Acute Kidney Injury (AKI) / Acute Renal Failure

Definition: Rapid decline in renal function. Classified into pre-renal, intra-renal, post-renal.

1. Pre-Renal AKI

• Cause: ↓ renal blood flow → ↓ GFR, ↓ Na⁺ filtration.

• Pathophysiology:

  • Less Na⁺ reabsorption (main O₂ consumer) → ↓ renal O₂ demand.

  • Results in oliguria.

• Reversible if blood flow restored before ischemic damage.

• Common causes:

  • Volume depletion: hemorrhage, diarrhea, vomiting, burns.

  • ↓ Cardiac output: MI, valvular disease.

  • Vasodilation: sepsis, anaphylaxis, anesthesia.

  • Renal artery stenosis, embolism, thrombosis.

2. Intra-Renal AKI

• Glomerular damage:

  • Vasculitis, malignant HTN, cholesterol emboli.

  • Post-strep glomerulonephritis (1–3 wks after Group A strep) → immune complex deposits.

• Tubular injury:

  • Ischemia or toxins → acute tubular necrosis (ATN).

• Interstitial injury:

  • Acute pyelonephritis.

  • Interstitial nephritis.

3. Post-Renal AKI

• Cause: Urinary tract obstruction.

• Sites:

  • Bilateral ureteral obstruction (stones, clots).

  • Bladder outlet obstruction.

  • Urethral obstruction.

  • Foley catheter obstruction.

Clinical Features of AKI

• Retention of: water, electrolytes, wastes.

• Complications: edema, HTN, hyperkalemia, metabolic acidosis.

• Anuria → death within weeks unless treated (restored function or dialysis).

Chronic Kidney Disease (CKD)

Definition: Loss of ~75% of nephrons; usually irreversible.

Causes

• Metabolic: diabetes, obesity, amyloidosis.

• Hypertension.

• Renovascular disease: atherosclerosis, nephrosclerosis.

• Immune: chronic glomerulonephritis, lupus.

• Infections.

• Nephrotoxins.

• Obstruction: post-renal.

• Congenital disorders.

Pathophysiology

• Remaining nephrons hyperfunction → rapid tubular flow.

• Kidneys can still make urine, but it is dilute (poorly concentrated).

• Progression → end-stage renal disease (ESRD).

Common U.S. Causes of ESRD

• Diabetes.

• Hypertension.

Manifestations of CKD

• Fluid & electrolytes: edema, HTN, acidosis, hyperkalemia.

• Nitrogenous waste: uremia (↑ urea, creatinine, uric acid).

  • Uremic platelet dysfunction → bleeding.

• Other retained toxins: phenols, sulfates, phosphates, potassium, guanidine.

• Endocrine/metabolic:

  • ↓ Erythropoietin → anemia.

  • ↓ Vitamin D activation → osteomalacia.

  • ↑ Phosphate retention → ↓ Ca²⁺ → ↑ PTH → secondary hyperparathyroidism → bone demineralization.

• Hypertension: both cause and consequence (salt/water retention, ↑ renin/Ang II).

Dialysis and Renal Replacement Therapy

Indications (Mnemonic: AEIOU)

• A: Acidosis.

• E: Electrolyte disturbances (K⁺, Na⁺, Ca²⁺).

• I: Intoxication (methanol, ethylene glycol, lithium, aspirin, drugs).

• O: Overload (volume).

• U: Uremia (symptoms: nausea, seizures, pericarditis, bleeding).

Hemodialysis

• Blood removed, passed across a semipermeable membrane against dialysate → solutes/water exchange.

• Typical schedule: 4–6 hrs, 3x/week.

• Access types:

  • Fistula: artery–vein connection; best option but needs months to mature.

  • Graft: synthetic tubing connecting artery–vein; usable immediately.

  • Central dialysis catheter: temporary, immediate use.

Peritoneal Dialysis

• Catheter placed in peritoneal cavity → dialysate instilled.

• Solutes diffuse across peritoneum.

• Types:

  • Continuous ambulatory (manual exchanges).

  • Automated (cycler overnight).

• Advantages: better tolerated fluid shifts, useful when vascular access is difficult.

• Risks: peritonitis (abdominal pain, fever).

Anesthesia Considerations in CKD/ESRD

• Pre-op:

  • Check serum creatinine for renal function.

  • Check serum potassium, often required on day of surgery.

  • Assess comorbidities (diabetes, HTN).

• Medications:

  • Avoid drugs heavily dependent on renal clearance (dose-adjust).

  • Succinylcholine hyperkalemia not exaggerated in CKD.

• Hematology:

  • May have anemia (↓ EPO).

  • Uremic platelet dysfunction → may respond to desmopressin.

• Hemodynamics:

  • Impaired vasoconstriction → hypotension risk (hypovolemia, PPV, anesthesia).

• Vascular access precautions:

  • Avoid BP cuff, IV, arterial line on arm/leg with dialysis access.

  • Monitor fistula/graft thrill during surgery.

• Fluid management:

  • Avoid K⁺-containing fluids (e.g., LR).

  • NS may cause acidosis.

  • Fluids used sparingly—balance risk.

• Volume assessment:

  • Compare weight to dry weight (post-dialysis baseline).

  • Recently dialyzed → may behave hypovolemic → sensitive to anesthetics.

• Monitoring:

  • Consider arterial line or central line for closer hemodynamic control.

 Takeaways

• AKI = reversible, classified into pre-renal, intra-renal, post-renal.

• CKD = progressive, irreversible nephron loss → ESRD.

• Dialysis indicated by AEIOU.

• Anesthesia in CKD requires careful attention to electrolytes, fluid status, vascular access, and drug dosing.