Chronic kidney disease (CKD) affects many adults worldwide. Persistent low-grade inflammation is a substantial factor in its development and progression and has correlated with increased mortality and cardiovascular problems. This low-grade inflammation is a product of dysregulation of the normal balance between pro- and anti-inflammatory markers. Various factors such as increased innate immune system activation, reactive oxygen species production, periodontal disease, dysregulation of anti-inflammatory systems and intestinal dysbiosis result in the dysregulation of this balance. Furthermore, this low-grade inflammation has down-effects such as hypertension, renal fibrosis and acceleration of renal function decline. Moreover, low-grade inflammation over time has been linked to malignancy in CKD. As CKD progresses, many patients require dialysis, which has a negative bidirectional relationship with persistent inflammation. Treatment options for inflammation in CKD are vast, including cytokine inhibitors, statins and diets. However, more research is needed to create a standardized management plan. In this review, we will examine the normal physiology of the kidney and its relationship with the immune system. We will then delve into the pathology behind persistent inflammation, the various causes of inflammation, the downstream effects of inflammation, dialysis and potential treatments for inflammation in CKD.

Hyperammonaemia in children can lead to grave consequences in the form of cerebral oedema, severe neurological impairment and even death. In infants and children, common causes of hyperammonaemia include urea cycle disorders or organic acidaemias. Few studies have assessed the role of extracorporeal therapies in the management of hyperammonaemia in neonates and children. Moreover, consensus guidelines are lacking for the use of non-kidney replacement therapy (NKRT) and kidney replacement therapies (KRTs, including peritoneal dialysis, continuous KRT, haemodialysis and hybrid therapy) to manage hyperammonaemia in neonates and children. Prompt treatment with KRT and/or NKRT, the choice of which depends on the ammonia concentrations and presenting symptoms of the patient, is crucial. This expert Consensus Statement presents recommendations for the management of hyperammonaemia requiring KRT in paediatric populations. Additional studies are required to strengthen these recommendations.

Rickets is a common bone disease worldwide that is associated with disturbances in calcium and phosphate homeostasis and can lead to short stature and joint deformities. Rickets can be diagnosed based on history and physical examination, radiological features, and biochemical tests. It can be classified into 2 major groups based on phosphate or calcium levels: phosphopenic and calcipenic. Knowledge of categorization of the type of rickets is essential for prompt diagnosis and proper management. Nutritional rickets is a preventable disease through adequate intake of vitamin D through both dietary and sunlight exposure. There are other subtypes of rickets, such as vitamin D–dependent type 1 rickets and vitamin D–dependent type 2 rickets (due to defects in vitamin D metabolism), renal rickets (due to poor kidney function), and hypophosphatemic rickets (vitamin D–resistant rickets secondary to renal phosphate wasting wherein fibroblast growth factor-23 (FGF-23) often plays a major role), which requires closer monitoring and supplementation with activated vitamin D with or without phosphate supplements. An important development has been the introduction of burosumab, a human monoclonal antibody to FGF-23, which is approved for the treatment of X-linked hypophosphatemia among children 1 year and older.

Background: A common practice in the management of critically ill patients is fluid resuscitation. An excessive administration of fluids can lead to an imbalance in fluid homeostasis and cause fluid overload (FO). In pediatric critical care patients, FO can lead to a multitude of adverse effects and increased risk of morbidity. Objectives: To review the literature highlighting impact of FO on a multitude of outcomes in critically-ill children, causative vs. associative relationship of FO with critical illness and current pediatric fluid management guidelines. Data Sources: A literature search was conducted using PubMed/Medline and Embase databases from the earliest available date until June 2017. Data Extraction: Two authors independently reviewed the titles and abstracts of all articles which were assessed for inclusion. The manuscripts of studies deemed relevant to the objectives of this review were then retrieved and associated reference lists hand-searched. Data Synthesis: Articles were segregated into various categories namely pathophysiology and sequelae of fluid overload, assessment techniques, epidemiology and fluid management. Each author reviewed the selected articles in categories assigned to them. All authors participated in the final review process. Conclusions: Recent evidence has purported a relationship between mortality and FO, which can be validated by prospective RCTs (randomized controlled trials). The current literature demonstrates that “clinically significant” degree of FO could be below 10%. The lack of a standardized method to assess FB (fluid balance) and a universal definition of FO are issues that need to be addressed. To date, the impact of early goal directed therapy and utility of hemodynamic parameters in predicting fluid responsiveness remains underexplored in pediatric resuscitation.

Pediatric acute kidney injury (AKI) is a frequently missed complication. AKI has a significant impact on both short- and long-term outcomes in children. Within the last decade, there have been major landmark developments in this field of critical care pediatric nephrology. The topic was searched by two independent researchers using Google Scholar and PubMed and related studies published in the last 10 years. The terms used for the search were 'pediatric acute kidney injury,' 'pediatric acute renal failure,' 'pediatric dialysis,' 'biomarkers,' 'nephrotoxins,' 'nephrotoxicity in children,' and 'pediatric critical care nephrology.' We found that AKI is common in critically ill neonates and children. Among the various definitions, the Kidney Disease: Improving Global Outcomes (KDIGO) definition is most commonly used. In addition, it is imperative to risk stratify sick children at admission in the hospital to predict AKI and worse outcomes as this aids in early management. There are now major landmark trials that describe the epidemiology, prevention, and management guidelines in this field and health care professionals need to be aware they should diagnose AKI early. Overall, this review highlights the landmark studies in the last decade and shows that early diagnosis and management of AKI in 'at risk' children can improve outcomes.