Notes

Any likelihood-based deconvolution regarding mass gene appearance info making use of single-cell personal references.
The association of phenylacetylglutamine with shortness of breath was consistent in both sexes, although it only reached statistical significance in the full population. In contrast, TMAO (fatigue) and PCS and phenylacetylglutamine (constipation) were only associated with symptoms in men, who presented higher serum levels than women.

Only a limited number of toxins were associated with symptoms in persons with stage 4/5 CKD. Other uremic toxins, uremia-related factors or psychosocial factors not yet explored might contribute to symptom burden.
Only a limited number of toxins were associated with symptoms in persons with stage 4/5 CKD. Other uremic toxins, uremia-related factors or psychosocial factors not yet explored might contribute to symptom burden.The association between cardiovascular (CV) disease and anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is well documented. The recent work by Massicotte-Azarniouch et al. confirms the risk and adds to the existing evidence by describing the highest risk in the first 3 months after diagnosis. In this review, we aim to put their findings into perspective and formulate implications for the care of AAV patients. We discuss mechanisms for increased CV disease in AAV, including the impact of traditional risk factors and disease-related risks such as renal impairment and anti-myeloperoxidase (MPO) ANCA serotype. We also provide a brief primer on the impact of inflammatory-driven endothelial dysfunction and platelet activation on accelerated atherosclerosis in AAV patients. These features alongside the impact of disease activity and systemic inflammation provide potential explanations to why the incidence of CV events is highest in the first 3 months from diagnosis. We suggest future avenues of research, provide some suggestions to address and treat CV risk based on current evidence, and highlight the importance of addressing this topic early on. Addressing modifiable risk factors, dialogue with patients, patient information and a structured approach overall will be key to improve CV outcomes in AAV.Albumin is the most abundant protein in blood plasma and acts as a carrier for many circulating molecules. Hypoalbuminaemia, mostly caused by either renal or liver disease or malnutrition, can perturb vascular homeostasis and is involved in the development of multiple diseases. Here we review four functions of albumin and the consequences of hypoalbuminaemia on vascular homeostasis. (i) Albumin is the main determinant of plasma colloid osmotic pressure. Hypoalbuminaemia was therefore thought to be the main mechanism for oedema in nephrotic syndrome (NS), however, experimental studies showed that intrarenal mechanisms rather than hypoalbuminaemia determine formation and, in particular, maintenance of oedema. (ii) Albumin functions as an interface between lysophosphatidylcholine (LPC) and circulating factors (lipoproteins and erythrocytes) and the endothelium. Consequently, hypoalbuminaemia results in higher LPC levels in lipoproteins and erythrocyte membrane, thereby increasing atherosclerotic properties of low-density lipoprotein and blood viscosity, respectively. Furthermore, albumin dose-dependently restores LPC-induced inhibition of vasodilation. (iii) Hypoalbuminaemia impacts on vascular nitric oxide (NO) signalling by directly increasing NO production in endothelial cells, leading to reduced NO sensitivity of vascular smooth muscle cells. (iv) Lastly, albumin binds free fatty acids (FFAs). FFAs can induce vascular smooth muscle cell apoptosis, uncouple endothelial NO synthase and decrease endothelium-dependent vasodilation. Unbound FFAs can increase the formation of reactive oxygen species by mitochondrial uncoupling in multiple cell types and induce hypertriglyceridemia in NS. In conclusion, albumin acts as an interface in the circulation and hypoalbuminaemia impairs multiple aspects of vascular function that may underlie the association of hypoalbuminaemia with adverse outcomes. However, hypoalbuminaemia is not a key to oedema in NS. These insights have therapeutic implications.Monogenic causes of paediatric nephrocalcinosis are associated with extensive phenotypic variability. We report a 14-year-old male who presented at 8 years of age with incidentally identified nephrocalcinosis alongside growth impairment and dental anomalies. Extensive genetic investigation confirmed a molecular diagnosis of Bartter syndrome type II. This is exceptional in both late presentation and the presence of amelogenesis imperfecta, a very rare association of inherited tubulopathies. Details of the nephrocalcinosis gene panel analysed and associated phenotypes are presented to highlight the utility of a phenotype-driven genetic panel in resolving an atypical presentation of nephrocalcinosis, allowing precise diagnosis, tailored therapy and prognostication.
With the ageing population and changes in the indications of diagnostic and protocol biopsies in systemic lupus erythematosus in recent years, an impact on the incidence and presentation of lupus nephritis (LN) is expected. The aim of this study was to analyse the epidemiological changes regarding clinical and histological presentation of LN in kidney biopsies performed from 1994 to 2019 included in the Spanish Registry of Glomerulonephritis.

