Prevention

Four important practical steps to reduce the risk of acute kidney injury (AKI) in hospitalized patients:

• Adequate hydration.
• Avoiding hypotension.
• Detecting and treating urine retention early.
• Limiting the use of nephrotoxins.

Let’s break down these points a bit…

Adequate hydration

For most, adequate oral intake provides sufficient hydration. Use IV fluids only when necessary—like in cases of volume depletion or prolonged NPO status.

Precautions:

• Patients with vomiting, diarrhea, fever, or decreased oral intake for any reason have a degree of volume depletion. We must optimize their volume status with IV fluids before introducing nephrotoxic medications, even if their kidney function looks normal.
• Patients on diuretics are at higher risk of dehydration and electrolyte imbalances due to over-diuresis. I always advise my patients to stop taking diuretics if they develop vomiting, diarrhea, fever, or significantly reduced oral intake.
• Patients with rhabdomyolysis and hemolysis are at risk of developing pigment-induced nephropathy particularly when CK > 5000, aggressive IV fluid hydration should be provided to prevent that.
• Patients at risk for contrast-induced nephropathy (CIN) such as those with preexisting renal impairment, should receive IVF hydration with isotonic solutions 1 mL/kg/hour starting 6-12 hours before and continuing for 12-24 hours after the procedures.

Avoiding hypotension.

The kidneys are susceptible to low blood pressure, and even brief episodes of hypotension can cause AKI. We must act quickly to stabilize blood pressure and address hemodynamic instability.

Detecting and treating urine retention early.

Routinely palpate the lower abdomen for bladder distension, especially in elderly males with dementia or encephalopathy. If a Foley catheter is in place, confirm it is patent and draining properly.

Limiting the use of nephrotoxins

• Several medications may cause nephrotoxicity! NSAIDs, IV vancomycin, aminoglycosides, amphotericin B, acyclovir, methotrexate, Cyclosporins, tacrolimus, and IVIG are just some of the medications.
• Among NSAIDs, Ketorolac is the most nephrotoxic and should not be used for more than 5 days.
• IV Vancomycin and aminoglycoside levels should be closely monitored, I typically have our pharmacy handle that. We must switch to less nephrotoxic antibiotics as soon as we can.
• IV Acyclovir can cause crystal-induced nephropathy, particularly at higher doses. Ensure patients are well-hydrated before starting therapy and continue IV fluids during treatment unless contraindicated.

• Always opt for a less nephrotoxic alternative when an equally effective medication is available.
• Kidney function and urine output should be closely monitored whenever nephrotoxic medications are administered.

In patients with CKD, it’s important to avoid nephrotoxins whenever possible. NSAIDs should be avoided entirely, and contrast agents should only be used if necessary. Additionally, ensure all medications are dosed appropriately for renal impairment.

Diagnosis of AKI

AKI is an abrupt decline in kidney function, reflected by a decline in theGFR. Since direct GFR measurement isn’t practical, AKI is diagnosed based on creatinine accumulation or decreased urine output, using the following criteria:

• Increase in serum creatinine by ≥0.3 mg/dL within 48 hours.
• Increase in serum creatinine to ≥1.5 times baseline within 7 days.
• Urine output ≤0.5 mL/kg/hr for 6 hours.

I have three comments on this definition:

1. Trend Over Time Matters – AKI is diagnosed based on serial changes, not a single isolated value. Always compare current kidney function to previous results. If prior values are unavailable and the patient presents with abnormal kidney function, assume AKI until proven otherwise.
2. BUN is Not Included – Serum creatinine is the preferred marker as it more accurately reflects GFR. BUN levels can be influenced by protein intake, catabolism, GI bleeding, or liver dysfunction, making them less specific for AKI.
3. No Creatinine Cutoff – A normal BUN/Cr ratio does not necessarily mean normal kidney function, while an abnormal ratio may indicate chronic kidney disease (CKD) rather than AKI.

