Background: The optimal time to initiate renal replacement therapy (RRT) in cardiac surgery-associated acute kidney injury (CSA-AKI) is unknown. Evidence suggests that the early use of RRT in critically ill patients is associated with improved outcomes. We studied the effects of time to initiation of RRT on outcome in patients with CSA-AKI. Methods: This was a retrospective observational multicenter study (24 Spanish hospitals). We analyzed data on 203 patients who required RRT after cardiac surgery in 2007. The cohort was divided into 2 groups based on the time at which RRT was initiated: in the early RRT group, therapy was initiated within the first 3 days after cardiac surgery; in the late group, RRT was begun after the 3rd day. Multivariate nonconditional logistic and linear regression models were used to adjust for potential confounders. Results: In-hospital mortality was significantly higher in the late RRT group compared with early RRT patients (80.4 vs. 53.2%; p < 0.001; adjusted odds ratio of 4.1, 95% CI: 1.6–10.0). Also, patients in the late RRT group had longer adjusted hospital stays by 11.6 days (95% CI: 1.4–21.9) and higher adjusted percentage increases in creatinine at discharge compared with baseline by 67.7% (95% CI: 28.5–106.4). Conclusions: Patients who undergo early initiation of RRT after CSA-AKI have improved survival rates and renal function at discharge and decreased lengths of hospital stay.

In this external validation, the CPRPC performed poorly despite its simplicity. The CPRPC was not a useful scale in our cohort. In contrast, we used a more accurate score to predict the occurrence of PPCs in our cohort. It is based on age, smoking status and predicted postoperative forced expiratory volume in 1 s. We propose that our formula should be externally validated.

Acute kidney injury (AKI) is defined as an abrupt decline in the glomerular filtration rate with accumulation of nitrogenous waste products and the inability to maintain fluid and electrolyte homeostasis. Occurring in 7% of all hospitalized patients and 28% to 35% of those in intensive care units, AKI increases hospital mortality. Early evaluation should include differentiating prerenal and postrenal components from intrinsic renal disease. Biological markers can give early warning of AKI and assist with differential diagnosis and assessment of prognosis. The most effective preventive measure is to maintain adequate circulation and cardiac output, avoiding ischemia- or nephrotoxin-induced injury. To that end, patients and situations of risk must be identified, hemodynamics and diuresis monitored, hypovolemia reversed, and nephrotoxins avoided. Protective agents such as sodium bicarbonate, mannitol, prostagiandins, calcium channel blockers, N-acetyl-L-cysteine, sodium deoxycholate, allopurinol, and pentoxifylline should be used. Treatment includes the elimination of prerenal and postrenal causes of AKI; adjustment of doses according to renal function; avoidance of both overhydration and low arterial pressure; maintenance of electrolytic balance, avoiding hyperkalemia and correcting hyperglycemia; and nutritional support, assuring adequate protein intake. For severe AKI, several modalities of renal replacement therapy, differentiated by mechanism and duration, are available. Timing--neither the best moment to start dialysis nor the optimal duration--has been not established. Early detection of AKI is necessary for preventing progression and starting renal replacement therapy at adjusted doses that reflect metabolic requirements.

No author has a financial or proprietary interest in any material or method mentioned.

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