5. Renal Replacement Therapy in ICU

Learning Objectives

• Identify the indications for initiating renal replacement therapy (RRT) in critically ill patients
• Compare CRRT, intermittent hemodialysis (IHD), and SLED in terms of mechanism, hemodynamic tolerance, and clinical use
• Describe the components of a CRRT circuit and the parameters that must be monitored during treatment
• Explain anticoagulation strategies used to maintain circuit patency, including citrate and heparin protocols
• Recognize common complications of RRT and how to prevent or manage them
• Apply RRT principles to a clinical vignette involving AKI with hyperkalemia and volume overload

Quick Answer

Renal replacement therapy (RRT) is the use of an extracorporeal circuit to perform the kidney's core jobs — clearing uremic toxins, correcting electrolyte and acid-base derangements, and removing excess fluid — when native renal function fails to keep up. In the ICU, the three workhorse modalities are continuous renal replacement therapy (CRRT), intermittent hemodialysis (IHD), and sustained low-efficiency dialysis (SLED). The choice between them hinges almost entirely on hemodynamic stability: CRRT removes solutes and fluid slowly and continuously, so it is tolerated by patients in shock, while IHD clears faster but causes larger swings in blood volume that unstable patients cannot buffer. RRT is not started for a lab number alone — it is started when a specific, refractory problem (severe hyperkalemia, refractory acidosis, diuretic-resistant volume overload, uremic encephalopathy or pericarditis, or certain toxin ingestions) demands it.

Overview

The kidneys quietly do three jobs every minute of every day: clear nitrogenous waste, balance electrolytes and acid-base status, and regulate fluid volume. When acute kidney injury (AKI) is severe enough that the kidneys can no longer keep pace — especially in a critically ill patient already fighting sepsis, hypotension, or multi-organ failure — an artificial circuit has to take over. That circuit is renal replacement therapy.

It helps to think of RRT less as "dialysis" (a single fixed procedure) and more as a family of techniques that all rely on the same two physical principles: diffusion (solutes move across a semipermeable membrane down a concentration gradient, which is how dialysis clears small molecules like potassium and urea) and convection (fluid is pushed across the membrane under pressure, dragging solutes with it, which is how ultrafiltration and hemofiltration work). Different RRT modalities simply combine these two principles in different proportions and at different speeds, and that combination is what determines whether a modality suits a hemodynamically fragile ICU patient or a stable ward patient.

Roughly 5–10% of ICU patients develop AKI severe enough to need RRT, and mortality in this group remains high (40–60%) — not usually because of the RRT itself, but because RRT is a marker of how sick the underlying illness (sepsis, cardiogenic shock, major surgery) already is. Understanding RRT well means understanding it as one tool within a much larger critical illness picture, not an isolated technical skill.

Why RRT Matters in the ICU

RRT is one of the few ICU interventions that can immediately reverse a life-threatening derangement rather than just supporting the patient through one. That is why it earns a place alongside mechanical ventilation and vasopressors as core organ-support therapy.

• Fluid balance — removes litres of accumulated fluid that diuretics can no longer touch, which matters enormously for oxygenation in a fluid-overloaded, ventilated patient
• Electrolyte correction — clears potassium fast enough to prevent fatal arrhythmias when medical therapy (insulin/glucose, calcium, beta-agonists) has only bought time
• Toxin and waste removal — clears urea, creatinine, and other uremic toxins that cause encephalopathy, platelet dysfunction, and pericarditis
• Acid-base correction — corrects severe metabolic acidosis that is dragging down cardiac contractility and vascular tone
• Buying time for renal recovery — most ICU AKI is potentially reversible; RRT is a bridge, not a cure, while the kidneys heal

Types of RRT

Continuous Renal Replacement Therapy (CRRT)

CRRT runs 24 hours a day at a slow, steady rate, removing fluid and solute gradually rather than in a rapid burst. Because the rate of change is gentle, it is the default choice for hemodynamically unstable ICU patients — those on vasopressors, in septic shock, or with labile intracranial pressure who cannot tolerate the rapid fluid shifts of intermittent dialysis. Several sub-modes exist depending on which physical principle dominates:

• CVVH (continuous venovenous hemofiltration) — pure convection; a replacement fluid is infused and ultrafiltrate is removed
• CVVHD (continuous venovenous hemodialysis) — pure diffusion; dialysate flows countercurrent to blood
• CVVHDF (continuous venovenous hemodiafiltration) — combines both; the most commonly used mode in practice

Intermittent Hemodialysis (IHD)

IHD is the same technology used for outpatient dialysis, run in short, intense sessions of 3–4 hours, several times a week. Blood and dialysate flow rates are far higher than CRRT, so clearance per session is much faster — but so is the volume shift, which is exactly why it is reserved for patients who are hemodynamically stable enough to tolerate rapid fluid removal. It is also useful when urgent, fast correction is needed (e.g., life-threatening hyperkalemia or a dialyzable toxin ingestion) because it works quickly.

