# Acute Kidney Injury After Cardiac Surgery

## Introduction

Cardiac surgery-associated acute kidney injury (CSA-AKI) is one of the most common and consequential complications following cardiac operations, affecting 20-40% of patients. Severe AKI requiring renal replacement therapy (RRT) occurs in 2-6% of cases and carries a mortality rate exceeding 50%. Understanding the multifactorial pathophysiology and implementing preventive strategies are essential competencies for the cardiothoracic surgeon.

## Definition and Staging

### KDIGO Classification

| KDIGO Stage | Serum Creatinine Criteria | Urine Output Criteria | Incidence After Cardiac Surgery |
|-------------|--------------------------|----------------------|-------------------------------|
| Stage 1 | 1.5-1.9x baseline OR ≥0.3 mg/dL increase within 48 hrs | <0.5 mL/kg/hr for 6-12 hours | 15-25% |
| Stage 2 | 2.0-2.9x baseline | <0.5 mL/kg/hr for ≥12 hours | 3-8% |
| Stage 3 | ≥3.0x baseline OR ≥4.0 mg/dL OR initiation of RRT | <0.3 mL/kg/hr for ≥24 hrs OR anuria ≥12 hrs | 2-6% |

Stage 1 AKI is defined by a serum creatinine increase of 1.5-1.9x baseline or an increase of 0.3 mg/dL or more within 48 hours, with urine output below 0.5 mL/kg/hr for 6-12 hours. Stage 2 involves a creatinine increase of 2.0-2.9x baseline with urine output below 0.5 mL/kg/hr for 12 hours or more. Stage 3 is defined by a creatinine increase of 3.0x or more baseline, or an increase to 4.0 mg/dL or more, or initiation of RRT, with urine output below 0.3 mL/kg/hr for 24 hours or more, or anuria for 12 hours or more.

## Pathophysiology

### Mechanisms of Renal Injury

Ischemia-reperfusion injury from hypoperfusion during CPB followed by reperfusion generates reactive oxygen species and endothelial damage. Hemolysis and hemoglobinuria from mechanical destruction of red blood cells in the CPB circuit releases free hemoglobin, which is directly nephrotoxic. The inflammatory cascade activated by CPB, including complement, neutrophils, and cytokines, causes renal tubular and endothelial injury. Atheroembolic disease from manipulation of a calcified aorta releases cholesterol emboli to the renal vasculature. Venous congestion from elevated central venous pressure due to right heart dysfunction impairs renal venous drainage. Nephrotoxic agents including contrast dye, aminoglycosides, NSAIDs, and vancomycin contribute to tubular injury.

### Hemodynamic Factors

Mean perfusion pressure during CPB should target MAP above 65 mmHg, with higher targets for patients with chronic hypertension. Non-pulsatile flow during CPB may reduce renal cortical blood flow. Hemodilution on CPB reduces oxygen delivery, and a hematocrit below 21% is associated with increased AKI risk. Postoperative low cardiac output syndrome and vasoplegia compound renal hypoperfusion.

![Diagram of the pathophysiological mechanisms contributing to cardiac surgery-associated acute kidney injury](/images/csa-aki-pathophysiology.png)

## Risk Factors

### Preoperative

Baseline chronic kidney disease (eGFR below 60 mL/min) is the strongest predictor. Other preoperative risk factors include diabetes mellitus and hypertension, advanced age (above 70 years), congestive heart failure and reduced ejection fraction, preoperative anemia (hemoglobin below 12 g/dL), and recent contrast exposure (within 72 hours before surgery).

### Intraoperative

Intraoperative risk factors include prolonged CPB time (above 120 minutes) and aortic cross-clamp time, intraoperative hypotension (MAP below 60 mmHg for more than 10 minutes), excessive hemodilution (nadir hematocrit below 21%), blood transfusion (more than 2 units packed RBCs), and aortic manipulation with atheroembolism.

### Postoperative

Postoperative risk factors include low cardiac output syndrome requiring inotropes or mechanical support, need for re-exploration (bleeding or tamponade), sepsis and multiorgan dysfunction, and nephrotoxic drug exposure.

## Prevention Strategies

### Preoperative

Volume status should be optimized and nephrotoxins discontinued 48-72 hours before surgery. Surgery should be delayed more than 72 hours after contrast administration when feasible. Anemia can be corrected with iron supplementation or erythropoietin when time permits. Risk stratification using validated scoring systems (Cleveland Clinic Score, STS risk calculator) guides planning.

