Systematic review of microRNAs in human acute kidney injury.

Introduction: Early diagnosis of acute kidney injury (AKI) is limited with current tools. MicroRNAs (miRNAs) are implicated in AKI pathogenesis in preclinical models, but less is known about their role in humans. We conducted a systematic review to identify dysregulated miRNAs in humans with AKI.

miR-486-5p protects against rat ischemic kidney injury and prevents the transition to chronic kidney disease and vascular dysfunction.

Aim: Acute kidney injury (AKI) increases the risk for progressive chronic kidney disease (CKD). MicroRNA (miR)-486-5p protects against kidney ischemia-reperfusion (IR) injury in mice, although its long-term effects on the vasculature and development of CKD are unknown. We studied whether miR-486-5p would prevent the AKI to CKD transition in rat, and affect vascular function.

Protecting the kidney in sepsis: resident macrophages to the rescue.

Kidney resident macrophages exert pro-inflammatory or reparative effects in experimental acute kidney injury, but their role in sepsis is unclear. In a mouse model of sepsis, Privratsky et al. show that kidney resident F4/80 macrophages protect against kidney injury by expressing interleukin-1 receptor antagonist, which blocks interleukin-6 production selectively from endothelial cells.

miRNA-486-5p: signaling targets and role in non-malignant disease.

MicroRNAs (miRNAs) are short non-coding RNAs, highly conserved between species, that are powerful regulators of gene expression. Aberrant expression of miRNAs alters biological processes and pathways linked to human disease. miR-486-5p is a muscle-enriched miRNA localized to the cytoplasm and nucleus, and is highly abundant in human plasma and enriched in small extracellular vesicles.

Page kidney: Rare cause of acute kidney injury after complicated renal artery angioplasty.

The authors present a case of a patient who experienced a rare complication after attempted renal angioplasty and stenting, Page kidney. This patient presented with new onset hypertension secondary to bilateral renal artery stenosis and was referred for revascularization given hypertension refractory to medical management. The right renal artery underwent successful angioplasty and stenting; however, the left renal artery experienced recoil stenosis.

micro-RNA-486-5p protects against kidney ischemic injury and modifies the apoptotic transcriptome in proximal tubules.

Acute kidney injury (AKI) carries high morbidity and mortality, and effective treatments are lacking. Preclinical models support involvement of micro-RNAs (miRs) in AKI pathogenesis, although effects on the kidney transcriptome are unclear. We previously showed that injection of cord blood endothelial colony forming cell-derived exosomes, enriched in miR-486-5p, prevented ischemic AKI in mice.

MicroRNA in Human Acute Kidney Injury: A Systematic Review Protocol.

Background: Acute kidney injury (AKI) is a common complication of hospitalization with high morbidity and mortality for which no effective treatments exist and for which current diagnostic tools have limitations for earlier identification. MicroRNAs (miRNAs) are small non-coding RNAs that have been implicated in the pathogenesis of AKI, and some miRNAs have shown promise as therapeutic tools in animal models of AKI. However, less is known about the role of miRNAs in human AKI.

Sex diversity in proximal tubule and endothelial gene expression in mice with ischemic acute kidney injury.

Female sex protects against development of acute kidney injury (AKI). While sex hormones may be involved in protection, the role of differential gene expression is unknown. We conducted gene profiling in male and female mice with or without kidney ischemia-reperfusion injury (IRI).

Mechanisms for hemodynamic instability related to renal replacement therapy: a narrative review.

Hemodynamic instability related to renal replacement therapy (HIRRT) is a frequent complication of all renal replacement therapy (RRT) modalities commonly used in the intensive care unit. HIRRT is associated with increased mortality and may impair kidney recovery. Our current understanding of the physiologic basis for HIRRT comes primarily from studies of end-stage kidney disease patients on maintenance hemodialysis in whom HIRRT is referred to as 'intradialytic hypotension'.

Safety Lapses Prior to Initiation of Hemodialysis for Acute Kidney Injury in Hospitalized Patients: A Patient Safety Initiative.

Safety lapses in hospitalized patients with acute kidney injury (AKI) may lead to hemodialysis (HD) being required before renal recovery might have otherwise occurred. We sought to identify safety lapses that, if prevented, could reduce the need for unnecessary HD after AKI; We conducted a retrospective observational study that included consecutive patients treated with HD for AKI at a large, tertiary academic center between 1 September 2015 and 31 August 2016. Exposures of interest were pre-specified iatrogenic processes that could contribute to the need for HD after AKI, such as nephrotoxic medication or potassium supplement administration.

Interventions to prevent hemodynamic instability during renal replacement therapy in critically ill patients: a systematic review.

Background: Hemodynamic instability related to renal replacement therapy (HIRRT) may increase the risk of death and limit renal recovery. Studies in end-stage renal disease populations on maintenance hemodialysis suggest that some renal replacement therapy (RRT)-related interventions (e.g.

Interventions to prevent hemodynamic instability during renal replacement therapy for acute kidney injury: a systematic review protocol.

Background: Hemodynamic instability during renal replacement therapy (HIRRT) in the form of intradialytic hypotension (IDH) is a frequent complication of hemodialysis in end-stage kidney disease (ESKD), and most studies have focused on this chronic population. However, HIRRT is also an important concern for critically ill ICU patients with acute kidney injury (AKI), complicating an estimated 30% of dialysis treatments in this population. HIRRT can exacerbate organ hypoperfusion in the setting of critical illness and may negatively impact renal recovery in the AKI population.

Functional analysis of the TRIB1 associated locus linked to plasma triglycerides and coronary artery disease.

Background: The TRIB1 locus has been linked to hepatic triglyceride metabolism in mice and to plasma triglycerides and coronary artery disease in humans. The lipid-associated single nucleotide polymorphisms (SNPs), identified by genome-wide association studies, are located ≈30 kb downstream from TRIB1, suggesting complex regulatory effects on genes or pathways relevant to hepatic triglyceride metabolism. The goal of this study was to investigate the functional relationship between common SNPs at the TRIB1 locus and plasma lipid traits.