acute kidney injury

Acute Kidney Injury“Laying Siege to Life”

2020 NURSING SYMPOSIUM

DisclosuresRelevant Financial Relationships:◦ None

Relevant Non-Financial Relationships:◦ Medical Director at a Fresenius Kidney Care Center

Acute kidney injury - Facts

Complicates 5% of hospital admissions

Affects 30-50% of intensive care patients

Prerenal failure is most common etiology

Hospital mortality as high as 20-25%

Death remains high in the first year after hospitalization (28% in a study from Ontario, CA)

BMJ 2015;351:h5639

Risk of postoperative acute kidney injury in patients undergoing orthopaedic surgery—development and validation of a risk score and effect of acute kidney injury on survival: observational cohort study

Acute kidney injury - Facts

Average duration of AKI is 7 to 21 days - although

highly variable

Recurrent AKI is associated with higher

risk of CKD and/or death

AKI is associated with a higher mortality

Acute Kidney Injury may lead to CKDRisk factors that may increase risk of chronic injury:◦ Preexisting chronic kidney disease

◦ Prolonged ischemia

◦ Repeated injuries

◦ Older age

◦ Heart or liver failure

◦ Albuminuria

Acute kidney injury after cardiac surgery in eastern Saudi Arabia

EMHJ, 2011, 17(6): 495-500

Acute Kidney Injury IncreasingAging of the population

More interventions (chemotherapy, surgery, contrast procedures)

Rising incidence of co-morbid conditions (heart failure, diabetes)

Rising awareness of kidney injuries

Acute vs Chronic Kidney InjuryCharacteristic AKI CKD

Duration Short Permanent

Onset Recent Slow and Prolonged

Progression Rapid Gradual

SymptomsFrequent and driven by rapid

changesFew, unless driven by

associated disease

Recovery Common Uncommon

Acute Kidney Injury – Blood FlowOrgan Blood flow rate Percent of Cardiac Output

Kidneys 1200-1300 ml/min 25%

Brain 750 ml/min 15%

Intestines 500-1750 ml/min 10-35%

Skeletal muscles 1000 ml/min (rest) to 4000 ml/min

20-80%

AKI Evaluation

Laboratory Data◦ BUN and creatinine *◦ Urine analysis *◦ Others (Hgb, PTH, uric acid, CK, sodium, CO2)

Imaging studies◦ IV contrast given◦ Structural analysis

Symptoms *

Vitals and Urine output *

Medication *

ATN41%

PRERENAL19%

OBSTRUCTION9%

NEPHRITIS6%

AKI w/ CKD12%

OTHER13%

AKI CAUSES

ATN PRERENAL OBSTRUCTION NEPHRITIS AKI w/ CKD OTHER

Important Factors in AKI

Insufficient renal circulation (hypotension, hemorrhage)

Medication (RAS inhibitors, NSAIDS, PPI drugs, chemotherapy)

Iodinated contrast agents

Obstruction

Inflammation◦ Muscle damage

◦ Cellular injury (uric acid)

◦ Autoimmune conditions (lupus, scleroderma, vasculitis)

◦ Infection (sepsis, thrombotic microangiopathy)

Acute Kidney Failure

Vasocontrictors Vasodilators

Angiotensin II Nitric Oxide

Endothelin I Prostaglandin E2

Thromboxane A2 Prostacyclin

Adenosine Atrial natriuretic peptide

Sympathetic nerve activity

Pre-Renal Injury◦ Unable to optimize filtration efficiency◦ Reduces waste clearance◦ Reversible◦ Since tubular function is intact, urinary sodium will be low – the

kidney is trying to restore intravascular volume◦ Clinically, patient may have hypovolemia, euvolemia, or

hypervolemia◦ “Effective renal blood flow” may be decreased◦ Treatment is directed at restoring glomerular blood flow to enable

filtration

Acute Tubular Injury Treatment

Eliminate Threats◦ Correct blood pressure or eliminate obstruction

◦ Stop offending medication

Avoid new insults (iodinated contrast, hypotension)

Optimize renal perfusion◦ Restore central volume

◦ Support systemic blood pressure (pressors, reduce afferent arteriolar vasocontriction)

Loop diuretics◦ Mainly used to augment urine, but may help with dislodgement of intratubular casts

Eliminate triggers (Treat infections)

AKI Treatment◦ Atrial natriuretic peptide (block tubular reabsorption of sodium,

vasodilate afferent arterioles, and inhibit the renin-angiotensin system)

