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Heart ◽  
2021 ◽  
pp. heartjnl-2021-320047
Author(s):  
Tom Norris ◽  
Cameron Razieh ◽  
Francesco Zaccardi ◽  
Thomas Yates ◽  
Nazrul Islam ◽  
...  

ObjectiveUsing a large national database of people hospitalised with COVID-19, we investigated the contribution of cardio-metabolic conditions, multi-morbidity and ethnicity on the risk of in-hospital cardiovascular complications and death.MethodsA multicentre, prospective cohort study in 302 UK healthcare facilities of adults hospitalised with COVID-19 between 6 February 2020 and 16 March 2021. Logistic models were used to explore associations between baseline patient ethnicity, cardiometabolic conditions and multimorbidity (0, 1, 2, >2 conditions), and in-hospital cardiovascular complications (heart failure, arrhythmia, cardiac ischaemia, cardiac arrest, coagulation complications, stroke), renal injury and death.ResultsOf 65 624 patients hospitalised with COVID-19, 44 598 (68.0%) reported at least one cardiometabolic condition on admission. Cardiovascular/renal complications or death occurred in 24 609 (38.0%) patients. Baseline cardiometabolic conditions were independently associated with increased odds of in-hospital complications and this risk increased in the presence of cardiometabolic multimorbidity. For example, compared with having no cardiometabolic conditions, 1, 2 or ≥3 conditions was associated with 1.46 (95% CI 1.39 to 1.54), 2.04 (95% CI 1.93 to 2.15) and 3.10 (95% CI 2.92 to 3.29) times higher odds of any cardiovascular/renal complication, respectively. A similar pattern was observed for all-cause death. Compared with the white group, the South Asian (OR 1.19, 95% CI 1.10 to 1.29) and black (OR 1.53 to 95% CI 1.37 to 1.72) ethnic groups had higher risk of any cardiovascular/renal complication.ConclusionsIn hospitalised patients with COVID-19, cardiovascular complications or death impacts just under half of all patients, with the highest risk in those of South Asian or Black ethnicity and in patients with cardiometabolic multimorbidity.


2021 ◽  
Vol 12 ◽  
Author(s):  
Kirsty Crowe ◽  
Terence J. Quinn ◽  
Patrick B. Mark ◽  
Mark D. Findlay

Cognitive impairment is independently associated with kidney disease and increases in prevalence with declining kidney function. At the stage where kidney replacement therapy is required, with dialysis or transplantation, cognitive impairment is up to three times more common, and can present at a younger age. This is not a new phenomenon. The cognitive interactions of kidney disease are long recognized from historical accounts of uremic encephalopathy and so-called “dialysis dementia” to the more recent recognition of cognitive impairment in those undergoing kidney replacement therapy (KRT). The understanding of cognitive impairment as an extra-renal complication of kidney failure and effect of its treatments is a rapidly developing area of renal medicine. Multiple proposed mechanisms contribute to this burden. Advanced vascular aging, significant multi-morbidity, mood disorders, and sleep dysregulation are common in addition to the disease-specific effects of uremic toxins, chronic inflammation, and the effect of dialysis itself. The impact of cognitive impairment on people living with kidney disease is vast ranging from increased hospitalization and mortality to decreased quality of life and altered decision making. Assessment of cognition in patients attending for renal care could have benefits. However, in the context of a busy clinical service, a pragmatic approach to assessing cognitive function is necessary and requires consideration of the purpose of testing and resources available. Limited evidence exists to support treatments to mitigate the degree of cognitive impairment observed, but promising interventions include physical or cognitive exercise, alteration to the dialysis treatment and kidney transplantation. In this review we present the history of cognitive impairment in those with kidney failure, and the current understanding of the mechanisms, effects, and implications of impaired cognition. We provide a practical approach to clinical assessment and discuss evidence-supported treatments and future directions in this ever-expanding area which is pivotal to our patients' quality and quantity of life.


QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Ahmed Refaat Mohamed Refaat ◽  
Gamal Samy ◽  
Faisal Morad ◽  
Nabil Abd Gawad

Abstract Background ​ In the era of minimal invasive cardiac surgery, Ministernotomy Aortic valve .replacement have been proposed as an alternative to conventional full sternotomy approach Aim of the Work ​: ​​To evaluate the safety and efficacy of AVR through ministernotomy in comparison to full sternotomy AVR in terms of Cardiac cause mortality, Neurological and .Renal complication​s Patients and Methods ​After gaining the institutional ethical committee approval, the study included all patients who underwent isolated, DE novo, open aortic valve replacement during the period from June 2017 till June 2019 performed by multiple surgeons at cardiothoracic .academy Ain Shams University Results ​ The study included 60 patients; 32 patients performed through full sternotomy (53.3%) and 28 patients through ministernotomy (46.6%).​ ​Post-operative arrhythmias occurred in full sternotomy in 6 cases (18.8%) where in mini-sternotomy, only 3 cases (12%) developed arrhythmias with no significant statistical difference (p value = ​0.558)​. Cerebrovascular stroke was recorded 1 patient (3%) versus 4 cases (14.3%) in the full sternotomy versus the ministernotomy groups respectively with no Statistical difference between the 2 groups (p value = 0.119).​ Postoperative acute renal impairment was recorded​ in 3 cases (9.4%) vs 2 patients (7.1%) in the full sternotomy vs the ministernotomy groups respectively (p value = 0.755). There was no​ mortality in either groups. Mean post-operative Ventilation hours were 17.21hrs with SD ± 11.026 versus 14.97hrs with SD ​± ​6.473 (p value is 0.35) for the full sternotomy versus the ministernotomy groups respectively. Mean blood loss was 305.51ml with SD ± 282.662 versus 230.36ml with SD ​± ​247.708 (p value is 0.277) for the full versus the ministernotomy groups respectively. Mean units of blood transfused was 2.31Units with SD ​± ​0.926 versus 1.14Units with SD ​±​ 0.591 in the full sternotomy versus the ministernotomy groups with high statistical significance between both groups (p value less than 0.01). Mean ICU stay was 2.66 days with SD ​±​ 0.915 and was 3.1days with SD ​±​ 2.743 (p .value is 0.424) for the full sternotomy versus the ministernotomy groups respectively Conclusion ​ Ministernotomy Aortic valve replacement was found to be a safe procedure​ compared to full sternotomy approach. Patients who had their surgery through the mini approach had less amount of blood loss, blood transfusion requirements, ventilation time which all led to less duration of ICU and hospital stay, resulting in a better outcome for the .patients


2021 ◽  
Vol 47 (1) ◽  
Author(s):  
Luisa Santangelo ◽  
Giuseppe Stefano Netti ◽  
Diletta Domenica Torres ◽  
Giovanni Piscopo ◽  
Vincenza Carbone ◽  
...  

Abstract Background The Neurological involvement is the most common extra-renal complication of Shiga toxin-producing E. coli-hemolytic uremic syndrome (HUS) or typical HUS. On brain magnetic resonance examination, main neurological signs encompass acute lesions of the basal ganglia and the white matter, which could usually regress after Eculizumab infusion. In contrast, peripheral nervous system (PNS) manifestations in typical HUS are very rare and, when occurring, they require a careful management of neurological sequelae and an intensive multidisciplinary neuro-rehabilitation program. Case presentation Here, we present two pediatric cases of severe and complicated typical HUS with PNS manifestations who required therapeutic treatment and an intensive multidisciplinary neuro-rehabilitation program. In both cases, PNS manifestations were followed by the recovery from typical HUS-related severe central neurological damage and manifested mainly with marked bilateral motor deficit and hyporeflexia/areflexia in the lower limbs. The peripheral polyneuropathy was treated with immunosuppressive therapy (methylprednisolone boluses, i.v. immunoglobulins, plasma exchange), followed by a prolonged intensive neuro-rehabilitation program. After 8 months of rehabilitation, both patients gained complete functional recovery. Conclusions PNS manifestations during typical HUS are a rare event and potentially leading to severe disability. A timely clinical assessment is mandatory to set up a prompt therapeutic and rehabilitation program and to obtain a complete clinical and functional recovery.


