For patients with chronic kidney disease (CKD) and atrial fibrillation, treatment with a direct oral anticoagulant (DOAC) provides similar protection against stroke as warfarin, but poses a higher risk of bleeding, according to results of an observational study.
Reuters Health Information

Multiple studies show that dietary supplements result in little more than expensive urine and in some cases may even cause harm. Melissa Walton-Shirley thinks it's high time they were better regulated.
theheart.org on Medscape

Hope that observed renoprotective effects of SGLT2 inhibitors will delay worsening of kidney disease in type 2 diabetes seems to be borne out, as the CREDENCE trial is stopped early.
Medscape Medical News

Guidelines were meant to make treatment decisions easier and more evidence-based, but it hasn't quite worked out that way, says Dr Lundberg.
Medscape Internal Medicine

Mandrola and Prasad fear that a study showing high cost of care at end of life but little ability to predict who will die will be misinterpreted and worsen the crisis of end-of-life care.
Medscape

Background: Pyrrolidine dithiocarbamate (PDTC) reduces renal cyst growth in a rodent model of polycystic kidney disease (PKD) but the mechanism of action is not clear. Here, we investigated the hypothesis that PDTC reduces the proliferation of cystic epithelial cells in vitro in a nuclear factor (NF)-κB-dependent manner. Methods: Immortalized autosomal dominant PKD (ADPKD) cells that are heterozygous (WT9-7) and homozygous (WT-9-12) for a truncating Pkd1 mutation, and immortalized normal human tubular cells (HK-2), were exposed to NF-κB-inducing agents with or without PDTC. Cell proliferation and apoptosis were assessed by bromodeoxyuridine assay and Annexin V flow cytometry, respectively. NF-κB activity was assessed by luciferase reporter assay and western blotting for nuclear p65, p50, and RelB subunits and cytoplasmic phosphorylated-IκBα. Results: Serum-induced proliferation was similar in all cell lines over 72 h. PDTC demonstrated anti-proliferative effects that were delayed in ADPKD cells compared to HK-2. Basal NF-κB-dependent luciferase reporter activity was lower in ADPKD cells compared to normal cells. Classical NF-κB stimulants, lipopolysaccharide (LPS) and tumor necrosis factor (TNF)-α, increased NF-κB luciferase activity in HK-2, whereas in PKD cell lines, NF-κB activity was only induced by TNF-α. However, neither stimulant altered proliferation in any cell line. PDTC reduced TNF-α-stimulated NF-κB activity in HK-2 only. Conclusions: PDTC reduced proliferation in ADPKD cells but did not consistently alter NF-κB activation, suggesting that other signalling pathways are likely to be involved in its ability to attenuate renal cyst growth in vivo.

Background: Reports on the histopathology of childhood nephrotic syndrome (NS) had emanated from our Centre since the 1960s and by the late 1980s and early 1990s, a change was observed and reported. Taking into consideration the worldwide changing trend in the histopathology of the NS and our Unit policy change in the indications for renal biopsy, a change was envisaged. We therefore evaluated the current histologic pattern of childhood NS in Ibadan with the view to highlighting any variations from the past and comparing the findings with regional and global trends.MethodologyWe reviewed our database and analyzed the renal biopsy findings in patients who were biopsied before treatment was administered between 1997 and 2001 and those with mostly idiopathic steroid resistant NS (SRNS) and secondary NS, managed between 2006 and 2013. A comparative analysis of the findings from the present study was carried out with two previous reports from our Unit in the 1970s and early 1990s and also with reports from other Centres. Results: A total of 78 patients had successful biopsies done during the study period in children aged between 2 ½ and 16 years. In both pre-treatment biopsy era (1997–2001) and post-treatment biopsy era (2006–2013), focal segmental glomerulosclerosis (FSGS) predominated. 75 % of the patients had idiopathic NS and among the patients that had idiopathic steroid resistant NS, FSGS was the most common followed by MPGN. For secondary NS, MCD was the most common but could be the early stages of either membranous nephropathy (MN) or FSGS. Chronic pyelonephritis and chronic interstitial nephritis occurred in 25 % of the study population but they were more prevalent in secondary nephrotic syndrome. Conclusion: FSGS is the most common histopathology in children requiring renal biopsy in Ibadan presently. FSGS is also the most common histopathology in idiopathic SRNS, which is in keeping with reports from most parts of the world.There has been a transition from the preponderance of Quartan Malarial Nephropathy (QMN) in the 1960s to MPGN in the 1980s to FSGS presently. This has great implications with regards to searching for new aetiologic factors, providing more efficacious treatment modalities and ensuring facilities for immunofluorescence, electron microscopic and genetic studies.

