A device for measuring human breath ammonia was developed based on a single use, disposable, inkjet printed ammonia sensor fabricated using polyaniline nanoparticles. The device was optimized for sampling ammonia in human breath samples by addressing issues such as variations in breath sample volume, flow rate, sources of oral ammonia, temperature and humidity. The resulting system was capable of measuring ammonia in breath from 40 to 2993 ppbv (r(2 )= 0.99, n = 3) as correlated with photoacoustic laser spectroscopy and correlation in normal human breath samples yielded a slope of 0.93 and a Pearson correlation coefficient of 0.9705 (p < 0.05, n = 11). Measurement of ammonia in the breath of patients with end-stage kidney disease demonstrated its significant reduction following dialysis, while also correlating well with blood urea nitrogen (BUN) (r = 0.61, p < 0.01, n = 96). Excellent intraindividual correlations were demonstrated between breath ammonia and BUN (0.86 to 0.96), which demonstrates the possibility of using low cost point of care breath ammonia systems as a noninvasive means of monitoring kidney dysfunction and treatment.

Successful cannulation of the arteriovenous access for patients with end-stage kidney failure to allow catheter-free hemodialysis is associated with superior patient outcomes. With an increasing rate of arteriovenous access creation, coupled with increasing dialysis patient age, the "difficult-to-cannulate" access is becoming more commonplace. Ultrasound-guided cannulation aims to improve first-time successful cannulations and minimize cannulation-associated complications such as infiltration and hematoma formation, minimizing delays in access use and reducing catheter dependency. Ultrasound-guided cannulation has the potential to not only improve patient experience but also reduce morbidity associated with complications, dialysis catheter dependency, and subsequent healthcare costs. A smooth and complication-free dialysis initiation is also important for the longevity of technique survival and self-cannulation in home hemodialysis patients. Appropriate training of the ultrasound operator is required to ensure competent image acquisition with simultaneous needling. There are various approaches and considerations in choosing how to apply the ultrasound probe and needle the access, which are often governed by personal choice, training, and institutional patterns of practice more than a robust evidence base. Future research should focus on providing more clarity on the optimal method of utilizing ultrasound guidance in arteriovenous access cannulation, the precise indications for its use and, lastly, the benefits it confers compared to traditional blind cannulation.

The outcome of lupus nephritis (LN) has changed since the introduction of glucocorticoids (GCs), which dramatically reduced the mortality related to one of the most severe complications of systemic lupus erythematosus (SLE). Since the 1950's, other immunosuppressants, including biologic drugs (i.e. rituximab) have aided in maintaining remission, preserving kidney function, but not preventing treatment-related toxicity. GCs still remain the cornerstone in the treatment of SLE, including LN, and they are widely used in clinical practice. However, GC administration represents a double-edged sword. Indeed, from one side they allow a fast and effective control of disease activity by dampening inflammation; from the other side, they have many and severe side effects leading to organ damage. In this paper, we will discuss pros and cons of the chronic use of GCs, especially focusing on LN.

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Chronic kidney disease (CKD) is associated with significant morbidity and mortality, impacted not alone by progression to end-stage kidney disease, but also by the high associated incidence of cardiovascular events and related mortality. Despite our current understanding of the pathogenesis of CKD and the treatments available, the reported incidence of CKD continues to rise worldwide, and is often referred to as the silent public healthcare epidemic. The significant cost to patient wellbeing and to the economy of managing the later stages of CKD have prompted efforts to develop interventions to delay the development and progression of this syndrome. In this article, we review established and novel agents that may aid in delaying the progression of CKD and improve patient outcomes. KEYWORDS: Chronic kidney disease, progression, drug therapy IntroductionChronic kidney disease (CKD), as defined by proteinuria or a reduced glomerular filtration rate (GFR) below 90 mL/min/1.73 m 2 persisting for greater than 3 months, is reported to affect 13% of US adults.1 There is a significantly higher prevalence in the elderly and those with hypertension or diabetes, and with these comorbidities increasing in prevalence and the population ageing, CKD is projected to affect up to 16% of adults by 2030.2,3 Even in its early stages, CKD is associated with accelerated cardiovascular disease and increased mortality, with an exponential increase in attributable risk as GFR declines to end-stage kidney disease (ESKD). 4,5 The mortality rate in ESKD patients maintained on dialysis is striking, with a life expectancy less than one-third that of their counterparts without ESKD, and a 5-year survival rate on dialysis of only 40%. 6 There is also a substantial healthcare cost associated with provision of ESKD care, currently estimated at $33 billion annually in the US, ABSTRACT equating to 6.3% of the Medicare Budget. 6 Hence, there may be significant healthcare and economic benefits to be garnered from halting or delaying CKD progression. In this article, we discuss recent evidence for established and emerging therapies that may alter the progression of CKD. Non disease-specific drug therapies Sodium bicarbonateCKD is associated with a metabolic acidosis, particularly at lower levels of GFR <25 mL/min/1.73 m 2 , which is predominantly attributed to reduced hydrogen ion excretion as titratable acids or ammonium in the urine. Chronic metabolic acidosis exacerbates CKD-related mineral bone disease, leads to muscle atrophy, and is associated with other complications such as abnormal albumin synthesis, thyroid dysfunction and insulin resistance. 7,8 Observational data demonstrate a strong risk of progression of CKD in those with a lower serum bicarbonate level, as well as an increased mortality risk. 9,10 Possible mechanisms for the deleterious effect of acidosis on GFR may be the inadvertent pro-fibrotic effects of inducing regulatory mechanisms in the kidney, such as increased renal ammonium production, endothelin-A receptor activation and pr...