treaatment of hepato renal syndrome

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2024 AASLD hepatorenal syndrome acute kidney injury treatment terlipressin albumin guidance

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https://pmc.ncbi.nlm.nih.gov/articles/PMC10524408

Hepatorenal syndrome treatment

Hepatorenal syndrome-acute kidney injury (HRS-AKI) is an emergency in advanced cirrhosis, usually with ascites. It requires hospital management, early hepatology input, and assessment for liver transplantation, the only definitive treatment.

1. Confirm HRS-AKI and correct reversible causes

Before labeling AKI as HRS, clinicians should:

Stop nephrotoxic drugs, especially NSAIDs, ACE inhibitors/ARBs, and avoid IV contrast where possible.
Hold diuretics temporarily if volume depletion is possible.
Look for and promptly treat triggers: spontaneous bacterial peritonitis, other infections, GI bleeding, diarrhea/vomiting, excessive paracentesis without albumin, and shock.
Exclude obstruction and intrinsic renal injury, including acute tubular necrosis.
Give an albumin volume challenge when appropriate, commonly 1 g/kg/day of 20-25% albumin, maximum 100 g/day, for 2 days, while carefully checking for pulmonary edema or fluid overload.

2. Vasoconstrictor plus albumin: first-line disease-specific therapy

The usual preferred treatment for confirmed HRS-AKI is terlipressin plus IV albumin. Terlipressin constricts the splanchnic circulation, improving effective arterial volume and renal perfusion. AASLD-based guidance identifies terlipressin plus albumin as the preferred regimen. AASLD-based management review

Terlipressin: dose depends on local protocol/product labeling. In the US, a commonly used label-based regimen starts at 0.85 mg IV every 6 hours for 3 days, then is adjusted according to serum-creatinine response, for a maximum of 14 days.
Albumin during treatment: often 20-40 g/day, individualized to volume status. Do not give albumin indiscriminately if there is pulmonary edema or major volume overload. AASLD albumin review

Monitor closely: blood pressure, urine output, serum creatinine, sodium, fluid balance, ischemic symptoms, and oxygen saturation.

Important safety issue: terlipressin may cause serious or fatal respiratory failure and can cause coronary, mesenteric, or peripheral ischemia. Avoid or stop it in hypoxia, worsening respiratory symptoms, or ongoing ischemia; continuous pulse-oximetry monitoring is recommended. The textbook likewise identifies terlipressin plus albumin as a bridge to transplant but warns about respiratory failure. Goldman-Cecil Medicine, Hepatorenal Syndrome section.

3. If terlipressin is unavailable or unsuitable

Norepinephrine plus albumin: preferred alternative, generally given in an ICU because it requires continuous vasopressor infusion and close hemodynamic monitoring.
Midodrine plus octreotide plus albumin: an option if neither terlipressin nor norepinephrine can be used, but it is less effective than the other two approaches.

4. Treat complications and consider renal replacement therapy

Treat sepsis, GI bleeding, hypotension, encephalopathy, and electrolyte disturbances.
Dialysis/continuous renal replacement therapy is used for standard urgent indications: refractory hyperkalemia, severe acidosis, pulmonary edema/volume overload, or uremic complications.
Dialysis is mainly a bridge to liver transplant or recovery from a reversible acute insult. It does not correct the underlying circulatory/liver failure.

5. Liver transplantation

Urgently refer or reassess for liver transplantation. Vasoconstrictor therapy may reverse AKI in some people and improve pre-transplant stability, but it does not cure the liver disease. HRS is a transplant-priority condition. Current management review

6. Procedures

TIPS may help selected patients with portal-hypertension complications, but it is not routine acute treatment for HRS-AKI and is unsuitable in many patients with severe liver failure, encephalopathy, or cardiac dysfunction.
Extracorporeal albumin dialysis is experimental or highly specialized, not standard first-line management.

Recent evidence

Recent systematic reviews continue to support terlipressin-based therapy for HRS reversal, though respiratory and ischemic adverse effects require careful patient selection and monitoring: 2025 meta-analysis, PMID 40207491 and 2024 systematic review, PMID 39295934.

Practical summary:
Stop precipitants and nephrotoxins -> albumin challenge and infection evaluation -> terlipressin + albumin if HRS-AKI persists -> norepinephrine if terlipressin cannot be used -> dialysis only when indicated/bridge -> urgent transplant evaluation.