2021 ◽  
pp. ASN.2020111579
Author(s):  
Theresa Wewers ◽  
Annika Schulz ◽  
Ingo Nolte ◽  
Hermann Pavenstaedt ◽  
Marcus Brand ◽  
...  

Soluble Fms-like tyrosine kinase (sFlt-1/sVEGFR1) is a natural occurring antagonist of vascular endothelial growth factor (VEGF). Despite being a secreted, soluble protein lacking cytoplasmic and transmembrane domains, sFlt-1 can act locally and be protective against excessive microenvironmental VEGF concentration, or exert autocrine functions independently of VEGF. Circulating sFlt-1 may indiscriminately affect endothelial function and the microvasculature on distant target organs. The clinical significance of excess sFlt-1 in kidney disease was first shown in preeclampsia, a major renal complication of pregnancy. However, circulating sFlt-1 levels appear to be increased in different diseases with varying degrees of renal impairment. Relevant clinical associations between circulating sFlt-1 and severe outcomes (e.g., endothelial dysfunction, renal impairment, cardiovascular disease, and all-cause mortality) have been observed in patients with chronic kidney disease and following kidney transplantation. However, sFlt-1 appears to be protective against renal dysfunction-associated aggravation of atherosclerosis and diabetic nephropathy. Therefore, in this review, we provide an update on sFlt-1 in several kidney diseases other than preeclampsia, discuss clinical findings and experimental studies, and briefly consider its use in clinical practice.


2021 ◽  
Author(s):  
Luisa Santangelo ◽  
Giuseppe Stefano Netti ◽  
Diletta Domenica Torres ◽  
Giovanni Piscopo ◽  
Vincenza Carbone ◽  
...  

Abstract Background. The Neurological involvement is the most common extra-renal complication of Shiga toxin-producing Escherichia coli-hemolytic uremic syndrome (STEC-HUS). On brain magnetic resonance examination, main neurological signs encompass acute lesions of the basal ganglia and the white matter, which could usually regress after Eculizumab infusion. In contrast, STEC-HUS-related peripheral nervous system (PNS) involvement is very rare and, when occurring, it requires a careful management of neurological sequelae and an intensive multidisciplinary neuro-rehabilitation program.Case presentation. Here, we present two cases of severe and complicated STEC-HUS patients with PNS-involvement who successfully required therapeutic treatment and an intensive multidisciplinary neuro-rehabilitation program.In both cases, PNS-involvement followed the recovery from STEC-HUS-related severe central neurological damage and manifested mainly with marked bilateral motor deficit and hyporeflexia/areflexia in the lower limbs. The peripheral polyneuropathy was treated with immune-suppressive therapy (methylprednisolone pulses, i.v. immunoglobulins, therapeutic plasma exchange), followed by a prolonged intensive neuro-rehabilitation program. After 8 months of neuro-rehabilitation, both patients gained complete functional recovery.Conclusions. PNS involvement during STEC-HUS is a rare event and potentially leading to severe disability. A timely clinical assessment is mandatory to set up a prompt therapeutic and neuro-rehabilitation program and to obtain a complete clinical and functional recovery.


Rheumatology ◽  
2020 ◽  
Author(s):  
Maurizio Bruschi ◽  
Gabriella Moroni ◽  
Renato Alberto Sinico ◽  
Franco Franceschini ◽  
Micaela  Fredi ◽  
...  

