5.3 AKI, CKD/ESRD & Electrolyte Imbalances
Key Takeaways
- AKI is classified as pre-renal (fluid-responsive), intrinsic/ATN (muddy brown casts, not simply fluid-responsive), or post-renal (obstruction)
- KDIGO Stage 3 AKI includes creatinine >=3x baseline, RRT initiation, or urine output <0.3 mL/kg/hr for >=24 hours
- IV calcium gluconate is the first-line treatment for hyperkalemia with ECG changes because it stabilizes the cardiac membrane, even though it does not lower serum potassium
- Hemodialysis carries a risk of disequilibrium syndrome; peritoneal dialysis carries a risk of peritonitis, signaled by cloudy effluent
- CKD/ESRD commonly causes hypocalcemia and hyperphosphatemia, managed with phosphate binders and dietary restriction
5.3 AKI, CKD/ESRD & Electrolyte Imbalances
Renal content is only 4% of the blueprint by itself, but electrolyte derangements caused by kidney dysfunction show up throughout the exam's cardiovascular, endocrine, and multisystem questions — a hyperkalemic dysrhythmia or a dialysis complication can just as easily appear in a cardiac scenario as a renal one.
Acute Kidney Injury (AKI)
AKI is staged using KDIGO criteria, based on the change in serum creatinine and urine output: Stage 1 — creatinine increase ≥0.3 mg/dL within 48 hours, or 1.5–1.9× baseline within 7 days, or urine output <0.5 mL/kg/hr for 6–12 hours; Stage 2 — creatinine 2.0–2.9× baseline, or urine output <0.5 mL/kg/hr for ≥12 hours; Stage 3 — creatinine ≥3× baseline or ≥4.0 mg/dL, initiation of renal replacement therapy, or urine output <0.3 mL/kg/hr for ≥24 hours or anuria for ≥12 hours.
AKI is classified into three categories by cause:
- Pre-renal (most common, roughly 60–70% of cases): decreased renal perfusion from hypovolemia, hypotension, heart failure, sepsis, or drugs that reduce glomerular perfusion (NSAIDs, ACE inhibitors). Typical findings: FENa <1%, BUN:creatinine ratio >20:1. This category is fluid-responsive — it improves once perfusion and volume status are restored.
- Intrinsic (renal): direct damage to nephron structures. Acute tubular necrosis (ATN) is the most common intrinsic cause, resulting from either prolonged untreated pre-renal ischemia or nephrotoxins (IV contrast, aminoglycosides, vancomycin, NSAIDs, or myoglobin released in rhabdomyolysis). The classic finding is muddy brown granular casts on urinalysis, with FENa >2% and a BUN:creatinine ratio closer to 10–15:1. Unlike pre-renal azotemia, intrinsic AKI is not simply fluid-responsive — the damaged tubules need time (days to weeks) to heal.
- Post-renal: obstruction of urine outflow from benign prostatic hyperplasia, pelvic or prostate malignancy, nephrolithiasis, a blocked urinary catheter, or a neurogenic bladder. Because one functioning kidney can compensate, a bilateral obstruction (or obstruction in a solitary kidney) is needed to raise creatinine. This category often reverses quickly once the obstruction is relieved (bladder scan, catheter placement, or nephrostomy).
Nursing priorities: identify and treat the underlying cause, maintain strict intake/output and daily weights, avoid nephrotoxic drugs and contrast when possible, dose-adjust renally cleared medications, and monitor closely for fluid overload, electrolyte derangements (hyperkalemia is the most dangerous), and signs of uremia (altered mental status, pericarditis, platelet dysfunction with bleeding).
Chronic Kidney Disease (CKD) and ESRD
CKD is defined as kidney damage or a GFR below 60 mL/min/1.73m² persisting for three months or more, staged 1 through 5 by GFR. Stage 5 (ESRD) is a GFR below 15 mL/min/1.73m², requiring renal replacement therapy or transplant to sustain life. Diabetes and hypertension are the leading causes of CKD.