The underlying cause

• History and physical exams remain the single most important element in finding out the underlying cause of AKI.
  • Patients who are volume-depleted such as those with vomiting, diarrhea, decreased oral intake, and bleeding are likely to have AKI due to renal hypoperfusion or what we call prerenal AKI.
  • Patients with signs of volume overload such as peripheral edema and ascites are likely to have a prerenal AKI due to decreased effective circulatory volume. When this happens in patients with congestive heart failure with decreased cardiac output we call it cardiorenal syndrome.
  • The development of AKI in patients with decompensated liver cirrhosis suggests possible hepatorenal syndrome.
  • AKI with urine retention suggests obstructive uropathy or what we call post-renal, this is mainly seen in elderly male patients and those with urinary catheters.
  • AKI after hypotension suggests ATN! Remember that even transient episodes of hypotension can cause AKI.
  • Medications can cause AKI via different mechanisms:
    • ATN such as with vancomycin and aminoglycosides.
    • Crystal-induced nephropathy such as methotrexate, acyclovir, amoxicillin, and sulphamethoxazole.
    • AIN (Acute interstitial nephritis) such as with beta-lactam antibiotics, NSAIDs, and PPI.

• The development of AKI in the setting of rhabdomyolysis especially when CK level > 5000 suggests possible pigment-induced nephropathy. Think of rhabdomyolysis in patients with prolonged immobilized state, heat exertion, trauma, and some drugs. Remember that rhabdomyolysis may cause elevated AST/ALT as well.
• AKI that develops within 48 to 72 hours after contrast exposure suggests contrast-induced nephropathy.

W/U

Even when the cause of AKI seems clear based on the history and physical exam, I always perform a urinalysis and renal ultrasound to look for any evidence of obstruction. I reserve additional urine tests—such as FENa, FEUrea, urine creatinine, cast analysis, and sometimes renal biopsy for cases where the etiology of AKI remains unclear after my initial assessment.

Management of AKI

• When my patient develops AKI, I reflexively do these five things:
  • Discontinue any potential nephrotoxin and offending agents.
  • Correct and avoid hypotension.
  • Ask the pharmacy to renally adjust all medication.
  • Switch to a renally safe alternative if possible, for example, switch to LMWH to UFH for DVT prophylaxis or anticoagulation.
  • Palpate the patient’s lower abdomen to check for any bladder distension and place a Foley catheter if detected. This is particularly important in elderly gentlemen.

Obstructive uropathy

• The treatment of obstructive uropathy involves relieving the obstruction and managing volume and electrolytes.
• Urinary catheterization relieves the obstruction in most cases. I always consult urology with these patients.
• If the obstruction is due to BPH, alpha-blockers such as tamsulosin must be initiated.
• Volume management is crucial in these patients given potential post-obstructive diuresis.
  • There is no set rule for a fluid replacement here! Ensuring the patient remains hemodynamic stability is the main goal.
  • Some may opt to track UO and replace it with fluids, a 50–75% strategy can be used which means replacing 50-75% of the previous hour’s urine output with IV fluid.
• Post-decompression hematuria may develop with rapid bladder decompression.

Prerenal AKI

• The management of prerenal AKI depends on the cause of decreased renal perfusion.
• Volume depletion:
  • Aggressive IV fluid resuscitation with isotonic crystalloid solutions, don’t shy away from using LR or plasmalyte because of the concern of hyperkalemia!
  • Bicarb drip should be used instead if metabolic acidosis is present, I use bicarb drip when HCO3 < 22.
• Volume overload:
  • IV loop diuretics. Patients with AKI require higher doses of loop diuretics, the starting dose of furosemide is 80 mg once or twice daily, and 2 mg once or twice daily for bumetanide.

• Patients with congestive heart failure and low CO syndrome may require inotropes as well. Please consult cardiology in addition to nephrology if you decide to use inotropes.
• Albumin along with terlipressin or norepinephrine is the treatment of choice for hepato-renal syndrome.

Acute interstitial nephritis

• Discontinue any potential offending agents as this can lead to partial or complete recovery of renal function.
• If no improvement in kidney function within 5-7 days after stopping the offending drug, corticosteroids are recommended. Prednisone is commonly used, starting at 1 mg/kg/day for 1-2 weeks, followed by a taper over 4-6 weeks. Early initiation of steroids is associated with better outcomes and reduced risk of chronic kidney disease.

