7.1 Acute Kidney Injury, Electrolytes & Acid-Base

Acute Kidney Injury: Classifying the Insult

Acute kidney injury (AKI) is an abrupt (hours to days) fall in renal function marked by retention of nitrogenous waste and loss of fluid, electrolyte, and acid-base control. On the CCRN, AKI lives inside the 21% cross-system domain, and almost every item hinges on naming the category of injury, because the category dictates the intervention.

The Three Categories

Prerenal AKI comes from decreased renal perfusion - hypovolemia, hemorrhage, heart failure, sepsis/vasodilation, or renal artery stenosis. The nephrons are structurally intact, so restoring perfusion (crystalloid for hypovolemia, cardiac output for heart failure) reverses it. Laboratory clues: BUN:creatinine ratio >20:1, urine sodium <20 mEq/L, fractional excretion of sodium (FENa) <1%, and concentrated urine with high specific gravity.

Intrarenal (intrinsic) AKI is direct parenchymal damage, most often acute tubular necrosis (ATN) from prolonged ischemia or nephrotoxins (aminoglycosides, IV contrast, or myoglobin from rhabdomyolysis). Urine shows muddy-brown granular casts, urine sodium >40 mEq/L, FENa >2%, and a BUN:creatinine ratio nearer 10-15:1 because damaged tubules cannot reabsorb sodium or urea.

Postrenal AKI is mechanical obstruction below the kidney - benign prostatic hyperplasia, tumor, bilateral stones, or a clotted or kinked Foley catheter. The fix is to relieve the obstruction; suspect it when sudden anuria alternates with polyuria.

Staging and Baseline Numbers

Three consensus systems stage AKI: RIFLE (Risk, Injury, Failure, Loss, End-stage), AKIN, and the current standard KDIGO. KDIGO Stage 1 = creatinine rise >=0.3 mg/dL in 48 hours or 1.5-1.9x baseline, or urine output <0.5 mL/kg/h for 6-12 hours. Oliguria is <400-500 mL/day; anuria is <100 mL/day. Normal BUN is 10-20 mg/dL and creatinine 0.6-1.2 mg/dL. Classic ATN evolves through onset, an oliguric phase, a diuretic phase (where the danger flips to hypokalemia and dehydration), and recovery.

Critical Electrolyte Derangements

Potassium (3.5-5.0 mEq/L)

Potassium is the deadliest ICU electrolyte because it controls cardiac excitability. Hyperkalemia (>5.0; critical >6.5) marches through the ECG: peaked T waves -> prolonged PR -> widened QRS -> loss of P wave -> sine wave -> ventricular fibrillation/asystole. Treatment follows a strict sequence:

1. Calcium gluconate or calcium chloride - stabilizes the myocardial membrane within minutes but does NOT lower potassium. Give it FIRST whenever ECG changes are present.
2. Shift potassium into cells: regular insulin 10 units with D50, nebulized albuterol, and sodium bicarbonate if acidotic.
3. Remove potassium from the body: loop diuretics, sodium polystyrene sulfonate (Kayexalate) or patiromer, and hemodialysis for refractory or ESRD patients.

Hypokalemia (<3.5) causes flattened T waves, U waves, ST depression, PVCs, and torsades de pointes. Replace potassium and always check magnesium - hypomagnesemia drives refractory hypokalemia that will not correct until the magnesium is repleted.

Sodium (135-145 mEq/L)

Hyponatremia (<135) produces cerebral edema, confusion, and seizures. Severe symptomatic hyponatremia (for example Na 112 with active seizures) is treated with 3% hypertonic saline, but correction must not exceed ~8 mEq/L per 24 hours to avoid osmotic demyelination syndrome (central pontine myelinolysis). Hypernatremia (>145) causes thirst, lethargy, and seizures; correct slowly (<10-12 mEq/L/day) to prevent rebound cerebral edema.

Calcium, Magnesium, Phosphate

• Ionized calcium 4.5-5.6 mg/dL (total 8.5-10.5): hypocalcemia from citrate (massive transfusion, CRRT) causes a prolonged QT, Chvostek and Trousseau signs, and tetany; hypercalcemia causes a shortened QT and "stones, bones, groans, and moans."
• Magnesium 1.5-2.5 mg/dL: hypomagnesemia triggers torsades and refractory K/Ca; hypermagnesemia causes loss of deep-tendon reflexes and respiratory depression (treat with IV calcium).
• Phosphate 2.5-4.5 mg/dL: hyperphosphatemia in tumor lysis syndrome; hypophosphatemia in refeeding syndrome, which weakens respiratory muscles.

Acid-Base Interpretation

Normal values: pH 7.35-7.45, PaCO2 35-45 mmHg, HCO3 22-26 mEq/L. Read every ABG stepwise: pH (acidemia vs alkalemia) -> primary disorder (respiratory if PaCO2 drives it, metabolic if HCO3 does) -> compensation. Then compute the anion gap = Na - (Cl + HCO3) (normal 8-12).

• High-anion-gap metabolic acidosis (MUDPILES): methanol, uremia, DKA, lactic acidosis, salicylates.
• Normal-gap metabolic acidosis: diarrhea and renal tubular acidosis (direct bicarbonate loss).
• Metabolic alkalosis: vomiting/NG suction and diuretics.

Worked example: pH 7.28, PaCO2 30, HCO3 14, Na 140, Cl 100. The low pH with low HCO3 is a metabolic acidosis; the low PaCO2 is appropriate respiratory compensation. Anion gap = 140 - (100 + 14) = 26 -> a high-gap acidosis consistent with DKA or lactic acidosis. A common CCRN trap is treating the compensating low PaCO2 as a separate problem - it is the lungs protecting the patient, not a second disorder.

Interpretation Caveats and Common Traps

FENa is unreliable after diuretics - loop diuretics force sodium into the urine, so a patient on furosemide can show a high FENa despite true prerenal physiology. In that setting, use the fractional excretion of urea (FEUrea <35% suggests prerenal) instead. Do not anchor on a single number: correlate the labs with volume status, medications, and the urine sediment. Another frequent trap is giving potassium to a patient whose ECG shows peaked T waves and rising QRS while awaiting a serum level - always suspect and treat hyperkalemia before the value returns when the clinical picture fits. Finally, remember the ATN diuretic phase: as tubules recover they cannot concentrate urine, so the patient swings from oliguria to large-volume diuresis and the risk reverses to hypokalemia, hypomagnesemia, and hypovolemia - keep replacing losses and rechecking electrolytes frequently until the concentrating ability returns.