regression analysis showed previous valvular heart diseases (OR: 20.1; p&lt;0.001), a higher peak CRP (OR:1.01; p=0.001), and a longer duration of catheter use (OR: 1.01; p=0.035) as significant predictors for infective endocarditis (table 2). Conclusion Bacteremia in patients receiving hemodialysis through a catheter as access should be actively investigated with a high index of suspicion for IE particularly those having valvular heart diseases, hypertension, higher peak CRP, and those with a longer duration of dialysis catheter usage. Work up may need to include invasive investigations such as transesophageal echocardiogram to confirm or reliably rule out this devastating condition.

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