Which ONE of the following statements regarding the modality of RRT in this clinical setting is evidence based? A. CRRT would be associated with a greater probability of survival compared with intermittent hemodialysis. B. Intermittent hemodialysis would be associated with an increased risk of combined death and irreversible renal function. C. SLED would provide more rapid correction of metabolic acidosis than CRRT. D. CRRT would be associated with a greater probability of achieving negative net fluid balance than SLED.

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cirrhosis acute kidney injury renal replacement therapy CRRT SLED intermittent hemodialysis survival fluid balance evidence

C. SLED would provide more rapid correction of metabolic acidosis than CRRT.

SLED is an extended intermittent modality with higher solute clearance over a treatment session than CRRT, so it can correct severe metabolic acidosis more quickly. Guidelines suggest IHD or SLED over CRRT for rapid correction of metabolic acidosis. ICU AKI/RRT guideline summary

Why the others are incorrect:

A: CRRT has no proven survival advantage over intermittent hemodialysis.
B: IHD has not been shown to increase the combined outcome of death and irreversible loss of renal function compared with CRRT.
D: CRRT permits gradual, precise fluid removal, but evidence does not show it achieves a greater net negative fluid balance than SLED.

CRRT or SLED is generally chosen over IHD when the patient is hemodynamically unstable; modality selection should be individualized. Brenner and Rector’s The Kidney, SLED section.

A 7-year-old girl is to begin chemotherapy for a poorly differentiated non-Hodgkin lymphoma. Which ONE of the following is NOT effective at reducing her risk of developing AKI as a result of induction chemotherapy? A. Furosemide. B. Rasburicase. C. Allopurinol. D. Isotonic saline. E. Sodium bicarbonate.

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pediatric tumor lysis syndrome prevention bicarbonate furosemide hydration rasburicase allopurinol guideline

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https://www.ncbi.nlm.nih.gov/books/NBK518985

E. Sodium bicarbonate

Routine urine alkalinization with sodium bicarbonate is not recommended for prevention of tumor lysis syndrome-associated AKI. Although it increases uric acid solubility, it can promote calcium-phosphate precipitation in renal tubules and worsen hypocalcemia. It is generally reserved only for specific situations such as significant metabolic acidosis when rasburicase is unavailable.

Effective preventive measures are:

Isotonic saline to maintain renal perfusion and high urine flow
Rasburicase for rapid uric-acid reduction in high-risk TLS
Allopurinol to prevent new uric-acid formation
Furosemide may be used selectively to maintain urine output after adequate hydration, not in hypovolemia

The primary TLS prophylaxis strategies are hydration plus allopurinol or rasburicase, while bicarbonate is no longer routinely advised. TLS management review

Urinary alkalinization using sodium bicarbonate has also been recommended as a prophylactic measure to increase the urinary solubility of uric acid; however, urinary alkalinization may increase the risk of calcium phosphate precipitation in patients with concomitant hyperphosphatemia. There is, however, no role for loop-acting diuretics such as furosemide for the prevention of AKI in the tumor lysis syndrome. is this true ??

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tumor lysis syndrome prophylaxis furosemide loop diuretic no role AKI prevention guideline urine alkalinization sodium bicarbonate

Yes, that statement is true. My previous answer was incorrect.

For the MCQ, the best answer is:

A. Furosemide

Loop diuretics do not prevent tumor lysis syndrome-associated AKI. They should not be given routinely to force diuresis, because they can worsen intravascular volume depletion. They may be considered only after adequate hydration in a patient with fluid overload or inadequate urine output, after excluding hypovolemia and urinary obstruction. TLS management review

How to reconcile sodium bicarbonate

Sodium bicarbonate/urinary alkalinization was historically recommended because it raises uric-acid solubility.
However, modern practice generally does not recommend it routinely, because alkaline urine may promote calcium-phosphate precipitation, especially with hyperphosphatemia, and may worsen AKI and hypocalcemia. Haematologica review
In an exam framed around older or traditional prophylactic measures, bicarbonate may still be listed as a measure that has been recommended, whereas furosemide is the clearly incorrect prophylactic intervention.

High-yield answer:
Hydration with isotonic saline + allopurinol or rasburicase are preventive measures. Do not use furosemide routinely to prevent AKI.

