Acute Kidney Injury and Kidney Replacement Therapy in the Critically Ill Patient

IHD is the most common form of KRT used in the acute setting for treating patients with AKI or end-

stage renal disease needing dialysis.

Intradialytic hypotension occurs in up to 30% of patients, which can lead to early dialysis termination

or compromise of residual renal function. Several strategies to improve hemodynamics during

IHD have been suggested, including fluid administration, ultrafiltration and sodium modeling,

periprocedural antihypertensive hold, and midodrine or vasopressor therapy. Selection among

these options is patient-specific and should only be done in conjunction with a careful evaluation of

underlying etiologies for hypotension, including potential infection and cardiac dysfunction.

Patients with preexisting hypotension before IHD (e.g., septic shock), may not tolerate the large fluid

and electrolyte shifts during IHD resulting in further hemodynamic alterations.

In patients with head trauma or hepatic encephalopathy, hypotension can reduce cerebral perfusion.

Changes in solute concentrations can also worsen cerebral edema. Rapid plasma clearance of solutes

acutely decreases their systemic intravascular concentrations while intracranial concentrations

remain unchanged. This relatively high intracranial concentration of solute results in water transport

back across the blood-brain barrier, which contributes to cell swelling, cerebral edema, and increased

intracranial pressure. Careful consideration of IHD use in these populations is warranted.

Continuous KRT is the most commonly used modality of KRT in hemodynamically unstable ICU

patients. Past nomenclature of continuous KRT is continuous renal replacement therapy (CRRT) and

may still be referred to as such in clinical practice or in historical literature.

venovenous hemodialysis (CVVHD), and continuous venovenous hemodiafiltration (CVVHDF).

SCUF, or slow continuous ultrafiltration, is another type of continuous KRT that removes fluid without

the need for replacement solutions. This therapy has limited effect on removal of waste products (e.g.,

BUN) or electrolytes and cannot correct acid-base abnormalities.

Solute clearance during CVVH occurs by convection, and the ultrafiltration rate determines the

clearance rate for most solutes.

Solute clearance during CVVHD occurs by diffusion.

For CVVHDF, solute removal occurs by both convection and diffusion, with diffusion commonly

the dominant waste removal modality.

Because of the continuous nature of continuous KRT and prolonged exposure of blood to foreign surfaces

of the extracorporeal circuit, anticoagulation is often required to prevent circuit clotting, maintain

membrane permeability, and prevent blood loss in the clotted filter. Unfractionated heparin and regional

citrate anticoagulation (RCA) are the most common anticoagulant options. Compared with systemic

unfractionated heparin, RCA has been shown to increase filter life span and decrease bleeding, but

with no difference in mortality. Challenges associated with RCA include accumulation in patients with

reduced liver function and shock states, metabolic complications (acidosis, alkalosis, hypernatremia,

hypocalcemia, and hypercalcemia), increased complexity, and need for use of a strict protocol. Systemic

unfractionated heparin infusion remains an option for anticoagulation when unable to administer RCA.

The recommended dose and monitoring is variable; however, it may be reasonable to titrate to a target

activated partial thromboplastin time of 45–60 seconds or anti-Xa activity of 0.3–0.6 IU/mL. Heparin

may also be administered regionally via infusion into the arterial line of the circuit with administration

of continuous protamine post-filter to inactivate the unfractionated heparin.