CRRT and Acute Kidney Therapies
Key Takeaways
- CRRT provides slow, continuous fluid and solute removal over 24 hours, making it preferred for hemodynamically unstable ICU patients who cannot tolerate rapid shifts of intermittent hemodialysis.
- SLED (sustained low-efficiency dialysis) runs 8–12 hours with low blood and dialysate flows, offering better hemodynamic tolerance than conventional HD with greater efficiency than CRRT.
- Urgent dialysis indications in AKI include refractory hyperkalemia, severe metabolic acidosis, volume overload unresponsive to diuretics, uremic encephalopathy, and pericarditis.
- Prerenal AKI shows FENa under 1% and responds to volume; acute tubular necrosis shows muddy brown casts and FENa over 2%; postrenal AKI follows obstruction.
- CRRT nursing priorities include hourly fluid balance, filter pressure monitoring, anticoagulation management, and micronutrient loss awareness in critically ill patients.
CRRT and Acute Kidney Therapies
Quick Answer: Continuous renal replacement therapy (CRRT) runs slowly around the clock to remove fluid and solutes without the rapid shifts of intermittent hemodialysis — the hemodynamic advantage CDN items test most often. Know when AKI needs urgent dialysis, how CRRT differs from SLED and conventional HD, and what ICU nurses monitor hourly at the bedside.
Acute kidney injury (AKI) is a sudden decline in kidney function over hours to days, often in hospitalized or critically ill patients. Unlike chronic kidney disease, AKI may be reversible if the underlying cause is treated promptly. The CDN exam expects you to distinguish prerenal, intrinsic, and postrenal causes, recognize urgent dialysis indications, and compare acute renal replacement modalities — especially CRRT versus intermittent HD.
AKI Definition and KDIGO Staging
KDIGO defines AKI by any of: creatinine rise ≥0.3 mg/dL within 48 hours, creatinine ≥1.5 times baseline within 7 days, or urine output <0.5 mL/kg/hour for 6 hours. Staging guides severity and prognosis:
| KDIGO Stage | Creatinine criteria | Urine output |
|---|---|---|
| Stage 1 | 1.5–1.9× baseline or ≥0.3 mg/dL rise | <0.5 mL/kg/h for 6–12 h |
| Stage 2 | 2.0–2.9× baseline | <0.5 mL/kg/h for ≥12 h |
| Stage 3 | 3× baseline or ≥4.0 mg/dL or RRT | <0.3 mL/kg/h for ≥24 h or anuria ≥12 h |
Prerenal, Intrinsic, and Postrenal AKI
Prerenal AKI results from decreased renal perfusion — sepsis, dehydration, heart failure, NSAIDs, or ACE inhibitors in bilateral renal artery stenosis. Urine sodium is low, fractional excretion of sodium (FENa) is under 1%, and the sediment is bland. Volume resuscitation often reverses injury.
Intrinsic AKI — most commonly acute tubular necrosis (ATN) from ischemia or nephrotoxins — shows muddy brown casts, FENa over 2%, and oliguria in the classic presentation. Contrast-induced nephropathy and aminoglycoside toxicity are frequent hospital triggers.
Postrenal AKI follows urinary tract obstruction — stones, BPH, malignancy, or catheter occlusion. Imaging may show hydronephrosis; output can be fluctuating. Relief of obstruction can produce a dramatic polyuric recovery phase with high urine volumes and electrolyte losses requiring close monitoring.
Phases of AKI and Urine Output
The oliguric phase (typically urine output under 400 mL/day) concentrates toxins and raises hyperkalemia risk. The polyuric (diuretic) phase during recovery can exceed 3–5 L/day — nurses must replace fluids judiciously and watch for hypokalemia and hypomagnesemia. Serum creatinine and cystatin C track function; NGAL and other biomarkers are sensitive early markers tested conceptually on certification exams.
Urgent Dialysis Indications in AKI
Use the mnemonic AEIOU for emergent dialysis needs:
| Letter | Indication | Why it is urgent |
|---|---|---|
| A | Severe acidosis (pH <7.1–7.2) unresponsive to medical therapy | Cardiovascular instability |
| E | Electrolyte emergency — refractory hyperkalemia with ECG changes | Arrhythmia risk |
| I | Intoxication with dialyzable toxins | Methanol, ethylene glycol, lithium |
| O | Overload — pulmonary edema despite diuretics | Hypoxemia |
| U | Uremic complications — encephalopathy, pericarditis, intractable vomiting | Life-threatening |
CRRT vs Intermittent HD vs SLED
Conventional intermittent hemodialysis in the ICU removes fluid and solutes rapidly over 3–4 hours. Rapid ultrafiltration can precipitate hypotension in septic or cardiogenic shock — a key limitation CDN items exploit.
CRRT (continuous renal replacement therapy) operates 24 hours with low blood flows (typically 100–200 mL/min) and gentle ultrafiltration. Modes include:
- CVVH — continuous venovenous hemofiltration (convection-dominant)
- CVVHD — continuous venovenous hemodialysis (diffusion-dominant)
- CVVHDF — combines convection and diffusion
Primary CRRT advantage: better hemodynamic stability because fluid and solute shifts are slow and continuous. Tradeoffs: ICU resource intensity, anticoagulation needs, electrolyte and micronutrient losses, and higher cost — not faster toxin removal (a common distractor).
SLED (sustained low-efficiency dialysis) bridges ICU needs: treatments run 8–12 hours with low blood and dialysate flows, offering better hemodynamic tolerance than conventional HD while clearing solutes more efficiently than CRRT in some protocols. Expect CDN comparisons among all three modalities.
CRRT Nursing Management
Hourly nursing responsibilities on CRRT include:
- Fluid balance — net ultrafiltration goal versus actual; avoid unintended hypovolemia.
- Filter pressures — rising venous or transmembrane pressure signals clotting; notify provider per protocol.
- Anticoagulation — systemic heparin or regional citrate; monitor aPTT or ionized calcium per citrate protocol.
- Access integrity — double-lumen central catheter care; avoid line draws from dialysis ports when policy prohibits.
- Electrolytes and acid-base — phosphate and potassium shifts; replace per ICU protocol.
- Nutrition coordination — critical illness plus CRRT increases protein and micronutrient losses.
Worked Scenario: Septic Shock with AKI
A 64-year-old ICU patient with septic shock has creatinine rising from 1.0 to 3.8 mg/dL, urine output 15 mL/hour, potassium 6.2 mEq/L with peaked T waves, and mean arterial pressure 58 mmHg on norepinephrine. Priority sequence: administer IV calcium for cardiac membrane stabilization, initiate potassium-lowering therapy per protocol, and consult nephrology for urgent renal replacement. CRRT is preferred over aggressive intermittent HD because rapid fluid removal would worsen hypotension. This integrates AKI staging, hyperkalemia urgency, and modality selection — a high-value CDN composite stem.
Exam Traps for Acute Therapies
Do not select CRRT because it is cheaper, needs no anticoagulation, or removes toxins faster — those are wrong on NNCC forms. Do not confuse oliguric urine volumes with polyuric recovery. Remember FENa under 1% supports prerenal physiology, while muddy brown casts point to ATN. Acute therapy items are few but highly patterned; drill them the week before your PSI appointment.
What is the primary advantage of CRRT over conventional intermittent hemodialysis in a hemodynamically unstable ICU patient?
Which urinalysis finding is most consistent with acute tubular necrosis?
A critically ill patient with AKI needs renal replacement therapy but cannot tolerate rapid ultrafiltration. Which modality best balances solute clearance with hemodynamic tolerance when CRRT is unavailable overnight?