Acute Kidney Injury (AKI)

Acute Kidney Injury (AKI)

• AKI involves a sudden and often reversible loss of renal function, developing over days to weeks.
• It often occurs with a decrease in urine output.

Epidemiology

• Approximately 20% of acutely ill patients, especially the elderly, develop AKI.

KDIGO Definition

• AKI is diagnosed when at least one of the following criteria is met:
  • Serum creatinine increases to ≥1.5 times the baseline level within 7 days.
  • Serum creatinine increases by ≥0.3 mg/dL within 48 hours.
  • Urine output is <0.5 mL/kg/hour for 6 hours.

Etiology and Pathophysiology

• AKI has various causes and is frequently multifactorial.
• AKI is classified into three main types:
  • Pre-renal: reduced perfusion to the kidneys
  • Renal (Intrinsic): intrinsic kidney disease
  • Post-renal: obstruction to urine flow, also known as obstructive uropathy

Pre-Renal AKI

• In pre-renal AKI, the kidney is not damaged.
• Glomerular filtration rate (GFR) can improve rapidly if renal perfusion is restored.

Clinical Presentation

• Includes patient history.
• All acutely ill patients should be assessed for hemodynamic status, temperature, renal function tests (RFT), comorbidities, and medications used.
• If serum creatinine is elevated, it's important to determine if it's acute or AKI on top of chronic kidney disease, using previous patient data if available.

Symptoms

• AKI can be asymptomatic until significant loss of renal function.
• Oliguria or anuria, a frequent complaint, may occur.
• Uremic symptoms include anorexia, altered taste (dysguesia), nausea, vomiting, weight loss, fatigue, muscle cramps, restless legs, altered mental status, itching (pruritus), bleeding, hiccups, and chest pain.
• Fluid retention symptoms include swelling and breathlessness.

Signs of AKI

• Confusion, convulsions, asterixis (flapping tremor), coma (uremic encephalopathy).
• Pericardial rub (uremic pericarditis)
• Scratch marks, bleeding manifestations
• Dyspnea, orthopnea, acidotic breathing (Kussmaul breathing), uremic fetor, crackles, pleural rub, pleural effusion.
• Edema (dependent and/or orbital and genital), elevated jugular venous pressure (JVP).
• Hypertension

Diagnosis

• High RFT (blood urea, serum creatinine levels).
• Previous data indicating elevated creatinine for ≥3 months suggests chronicity.

Causes of AKI

• Pre-renal
  • Volume depletion: GI loss, renal loss, hemorrhage, burns.
  • Reduced cardiac output: heart failure (HF), acute coronary syndrome (ACS), massive pulmonary embolism (PE).
  • Systemic vasodilation: sepsis, anaphylaxis, cirrhosis.
  • Intrarenal vasoconstriction: NSAIDs, contrast agents, hypercalcemia, hepatorenal syndrome (HRS).
  • Efferent arteriolar vasodilation: ACE inhibitors (ACEi), angiotensin receptor blockers (ARB).
• Renal (Intrinsic)
  • Acute tubular necrosis (ATN).
  • Acute interstitial nephritis (AIN).
  • Acute glomerulonephritis (AGN).
  • Acute vascular syndromes (macro and microvascular).
  • Tubular obstruction.

Acute Tubular Necrosis (ATN)

• Can be ischemic, from prolonged pre-renal AKI.
• Drug-induced: aminoglycosides, amphotericin B, tenofovir, NSAIDs, contrast agents, immunoglobulins.
• Pigments: rhabdomyolysis, intravascular hemolysis.

Acute Interstitial Nephritis (AIN)

• More common in the elderly.
• Drug-induced: penicillins, cephalosporins, sulfonamides, quinolones, NSAIDs, proton pump inhibitors (PPIs), diuretics.
• Infection: pyelonephritis, leptospirosis, tuberculosis (TB).
• Autoimmune: systemic lupus erythematosus (SLE), sarcoidosis, Sjogren's syndrome.
• Malignancy: leukemia, lymphoma.

Acute Glomerulonephritis (AGN)

• Infection-related GN (IRGN).
• Rapidly progressive GN (RPGN).
• Lupus nephritis (SLE).
• Anti-glomerular basement membrane (GBM) disease.
• Renal vasculitis.

Acute Vascular Syndromes

• Renal artery occlusion.
• Renal vein thrombosis (Nephrotic).
• Cholesterol emboli (after catheterization).
• Scleroderma renal crisis.
• Emergency hypertension.
• Thrombotic microangiopathy (TMA): hemolytic uremic syndrome (HUS) / thrombotic thrombocytopenic purpura (TTP).
• HELLP syndrome (hemolysis, elevated liver enzymes, low platelet count).

Tubular Obstruction

• Cast nephropathy from paraprotein (myeloma).
• Crystal nephropathy due to tumor lysis syndrome (TLS), acyclovir use, ethylene glycol.

Post-Renal Causes

• Calculi (stones), bilateral.
• Clot in urinary tract.
• Retroperitoneal fibrosis.
• Tumors of the bladder, prostate, or cervix.
• Urethral stricture.
• Meatal stenosis.

Signs and Investigation Results

• Pre-renal
  • Tachycardia, hypotension (including orthostatic), delayed capillary refill, dry mucous membranes, delayed skin turgor.
  • Labs: Urine Na < 20 mmol/L, FENa < 1%, high urea:creatinine ratio, bland urinalysis.
• ATN
  • Labs: Urine Na > 40 mmol/L, FENa ≥ 1%, granular (muddy brown) casts.
• GN
  • Hypertension, edema, rash, arthritis.
  • Labs: hematuria, dysmorphic RBCs, RBC casts, proteinuria.
• AIN
  • Fever, rash, arthralgia (mainly drug-induced).
  • Labs: leucocyturia (pyuria), WBC casts, eosinophiluria, eosinophilia.
• Post-renal
  • Flank pain / suprapubic pain, hematuria.
  • Palpable kidney(s), distended bladder.
  • Imaging is required to identify obstructive lesion, hydronephrosis/hydroureter.