Hemodialysis (HD) uses an AV fistula, AV graft, or central venous catheter for rapid solute and fluid removal, typically over 3–4 hour sessions three times a week. Key risks include disequilibrium syndrome — rapid urea shifts causing cerebral edema with headache, nausea, confusion, or seizures during or shortly after treatment — and intradialytic hypotension. Vascular access must be protected: no blood pressure measurements or venipuncture in the fistula/graft arm, and the nurse should routinely palpate for a thrill and auscultate for a bruit to confirm patency.
Peritoneal dialysis (PD) uses the peritoneal membrane and a surgically placed catheter for a more gradual exchange. The signature complication to monitor for is peritonitis — cloudy dialysate effluent, abdominal pain, and fever — along with catheter-site infection.
Nephrotoxicity and renal protection: minimize NSAIDs, aminoglycosides, and IV contrast whenever possible. When contrast is necessary, use periprocedural IV isotonic fluids, the lowest effective contrast volume, and follow facility protocol for holding nephrotoxic or renally cleared medications (such as metformin) around the procedure. Monitor trough levels for nephrotoxic antibiotics.
Electrolyte Imbalances
| Electrolyte | Normal range | Key derangement and nursing action |
|---|---|---|
| Potassium | 3.5–5.0 mEq/L | Hyperkalemia (>5.0): peaked T waves progress to loss of P waves, widened QRS, then a sine wave pattern and asystole. Treat with IV calcium gluconate first to stabilize the cardiac membrane (it does not lower potassium), then shift potassium intracellularly with insulin/dextrose and albuterol, and remove potassium with sodium polystyrene sulfonate, patiromer, or dialysis. Hypokalemia (<3.5): flattened T waves, U waves, dysrhythmias, muscle weakness; replace potassium cautiously — IV potassium is never given by push and infusion rates are capped with continuous cardiac monitoring. |
| Sodium | 135–145 mEq/L | Hypernatremia (e.g., DI, dehydration) causes thirst, confusion, and seizures; correct slowly with free water or hypotonic fluids matched to losses. Hyponatremia (e.g., SIADH) is corrected slowly as described in 5.2. |
| Calcium (total) | 8.5–10.5 mg/dL | Hypocalcemia is common in CKD from impaired vitamin D activation and phosphorus retention — watch for Chvostek's and Trousseau's signs, tetany, and a prolonged QT interval. Hypercalcemia (malignancy, immobility) causes lethargy, constipation, and a shortened QT interval. |
| Magnesium | 1.5–2.5 mg/dL | Renally excreted, so it is retained in AKI/CKD. Hypermagnesemia causes loss of deep tendon reflexes, respiratory depression, and cardiac arrest — calcium gluconate is the antidote, with dialysis for severe cases. Hypomagnesemia causes tremors, seizures, and dysrhythmias (including torsades de pointes) and often coexists with hypokalemia or hypocalcemia that resists correction until magnesium is repleted. |
| Phosphorus | 2.5–4.5 mg/dL | Hyperphosphatemia is common in CKD/ESRD from impaired excretion and is managed with phosphate binders (calcium acetate, sevelamer) taken with meals plus dietary restriction; it drives secondary hyperparathyroidism and vascular calcification. Hypophosphatemia is associated with refeeding syndrome and respiratory/cardiac muscle weakness. |
Electrolyte questions on the PCCN reward recognizing the ECG pattern first and matching the correct first-line intervention — calcium gluconate for cardiac-membrane stabilization is a frequent trap because it is often confused with a potassium-lowering therapy when it is actually cardioprotective only.
The nurse reviews a urinalysis on a patient with new-onset AKI and finds muddy brown granular casts. This finding is most consistent with which category of AKI?
A patient's serum potassium is 6.8 mEq/L with peaked T waves and a widened QRS on the monitor. Which intervention should the nurse anticipate administering first?