To prevent prerenal acute kidney injury, which person is encouraged to increase fluid consumption?

Summary
To prevent prerenal acute kidney injury, which person is encouraged to increase fluid consumption?

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.

Etiology

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)
  • Acute interstitial nephritis
  • Vascular diseases
  • Glomerulonephritis: e.g., rapidly progressive glomerulonephritis

Overview of nephrotoxic medications
ClassExamples
Antimicrobials
  • Antibiotics
    • Aminoglycosides
    • Vancomycin
    • Cephalosporins
    • Colistin
    • Sulfonamides
    • Streptomycin
  • Antivirals
    • Acyclovir
    • Foscarnet
    • Cidofovir
    • Tenofovir
  • Antifungals
    • Amphotericin B
Antimetabolites
  • Methotrexate
  • Cladribine
Chemotherapeutic agents
  • Platinum-based chemotherapeutic agents
    • Cisplatin
    • Carboplatin
Antiinflammatories and immunosuppressants
  • NSAIDs
  • Cyclosporine
  • Calcineurin inhibitors
Others
  • Inhalational anesthetics
  • Lithium
  • Herbal remedies
  • Phosphate-containing bowel preparations

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.

Pathophysiology

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 nephronnecrosis 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

Overview of the four phases of AKI
Phase Characteristic features (some patients may not undergo all phases)Duration

Initiating event (kidney injury)

  • Symptoms of the underlying illness causing AKI may be present.
  • Hours to days

Oliguric or anuric phase (maintenance phase)

  • Progressive deterioration of kidney function
    • Reduced urine production (oliguria), < 50 ml/24 hrs = anuria
    • Increased retention of urea and creatinine (azotemia)
  • Complications: fluid retention (pulmonary edema), hyperkalemia, metabolic acidosis, uremia, lethargy, asterixis
  • 1–3 weeks

Polyuric/diuretic phase

  • Glomerular filtration returns to normal, which increases urine production (polyuria), while tubular reabsorption remains disturbed.
  • Complications: loss of electrolytes and water (dehydration, hyponatremia, and hypokalemia)
  • ∼ 2 weeks

Recovery phase

  • Kidney function and urine production normalize.
  • Months to years

References:[2][4]

Clinical features

  • May be asymptomatic.
  • Oliguria or anuria
  • Signs of volume depletion (in prerenal AKI caused by volume loss)
  • Signs of fluid overload (from Na+ and H2O retention)
    • Peripheral and pulmonary edema
    • Hypertension
    • Heart failure
    • Shortness of breath
  • Signs of uremia
  • 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).

Subtypes and variants

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
    • 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

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 after 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

References:[2][3][6]

Diagnostics

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.

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.

Initial evaluation

Laboratory studies

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)
  • Clinical findings: rapid improvement in renal function following resolution of the obstruction

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.

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]

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.

Management

Supportive care and follow-up

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]

Hemodynamic support in patients with AKI according to presumed intravascular volume status

Hypovolemia (and/or hypotension)
  • Start IV fluid resuscitation.
  • Consider vasopressors to maintain mean arterial pressure (MAP) ≥ 65 mmHg in patients with persistent hypotension despite fluid resuscitation. [8][9]
Hypervolemia
  • Start fluid restriction.
  • Consider loop diuretics: e.g., furosemide
Euvolemia or indeterminate volume status
  • Consider an IV fluid challenge to assess if the patient responds to fluids (e.g., improvement in creatinine, urine output, and/or blood pressure)
    • Responsive: Carefully continue IV fluid challenges until the patient is no longer responsive.
    • No response: Stop IV fluid challenges but ensure continued fluid needs are met.

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]

Acute management checklist

  • 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)

Prevention

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

Prevention of acute kidney injury
Risk factorsPreventive strategies
Acute illness
  • Consider temporarily holding ACE-Is, ARBs, and diuretics in the setting of vomiting, diarrhea, and/or sepsis. [22]
  • Prevent hypovolemia and hypotension by optimizing fluid volume and hemodynamic status. [7][8]
    • Fluid resuscitation: Avoid colloids; balanced crystalloid solutions (e.g., lactated Ringer's, Plasma-Lyte A) are preferred over normal saline. [8][9]
    • Maintain adequate MAP (> 65 mmHg is appropriate for most patients).
Nephrotoxic medication exposure
  • Avoid nephrotoxic medication whenever possible.
  • Single daily dosing of aminoglycosides is preferred over multiple daily dosing if no suitable antibiotic alternatives are available. [7]
  • Alternative antifungals (e.g., azoles or echinocandins) or lipid formulations of amphotericin B are preferred over conventional amphotericin B. [7]
Iodinated radiocontrast agent exposure
  • Screen for reduced eGFR if risk factors are present.
  • See “Prevention of contrast-induced nephropathy” for details (e.g., IV hydration, discontinuation of medication).
Liver failure
  • Recognize and manage ascites, SBP, and GI bleeding early.
  • Administer IV albumin supplementation in patients with spontaneous bacterial peritonitis or following large-volume therapeutic paracentesis.
Surgery
  • Perioperative management
    • Optimize fluid volume and hemodynamic status.
    • Consider holding ACE-Is, ARBs, and diuretics.
Endogenous nephrotoxins
  • Initiate aggressive IV fluid therapy targeting high urine output [39][41]
  • See also “Rhabdomyolysis” and “Tumor lysis syndrome.”

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References

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What can be done to prevent acute kidney injury?

However, there are very few interventions that have been shown to consistently prevent AKI. Measures such as adequate hydration, maintenance of adequate circulating blood volume and mean arterial pressure, and avoidance of nephrotoxins are still the mainstay of prevention.

How is Prerenal acute kidney injury treated?

Treatment / Management In the emergency department or the hospital setting, the mainstay of treatment of prerenal AKI is isotonic fluid administration. It is both therapeutic and diagnostic. A downtrend in creatinine after administration of isotonic fluids is the gold standard in diagnosis.

What are the most common Prerenal causes of acute kidney injury?

Causes of prerenal acute kidney injury include: Severe blood loss and low blood pressure related to major cardiac or abdominal surgery, severe infection (sepsis), or injury.

Which patients are at increased risk for acute kidney injury?

Conclusions: AKI is a common and serious complication of COVID-19. Overall, male sex, age, smoking, obesity, hypertension, diabetes, pneumopathy, cardiovascular disease, cancer, CKD, mechanical ventilation and the use of vasopressors were independent risk factors for AKI in adult patients with COVID-19.