Acute kidney injury

Acute kidney injury (AKI) is a sudden loss of renal function with a subsequent rise in creatinine and blood urea nitrogen (BUN). It is most frequently caused by decreased renal perfusion (prerenal) but may also be due to direct damage to the kidneys (intrarenal or intrinsic) or inadequate urine drainage (postrenal). In AKI, the acid-base, fluid, and electrolyte balances are disturbed and the urinary excretion of substances such as drugs is impaired. AKI may be asymptomatic or manifest with oliguria or anuria and, when kidney dysfunction is severe, it may manifest with symptoms and signs of uremia; in some cases, polyuria may occur as a result of impaired tubular reabsorption. A diagnosis of AKI can be made based on an increase in serum creatinine concentration and/or decrease in urine output. Initial evaluation includes blood and urine studies, which may help identify the mechanism of kidney injury and any metabolic complications of AKI. Additional specific investigations are guided by the suspected cause. Rapid evaluation, diagnosis, and treatment are necessary to prevent irreversible loss of renal function. Management is based on the mechanism of kidney injury and the underlying causes. Treatment is primarily supportive and aims to ensure adequate kidney perfusion and prevent complications and further kidney damage.

Prerenal acute kidney injury ^[1][2][3]

Prerenal causes include any condition that leads to decreased renal perfusion (∼ 60% of cases of AKI). ^[1][2][3]

• Hypovolemia: e.g., due to hemorrhage, vomiting, diarrhea, sweating, burns, diuretics, poor oral intake, dehydration, hypercalcemia
• Hypotension: e.g., due to sepsis, cardiogenic shock (decreased cardiac output), anaphylactic shock
• Decreased circulating volume (↓ effective arterial volume)
  • Cardiorenal syndrome: e.g., in congestive heart failure
  • Hepatorenal syndrome: e.g., in cirrhosis, liver failure
  • Abdominal compartment syndrome
  • Nephrotic syndrome
  • Acute pancreatitis
• Renal artery stenosis
• Drugs that affect glomerular perfusion: e.g., cyclosporine, tacrolimus, NSAIDs , ACE inhibitors (ACE-Is)

Prolonged prerenal injury leads to intrinsic injury, as decreased renal perfusion causes tubular necrosis.

Intrinsic acute kidney injury

Intrinsic causes include any condition that leads to severe direct kidney damage (∼ 35% of cases of AKI). ^[1][2][3]

• Acute tubular necrosis (causes ∼ 85% of intrinsic AKIs)
  • Ischemia: e.g., due to prolonged hypotension
  • Nephrotoxic drugs: e.g., radiographic contrast agents, aminoglycosides, cisplatin, methotrexate, ethylene glycol, amphotericin B
  • Endogenous toxins: e.g., hemoglobin in intravascular hemolysis, myoglobin in rhabdomyolysis, uric acid in TLS, Bence-Jones protein light chains in multiple myeloma
• Acute interstitial nephritis
  • Medication: e.g., antibiotics , phenytoin, interferon, PPIs, NSAIDs, cyclosporine
  • Infection
    • Bacterial: e.g., Legionella spp., Streptococcus spp.
    • Fungi: Candida, Histoplasma
    • Viral: e.g., hepatitis C virus, cytomegalovirus, HIV
  • Infiltrative diseases: e.g., sarcoidosis, amyloidosis
• Vascular diseases
  • Hemolytic uremic syndrome (HUS)
  • Thrombotic thrombocytopenic purpura (TTP)
  • Hypertensive emergency
  • Vasculitis, scleroderma renal crisis
  • Renal vein thromboses, renal atheroemboli, renal infarction
• Glomerulonephritis:e.g., rapidly progressive glomerulonephritis

Postrenal acute kidney injury

Postrenal causes include any condition that results in bilateral obstruction of urinary flow from the renal pelvis to the urethra (∼ 5% of cases of AKI). ^[1][2][3]

• Acquired obstructions
  • Benign prostatic hyperplasia (BPH)
  • Iatrogenic: e.g., catheter-associated injuries
  • Tumors: e.g., bladder, prostate, cervical, metastases
  • Stones
  • Bleeding with subsequent blood clot formation
• Neurogenic bladder: e.g., due to multiple sclerosis, spinal cord lesions, or peripheral neuropathy
• Congenital malformations: e.g., posterior urethral valves

As long as the contralateral kidney remains intact, patients with unilateral ureteral obstruction typically maintain normal serum creatinine levels.

