The practical implications are balancing the theoretical assumption that early initiation of RRT may lead to earlier removal of uraemic toxins, against the possibility that delayed treatment may result in spontaneous recovery and avoidance of RRT entirely. With evidence that no added benefit is derived from early therapy, in the absence of emergent indications a serum urea level of 40 mmol/L is therefore not unreasonable. The recently examined upper limit was > 35.7 mmol/L to the onset of clinical signs or symptoms, although most studies initiated treatment no higher than 40 mmol/L. Most recent studies did, however, implement an upper limit at which interventional RRT was initiated Table Table1 1.Īs no recent RCTs assess urea independently, it is reasonable to extrapolate the correlating urea levels to make a plausible appraisal of what level is acceptable to commence RRT. The only study found to consider serum urea in isolation confirmed a declining trend of threshold urea level for RRT initiation and no association with in-hospital mortality. Older studies have demonstrated increased mortality when serum urea reaches higher ranges (50.7–71.4 mmol/L), which perhaps established the tendency to initiate RRT therapy at lower levels.Įvaluation of the available data led to the proposal of serum urea > 35.7 mmol/L as an absolute indication for RRT but no recent RCTs have looked at urea as an independent variable for initiation. The most comprehensive data regarding optimal timing for RRT initiation comes from a 2017 meta-analysis of RCTs assessing early versus late initiation of RRT in patients with AKI that concluded there was no added benefit of early initiation with respect to 30, 60, and 90-day mortality, overall ICU and hospital mortality, and dialysis dependence. However, the question remains, when is the most appropriate time to initiate therapy based on serum urea levels without other apparent indications?ĭespite early meta-analysis suggesting early RRT improves survival in critical illness, more recent analysis does not support that view. It is also common practice to delay haemodialysis for an indefinite period in the absence of these specific uraemic complications due to the risks associated with RRT.
The clinical signs of pathological uraemia (pericarditis, pleuritis, encephalopathy and bleeding) are well established as indications to start haemodialysis, but therapy often commences prior to their development. ĭespite the common assumption that elevated urea requires urgent dialysis, treating AKI on serum urea alone is difficult due to variations in the base urea level in the presence of metabolic instability and variations in urea generation.
The issue is further complicated by several randomised control trials (RCTs) that investigated early versus delayed prescription of RRT producing conflicting results. Without clinically significant ureamic symptoms or emergent indications (electrolyte abnormalities, volume overload) the timing of RRT initiation remains contentious and inconsistent across health providers. The decision to initiate renal replacement therapy (RRT) and the optimal timing for commencement is a difficult decision clinicians face when treating acute kidney injury (AKI) in the intensive care setting.
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