Sustained Low-Efficiency Dialysis (SLED)

SLED is the hybrid: it runs for 8–12 hours using lower blood and dialysate flow rates than IHD but is not continuous like CRRT. It gives much of CRRT's hemodynamic gentleness while freeing the patient (and the machine) for procedures, imaging, or transport during the rest of the day — a practical compromise increasingly used in resource-limited ICUs.

Indications for RRT

Students often try to memorize a lab cutoff for "when to dialyze." That is the wrong mental model — RRT is indicated when a specific problem is refractory to medical management, not simply because a number crossed a threshold. The classic mnemonic AEIOU captures this well:

• Acidosis — severe metabolic acidosis (pH < 7.1–7.2) refractory to bicarbonate therapy
• Electrolyte abnormalities — life-threatening hyperkalemia unresponsive to medical therapy
• Intoxication — certain dialyzable poisons/drugs (e.g., methanol, ethylene glycol, lithium, salicylates)
• Overload — volume overload causing pulmonary edema or hypoxemia, resistant to diuretics
• Uremia — uremic encephalopathy, uremic pericarditis, or uremic bleeding

Contraindications

RRT is rarely absolutely contraindicated because it can be life-saving, but certain situations demand caution or a modified approach:

• Active, uncontrolled hemorrhage (anticoagulation for the circuit becomes dangerous)
• Severe hemodynamic instability that even CRRT cannot buffer (may need to correct shock first)
• Lack of vascular access
• Patient or surrogate refusal after informed discussion of goals of care

Equipment and the CRRT Circuit

Understanding the circuit demystifies the whole therapy. Blood is drawn from a large-bore dual-lumen catheter (usually internal jugular or femoral), pumped through the circuit by a blood pump, passed across the hemofilter/dialyzer (the semipermeable membrane where diffusion and/or convection happens), and returned to the patient. Along the way:

1. Dialyzer/hemofilter — the actual filtration membrane; the workhorse of the circuit
2. Blood pump — drives blood flow, typically 150–250 mL/min in CRRT
3. Dialysate pump — delivers dialysis fluid on the opposite side of the membrane (in CVVHD/CVVHDF)
4. Replacement fluid pump — infuses replacement fluid pre- or post-filter (in CVVH/CVVHDF)
5. Ultrafiltration pump — controls the net fluid removal rate independently of solute clearance
6. Pressure and air-bubble monitors — safety systems that stop the pump if pressures are abnormal or air is detected

Key Parameters Monitored During RRT

• Blood flow rate and dialysate/replacement fluid flow rate
• Net ultrafiltration rate (the actual fluid removed per hour)
• Circuit pressures (access, return, filter, and transmembrane pressure) — rising pressures often signal filter clotting
• Electrolytes (potassium, calcium, sodium, phosphate) — checked every 4–6 hours during CRRT
• Acid-base status (pH, bicarbonate)
• Anticoagulation markers — ionized calcium for citrate protocols, aPTT for heparin protocols
• Patient temperature (CRRT circuits can cause significant heat loss)

Anticoagulation

The extracorporeal circuit exposes blood to foreign surfaces, activating the clotting cascade, so without anticoagulation the filter clots and stops working within hours.

• Regional citrate anticoagulation — citrate is infused pre-filter, chelating ionized calcium and preventing clotting only within the circuit; calcium is then replaced systemically post-filter. This is now the preferred method in most ICUs because it does not increase the patient's systemic bleeding risk — a major advantage in septic or post-surgical patients. It requires careful monitoring of ionized calcium (both systemic and post-filter) and can cause citrate accumulation (metabolic alkalosis, rising total-to-ionized calcium ratio) in patients with severe liver failure who cannot metabolize citrate.
• Systemic heparin — simpler to run but anticoagulates the whole patient, increasing bleeding risk; monitored with aPTT. Used when citrate is contraindicated (e.g., severe liver failure) or unavailable.
• No anticoagulation — an option in patients who are already coagulopathic or actively bleeding, accepting a shorter filter lifespan in exchange for not worsening hemorrhage.