The differential diagnosis of AKI in a patient with advanced liver disease includes prerenal azotemia, acute tubular necrosis, hepatorenal syndrome, and glomerular disease. In this patient, the primary differentiation is between prerenal azotemia and hepatorenal syndrome. Glomerular disease is unlikely given the absence of proteinuria and hematuria. Acute tubular necrosis is unlikely given the very low urine sodium concentration. Hepatorenal syndrome is differentiated from a prerenal state based on an assessment of effective intravascular volume and/or the response to a volume challenge. The appropriate intervention should therefore be intravascular volume expansion as both a diagnostic and therapeutic trial.1 There is no evidence to support the administration of hypertonic albumin or other colloid solutions in the routine management of renal dysfunction in patients with advanced liver disease (choice B is incorrect). The combination of octreotide and midodrine is of potential benefit in patients with hepatorenal syndrome; however, this diagnosis has not yet been established in this patient (choice D is incorrect). Placement of a transjugular intrahepatic portosystemic shunt may be of benefit in some patients with hepatorenal syndrome, particularly if they have responded to vasoconstrictor therapy, but should not be used before establishment of the diagnosis and should probably be withheld until after a trial of vasoconstrictors (choice E is incorrect). is this true ??

Differential diagnosis of AKI in advanced cirrhosis
Prerenal azotemia, HRS-AKI, acute tubular necrosis, and glomerular disease.
Distinguishing prerenal AKI from HRS-AKI
Volume status, removal of precipitants, albumin challenge, and diagnostic criteria.
Role of urine sodium and urinalysis
Their limitations in cirrhosis, including why low urine sodium does not reliably exclude ATN.
Initial treatment of AKI in advanced liver disease
Diuretic/nephrotoxin withdrawal, infection and bleeding assessment, crystalloid versus albumin, and monitoring for overload.
Therapy after HRS-AKI is established
Terlipressin plus albumin, norepinephrine, midodrine-octreotide, transplant referral, and restricted roles for TIPS and dialysis.

At a high level, the quoted passage is broadly correct in prioritizing volume assessment and a response-to-volume strategy before diagnosing HRS-AKI. However, it is dated or oversimplified in important ways: current HRS-AKI work-up commonly uses an albumin-based volume challenge in appropriate patients, and low urine sodium alone does not reliably rule out ATN in cirrhosis.

The passage is also right that vasoconstrictor therapy and TIPS should not routinely precede confirmation of HRS-AKI. The precise choice and amount of volume expansion, especially albumin, depends on whether the patient is depleted, infected, bleeding, or fluid overloaded.

Asking for Preferences

Which part should I examine in detail against current evidence?

Your credits are exhausted. You can purchase a top-up or subscribe to a plan to continue using Orris. If you're already subscribed, your daily credits will reset tomorrow.## Hepatorenal syndrome treatment

Hepatorenal syndrome-acute kidney injury (HRS-AKI) is an emergency in advanced cirrhosis, usually with ascites. It requires hospital management, early hepatology input, and assessment for liver transplantation, the only definitive treatment.

1. Confirm HRS-AKI and correct reversible causes

Before labeling AKI as HRS, clinicians should:

Stop nephrotoxic drugs, especially NSAIDs, ACE inhibitors/ARBs, and avoid IV contrast where possible.
Hold diuretics temporarily if volume depletion is possible.
Look for and promptly treat triggers: spontaneous bacterial peritonitis, other infections, GI bleeding, diarrhea/vomiting, excessive paracentesis without albumin, and shock.
Exclude obstruction and intrinsic renal injury, including acute tubular necrosis.
Give an albumin volume challenge when appropriate, commonly 1 g/kg/day of 20-25% albumin, maximum 100 g/day, for 2 days, while carefully checking for pulmonary edema or fluid overload.

2. Vasoconstrictor plus albumin: first-line disease-specific therapy

The usual preferred treatment for confirmed HRS-AKI is terlipressin plus IV albumin. Terlipressin constricts the splanchnic circulation, improving effective arterial volume and renal perfusion. AASLD-based guidance identifies terlipressin plus albumin as the preferred regimen. AASLD-based management review

Terlipressin: dose depends on local protocol/product labeling. In the US, a commonly used label-based regimen starts at 0.85 mg IV every 6 hours for 3 days, then is adjusted according to serum-creatinine response, for a maximum of 14 days.
Albumin during treatment: often 20-40 g/day, individualized to volume status. Do not give albumin indiscriminately if there is pulmonary edema or major volume overload. AASLD albumin review

Monitor closely: blood pressure, urine output, serum creatinine, sodium, fluid balance, ischemic symptoms, and oxygen saturation.