Overview of nephrotoxic medications

Prerenal

• Decreased blood supply to kidneys (due to hypovolemia, hypotension, or renal vasoconstriction); → failure of renal vascular autoregulation to maintain renal perfusion → decreased GFR → activation of renin-angiotensin system → increased aldosterone release → increased reabsorption of Na⁺, H₂O → increased urine osmolality → secretion of antidiuretic hormone → increased reabsorption of H₂O and urea
• Creatinine is still secreted in the proximal tubules, so the blood BUN:creatinine ratio increases.

Intrinsic

• Damage to a vascular or tubular component of the nephron → necrosis or apoptosis of tubular cells → decreased reabsorption capacity of electrolytes (e.g., Na⁺), water, and/or urea; (depending on the location of injury along the tubular system) → increased Na⁺ and H₂O in the urine → decreased urine osmolality

Postrenal

• Bilateral urinary outflow obstruction (e.g., stones, BPH, neoplasia, congenital anomalies) → increased retrograde hydrostatic pressure within renal tubules → decreased GFR and compression of the renal vasculature → acidosis, fluid overload, and increased BUN, Na⁺, and K⁺.
• A normal GFR can be maintained as long as one kidney functions normally.

Four phases of AKI

References:^[2][4]

• May be asymptomatic.
• Oliguria or anuria
• Signs of volume depletion (in prerenal AKI caused by volume loss)
  • Orthostatic or frank hypotension and tachycardia
  • Reduced skin turgor
• Signs of fluid overload (from Na⁺ and H₂O retention)
  • Peripheral and pulmonary edema
  • Hypertension
  • Heart failure
  • Shortness of breath
• Signs of uremia
  • Anorexia, nausea
  • Encephalopathy, asterixis
  • Pericarditis
  • Platelet dysfunction
• Signs of renal obstruction (in postrenal AKI)
  • Distended bladder
  • Incomplete voiding
  • Pain over the bladder or flanks
• Fatigue, confusion, and lethargy
• In severe cases: seizures or coma
• Affected individuals have a higher risk of secondary infection throughout all phases (most common reason for fatalities).

Acute tubular necrosis

• Epidemiology: : causes ∼ 85% of intrinsic AKIs
• Location
  • The straight segment of the proximal tubule and the straight segment of the distal tubule (i.e., the thick ascending limb) are particularly susceptible to ischemic damage.
  • The convoluted segment of the proximal tubule is particularly susceptible to damage from toxins.
• Etiology
  • Ischemic: Injury occurs secondary to decreased renal blood flow.
    • Severe hypotension, especially in the context of shock: hypovolemic (e.g., hemorrhage, severe dehydration), septic, cardiogenic (e.g., heart failure), or neurogenic shock
    • Thromboembolism
    • Thrombotic microangiopathy
    • Cholesterol embolism (atheroemboli)
  • Toxic: Injury occurs directly due to nephrotoxic substances.
    • Contrast-induced nephropathy
    • Medication: aminoglycosides, cisplatin, amphotericin, lead, ethylene glycol
    • Pigment nephropathy: an acute kidney injury that occurs as a result of the toxic effects of heme-containing pigments (e.g., hemoglobin, myoglobin) on proximal renal tubular cells (toxin-induced acute tubular necrosis)
      • Myoglobinuria due to rhabdomyolysis (crush syndrome)
      • Hemoglobinuria associated with hemolysis
    • Acute uric acid nephropathy
  • Other: sepsis, infections
• Pathophysiology: necrotic proximal tubular cells fall into the tubular lumen → debris obstructs tubules → decreased GFR → sequence of pathophysiological events similar to prerenal failure (i.e., activation of RAAS; see “Pathophysiology” above)
• Clinical features: same as AKI (see “Clinical features” and four phases of AKI above)
• Diagnostics (see “Diagnostics” below)
  • Blood findings: azotemia, hyperkalemia, and metabolic acidosis
  • Urinary findings
    • ↑ Fractional excretion of sodium (FENa)
    • Myoglobinuria, hemoglobinuria
  • Urinary sediment
    • Muddy brown granular casts
    • Epithelial cell casts
    • Free renal tubular epithelial cells (due to denudation of the tubular basement membrane)
• Management: See “Management” below.
• Prognosis
  • After 1–3 weeks, most patients with ATN will experience tubular re-epithelialization and spontaneous full recovery is common.
  • Can be lethal; if AKI is severe and not managed adequately (e.g., dialysis may be required in oliguric patients with volume overload or severe hyperkalemia)

