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Acute Kidney Injury (AKI)

Table of Contents

  • Key Points ⚡
  • Introduction
  • Aetiology
  • Risk Factors
  • Clinical Features
  • Investigations
  • Diagnosis
  • Management
  • Complications
  • References
  • Related Notes
  • Test Yourself

Key Points ⚡

  • AKI is a rapid deterioration in kidney function, common in hospitalized patients (up to 20%).
  • Classified into pre-renal (reduced perfusion), intra-renal (nephron damage), and post-renal (obstruction).
  • Risk factors include CKD, heart failure, liver disease, diabetes, nephrotoxic drugs, sepsis, age >65, and urological obstruction.
  • Symptoms often nonspecific or absent; may show volume overload, uraemia signs, or obstruction.
  • Diagnosis based on KDIGO criteria: urine output <0.5 ml/kg/hr for 6 hrs, creatinine rise ≥1.5x baseline or 0.3 mg/dL within 48 hrs.
  • Management includes withdrawal of nephrotoxic agents, optimizing fluids, addressing causes, and renal replacement therapy (RRT) when indicated.
  • Complications include fluid overload, electrolyte imbalance, metabolic acidosis, progression to CKD or ESRD, and death.

Introduction

AKI is characterized by a rapid decline in kidney function causing accumulation of waste products and dysregulation of fluid, electrolytes, and acid-base balance. It is frequent in hospitalized patients and requires prompt recognition and management.

Aetiology

Pre-renal AKI

  • Due to reduced kidney perfusion from:
  • Hypovolemia (bleeding, vomiting, diarrhea, over-diuresis)
  • Low effective circulating volume (heart failure, liver failure)
  • Renal artery stenosis
  • Drugs (NSAIDs, ACE inhibitors, diuretics)

Intra-renal AKI

  • Structural or functional nephron damage:
  • Acute tubular necrosis (ischemic or toxic injury)
  • Acute interstitial nephritis (drug-induced, infectious, immune-mediated)
  • Glomerular diseases (nephritic/nephrotic syndromes)
  • Intra-tubular obstruction (myeloma, rhabdomyolysis)
  • Other (scleroderma renal crisis, malignant hypertension)

Post-renal AKI

  • Obstruction at any level from ureters to urethra causing bilateral kidney congestion:
  • Nephrolithiasis, retroperitoneal fibrosis
  • Bladder/prostate cancer, BPH
  • Urethral stricture, external compression (tumors)

Risk Factors

  • Chronic kidney disease (eGFR <60)
  • Heart failure, liver disease, diabetes
  • Previous AKI episodes
  • Oliguria
  • Cognitive impairment
  • Hypovolemia
  • Nephrotoxic drugs (NSAIDs, ACEi/ARBs, aminoglycosides, amphotericin B, cisplatin, tacrolimus)
  • Iodinated contrast media exposure
  • Urological obstruction
  • Sepsis
  • Age ≥65 years

Clinical Features

History

  • Often asymptomatic or nonspecific symptoms (nausea, confusion)
  • Important to assess recent hospital admission reason, medication use, urinary symptoms, and solitary kidney

Examination

  • Oliguria/anuria
  • Signs of hypovolemia (dry mucous membranes, hypotension, tachycardia)
  • Signs of fluid overload (pulmonary/peripheral edema, elevated JVP)
  • Uremic signs (ecchymosis, asterixis, encephalopathy)
  • Bladder distension if obstruction suspected

Investigations

Laboratory

  • Urea and electrolytes (creatinine, BUN, calcium, phosphate, potassium, sodium)
  • Full blood count (anemia, leukopenia, thrombocytopenia)
  • Liver function tests (albumin)
  • Venous blood gas (acidosis)

Urine Studies

  • Urinalysis (proteinuria, hematuria, WBCs)
  • Urine volume measurement
  • Microscopy (casts, crystals)
  • Urine osmolarity and specific gravity
  • Urinary eosinophils (rare, for AIN)

Imaging

  • Bladder scan (post-void residual volume)
  • Renal ultrasound (kidney size, hydronephrosis, obstruction)
  • Non-contrast CT (calculi, obstruction)
  • CT urography/triphasic kidneys (bleeding, renal masses)

Renal Biopsy

  • Consider in suspected intra-renal AKI or rapidly progressive glomerulonephritis (RPGN)
  • Not routine for suspected ATN unless diagnosis unclear

Diagnosis

Based on KDIGO criteria:
- Urine output <0.5 ml/kg/hr for 6 hours
- Serum creatinine rise ≥1.5x baseline within 7 days or ≥0.3 mg/dL within 48 hours

Management

General

  • Withdraw nephrotoxic medications
  • Adjust drug dosages for renal clearance
  • Fluid resuscitation in hypovolemia
  • Urinary catheterization for obstruction
  • Initiate sepsis bundle if indicated
  • Use ABCDE checklist for systematic management

Targeted

  • Diuretics for volume overload
  • Immunosuppression (steroids) for AIN or RPGN
  • Relief of obstruction with catheter, nephrostomy, or stenting as needed

Renal Replacement Therapy (RRT)

Indications (AEIOU mnemonic):
- Acidosis (pH <7.15)
- Electrolyte abnormalities (e.g. K+ >6.5 mmol/L)
- Ingested toxins (e.g. lithium, toxic alcohols)
- Fluid overload refractory to diuretics
- Uremia causing complications (pericarditis, encephalopathy)

Complications

  • Fluid overload (pulmonary edema, pleural effusions)
  • Electrolyte imbalances (hyperkalemia, hyperphosphatemia)
  • Metabolic acidosis
  • Uremic end-organ damage
  • Progression to chronic kidney disease (CKD) or end-stage renal disease (ESRD)
  • Death

References

  • Wang HE et al. Acute kidney injury and mortality in hospitalized patients. Am J Nephrol. 2012;35(4):349-355.
  • Santos WJQ et al. Critical Care. 2006;10(2).
  • Zhu K et al. Transl Androl Urol. 2020;9(3):1232-1243.
  • Patel JB & Sapra A. StatPearls. 2021.
  • Mohsenin V. J Intensive Care. 2017;5(1).
  • KDIGO Clinical Practice Guideline for AKI. 2012.
  • González E et al. Kidney Int. 2008;73(8):940-946.
  • Negi S et al. Ren Replace Ther. 2016;2(1).
  • Saran R et al. Am J Kidney Dis. 2019;73(3).
  • Chronic Kidney Disease (CKD)
  • Glomerular Disease (Glomerulonephropathies)
  • Hemodialysis
  • Henoch-Schönlein Purpura (IgA Vasculitis)
  • Hyperkalemia

Test Yourself

  • [Link to quiz/flashcards on Acute Kidney Injury]

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