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    Acute Kidney Injury – Diagnosis & Treatment

    Urological

    Last Updated Mar 31, 2021
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    By Julian Marsden, Dave Zhu

    Context

    • Acute Kidney Injury (AKI) is defined as an acute loss of kidney function, with subsequent accumulation of metabolic waste products.
    • AKI can be divided into 3 subtypes:
      • Prerenal – Decrease in kidney perfusion
      • Intrarenal – Injury to kidney parenchyma
      • Postrenal – Urine obstruction
    • Clinical presentation of AKI is varied. Patients may be asymptomatic and be diagnosed incidentally on lab investigations or imaging, or present with overt signs and symptoms such as:
      • Oliguria/anuria
      • Pulmonary edema
      • Evidence of shock
    • Risk factors for AKI:
      • >65 years old
      • Volume depletion
      • Surgical procedures
      • Infections
      • Nephrotoxic agents
      • Hypertension
      • Diabetes
      • CHF
      • Atherosclerosis
      • Chronic Kidney Disease
      • Obstructive uropathy
    • Life threatening complications of AKI:
      • Severe metabolic acidosis
      • Hyperkalemia
      • Pulmonary edema
    • Recovery of kidney function may occur within days or require dialysis for many months depending on the severity, duration, and recurrence of the initial AKI.
    • Patients may require admission to monitor for recovery of renal function, and nephrology or urology consultation for further workup and management.

    Diagnostic Process

    • AKI is diagnosed based on serum creatinine (SCr) levels or decreased urine output.
      • eGFR is NOT applicable in AKI.
    • AKI Staging criteria based on Kidney Disease: Improving Global Outcomes definitions.

    • Baseline creatinine measurements may not be available. Patients at increased risk of AKI should have SCr and urine output monitored.

    Clinical Evaluation

    Try to determine the cause (prerenal, intrarenal, postrenal).

    • Prerenal and postrenal causes are the most common and attempts should be made to rule these causes out prior to workup for intrarenal causes.

    Prerenal

    • Hemorrhage
    • GI/urinary fluid loss
    • Sepsis
    • Postoperative hypotension
    • ACEi/ARBs
    • NSAIDs

    Postrenal

    • Prostate hypertrophy/cancer
    • Kidney stones
    • Neurogenic bladder

    Intrarenal

    • Nephritic syndrome
      • Hematuria
      • Proteinuria
      • HTN
    • Nephrotic syndrome
      • HTN
      • Periorbital swelling
      • Lower leg edema
    • Rhabdomyolysis
    • Nephrotoxic agents
    • Drug eruption
    • Infections

    Investigations

    Investigations are guided based on the likely cause (prerenal, intrarenal, postrenal). Postrenal causes CANNOT be ruled out based on urine output.

    Lab investigations:

    • Serum creatinine
    • BUN
    • Electrolytes
    • CBC
    • CK
    • ABG or VBG
      • pH
      • HCO3
      • pCO2
    • ECG:
      • Hyperkalemia causing ECG changes
    • Urinalysis:
      • Dipstick
      • Microscopy
      • Albumin or Protein to Creatinine ratio
      • Urine electrolytes
        • Urine sodium concentration < 20 mmol/L indicates prerenal cause (3)
      • Urine Osmolality
    • Imaging:
      • Ultrasound for postrenal obstruction and post-void volume
      • CT for obstruction or unexplained cause of AKI
    • Biopsy (consult nephrology)

    Recommended Treatment

    • Management of AKI is mostly supportive.
    • Life-threatening complications may arise and need to be treated promptly.
    • Early nephrology consultation may be beneficial.

    Discontinue Nephrotoxic Agents

    • Pharmacist review or use of a drug lookup database (e.g. Lexicomp, RxTx) may be beneficial.
    • Examples:
      • NSAIDs
      • ACEi/ARB
      • Aminoglycosides
    • Adjust Medications for Renal Dosing
      • Pharmacist review or use of a drug lookup database (e.g. Lexicomp, RxTx) may be beneficial.
    • Volume Status
      • Hypovolemia:
        • Renal perfusion needs to be balanced with fluid overload.
        • 9% normal saline or lactated Ringer’s solution are recommended over colloid solutions (1, 2). Plasmalyte can also be used.
        • Target Mean Arterial Pressure >65 mmHg.
        • Vasopressors may be used if fluid resuscitation is not successful (1, 2, 3).
      • Hypervolemia:
        • Furosemide:
          • Initial: 80 mg IV or double the patient’s usual dose if already on diuretic (5).
          • If no improvement in urine output within 2 hours, double initial dose (5).
        • Renal Replacement Therapy (Indications below)
      • Hyperkalemia
        • With ECG changes:
          • Calcium Gluconate 1 g IV, repeat as needed (3).
          • Insulin 10 Units IV with dextrose 25-50 g IV (3).
          • Salbutamol 10-20 mg nebulized (3).
          • Renal Replacement Therapy (Indications below)

    Potassium-restricted diet (<2g/day).

    Metabolic Acidosis

    • Treat underlying cause.
    • IV fluids:
      • Target serum bicarbonate 20-22 mmol/L and pH >7.2 (5).
      • 9% Normal Saline, plasmalyte or Lactated Ringer’s solution for acidosis due to reduced perfusion.
      • 3% Sodium Bicarbonate in D5W (3×50 mmol/50 mL ampules in 1L D5W) (5, 6).
        • May also decrease serum potassium.
        • Monitor for volume overload.
      • Renal Replacement Therapy preferred if hypervolemic (indications below).
    • Urinary Obstruction
      • Urethral catheterization
      • Consider Urology consultation
    • Glycemic Control
      • Target glucose 6.1 – 8.3 mmol/L (2)
    • Renal Replacement Therapy
      • Requires Nephrology consultation
      • Indications (1):
        • Despite adequate IV fluid administration:
          • Anuria (>6 hours) or severe oliguria (< 200mL in 12 hours)
          • Hyperkalemia (>6.5 mmol/L) despite treatments as mentioned above
          • Severe metabolic acidosis (pH <7.2)
        • Dialyzable toxin/drug
        • BUN > 30 mmol/L
        • Uremic complications (Encephalopathy, neuropathy, pericarditis)
        • Volume overload unresponsive to diuretics

    Quality Of Evidence?

    Justification

    Recommendations based off Kidney Disease: Improving Global Outcomes clinical practice guideline.

    High

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