Renal cortical necrosis

• Definition: rare cause of AKI caused by acute generalized ischemic necrosis of the renal cortex in both kidneys
• Etiology: septic shock, disseminated intravascular coagulation (DIC); , hemolytic uremic syndrome (HUS), obstetric complications; (e.g., abruptio placentae, septic abortion, postpartum hemorrhage)
• Pathophysiology: vasospasms and microvascular injury with vascular thrombosis → prolonged severe renal ischemia; → diffuse and/or patchy destruction of the renal cortex ^[5]
• Clinical features: flank pain, CVA tenderness and signs of AKI (see also “Clinical features” above and shock)
• Management: Dialysis can improve outcomes (see “Management” below).
• Prognosis: high mortality rates without treatment

Contrast-induced nephropathy

• Definition: AKI after IV administration of iodinated contrast medium
• Risk factors
  • Chronic kidney disease (CKD): esp. in patients with diabetes mellitus, multiple myeloma
  • Congestive heart failure, arterial hypotension
  • Nephrotoxic drugs: esp. NSAIDs
  • Anemia
  • Dehydration
• Clinical features/diagnostics: See “Clinical features” above and “Diagnostics” below.
• Course
  • Creatinine is highest 3–5 days after injury and usually falls back to the baseline level within 1 week.
  • The course is typically mild because end-stage renal disease usually only occurs in patients with pre-existing CKD.
• Prevention of contrast-induced nephropathy
  • Always evaluate kidney function before administering a contrast agent.
  • Use a low dose and low concentration of contrast medium.
  • The patient should discontinue nephrotoxic substances before administration.
  • Ensure hydration: isotonic NaCl before and after administration of contrast medium
  • Acetylcysteine (no clear recommendations )

References:^[2][3][6]

A diagnosis of AKI can be made based on an acute increase in serum creatinine and/or decrease in urine output in accordance with the definition of AKI.

Approach ^[7][8][9]

• Compare current and previous creatinine levels to determine if the process is acute.
• Check diagnostic criteria and perform staging of AKI.
• Determine the most likely mechanism of AKI (i.e., prerenal, intrinsic, or postrenal) based on:
  • A comprehensive chart review, history, and physical examination
  • Supportive diagnostic findings and response to initial interventions
• Consider further testing for specific underlying causes of AKI.

In the absence of previously documented creatinine levels, stable creatinine levels with findings such as chronic anemia and small hyperechoic kidneys on ultrasound suggest CKD rather than AKI.

Clinical presentation, laboratory tests, imaging, response to initial therapy, and, in some cases, histopathology are required to determine the underlying cause of AKI.