Complications of RRT

• Hypotension — especially with IHD's rapid fluid shifts; less common but still possible with CRRT if ultrafiltration is set too aggressively
• Bleeding — from anticoagulation or from the vascular access site
• Electrolyte disturbances — hypokalemia, hypophosphatemia, and hypocalcemia (especially with citrate) from over-correction
• Air embolism — rare but catastrophic; prevented by air-bubble detectors
• Catheter-related infection — the vascular access is a direct line into the bloodstream
• Filter clotting — interrupts therapy and wastes blood in the circuit when it happens
• Hypothermia — from large volumes of blood circulating outside the body, especially with CRRT run over many hours

Nursing and Team Considerations

RRT is a team sport, and bedside nursing vigilance often catches problems before they become emergencies:

• Continuous monitoring of vital signs, circuit pressures, and hourly fluid balance
• Vascular access site care to reduce catheter-related bloodstream infection
• Administering and titrating anticoagulation per protocol, coordinating calcium replacement with citrate infusions
• Recognizing early signs of filter clotting (rising transmembrane pressure, dark blood in the circuit) and troubleshooting promptly
• Communicating fluid balance goals with the intensivist so ultrafiltration targets are adjusted as the patient's hemodynamics change

Choosing a Modality: A Clinical Decision Pathway

Case Vignette: A 65-Year-Old Man with Septic AKI

Mr. Smith, 65, was admitted with septic shock secondary to pneumonia. Over 48 hours his creatinine rose from 1.2 to 3.5 mg/dL, his urine output fell to near-anuric, and his potassium climbed to 6.5 mmol/L despite insulin/glucose and calcium gluconate. He remained on norepinephrine to maintain a MAP above 65 mmHg.

Because he was hemodynamically unstable and had refractory hyperkalemia (an "E" in AEIOU), the team started CRRT (CVVHDF) with a blood flow rate of 200 mL/min and regional citrate anticoagulation, targeting a net ultrafiltration rate of 20 mL/hr initially given his marginal blood pressure. Potassium normalized within 6 hours of starting therapy. Over the next 72 hours his vasopressor requirement fell, his creatinine trended down to 2.0 mg/dL, and urine output returned. The team transitioned him off CRRT once he was hemodynamically stable and making adequate urine, confirming renal recovery over the following days.

This case illustrates the core teaching point: the modality was chosen by hemodynamic status and the specific refractory problem (hyperkalemia), not by the creatinine value alone, and RRT was stopped as soon as native kidney function recovered — RRT is a bridge, not a permanent fixture.

Key Terms

Term	Definition	Related Concept
CRRT	Continuous Renal Replacement Therapy — 24-hour dialysis for hemodynamically unstable patients	CVVH, CVVHD, CVVHDF
CVVHDF	Continuous venovenous hemodiafiltration — combines diffusion and convection; most common CRRT mode	Dialysate, replacement fluid
IHD	Intermittent Hemodialysis — short, high-efficiency sessions for stable patients	Rapid clearance, fluid shifts
SLED	Sustained Low-Efficiency Dialysis — hybrid of CRRT and IHD, 8–12 hour sessions	Intermediate stability
Ultrafiltration	Convective removal of fluid across the dialysis membrane driven by pressure	Fluid overload management
Regional Citrate Anticoagulation	Anticoagulates only the extracorporeal circuit by chelating calcium; calcium replaced systemically	Circuit patency, ionized calcium
AEIOU	Mnemonic for RRT indications — Acidosis, Electrolyte imbalance, Intoxication, Overload, Uremia	Indications for RRT
Transmembrane Pressure	Pressure gradient across the filter membrane; rises as the filter clots	Filter lifespan, circuit troubleshooting
Uremic Encephalopathy	Confusion/altered mental status from accumulated uremic toxins	Indication for urgent RRT

Common Mistakes

Misconception: RRT should be started as soon as creatinine crosses a fixed numeric threshold (e.g., creatinine > 4 mg/dL). Why it's wrong: There is no universal creatinine or BUN cutoff that mandates dialysis. Two patients with identical creatinine values may have very different clinical pictures — one stable and improving, the other with refractory hyperkalemia and pulmonary edema. Correct understanding: RRT is indicated by specific, refractory clinical problems (AEIOU: acidosis, electrolytes, intoxication, overload, uremia) that have failed medical management, not by a lab number in isolation.