### Intraoperative

MAP should be maintained above 65-75 mmHg during CPB, individualized to baseline blood pressure. Excessive hemodilution should be avoided with a target hematocrit above 24% on CPB. CPB time should be minimized using goal-directed perfusion strategies. Pulsatile flow on CPB may benefit high-risk patients. Blood transfusion should be minimized using cell salvage and antifibrinolytics. Aortic manipulation should be limited, with epiaortic ultrasound guiding cannulation.

### Postoperative

Goal-directed hemodynamic management maintains adequate cardiac output and MAP. Nephrotoxic agents should be avoided and renally cleared medications dose-adjusted. Euvolemia should be maintained, avoiding both hypovolemia and venous congestion. Urine output is monitored hourly and serum creatinine every 12-24 hours. Novel biomarkers including NGAL, KIM-1, TIMP-2, and IGFBP7 (NephroCheck) offer early detection.

![Flowchart showing a preventive care bundle for reducing cardiac surgery-associated acute kidney injury](/images/aki-prevention-bundle.png)

## Management of Established AKI

### Conservative Management

Fluid management avoids fluid overload, targeting neutral to slightly negative fluid balance. Furosemide infusion (1-10 mg/hr) addresses volume overload, but forced diuresis in euvolemic patients should be avoided. Hemodynamic optimization maintains cardiac output and perfusion pressure while avoiding excessive vasopressor use. Medications are dose-reduced or nephrotoxins avoided, with antibiotic dosing adjusted for renal function. Nutritional support provides adequate caloric intake (25-30 kcal/kg/day) with protein adjustment.

### Renal Replacement Therapy

Indications for RRT include refractory volume overload, severe hyperkalemia (above 6.5 mEq/L), metabolic acidosis (pH below 7.15), uremic symptoms, and anuria unresponsive to diuretics. Continuous RRT (CRRT) is preferred in hemodynamically unstable patients and provides gradual fluid and solute removal. Intermittent hemodialysis (IHD) is suitable for hemodynamically stable patients. Current evidence from the STARRT-AKI trial does not support routine early initiation; RRT should be initiated based on clinical indications. Vascular access uses a temporary dialysis catheter in the internal jugular vein (avoiding subclavian due to stenosis risk).

## Outcomes

Even Stage 1 AKI increases short-term mortality by 2-3 fold and long-term cardiovascular events. AKI requiring RRT has an in-hospital mortality of 40-60%. Twenty to thirty percent of patients with severe AKI progress to chronic kidney disease within 1 year. Survivors of CSA-AKI face increased long-term risk of end-stage renal disease and cardiovascular mortality.

![Kaplan-Meier survival curves comparing outcomes in patients with and without AKI after cardiac surgery](/images/aki-survival-outcomes.png)

## Key Clinical Pearls

Baseline renal function (eGFR) is the strongest predictor of postoperative AKI, making preoperative optimization paramount. A rise in creatinine of 0.3 mg/dL, though seemingly small, represents significant renal injury and should prompt immediate evaluation. Maintaining MAP above 65-75 mmHg during CPB and avoiding nadir hematocrit below 21% are modifiable intraoperative targets. Venous congestion (elevated CVP) is an underrecognized contributor to AKI, and right heart dysfunction should be monitored and treated aggressively. Novel biomarkers can detect AKI 12-24 hours before creatinine rises, allowing earlier intervention.

## References

1. Nadim MK, Forni LG, Bihorac A, et al. Cardiac and vascular surgery-associated acute kidney injury: the 20th International Consensus Conference of the ADQI Group. *Journal of the American Heart Association*. 2018;7(11):e008834.
2. Wang Y, Bhatt DL, Bhatt AB. Cardiac surgery-associated acute kidney injury: risk factors, pathophysiology, and treatment. *Transplantation Reviews*. 2022;36(2):100726.
3. Zarbock A, Koyner JL, Hoste EAJ, Kellum JA. Update on perioperative acute kidney injury. *Anesthesia & Analgesia*. 2018;127(4):921-933.
4. STARRT-AKI Investigators. Timing of initiation of renal-replacement therapy in acute kidney injury. *New England Journal of Medicine*. 2020;383(3):240-251.