Important safety issue: terlipressin may cause serious or fatal respiratory failure and can cause coronary, mesenteric, or peripheral ischemia. Avoid or stop it in hypoxia, worsening respiratory symptoms, or ongoing ischemia; continuous pulse-oximetry monitoring is recommended. The textbook likewise identifies terlipressin plus albumin as a bridge to transplant but warns about respiratory failure. Goldman-Cecil Medicine, Hepatorenal Syndrome section.

3. If terlipressin is unavailable or unsuitable

Norepinephrine plus albumin: preferred alternative, generally given in an ICU because it requires continuous vasopressor infusion and close hemodynamic monitoring.
Midodrine plus octreotide plus albumin: an option if neither terlipressin nor norepinephrine can be used, but it is less effective than the other two approaches.

4. Treat complications and consider renal replacement therapy

Treat sepsis, GI bleeding, hypotension, encephalopathy, and electrolyte disturbances.
Dialysis/continuous renal replacement therapy is used for standard urgent indications: refractory hyperkalemia, severe acidosis, pulmonary edema/volume overload, or uremic complications.
Dialysis is mainly a bridge to liver transplant or recovery from a reversible acute insult. It does not correct the underlying circulatory/liver failure.

5. Liver transplantation

Urgently refer or reassess for liver transplantation. Vasoconstrictor therapy may reverse AKI in some people and improve pre-transplant stability, but it does not cure the liver disease. HRS is a transplant-priority condition. Current management review

6. Procedures

TIPS may help selected patients with portal-hypertension complications, but it is not routine acute treatment for HRS-AKI and is unsuitable in many patients with severe liver failure, encephalopathy, or cardiac dysfunction.
Extracorporeal albumin dialysis is experimental or highly specialized, not standard first-line management.

Recent evidence

Recent systematic reviews continue to support terlipressin-based therapy for HRS reversal, though respiratory and ischemic adverse effects require careful patient selection and monitoring: 2025 meta-analysis, PMID 40207491 and 2024 systematic review, PMID 39295934.

Practical summary:
**Stop precipitants and nephrotoxins -> albumin challenge and infection evaluation -> terlipressin + albumin if HRS-AKI persists -> norepinephrine if terlipressin cannot be used -> dialysis only when indicated/bridge -> urgent transplant evaluation.**C. SLED would provide more rapid correction of metabolic acidosis than CRRT.

SLED is an extended intermittent modality with higher solute clearance over a treatment session than CRRT, so it can correct severe metabolic acidosis more quickly. Guidelines suggest IHD or SLED over CRRT for rapid correction of metabolic acidosis. ICU AKI/RRT guideline summary

Why the others are incorrect:

A: CRRT has no proven survival advantage over intermittent hemodialysis.
B: IHD has not been shown to increase the combined outcome of death and irreversible loss of renal function compared with CRRT.
D: CRRT permits gradual, precise fluid removal, but evidence does not show it achieves a greater net negative fluid balance than SLED.

CRRT or SLED is generally chosen over IHD when the patient is hemodynamically unstable; modality selection should be individualized. Brenner and Rector’s The Kidney, SLED section.E. Sodium bicarbonate

Routine urine alkalinization with sodium bicarbonate is not recommended for prevention of tumor lysis syndrome-associated AKI. Although it increases uric acid solubility, it can promote calcium-phosphate precipitation in renal tubules and worsen hypocalcemia. It is generally reserved only for specific situations such as significant metabolic acidosis when rasburicase is unavailable.

Effective preventive measures are:

Isotonic saline to maintain renal perfusion and high urine flow
Rasburicase for rapid uric-acid reduction in high-risk TLS
Allopurinol to prevent new uric-acid formation
Furosemide may be used selectively to maintain urine output after adequate hydration, not in hypovolemia

The primary TLS prophylaxis strategies are hydration plus allopurinol or rasburicase, while bicarbonate is no longer routinely advised. TLS management reviewYes, that statement is true. My previous answer was incorrect.