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Misconception: CRRT and IHD are interchangeable, and the choice is just about machine availability. Why it's wrong: The two modalities differ fundamentally in the rate of fluid and solute removal. Placing a hemodynamically unstable patient on IHD risks profound hypotension from rapid fluid shifts, which can worsen renal and end-organ perfusion — the opposite of what dialysis is meant to achieve. Correct understanding: Modality choice is driven primarily by hemodynamic stability. CRRT is default for unstable ICU patients; IHD suits stable patients or emergencies needing very fast correction; SLED is a practical middle ground.

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Misconception: Heparin is always required to keep an RRT circuit from clotting. Why it's wrong: Systemic heparin anticoagulates the entire patient, not just the circuit, which is a real problem in septic, post-surgical, or coagulopathic ICU patients who already have bleeding risk. Correct understanding: Regional citrate anticoagulation confines the anticoagulant effect to the circuit itself and has become the preferred first-line strategy in most modern ICUs specifically because it avoids systemic bleeding risk; heparin or no anticoagulation are reserved for specific situations (citrate contraindicated, or active bleeding).

Comparison and Connections

Feature	CRRT	Intermittent Hemodialysis (IHD)	SLED
Duration per session	Continuous (24 hr/day)	3–4 hours, 3x/week	8–12 hours
Best for	Hemodynamically unstable patients	Hemodynamically stable patients	Intermediate stability
Fluid/solute removal rate	Slow, gradual	Rapid	Moderate
Hemodynamic tolerance	Excellent	Poor in unstable patients	Good
Anticoagulation	Continuous (citrate preferred)	Brief, session-only	Moderate duration
Ability to correct severe hyperkalemia fast	Slower	Fastest	Intermediate
Resource/nursing burden	High (24-hr monitoring)	Lower (session-based)	Moderate
Typical ICU setting	First-line in ICU	More common outside ICU or for urgent correction	Flexible, resource-limited ICUs

Practice Questions

Recall

1. What does the AEIOU mnemonic stand for in the context of RRT indications? Answer guidance: Acidosis (severe, refractory metabolic acidosis), Electrolyte abnormalities (life-threatening hyperkalemia), Intoxication (dialyzable toxins like methanol, ethylene glycol, lithium, salicylates), Overload (diuretic-resistant volume overload), Uremia (encephalopathy, pericarditis, or bleeding).

2. Name the three main RRT modalities used in the ICU and roughly how long each session lasts. Answer guidance: CRRT (continuous, 24 hours/day), Intermittent Hemodialysis/IHD (3–4 hours, several times a week), SLED (8–12 hours, hybrid schedule).

Understanding

3. Explain why CRRT is better tolerated than IHD in a patient with septic shock on norepinephrine. Answer guidance: CRRT removes fluid and solutes slowly and continuously, so intravascular volume shifts gradually and the cardiovascular system can compensate. IHD removes a similar total volume much faster, causing rapid drops in intravascular volume that a vasopressor-dependent, already-vasodilated septic patient cannot buffer, risking severe hypotension and further renal/organ hypoperfusion.

4. Why is regional citrate anticoagulation generally preferred over systemic heparin in critically ill patients? Answer guidance: Citrate chelates calcium only within the extracorporeal circuit, preventing clotting there, while calcium is replaced systemically so the patient's own coagulation is not impaired. Heparin anticoagulates the entire patient, raising systemic bleeding risk, which is particularly dangerous in septic, post-operative, or coagulopathic ICU patients.

Application

5. A ventilated ICU patient in septic shock on two vasopressors develops potassium of 7.0 mmol/L with peaked T waves on ECG despite insulin/glucose and calcium gluconate. Which RRT modality should be started, and why? Answer guidance: CRRT, because the patient is hemodynamically unstable (on two vasopressors) and cannot tolerate the rapid fluid/solute shifts of IHD, even though IHD clears potassium faster. Immediate temporizing measures (calcium for cardiac membrane stabilization, insulin/glucose, possibly bicarbonate) continue while CRRT is set up; CRRT will steadily correct the hyperkalemia without worsening hemodynamics.

6. A patient with severe liver failure needs RRT for volume overload. The team is considering citrate anticoagulation. What complication should they anticipate, and what alternative might they use? Answer guidance: Patients with severe liver failure cannot metabolize citrate effectively, risking citrate accumulation — manifesting as metabolic alkalosis and a rising total-to-ionized calcium ratio ("citrate lock"). The team should monitor this ratio closely or consider using systemic heparin (if bleeding risk allows) or a no-anticoagulation strategy as an alternative.

