From the Guidelines
A patient with acute kidney injury (AKI) but normal lactate levels likely has adequate systemic perfusion despite the kidney injury. The normal lactate suggests that overall tissue perfusion is sufficient to prevent anaerobic metabolism, which would otherwise lead to lactate accumulation 1. AKI can occur due to various causes beyond hypoperfusion, including nephrotoxic medications, contrast agents, sepsis with inflammatory mediators, or obstruction. In this scenario, treatment should focus on identifying and addressing the specific cause of the AKI while maintaining hemodynamic stability.
Key Considerations
- Ensure adequate hydration (unless contraindicated)
- Discontinue nephrotoxic medications if possible
- Consider urinary obstruction as a potential cause requiring relief
- Monitor urine output, creatinine, and electrolytes closely The discrepancy between kidney injury and normal lactate suggests the AKI may be due to kidney-specific insults rather than global hypoperfusion, or that the kidney injury occurred earlier but perfusion has since improved 1. Remember that lactate is a late marker of tissue hypoperfusion, so other clinical parameters like urine output, capillary refill, and blood pressure should also be assessed to confirm adequate perfusion status.
Clinical Parameters to Assess
- Urine output
- Capillary refill
- Blood pressure These parameters will help confirm adequate perfusion status in a patient with AKI and normal lactate levels.
From the Research
Perfusion Status in Acute Kidney Injury (AKI) with Normal Lactate
- The perfusion status of a patient with AKI but normal lactate is a complex issue, and several factors need to be considered, including mean arterial pressure (MAP), mean perfusion pressure (MPP), and central venous pressure (CVP) 2, 3.
- Studies have shown that patients with AKI may have impaired renal perfusion, even with normal lactate levels, due to various factors such as hypovolemia, renal hypoperfusion, and venous congestion 4, 3.
- The relationship between lactate metabolism and AKI is not fully understood, but it is known that the kidney plays a crucial role in lactate metabolism, and alterations in lactate metabolism may contribute to the development and progression of AKI 5.
- In patients with septic AKI, the initial serum lactate level has been shown to be a predictor of AKI and mortality, and comorbidities such as liver disease, diabetes mellitus, and chronic kidney disease may also contribute to the development of AKI 6.
- The management of fluid balance is critical in patients with AKI, and a conservative strategy of fluid management may be beneficial in improving clinical outcomes, but accurate assessment of fluid status and careful definition of targets are needed to avoid hypovolemia and renal hypoperfusion 4.