Diagnostic criteria of acute kidney injury

• Acute kidney injury is defined as the presence of any of the following criteria: ; ^[7]
  • Increase in serum creatinine by ≥ 0.3 mg/dL (26.5 μmol/L) within 48 hours.
  • Increase in serum creatinine to ≥ 1.5 times baseline level within 7 days.
  • Decrease in urine output to < 0.5 mL/kg/hour for ≥ 6 hours.

Staging of acute kidney injury

• The KDIGO stages are widely used and correlate with the risk of death, need for renal replacement therapy, and long-term outcomes (e.g., CKD).
• Other classifications include: ^[7]
  • RIFLE criteria: A classification system for acute kidney injury
    • The acronym stands for Risk, Injury, Failure, Loss, and End-stage kidney disease.
    • For the first three categories, patients are classified according to the level of kidney injury (i.e., degree of increase in serum creatinine and/or decrease in GFR and urine output) and for the last two categories, according to the duration of complete loss of kidney function.
  • Acute Kidney Injury Network (AKIN) criteria

Initial evaluation

Laboratory studies

• Serum creatinine and BUN
• Serum electrolytes: sodium, potassium, magnesium, calcium, and phosphate
• CBC
• Blood gases: ABG or VBG
• Urinalysis with urine sediment microscopy
• Urine sodium, urea, creatinine, and osmolality
• Calculate excretion fractions: may help to differentiate prerenal AKI from intrinsic AKI ^[10]
  • Fractional excretion of sodium (FENa)
  • Fractional excretion of urea (FEUrea)

Overview of diagnostic findings

Despite the common use of BUN:creatinine ratio and urinary fractional excretions (i.e., FENa, FEUrea) in clinical practice, observational data suggest that they do not reliably distinguish prerenal AKI from intrinsic AKI. ^[10][11]

The most likely mechanism of AKI is primarily determined based on clinical presentation and response to therapy. Evaluating patients' response to initial interventions is key to confirming the mechanism of AKI and guiding further workup and management steps.

Prerenal AKI ^[8][9]

• Blood study findings
  • Elevated serum creatinine
  • Serum BUN:creatinine ratio ≥ 20:1 ^[12]
• Urine study findings
  • Normal urinalysis
  • Low urinary sodium and urea excretion
    • Low fractional excretion of sodium (FENa < 1%)
    • Low fractional excretion of urea (FEUrea < 35%)
  • High urine osmolality (> 500 mOsm/kg) and specific gravity (> 1.020) ^[13][14]
  • Urine sediment: hyaline casts due to concentrated urine in the setting of low renal perfusion
• Clinical findings: rapid improvement in renal function following acute intervention

Patients with prerenal AKI receiving diuretic therapy may have a falsely elevated FENa. Therefore, FEUrea may be more informative in this setting. ^[15]

Intrinsic AKI

• Blood study findings
  • Elevated serum creatinine concentration and rapidly rising serum creatinine level
  • BUN:creatinine ratio ≤ 15:1
• Urine study findings
  • High urinary sodium and urea excretion
    • High urine sodium concentration (> 40 mEq/L)
    • High fractional excretion of sodium (FENa > 2–3%) ^[8][15]
    • High fractional excretion of urea (FEUrea > 50%) ^[15]
  • Low urine osmolality (< 350 mOsm/kg)
  • Urine sediment: renal tubular epithelial cells or granular, muddy brown, or pigmented casts
• Biopsy: e.g., in suspected rapidly progressive glomerulonephritis
• Clinical findings: lack of response to acute intervention

A falsely low FENa may be seen in some patients with intrinsic AKI, e.g., due to glomerulonephritis, acute interstitial nephritis, rhabdomyolysis, or contrast-induced nephropathy. ^[15]

Postrenal AKI

• Blood study findings
  • Elevated serum creatinine concentration in bilateral obstruction
  • BUN:creatinine ratio varies; usually normal (i.e., 10:1–20:1)
• Urine study findings
  • Normal urinalysis; : e.g., when due to neurogenic bladder
  • Hematuria; : e.g., when due to stones, bladder cancer, clots
  • Urine osmolality varies. ^[16]
• Imaging (renal ultrasound or noncontrast CT scan)
  • Bladder distention, high postvoid residual volume, bilateral hydronephrosis, and/or obstructing stones
  • See “Imaging modalities” in “Urinary tract obstruction.”
• Clinical findings: rapid improvement in renal function following resolution of the obstruction

Additional evaluation

Imaging ^[17]

Imaging of the kidneys and urinary tract is not necessary to establish a diagnosis of AKI but may be needed to determine the etiology.