Background: The role of uric acid in development of renal dysfunction (RD) remains controversial. Earlier studies have reported inconsistent results, possibly because of their varying ability to adjust for confounding. The impact of longitudinal change in uric acid on renal outcome has not been assessed previously. We aimed to study the impact of change in serum uric acid (SUA) as well as baseline SUA on the development of RD. Methods: In a prospective cohort study, we assessed the associations between change in SUA during follow-up, baseline SUA and RD (defined as albumin-creatinine-ratio (ACR) ≥1.13 mg albumin/mmol creatinine and/or eGFR < 60 ml/min/1.73 m 2 ) in a large cohort from a general population participating in the Tromsø Study (n = 2637). Participants were stratified according to tertiles of change in SUA between baseline (1994/95) and follow-up 13 years later. (upper tertile: SUA increasing group, two lower tertiles: SUA non-increasing group). Logistic regression analysis was applied with RD and each component of RD after 7 and 13 years as the dependent variables. Adjustments were made for baseline eGFR, cardiovascular risk factors, and the use of antihypertensive drugs including diuretics. Results: After excluding participants with RD at baseline, SUA increasers, compared to SUA non-increasers, had a doubled risk of RD after 7 years (odds ratio 2.00, (95 % CI 1.45, 2.75)). Odds ratio for RD in SUA increasers after 13 years was 2.18 (95 % CI 1.71, 2.79). The risk of developing ACR ≥1.13 mg/mmol alone was not significantly increased after 7 years (odds ratio 1.30 (95 % CI 0.90, 1.89), but after 13 years (odds ratio 1.43 (95 % CI 1.09, 1.86)). An increase in baseline SUA of 59 μmol/L (1 mg/dL) gave an odds ratio for RD after 13 years of 1.16 (95 % CI 1.04, 1.29). Conclusion: An increase in SUA during follow-up was associated with an increased risk of developing RD after 7 and 13 years.

Background: Few studies have focused on investigating hypoalbuminemia in patients during earlier stages of chronic kidney disease (CKD). In particular, little is known about the role of gastrointestinal (GI) symptoms. Our goal in this paper is to study how GI symptoms relate to serum albumin levels in CKD, especially in the context of and compared with inflammation. Methods: We performed a cross-sectional study of 3599 patients with chronic kidney disease enrolled in the Chronic Renal Insufficiency Cohort (CRIC) study. All subjects were asked to complete the Modification of Diet in Renal Disease (MDRD) study patient symptom form. Our main predictor is GI symptom score. Serum level of C-reactive protein (CRP) was measured as well. Main outcome measures are serum albumin levels and prevalence of hypoalbuminemia. Results: Of the participants assessed, mean serum albumin was 3.95 ± 0.46 g/dL; 12.7 % had hypoalbuminemia. Patients with lower estimated glomerular filtration rate (eGFR) were likely to have more GI symptoms (apparent at an eGFR <45 ml/min/1.73 m 2 ). Patients with worse GI symptoms had lower dietary protein intake. GI symptoms, like inflammation, were risk factors for lower serum albumin levels. However, adding GI symptom score or CRP into the multivariable regression analysis, did not attenuate the association between lower eGFR and lower albumin or hypoalbuminemia. Conclusions: Increased prevalence of GI symptoms become apparent among CKD patients at relatively high eGFR levels (45 ml/min/1.73 m 2 ), long before ESRD. Patients with more severe GI symptoms scores are more likely to have hypoalbuminemia. But our data do not support GI symptoms/decreased protein intake or inflammation as being the main determinants of serum albumin level in CKD patients.

Background: Percutaneous renal biopsy (PRB) is an important diagnostic procedure. Despite advances in its safety profile there remains a small but significant risk of bleeding complications. Traditionally, operators train to perform PRB through tutor instruction and directly supervised PRB attempts on real patients. We describe an approach to teaching operators to perform PRB using cadaveric simulation. Methods: We devised a full day course hosted in the Clinical Anatomy Skills Centre, with places for nine candidates. Course faculty consisted of two Consultant Nephrologists, two Nephrology trainees experienced in PRB, and one Radiologist.Classroom instruction included discussion of PRB indications, risk minimisation, and management of complications. Two faculty members acted as models for the demonstration of kidney localisation using real-time ultrasound scanning. PRB was demonstrated using a cadaveric model, and candidates then practised PRB using each cadaver model. Results: Written candidate feedback was universally positive. Faculty considered the cadaveric model a realistic representation of live patients, while the use of multiple cadavers introduced anatomical variation. Conclusions: Our model facilitates safe simulation of a high risk procedure. This might reduce serious harm associated with PRB and improve patient safety, benefiting trainee operators and patients alike.