We analysed data from 28791 kidney biopsies from 130 Spanish hospitals comparing demographic, clinical and histological data. check details We divided the cohort according to the age of onset of LN into pediatric onset (<18 years), adult onset (18-50 years) and late onset (>50 years).

The incidence of LN has decreased from 9.6% of all kidney biopsies in the period 1994-2013 to 7% in the last quarter of the observation period (2014-2019) (P<0.001), despite an increase in the proportion of patients with LN that underwent repeat biopsies (16.6-24%; P<0.001). The age of onset of LN has increased from 32±14to 38±14years (P<0.001), with an increase in the proportion of late-onset LN (from 13% to 22% of incident LN; P<0.001). There were no differences in the distribution of histological features at presentation over the study period. Patients with late-onset LN showed fewer gender differences, had lower GFR and presented with less-proliferative forms of LN compared with early-onset LN.

The frequency of biopsy-proven LN has been decreasing in recent years, despite an increasing number of repeat biopsies. Late-onset LN is increasing, presenting with worse kidney function but fewer proliferative lesions compared with younger-onset LN.
The frequency of biopsy-proven LN has been decreasing in recent years, despite an increasing number of repeat biopsies. Late-onset LN is increasing, presenting with worse kidney function but fewer proliferative lesions compared with younger-onset LN.Calciphylaxis is a rare disorder characterized by vascular calcification and thrombosis of the subcutaneous microcirculation, leading to painful necrotic skin lesions and bearing a dreadfully high mortality rate. This syndrome is frequently also termed uraemic calcific arteriolopathy, since most cases are observed in patients with kidney failure. However, it is increasingly clear that calciphylaxis may also affect patients with normal or only slightly impaired renal function, including kidney transplant recipients. A precise definition of the characteristics and risk factors of calciphylaxis developing after kidney transplantation has been hindered by the extreme rarity of this condition, which also hampered the development of effective therapeutic strategies. In the present issue of CKJ, Guillén and colleagues report the largest case series of calciphylaxis in kidney transplant recipients to date, outlining several features that are apparently specific to this population. In this editorial, we briefly present the epidemiology and pathogenesis of calciphylaxis in different patient populations and discuss recent findings for its therapeutic management.
Patients receiving dialysis for end-stage kidney disease (ESKD) commonly co-exhibit risk factors for hepatic impairment. This systematic review and meta-analysis aimed to quantify the coexistence of chronic liver disease (CLD) and characterize risk factors and outcomes.

We searched the following databases from inception to May 2021 CINAHL, Cochrane Library, Embase, Kings Fund Library, MEDLINE and PubMed. The protocol was pre-registered on PROSPERO (study ID CRD42020206486). Studies were assessed against three inclusion criteria adults (>18 years) with ESKD receiving dialysis, primary outcome involving CLD prevalence and publications in English. Moderator analysis was performed for age, gender, study size and publication year. Sensitivity analysis was performed where applicable by removing outlier results and studies at high risk of bias.

Searches yielded 7195 articles; of these 15 met the inclusion criteria. A total of 320 777 patients were included. The prevalence of cirrhosis and non-alcoholic fatty liver disease (NAFLD) was 5% and 55%, respectively. Individuals with CLD had 2-fold higher mortality than those without odds ratio [OR] 2.19 [95% confidence interval (CI) 1.39-3.45]. Hepatitis B [OR 13.47 (95% CI 1.37-132.55)] and hepatitis C [OR 7.05 (95% CI 4.00-12.45)], but not diabetes, conferred increased cirrhosis risk. All studies examining NAFLD were judged to be at high risk of bias. We found no data on non-alcoholic steatohepatitis (NASH). Deaths from CLD, cancer and infection were greater among cirrhotic patients.

CLD is prevalent in dialysis patients. Hepatitis B and C confer increased risk of CLD. The impact of NAFLD and NASH cirrhosis requires further study. CLD is associated with an increased risk of mortality in this setting.
CLD is prevalent in dialysis patients. Hepatitis B and C confer increased risk of CLD. The impact of NAFLD and NASH cirrhosis requires further study. CLD is associated with an increased risk of mortality in this setting.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.
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