• Ultrasound
  • Obtain urgently to assess for hydronephrosis in patients with risk factors for urinary tract obstruction. ^[8][18]
  • Consider when evaluating renal dysfunction of unclear etiology.
• Noncontrast CT
  • Obtain if ultrasound shows hydronephrosis but does not reveal the cause of the obstruction.
  • Consider when clinical suspicion of obstruction remains high despite the absence of hydronephrosis on ultrasound.
  • See also “Imaging modalities” in “Urinary tract obstruction.”

Obtain an urgent ultrasound to rule out hydronephrosis in patients with risk factors for urinary tract obstruction.

While ultrasound is the initial test of choice to assess for urinary tract obstruction, CT has greater sensitivity for detecting obstructions and stones. ^[19]

Renal biopsy ^[8][20]

• Not routinely indicated
• Consider if:
  • The cause of AKI cannot be identified after a thorough initial evaluation
  • Diagnostic confirmation of the cause (e.g., glomerulonephritis, myeloma nephropathy) is needed prior to initiating disease-specific therapy

Additional specific testing

Usually reserved for cases in which intrinsic AKI is initially suspected or interventions aimed at reversing presumed prerenal AKI or postrenal AKI fail to improve renal function. Studies should be guided by clinical suspicion.

Approach ^[7][8][9]

• Initiate treatment for the underlying cause of AKI based on the presumed mechanism.
  • Prerenal: Correct adverse hemodynamic factors and replace the depleted volume as needed.
  • Postrenal: Relieve the urinary tract obstruction.
  • Intrinsic: Consider a trial of IV fluids; identify and treat underlying causes that require specific interventions.
• Consider indications for acute dialysis and early nephrology consultation.
• Provide supportive care to all patients.
  • Hold potentially nephrotoxic substances, ACE-Is, ARBs, NSAIDs, and nonessential medications.
  • Adjust the dosing of essential renally cleared medications.
  • Manage volume status and blood pressure to optimize kidney perfusion.
  • Identify and manage complications (e.g., electrolyte disturbances, acidosis, fluid overload).
  • Consider additional supportive care measures (e.g., nutritional support, VTE prophylaxis).
• Provide patient education and ensure adequate post-discharge follow-up.

AKI management is primarily supportive. Currently, there are no specific pharmacotherapies for AKI. ^[9]

Avoid coadministering RAAS inhibitors and NSAIDs in patients with reduced renal perfusion (e.g., in congestive heart failure, renal artery stenosis) because doing so can significantly decrease their GFR.

Early nephrology consult

• Common indications ^[22]
  • Indications for acute dialysis or renal biopsy
  • AKI stage 3
  • Inadequate response to initial treatment
  • Intrinsic AKI
  • Presence of CKD, if:
    • The patient has received a renal transplant
    • CKD category G4 or higher

Treatment of underlying causes ^[7][8][9]

The longer the underlying cause has been present, the greater the chance that AKI will progress to renal failure and/or CKD. Treat potential causes of AKI early.

Renal replacement therapy ^[7][9]

See also “Indications for acute dialysis.”