Acute tubular necrosis (ATN)

• Acute tubular necrosis (ATN) is probably the most common form of AKI in critically ill patients.
• It frequently results in oliguria, anuria, and the need for renal replacement therapy (RRT).

• Anuric or oligouric AKI always makes me nervous, I consult nephrology right away in these patients as life-threatening hyperkalemia and acidosis can develop quickly requiring RRT.
• Don’t be deceived by the initial normal K! As long as they are oliguric or anuric, potassium likely will rise despite hyperkalemia management, the same applies to metabolic acidosis.

Crystal-induced and pigment-induced nephropathy

The treatment of crystal-induced and pigment-induced nephropathy is similar and involves discontinuing the offending agent and providing supportive care with IV fluid resuscitation. In some cases, urine alkalinization may be necessary. Nephrology consultation is essential to optimize management and minimize the need for renal replacement therapy (RRT).

Initiating Renal replacement therapy (RRT)

• The Nephrology team typically decides when to initiate RRT, whether early or late, and whether to use CRRT or intermittent HD.
• CRRT is typically chosen in patients with hemodynamic instability who can’t handle the fluid shift used in regular HD.
• Critical hyperkalemia and severe metabolic acidosis are the two main reasons for emergent RRT in critically ill patients.

• Volume overload is another indication of RRT in ATN patients! Before starting RRT, if the patient is stable, a high-dose loop diuretic challenge can help assess responsiveness. Typically, we give IV furosemide at 1 mg/kg (or equivalent). If urine output remains ≤600 mL after 6 hours, it suggests poor response and a likely need for dialysis.
• RRT is also indicated for uremic complications such as encephalopathy, pericarditis, and bleeding. RRT is also used for some toxins removal.
• I understand that some of you may consult nephrology for every case of AKI, but that’s not always necessary. Many cases, such as AKI due to volume depletion, are straightforward and typically resolve with IV fluid resuscitation. Let’s reserve nephrology consults for more complex or severe cases, allowing them to focus on the situations that truly require their expertise!

Monitoring

• Patients with AKI should have their Urine output (UO), electrolytes, and kidney function closely monitored.
• While urine output is routinely monitored in critically ill patients, it may not be tracked as closely for those on the regular hospital floor. We must relay the importance of tracking urine output to patients and nurses.

• AKI is a dynamic process with a continuously changing GFR and creatinine clearance and for that reason, serial labs for kidney functions and electrolytes including HCO3 – labeled as CO2 on BMP/CMP- must be obtained!
  • For critically ill patients, particularly those with oliguria or anuria, key labs such as electrolytes, creatinine, and acid-base status should be monitored every 6–8 hours (or up to 12 hours, depending on clinical context). These patients are at high risk for rapid deterioration, including life-threatening hyperkalemia and metabolic acidosis. A single normal potassium (K) level or mildly elevated creatinine on a basic metabolic panel (BMP) should not provide false reassurance, as values can shift abruptly in unstable clinical conditions.
  • For stable inpatients with adequate urine output, daily laboratory monitoring is typically sufficient. However, more frequent testing (e.g., every 12–24 hours) is warranted if significant electrolyte imbalances, worsening renal function, or other clinical concerns arise.

Prognosis

• AKI due to volume depletion and obstructive uropathy resolves quickly if prompt intervention is provided.
• AKI from ATN may take weeks to months to recover, depending on the severity of tubular injury and comorbidities (e.g., diabetes, chronic kidney disease). Some patients may develop residual CKD or progress to ESRD.
• In AIN, Kidney function typically improves within weeks if the offending drug is stopped and steroids are initiated early.
• In crystal-induced nephropathy, recovery within days with early intervention including rapid hydration, urinary alkalinization, and discontinuing the offending drugs.
• In pigment-induced AKI, aggressive IV fluids to flush out nephrotoxic pigments (myoglobin, hemoglobin) can prevent permanent damage. However, severe cases may still progress to ATN or CKD.