For the MCQ, the best answer is:

A. Furosemide

Loop diuretics do not prevent tumor lysis syndrome-associated AKI. They should not be given routinely to force diuresis, because they can worsen intravascular volume depletion. They may be considered only after adequate hydration in a patient with fluid overload or inadequate urine output, after excluding hypovolemia and urinary obstruction. TLS management review

How to reconcile sodium bicarbonate

Sodium bicarbonate/urinary alkalinization was historically recommended because it raises uric-acid solubility.
However, modern practice generally does not recommend it routinely, because alkaline urine may promote calcium-phosphate precipitation, especially with hyperphosphatemia, and may worsen AKI and hypocalcemia. Haematologica review
In an exam framed around older or traditional prophylactic measures, bicarbonate may still be listed as a measure that has been recommended, whereas furosemide is the clearly incorrect prophylactic intervention.

High-yield answer:
Hydration with isotonic saline + allopurinol or rasburicase are preventive measures. Do not use furosemide routinely to prevent AKI.1. Differential diagnosis of AKI in advanced cirrhosis
Prerenal azotemia, HRS-AKI, acute tubular necrosis, and glomerular disease.

Distinguishing prerenal AKI from HRS-AKI
Volume status, removal of precipitants, albumin challenge, and diagnostic criteria.
Role of urine sodium and urinalysis
Their limitations in cirrhosis, including why low urine sodium does not reliably exclude ATN.
Initial treatment of AKI in advanced liver disease
Diuretic/nephrotoxin withdrawal, infection and bleeding assessment, crystalloid versus albumin, and monitoring for overload.
Therapy after HRS-AKI is established
Terlipressin plus albumin, norepinephrine, midodrine-octreotide, transplant referral, and restricted roles for TIPS and dialysis.

At a high level, the quoted passage is broadly correct in prioritizing volume assessment and a response-to-volume strategy before diagnosing HRS-AKI. However, it is dated or oversimplified in important ways: current HRS-AKI work-up commonly uses an albumin-based volume challenge in appropriate patients, and low urine sodium alone does not reliably rule out ATN in cirrhosis.

The passage is also right that vasoconstrictor therapy and TIPS should not routinely precede confirmation of HRS-AKI. The precise choice and amount of volume expansion, especially albumin, depends on whether the patient is depleted, infected, bleeding, or fluid overloaded.

: The CVVH method uses hydrostatic pressure across a semipermeable membrane for ultrafiltration using convection to filter solutes.1 Higher- and lower-molecular-weight solutes are transported with equal efficiency until the molecular radius of the solute exceeds the membrane pore size. A solute replacement fluid is required to allow sufficient solute clearance. The replacement fluid can be administered either before or after filtration. is this true ??

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continuous venovenous hemofiltration CVVH convection replacement fluid predilution postdilution solute clearance review

Mostly true, with one important qualification.

CVVH uses a transmembrane hydrostatic-pressure gradient to produce ultrafiltration.
Solutes are removed mainly by convection or solvent drag: solutes carried with filtered plasma water across the hemofilter.
The ultrafiltrate removed in excess of the desired net fluid loss is replaced with sterile replacement fluid to maintain volume and deliver the intended clearance dose.
Replacement fluid can be given prefilter (predilution) or postfilter (postdilution).

The inaccurate/overstated part is:

“Higher- and lower-molecular-weight solutes are transported with equal efficiency until the molecular radius exceeds the membrane pore size.”

In practice, convective clearance is not identical for all solutes below the pore cutoff. It depends on the sieving coefficient, which is affected by molecular size, shape/charge, protein binding, membrane characteristics, and filter fouling. Small solutes usually have sieving coefficients close to 1; clearance progressively falls as a solute's size approaches the membrane cutoff. Convection does generally remove larger, middle-molecular-weight solutes better than diffusion at comparable small-solute clearance.

Predilution vs postdilution

Predilution: replacement fluid is infused before the filter. It reduces hemoconcentration and clotting risk but dilutes blood entering the filter, so solute clearance is lower for a given effluent rate.
Postdilution: replacement is infused after the filter. It gives more efficient solute clearance but causes greater hemoconcentration within the filter.