Analysis

7. Compare the trade-offs of choosing SLED versus CRRT for a moderately stable ICU patient who needs a CT scan and other procedures during the day. Answer guidance: CRRT offers the gentlest, most continuous correction but ties the patient to the machine 24 hours a day, complicating transport for imaging or procedures. SLED offers most of CRRT's hemodynamic gentleness in a condensed 8–12 hour window, freeing the rest of the day for procedures — a practical trade-off when the patient is stable enough to tolerate the somewhat faster clearance rate of SLED.

8. A patient on CRRT develops rising transmembrane pressure and dark, sluggish blood in the circuit tubing over several hours. What is happening, and what are the downstream consequences if untreated? Answer guidance: This describes filter clotting, usually from inadequate anticoagulation or a kinked/malpositioned catheter. If untreated, the filter will clot off completely, stopping solute and fluid clearance, wasting the blood volume held in the circuit (a real blood loss for the patient), and requiring a new circuit setup — interrupting therapy and delaying correction of the underlying electrolyte or fluid problem.

FAQ

How do doctors decide when a patient no longer needs RRT? The main signal is renal recovery: rising urine output, falling creatinine, and resolution of the original indication (potassium, acidosis, or fluid overload corrected). Many ICUs use a trial of stopping RRT and watching urine output and labs over the next day; if the kidneys are recovering, RRT is not restarted. There is no single perfect predictive test, so this remains partly clinical judgment.

Can a patient be on more than one type of RRT during their ICU stay? Yes, and it is common. A patient often starts on CRRT while hemodynamically unstable, then transitions to SLED or IHD as vasopressors are weaned and blood pressure stabilizes. The modality is reassessed daily against the patient's current hemodynamic status, not fixed for the whole admission.

Does starting RRT mean the kidneys will never recover? No. Most ICU AKI, especially from sepsis or an ischemic insult, is potentially reversible. RRT is a bridge that supports the patient while the kidneys heal, not a marker of permanent kidney failure. Some patients do progress to chronic dialysis dependence, but this is the minority, and recovery is more likely when the underlying insult (e.g., septic shock) is treated promptly.

Why do CRRT patients sometimes get cold during treatment? Blood circulates through a large extracorporeal circuit continuously for many hours, losing heat to the environment along the way. This can cause measurable hypothermia, which is usually managed with an in-line blood warmer on the circuit and close temperature monitoring, since hypothermia can also mask fever from an underlying infection.

Is peritoneal dialysis ever used in the ICU? It can be, particularly in resource-limited settings or in pediatric ICUs, but it is far less common than CRRT, IHD, or SLED in adult critical care because it clears solutes more slowly and is harder to control precisely in a hemodynamically unstable patient. It remains an option when hemodialysis access or equipment is unavailable.

Quick Revision

• RRT replaces three kidney jobs: solute clearance, fluid removal, and acid-base/electrolyte correction
• Two physical principles: diffusion (dialysis, clears small solutes) and convection (ultrafiltration/hemofiltration, drags fluid and solute together)
• Three main modalities: CRRT (continuous, unstable patients), IHD (fast, stable patients), SLED (hybrid, 8–12 hr)
• Indications = AEIOU: Acidosis, Electrolyte imbalance, Intoxication, Overload, Uremia — not a fixed creatinine number
• CRRT is preferred in the ICU because slow, continuous removal avoids the hemodynamic swings of IHD
• CVVHDF (combined diffusion + convection) is the most commonly used CRRT sub-mode
• Regional citrate anticoagulation is now first-line; avoids systemic bleeding risk but requires calcium monitoring and caution in liver failure
• Rising transmembrane pressure signals impending filter clotting — a common cause of interrupted therapy
• Complications: hypotension, bleeding, electrolyte shifts, air embolism, catheter infection, hypothermia
• RRT is a bridge to renal recovery in most ICU AKI, not a permanent therapy
• Modality choice can and should change over the admission as the patient's hemodynamic status changes

Related Topics

Prerequisites: Renal physiology (GFR, tubular function), acid-base physiology, fluid and electrolyte balance, basic vascular access procedures

Related Topics: Intensive Care Unit Procedures, Acute Kidney Injury, Sepsis Management in ICU, Hemodynamic Monitoring, Electrolyte Emergencies

Next Topics: Acid-Base Disorders in Critical Care, Vasopressor and Inotrope Selection, Chronic Kidney Disease and Long-Term Dialysis, Toxicology and Extracorporeal Removal of Poisons