Abstract Objectives Serum anti-dsDNA and anti-nucleosome IgGs have been proposed as signatures for SLE and LN in limited numbers of patients. We sought to show higher sensitivity and specificity of the same antibodies with the IgG2 isotype and included IgG2 antibodies vs specific intracellular antigens in the analysis. Methods A total of 1052 SLE patients with (n = 479) and without (n = 573) LN, recruited at different times from the beginning of symptoms, were included in the study. Patients with primary APS (PAPS, n = 24), RA (RA, n = 24) and UCTD (UCTD, n = 96) were analysed for comparison. Anti-nucleosome (dsDNA, Histone2A, Histone3), anti-intracellular antigens (ENO1), anti-annexin A1 and anti-C1q IgG2 were determined by non-commercial techniques. Results The presence in the serum of the IgG2 panel was highly discriminatory for SLE/LN vs healthy subjects. Serum levels of anti-dsDNA and anti-C1q IgG2 were more sensitive than those of IgGs (Farr radioimmunoassay/commercial assays) in identifying SLE patients at low–medium increments. Of more importance, serum positivity for anti-ENO1 and anti-H2A IgG2 discriminated between LN and SLE (ROC T0–12 months), and high levels at T0–1 month were detected in 63% and 67%, respectively, of LN, vs 3% and 3%, respectively, of SLE patients; serum positivity for each of these was correlated with high SLEDAI values. Minor differences existed between LN/SLE and the other rheumatologic conditions. Conclusion Nephritogenic IgG2 antibodies represent a specific signature of SLE/LN, with a few overlaps with other rheumatologic conditions. High levels of anti-ENO1 and anti-H2A IgG2 correlated with SLE activity indexes and were discriminatory between SLE patients limited to the renal complication and other SLE patients. Trial registration The Zeus study was registered at https://clinicaltrials.gov, NCT02403115.


2020 ◽  
Author(s):  
Mònica Pérez-Mir ◽  
Laura Carreras-Planella ◽  
Francesc Borràs ◽  
Josep Bonet ◽  
Maribel Troya

Abstract Background: Autosomal dominant polycystic kidney disease (ADPKD) is a renal inherited disease characterized by the growth of bilateral renal cysts that lead to deterioration in renal function and end-stage renal disease (ESRD). These patients frequently present complications like urinary tract infection, acute pyelonephritis, acute or chronic pain, renal lithiasis or high blood pressure (HBP). The aim of this study is to compare the renal evolution in ADPKD patients with renal complications and/or HBP compared to those without complications nor HBP.Methods: Observational retrospective study of 29 ADPKD patients with normal renal function and <70 years followed up in our center. Clinical and analytical information of 2010, 2015 and 2017 were determined.Results: 29 patients were enrolled with a median age of 41 years [34-54], eighteen women (62,1%) and eleven men. Median of estimation of glomerular function rate (eGFR) was 85.8ml/min [70.7-115.6] in 2010, 76.0 ml/min [57.0-99.9] in 2015 and 63.1ml/min [45.0-95.8] in 2017. Eight patients (27.6%) have never had kidney complication nor HBP. Nine patients (31.0%) have normal blood pressure, 6 others (20.7%) have well controlled high blood pressure (HBP) and 14 (48.3%) have badly controlled HBP. When patients were divided between those who have never presented a complication (C-) and those who present renal complication and/or HBP (C+), the first group presented better kidney function. When patients were segregated into those who have never presented complication or well-controlled HBP (CHBP-) and those with renal complication and/or badly-controlled HBP (CHBP+) no differences were found at the initial eGFR, but a faster worsening of kidney function in CHBP+ group.Conclusions: In ADPKD patients, the decrease in eGFR is significantly important in individuals showing complications (including HBP) compared to those who did not present complications. Individuals with complications and badly-controlled HBP show even greater differences in kidney function decrease compared with patients without complications or well controlled HBP.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
MAROUA BAAZIZ ◽  
Eric Thervet ◽  
Dominique Nochy ◽  
KARRAS Alexandre