• Indications; consider urgently for:
  • Complications refractory to medical management
    • Refractory fluid overload
    • Electrolyte imbalances
    • Acid-base disturbances
  • Acute poisoning (e.g., by ethylene glycol); see “Approach to the poisoned patient.”
  • Uremic symptoms
• Modalities include: ^[7][9]
  • Hemodialysis and/or hemofiltration (i.e., by CRRT or intermittent hemodialysis)
  • Peritoneal dialysis ^[7]

The goal of supportive care is to avoid further renal insult and potentially aggravating factors, support adequate kidney perfusion, and ensure early identification and treatment of complications.

Medications and nephrotoxic substances ^[9]

• Medication management
  • Avoid nephrotoxic medications and drugs that may have a detrimental effect on glomerular perfusion.
  • Discontinue all nonessential renally cleared medications.
  • For essential medications that are renally cleared, adjust dosing daily based on the patient's presumed GFR, considering the following: ^[9]
    • Conventional eGFR formulas (e.g., Cockcroft-Gault, CKD-EPI equation, MDRD equation) are inaccurate in patients with AKI.
    • GFR should be reestimated daily based on the patient's urine output and the trajectory of serum creatinine.
    • The kinetic eGFR equation may provide an accurate estimation of GFR in this setting. ^[27][28][29]
• Contrasted imaging
  • Avoid iodinated contrast media to prevent contrast-induced nephropathy.
  • Avoid gadolinium-based contrast agents to prevent nephrogenic systemic fibrosis.

Calculating eGFR using conventional equations does not accurately predict the true GFR in patients with AKI. Reestimate GFR daily based on the patient's urine output and the trajectory of serum creatinine.

Noncontrast imaging studies are preferred if possible. When the use of iodinated contrast is required for a critical diagnostic study or procedure (e.g., for the treatment of STEMI), the lowest clinical diagnostic dose should be used.

Volume status and blood pressure ^[8][9]

• Goal: optimize renal perfusion and reverse prerenal insults while avoiding fluid overload
• Monitoring parameters
  • Clinical assessment of volume status
  • Fluid balance monitoring
  • Hemodynamic monitoring
  • Fluid responsiveness
• Management: Provide hemodynamic support and ensure continued fluid needs are met; see also “Daily fluid requirements for special patient groups.” ^[30]

Patients with AKI are at high risk of developing fluid overload, which can compromise renal function and may increase mortality. Avoid aggressive fluid resuscitation in patients who are not volume responsive.

Consider loop diuretics ONLY in patients with signs of fluid overload. Diuretics should not be used routinely to improve urine output in patients with AKI because of their lack of benefit and potential for harm. ^[7]

Choice of parenteral fluid ^[8][9][30]

• Use crystalloid solutions: Balanced IV fluid solutions, (e.g., lactated Ringer's, Plasma-Lyte A) may be preferred for most patients. ^[30]
• Avoid artificial colloids (e.g., hydroxyethyl starch). ^[8][9]
• Reserve IV albumin for select patients under specialist guidance. ^[31][32][33]

The use of balanced IV fluid solutions has been associated with lower mortality and better renal outcomes compared with the use of normal saline in patients with AKI.

Electrolyte and acid-base disorders

• Goals
  • To assess response to treatment and prevent complications of electrolyte disturbances
  • To assess for complications of parenteral fluid therapy
• Monitoring parameters: BMP, calcium, phosphorus, magnesium, and ABG or VBG
• Management ^[34]
  • Obtain an urgent ECG in patients with significant potassium, calcium, and/or magnesium abnormalities.
  • Address common metabolic complications of AKI.
    • Follow therapeutic approach to hyperkalemia.
    • Consider careful repletion regimens for hypocalcemia.
    • Restrict dietary phosphate and consider oral phosphate binders for significant hyperphosphatemia.
  • Acidemia: see “Indications for acute dialysis”

Obtain frequent (at least daily) laboratory studies to monitor for the presence of metabolic complications and response to treatment (e.g., improvement in creatinine levels).

Consider urgent renal replacement therapy for patients with refractory electrolyte or acid-base disturbances.