This is consistent with a CKRT prescribing review, which describes CVVH as hydrostatic-pressure-driven ultrafiltration with prefilter or postfilter replacement, and notes the clearance trade-off with predilution.

expand sled, CVVH , CRRT,IHD,CVVHD

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CRRT CVVH CVVHD SLED IHD definitions renal replacement therapy

Abbreviation	Full form	Key principle
SLED	Sustained Low-Efficiency Dialysis	Prolonged intermittent dialysis, usually 6-12 hours, with slower blood and dialysate flows than standard IHD.
CVVH	Continuous Veno-Venous Hemofiltration	A CRRT mode using convection. Plasma water is ultrafiltered across the membrane and replacement fluid is infused.
CRRT	Continuous Renal Replacement Therapy	Umbrella term for continuous 24-hour extracorporeal renal support used mainly in critically ill, hemodynamically unstable patients.
IHD	Intermittent Hemodialysis	Conventional dialysis, typically 3-4 hours per session, with rapid diffusion-based solute and fluid removal.
CVVHD	Continuous Veno-Venous Hemodialysis	A CRRT mode using diffusion. Dialysate flows countercurrent to blood across the membrane.

Also commonly tested:

Abbreviation	Full form	Principle
CVVHDF	Continuous Veno-Venous Hemodiafiltration	Combines convection from hemofiltration and diffusion from hemodialysis.
PIRRT	Prolonged Intermittent Renal Replacement Therapy	Broad name for hybrid therapies such as SLED.
SCUF	Slow Continuous Ultrafiltration	Mainly fluid removal, with little solute clearance.

Quick comparison

IHD: fastest correction of severe hyperkalemia or acidosis, but can cause hypotension due to rapid fluid/solute shifts.
SLED: intermediate modality. Gentler than IHD, more flexible and less resource-intensive than CRRT.
CRRT: continuous and gradual. Better tolerated during shock or unstable blood pressure; permits tightly controlled fluid balance.
CVVH: CRRT by convection.
CVVHD: CRRT by diffusion.
CVVHDF: CRRT by both convection and diffusion.

A memory aid:

HemoFILTRATION = convection = replacement fluid
HemoDIALYSIS = diffusion = dialysate
HemoDIAFILTRATION = both

Harrison’s Principles of Internal Medicine, AKI supportive measures section, describes CVVH as hydrostatic-pressure-driven convective clearance; Brenner and Rector’s The Kidney identifies SLED as a prolonged intermittent/hybrid modality.

A 2-year-old boy develops oliguric acute renal failure in the setting of multiple organ failure after a motor vehicle accident . with low bP with vasopresssor support Which ONE of the following statements regarding RRT in this setting is evidenced based? A. Intermittent hemodialysis is associated with increased mortality compared with CRRT. B. Survival with sustained low-efficiency hemodialysis is comparable to survival with CRRT. C. Intermittent hemodialysis should be prescribed to deliver a single-pool Kt/V of 1.2 on a 3-times-per-week schedule. D. CRRT should be prescribed to deliver an effluent flow rate of 25 mL/kg/h. E. CRRT will provide greater volume removal with less hemodynamic instability than intermittent hemodialysis

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pediatric acute kidney injury renal replacement therapy CRRT SLED survival effluent 25 mL kg hour guidelines

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D. CRRT should be prescribed to deliver an effluent flow rate of 25 mL/kg/h.

For a critically ill child with oliguric AKI, multiple-organ failure, hypotension, and vasopressor need, CRRT is generally preferred because it enables gradual solute and fluid removal with better hemodynamic tolerance.

The evidence-based CRRT dose is a delivered effluent dose of about 20-25 mL/kg/h. Because interruptions and circuit downtime reduce actual delivery, clinicians may prescribe a slightly higher rate, often 25-30 mL/kg/h. Current pediatric guidance supports an initial effluent volume of 25-30 mL/kg/h. KDIGO 2026 public-review draft

Why the others are not the best answer:

A: No convincing evidence shows higher mortality with IHD versus CRRT. Modality choice has not demonstrated a consistent survival difference.
B: SLED/PIRRT and CRRT have shown similar survival in mainly adult ICU studies, but this does not establish SLED as the evidence-based modality in a 2-year-old, and pediatric data are limited.
C: A thrice-weekly single-pool Kt/V target of 1.2 is a chronic maintenance hemodialysis prescription, not an appropriate standard prescription for severe AKI with ongoing metabolic and fluid demands.
E: CRRT is usually hemodynamically better tolerated than IHD, but it does not necessarily produce greater net volume removal. Net ultrafiltration must be individualized, and excessive removal can worsen shock.

Brenner and Rector’s The Kidney states that in critically ill AKI, CRRT effluent should be targeted at 25 mL/kg/hour.