Abstract Background and Aims Antineutrophil cytoplasmic antibody (ANCA) associated vasculitis (AAV) is a systemic disease characterized by inflammation of small vessels and presence of ANCA. Pauci-immune necrotizing crescentic glomerulonephritis is a severe renal complication of AAV. Despite immunosuppressive therapy, relapses are frequent during the course of the disease, affecting up to 50% of the patients. Kidney biopsy is routinely used to diagnose AAV at initial presentation and to predict renal prognosis. Although the activity of renal AAV is not easily evaluated by plasma or urine biomarkers, kidney biopsy is rarely performed when relapse is suspected. We herein analyze the clinical, laboratory and renal pathology data from patients who underwent repeated kidney biopsies during the course of AAV. Method We retrospectively reviewed data from 37 patients who underwent at least 2 kidney biopsies in our centre, between 2002 and 2018. The first renal biopsy (B1) was constantly performed at diagnosis. A follow-up biopsy (B2) was performed for purpose, either for suspicion of refractory disease or confirmation of renal relapse. Modifications of renal pathology between B1 and B2 were studied, by comparing presence of active and chronic lesions. Active lesions were defined by the presence of cellular crescents and/or fibrinoid necrosis. Chronic lesions were quantified by the percentage of globally sclerotic glomeruli and the percentage of interstitial fibrosis / tubular atrophy (IF/TA). Results Median age at diagnosis was 57 years, M/F ratio was 21/16. ANCA specificity was anti-MPO in 65% of cases, anti-PR3 in 32%. The median delay between B1 and B2 was 3,3 [0,9-5,8] years. B2 was done for suspicion of refractory disease (n=8) or of renal relapse (n=29). Causes of B2 were : persistence or reappearance of haematuria in 78% of cases, increase of creatinine in 43%, increase of ANCA titer in 67%. Systemic AAV activity was more important at B1 vs B2 (median BVAS 18 vs 9), as well as renal dysfunction (median sCreat 200 vs 156 μmol/l). Active glomerulonephritis was constantly found at B1 but was present in only 35% of B2. Presence of cellular crescents decreased from 71,4 to 29,7% (p = 0,002), whereas fibrinoid necrosis decreased from 80,6 to 35,1% (p = 0.0003). Five factors were significantly associated with the presence of active lesions : presence of at least one extra-renal AAV manifestation (p = 0.0006), increase of ANCA titer (p = 0.0022), CRP&gt;30mg/l (p = 0.001), absence of IF/TA (p=0,02) and high percentage of normal glomeruli (p=0,014) at B1. Interestingly, level of proteinuria and persistence of hematuria were not associated with histological activity at B2 (p =0,64 and 0,22 respectively). In contrast, chronic lesions such as glomerulosclerosis and IF/TA were more severe at B2 compared to B1 (p &lt;0,0001 and 0,014 respectively). The worsening of fibrotic lesions was not associated with ANCA specificity (anti-MPO vs -PR3). Conclusion This is the largest cohort reporting on repeated renal biopsy in AAV. Despite several clinical and laboratory signs suggesting active renal AAV, B2 revealed no relapse in 2/3 of cases, allowing avoidance of a new immunosuppressive induction treatment. Our results suggest that rebiopsy is crucial when renal relapse is suspected, as proteinuria and hematuria do not predict active disease, suggesting that their persistence could be explained by glomerular scarring.


2020 ◽  
Vol 21 (1) ◽  
pp. 44-56
Author(s):  
Warissara Jutidamrongphan ◽  
Pimporn Puttawibul

Crizotinib is one of the first generations of tyrosine kinase inhibitors targeting anaplastic lymphoma kinase(ALK) and is recently found to be associated with the development of complex renal cysts with inconclusive explanation up to this time. Hereby, we discuss the hypothesis of Crizotinib-associated complex renal cyst development and coexisting renal impairment after initiation of the treatment in a 75-year-old man with ALK-positive non-small cell lung cancer whose complex renal cysts evolved after initiation and cessation of Crizotinib treatment. The coexistence as renal impairment persisted even after switching from Crizotinib to Ceritinib.


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