◦ Dopamine (or Fenoldopam – selective dopamine-1 agonist)◦ N-acetylcysteine◦ Vasopressin◦ Steroids◦ Statins◦ Sodium bicarbonate

Acute Kidney Injury - TreatmentManage AKI

condition (dialysis, fluids,

nutrition)

Make an underlying diagnosis

Acute Kidney Injury - DialysisStart dialysis – “when the risks of dialysis are less than the risks of observation”◦ Hypervolemia

◦ Metabolic acidosis

◦ Uremia symptoms

◦ Electrolyte derangement (hyperkalemia, hyponatremia)

Other considerations:◦ Poisoning (ethylene glycol, lactic acidosis)

◦ CK levels in patients with rhabdomyolysis

◦ Urine output

◦ Weekends and evenings

Dialysis Risks

Line insertion with risk of bleeding, discomfort, or infection

Dialysis might prolong or compound tubular injury

Hypotension or arrythmias may occur during or after a dialysis session

Dialysis vs CRRT

Hemodialysis CRRT

Clearance √√√√ √√

Hemodynamic Stability √ √√√

Volume Removal √ √√√

Cost √√ √√√√

When to Stop Renal Replacement◦ Improving urine output

◦Creatinine not rising much between dialysis sessions

◦Creatinine falling spontaneously

◦Creatinine is below 3.5 mg/dl pre-dialysis

4.6 4.7

4.6 4.2

Special Circumstances

AKI in renal allograft

Hepatorenal syndrome

Rhabdomyolysis

NSAIDS

Allograft AKIAdditional prerenal conditions◦ Loss of afferent arteriole parasympathetic influence

◦ Continual calcineurin inhibitor (CNI) mediated vasocontriction

Initial ischemia (donor type, donor age, donor circulation)

Viral infection (polyoma BK, CMV)

Acute rejection (antibody-mediated rejection, cellular rejection)

Recurrence of primary renal disease (diabetes, FSGS, mesangial GN, membranoproliferative GN, lupus, crescentic GN)

Older donor age may be associated with greater sensitivity to CNI drugs

Allograft AKI

If creatinine is over 25% of baseline level:

• Adjust CNI dose if necessary

• Correct additional prerenal conditions

• Repeat lab including CNI level in 5-7 days

• If GFR not improved, then perform renal biopsy

Hepatorenal syndrome (HRS)◦ In the late 19th century, reports noted an association among advanced liver

disease, ascites, and oliguric renal failure in the absence of significant renal histologic changes

◦ Underlying mechanism of kidney failure is peripheral and splanchnic arterial vasodilation – combined with intense renal vasoconstriction mediated by renal sympathetic stimulation

◦ HRS kidneys work when transplanted – also kidney function may recover after liver transplantation

◦ Elevated nitric oxide synthesis particularly in splanchnic circulation

◦ Depressed prostaglandin synthesis

Frequent HRS Triggers

Bacterial infection

Large volume paracentesis

GI hemorrhage

Acute alcoholic hepatitis

Renal Circulatory Conditions

Hepatorenal syndrome

• Prerenal syndrome with internal derangement of renal autoregulation

Cardiorenal syndrome

Edematous conditions

• Severe pulmonary hypertension

• Severe venous insufficiency

• Abnormal capillary permeability (diabetes, sepsis, burns, trauma,

• Medication (NSAIDS, glucocorticoids, glitazones, insulin, estrogens, tamoxifen, vasodilators, calcium channel blockers, gabapentin, pregabalin, pramipexole)

• Lymphatic obstruction

• Nephrotic syndrome

Rhabdomyolysis

Crush injuries or direct muscle trauma

Exertional (non-traumatic) injury

• extreme exercise

• heat

Hyperkinetic conditions

• seizures

• amphetamine use

• delirium tremens

Metabolic causes

• carnitine palmitoyltransferase deficiency

• phosphorylase deficiency (McArdle disease)

• cocaine, alcohol, amphetamines

• statins, colchicine, volatile anesthetic agents

NSAIDS and the KidneyInhibit prostaglandins, thus leads to abnormal afferent arteriole autoregulation

If present during a period of hypoperfusion, then risk for acute tubular injury is much greater

May cause an interstitial nephritis

Associated with a glomerular disorder (minimal change nephropathy)

Impairs tubular potassium excretion and may cause a type IV renal tubular acidosis

Leads to sodium and water retention

May cause hyponatremia

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