10.1 AKI, CKD & Life-Threatening Electrolytes
Key Takeaways
- Pediatric AKI is staged with KDIGO using creatinine change from baseline and urine output in mL/kg/h — oliguria thresholds are weight-based, not adult daily volumes.
- Prerenal injury from hypovolemia or low cardiac output is the most common PICU pathway; intrinsic injury includes ATN, nephrotoxins, and glomerulonephritis, while postrenal injury often means congenital obstruction or a clogged catheter.
- Children with CKD in the PICU usually have congenital anomalies of the kidney and urinary tract (CAKUT), glomerular disease, or prior transplant failure — fluid, anemia, and growth issues compound critical illness.
- Symptomatic hyperkalemia with ECG changes gets IV calcium first to stabilize myocardium; insulin-dextrose, albuterol, and bicarbonate (if acidotic) shift potassium, and dialysis removes it.
- Severe hyponatremia is corrected cautiously (roughly ≤8 mEq/L in 24 hours) to avoid osmotic demyelination; ionized hypocalcemia prolongs the QT and can cause tetany after massive transfusion or citrate CRRT.
Pediatric AKI: Why the Child Is Not a Small Adult
Acute kidney injury (AKI) is an abrupt decline in glomerular filtration that retains nitrogenous waste and disrupts fluid, electrolyte, and acid-base balance. On the Pediatric CCRN, AKI sits inside the endocrine/hematology-immunology/GI/renal-GU/integumentary clinical judgment cluster. Almost every item turns on naming the category of injury and applying weight-based urine-output staging rather than adult milliliter-per-day cutoffs.
Normal pediatric creatinine is low because muscle mass is low — a neonate may run 0.2–0.4 mg/dL and a school-age child 0.4–0.7 mg/dL. A rise of ≥0.3 mg/dL within 48 hours or a 1.5× baseline climb still defines KDIGO Stage 1, even when the absolute number looks "normal" to an adult-trained eye. Always compare to the child's own baseline, not a generic adult reference range.
Causes You Must Sort in the PICU
Prerenal AKI is the most common PICU pathway: hypovolemia from gastroenteritis, hemorrhage, burns, or third-spacing; low cardiac output from cardiomyopathy or post–cardiac surgery; and distributive shock from sepsis. Tubules are intact, so the kidney avidly reabsorbs sodium and water. Classic clues: BUN:creatinine ratio >20:1, urine sodium <20 mEq/L, FENa <1%, and concentrated urine. Restore perfusion with isotonic fluid for hypovolemia or inotropes/afterload support for cardiogenic states — fixing the kidney starts with fixing delivery of oxygenated blood.
Intrinsic (intrarenal) AKI damages parenchyma. Prolonged ischemia produces acute tubular necrosis (ATN) with muddy-brown granular casts, urine sodium >40 mEq/L, and FENa >2%. Nephrotoxins common in pediatrics include aminoglycosides, vancomycin (especially with concurrent piperacillin-tazobactam), IV contrast, acyclovir crystal nephropathy, and calcineurin inhibitors. Glomerulonephritis, interstitial nephritis, and vascular insults (hemolytic uremic syndrome, cortical necrosis) also live here. Stop the toxin, support hemodynamics, and escalate to renal replacement when indicated.
Postrenal AKI is obstruction below the glomerulus. In infants and toddlers think posterior urethral valves, bilateral ureteropelvic junction obstruction, neurogenic bladder, stones, or a kinked/clotted Foley or ureteral stent. Sudden anuria alternating with overflow polyuria is a red flag. Relieve the obstruction — catheter irrigation, stent revision, or surgical decompression — before attributing oliguria to "just ATN."
