Acute kidney injury: prevention, detection, and management. Summary of updated NICE guidance for adults receiving iodine-based contrast media.

The National Institute for Health and Care Excellence (NICE) has recently updated the guideline for Acute kidney injury: prevention, detection and management (NG148), providing new recommendations on preventing acute kidney injury (AKI) in adults receiving intravenous iodine-based contrast media. The association between intravenous iodinated contrast media and AKI is controversial, particularly with widespread use of iso-osmolar agents. Associations between contrast media administration and AKI are largely based on observational studies, with inherent heterogeneity in patient populations, definitions applied, and timing of laboratory investigations. In an attempt to mitigate risk, kidney protection has typically been employed using intravenous volume expansion and/or oral acetylcysteine. Such interventions are in widespread use, despite lacking high-quality evidence of benefit. In the non-emergency setting, glomerular filtration rate (GFR) measurements should be obtained within the preceding 3 months before offering intravenous iodine-based contrast media. In the acute setting, adults should also have their risk of AKI assessed before offering intravenous iodine-based contrast media; however, this should not delay emergency imaging. Based on the evidence available from randomised controlled trials, the NICE committee recommends that oral hydration should be encouraged in adults at increased risk of AKI and that volume expansion with intravenous V fluids should only be considered for inpatients at particularly high risk.

Resolution of low-grade proteinuria is associated with improved outcomes after renal transplantation-a retrospective longitudinal study.

Low-grade proteinuria and systolic hypertension (SHT) are risk factors for allograft failure. Both are dynamic variables and their relationship is not independent. We have simultaneously analyzed the effects of proteinuria and SHT on graft outcomes in 805 adult Kidney Transplant Recipients and impact of their changes over time. Proteinuria and systolic blood pressure (SBP) were recorded for years 1 and 3 posttransplantation. Subjects with proteinuria >1 g/day were excluded. Patients were divided into groups based on proteinuria (Absent(A) <150 mg/day or low-grade(P)150 mg-1 g/day) and blood pressure (Normotensive-SBP <140 mmHg or hypertensive-SBP ≥ 140 mmHg). Graft survival was assessed in all four groups over 10 years by multivariate analysis. At the three annual time points (Year 1, 2 and 3) hypertensive patients with proteinuria had the worst graft survival. Patients with persistent proteinuria between years 1-2 and 2-3 had the poorest graft survival with an improvement if proteinuria regressed (P-A), especially in the Hypertensive group. The impact of proteinuria was highest in persistently hypertensive patients between years 1-3. Thus both proteinuria and SHT were associated with poor graft survival and the combination of the two led to the worst outcomes. Importantly, SHT was associated with significantly worse outcomes in patients with proteinuria. Patient cohort with SHT and low-grade proteinuria represent a selective group that might benefit from intervention.

Influenza A-induced rhabdomyolysis and acute kidney injury complicated by posterior reversible encephalopathy syndrome.

We report a case of Influenza A-induced rhabdomyolysis causing acute kidney injury in a young adult female who required invasive ventilation and renal replacement therapy. This case was further complicated by posterior reversible encephalopathy syndrome. Although this represents an extremely rare neurological complication of Influenza A infection, an appreciation of the condition and its management is important, given the high numbers of critically ill patients recently affected by H1N1 Influenza A in intensive care units in the UK.

Acute kidney injury.

Acute kidney injury (AKI) represents a medical emergency associated with poor clinical outcomes. The international guideline group Kidney Disease: Improving Global Outcomes (KDIGO) has defined AKI according to rises in serum creatinine and/or reductions in urine output. Any patient who meets the criteria for AKI should be reviewed to ascertain the cause of AKI and the severity of the injury should be staged. Patients with more severe AKI are at greater risk of progression to chronic kidney disease (CKD). The 2009 National Confidential Enquiry into Patient Outcomes and Death (NCEPOD) reported that only 50% of patients who died with a diagnosis with AKI received good care. The mortality from AKI has remained unchanged for the last four decades and there are currently no specific therapies for the majority of cases of AKI. Patients with rarer forms of AKI need urgent renal referral for specific therapy. At present, serum creatinine and urine output remain the best biomarkers for detecting AKI. However, significant kidney damage has usually occurred by the time changes in these biomarkers are manifest and newer biomarkers are under investigation. Management of AKI is based upon general supportive measures, which includes treatment of the underlying cause and the initiation of renal replacement therapy (RRT) in patients with complications refractory to medical management. The optimal choice of intravenous fluid therapy remains controversial. There is currently renewed interest in more specific therapies for AKI secondary to hypoperfusion and/or sepsis, which have been previously unsuccessful. A number of therapeutic strategies are presently being explored in clinical trials.