Additional considerations

• Nutritional support ^[7][35]
  • Ensure adequate protein and calorie intake.
  • Consider dietary potassium and/or phosphate restriction for patients with hyperkalemia and/or hyperphosphatemia. ^[36]
• Glucose management
  • Consider insulin therapy to maintain serum glucose between 110 and 149 mg/L (6.1 and 8.3 mmol/L) in critically ill patients. ^[7][9]
  • See also “Inpatient management of hyperglycemia.”
• Stress ulcer prophylaxis: Consider starting a PPI (e.g., pantoprazole) in critically ill patients who are at risk of GI bleeding. ^[37]
• VTE prophylaxis: If indicated, unfractionated heparin may be preferred over low molecular weight heparin (LMWH) or direct oral anticoagulants (DOACs) in patients with severe renal impairment.
• Uremia: Monitor for signs and symptoms; if present, consider renal replacement therapy.

The risk of GI bleeding may be increased in AKI due to uremic platelet dysfunction. ^[37]

Consider a nutrition consult for all patients with AKI. ^[35]

Follow-up care ^[38][39]

• Educate patients on medication management and the prevention of AKI.
• Monitor serum creatinine, eGFR, blood pressure, and weight following discharge. ^[38][40]
• Ensure that patients who require ongoing renal replacement therapy have access to outpatient dialysis services.
• Consider referral for outpatient nephrology follow-up in patients with significant residual renal dysfunction (i.e., eGFR < 60 mL/min).

Patients who recover from AKI are at high risk of readmission, mortality, cardiovascular events, progressive renal function deterioration, and developing de novo CKD. ^[38][39]

Adequate discharge planning and follow-up may help improve patient outcomes. ^[38][39]

• Confirm diagnosis (see “Diagnostic criteria for AKI”) and stage AKI (see “Staging of AKI”).
• Send initial laboratory evaluation
  • CBC, BMP, calcium, phosphate, magnesium, and ABG or VBG
  • Urine studies: urinalysis, urine microscopy, urine chemistry (sodium, urea, osmolality, creatinine)
• Consider urgent ultrasound and/or foley catheter placement (if urinary tract obstruction is suspected).
• Consider early nephrology consult.
• Optimize volume status.
• Identify and treat any metabolic complications (e.g., acidosis, hyperkalemia).
• Identify and treat the underlying cause.
• Hold nephrotoxic medications and renally-dose other medications.
• Strict input/output monitoring
• Provide additional supportive care (e.g., nutritional support, VTE prophylaxis)

Neonatal acute kidney injury ^[41][42][43]

• Epidemiology: AKI is common in critically ill newborns (approx. 30% of NICU patients). ^[43]
• Etiology ^[44]
  • ∼85% prerenal
  • ∼10% renal
  • ∼5% postrenal
• Infant risk factors
  • Perinatal: prematurity, low birth weight, asphyxia, congenital heart disease
  • Inflammatory: NEC, sepsis
  • Iatrogenic: nephrotoxic medications, cardiac surgery, ECMO therapy
• Diagnostics: Modifications to KDIGO staging ^[42]
  • Baseline serum creatinine in neonates is defined as the lowest previously measured value.
  • The cut-off for AKI stage 3 is a serum creatinine level ≥ 3 times baseline OR ≥ 2.5 mg/dL.
  • Accurate measurement of urine output in neonates poses challenges (esp. regarding urine collection) but is still being used to diagnose and stage AKI.
  • Other diagnostic biomarkers, e.g., cystatin C, are currently being investigated to improve early and accurate detection of AKI in neonates. ^[42]
  • See “Diagnostics” section above.
• Management
  • Monitor serum creatinine and urine output in at-risk neonates.
  • Treat underlying causes.
  • Avoid/adjust nephrotoxic medications.
  • Provide supportive management (e.g., fluid, electrolyte, and nutritional).
  • Consider renal replacement therapy.

Identify patients who are at risk of AKI and implement appropriate preventive strategies. ^[1][7][22]

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