| Category | Pediatric triggers | FENa / UNa | Sediment clue | First action |
|---|---|---|---|---|
| Prerenal | Dehydration, sepsis, low CO | FENa <1%; UNa <20 | Bland / hyaline | Restore perfusion |
| Intrinsic | ATN, nephrotoxins, GN, HUS | FENa >2%; UNa >40 | Muddy casts / RBC casts | Stop toxin; support; RRT if needed |
| Postrenal | PUV, UPJ, clogged Foley | Variable | Variable / crystals | Relieve obstruction |
Staging and Monitoring
KDIGO stages pediatric AKI by creatinine fold-change and urine output in mL/kg/h. Stage 1 includes urine output <0.5 mL/kg/h for 6–12 hours; deeper stages lengthen oliguria and raise creatinine further. Oliguria in infants is commonly framed as <1 mL/kg/h for clinical alerts even when formal staging uses the 0.5 threshold — know both conventions and chart hourly, weight-indexed totals. Anuria (<0.3 mL/kg/h or essentially no urine) demands urgent workup for obstruction, vascular catastrophe, or end-stage failure.
Daily weights, strict intake/output, blood pressure trends, and serial creatinine/electrolytes beat any single snapshot. FENa is unreliable after loop diuretics; use clinical volume assessment and, when available, fractional excretion of urea.
CKD in the PICU
Chronic kidney disease (CKD) in children is most often driven by congenital anomalies of the kidney and urinary tract (CAKUT), reflux nephropathy, focal segmental glomerulosclerosis, or failed prior transplant — not diabetic nephropathy. PICU admissions frequently involve fluid overload with hypertensive urgency, hyperkalemia, pericardial effusion from uremia, anemia of CKD, and mineral bone disease with secondary hyperparathyroidism.
Nursing priorities: protect residual function (avoid NSAIDs and unnecessary contrast), match fluid to residual urine plus insensible losses, dose renally cleared drugs by estimated GFR, and prepare for peritoneal dialysis or CRRT/hemodialysis when hyperkalemia, refractory acidosis, uremic symptoms, or pulmonary edema will not yield. Growth failure and developmental delay are chronic markers — they do not change the acute algorithm but explain why baseline creatinine and blood pressure norms differ from healthy peers.
Life-Threatening Electrolyte Crises
Potassium
Pediatric hyperkalemia (critical often >6.5 mEq/h, earlier if ECG changes) marches through peaked T waves → prolonged PR → widened QRS → sine wave → VF/asystole. Sequence matters:
- IV calcium (gluconate preferred peripherally; chloride via central line) — stabilizes myocardium within minutes; does not lower serum K+.
- Shift: regular insulin with dextrose (weight-based), nebulized albuterol, sodium bicarbonate if acidotic.
- Remove: loop diuretics if residual function, potassium binders, and dialysis for refractory or anuric children.
Hypokalemia flattens T waves, produces U waves, and predisposes to ventricular ectopy — always replete magnesium concurrently or potassium will not stick.
Sodium
Hyponatremia causes cerebral edema, seizures, and herniation risk, especially in infants with thin skull compliance margins. Symptomatic severe hyponatremia may need 3% hypertonic saline, but limit the rise to about 8 mEq/L per 24 hours to avoid osmotic demyelination. Hypernatremia from free-water loss (DI, osmotic diuresis, inadequate free water) is corrected slowly to prevent rebound cerebral edema.
Calcium
Track ionized calcium. Massive transfusion and citrate anticoagulation on CRRT bind calcium → prolonged QT, tetany, Chvostek/Trousseau signs, and poor contractility. Replace ionized calcium and pause or adjust citrate protocols. Hypercalcemia shortens QT and causes polyuria and constipation — less common acutely but tested in oncologic or hyperparathyroid contexts.
Integration Trap
Do not chase a "normal-looking" creatinine while ignoring oliguria in mL/kg/h, and do not give insulin for hyperkalemia before calcium when the QRS is widening — the heart fails first, the potassium number second.
A 14-kg toddler with septic shock has urine output of 5 mL over the last 8 hours, a creatinine rise from 0.3 to 0.6 mg/dL, FENa of 0.4%, and urine sodium of 12 mEq/L. These findings best support which AKI category?
A school-age child with anuria develops a potassium of 7.1 mEq/L, peaked T waves, and a widening QRS. Which intervention should the PICU nurse anticipate FIRST?
A toddler with chronic hyponatremia (Na 118 mEq/L) begins seizing and receives 3% hypertonic saline. The critical safety limit during correction is to: