AKI management & renal emergencies
Fix volume, stop NSAIDs/ACE/ARB if prerenal/AKI, avoid hyperglycemia and unnecessary contrast. Large-volume resuscitation: LR > NS (SMART/SALT-ED).
Management
- Optimize hemodynamics, avoid nephrotoxins. Correct volume: IVF and hold diuretics if hypovolemic; diurese if hypervolemic. Stop NSAIDs / ACE inhibitors / ARBs. Avoid hyperglycemia and contrast. No evidence of benefit for empiric diuretics in oliguria (). If large-volume resuscitation or critically ill, generally LR > NS (; ).
- Renally dose meds (Lexicomp by GFR). GFR calculations assume steady state: if creatinine is rising, assume clearance is lower than the reported eGFR; if anuric, assume GFR is 0. Run the MAR with pharmacy. Consider cystatin C if eGFR looks wrong ( CKD Guidelines).
- Manage complications — hyperK, hyperphos, metabolic acidosis, uremic bleeding.
- Dialyze when AEIOU is met.
| Complication | Move |
|---|---|
| Hyperkalemia | ECG, telemetry until improved. Stabilize with calcium gluconate, shift with insulin/dextrose and albuterol, then remove K with sodium zirconium cyclosilicate (Lokelma), bowel regimen, furosemide. Low-K diet. |
| Hyperphosphatemia | Sevelamer if P >5.5 mg/dL vs calcium acetate depending on calcium. Avoid IV calcium if Ca × Phos product >70 (precipitation). Low-phos diet. |
| Metabolic acidosis | Sodium bicarbonate PO/IV (see Acid-Base). |
| Uremic platelets / bleeding | DDAVP 0.3 mcg/kg IV; onset 1 h, lasts 4–8 h. |
- A
Acidosis
Especially pH <7.0, refractory to bicarbonate.
- E
Electrolytes
Refractory hyperkalemia.
- I
Intoxication
Lithium, ethylene glycol, metformin, salicylates, theophylline.
- O
Overload
Refractory volume overload.
- U
Uremia
Encephalopathy, neuropathy, pericarditis — not a BUN number.
Uremic emergencies, not a lab cutoff. Page renal when the temporizing moves are failing.
When to page the renal fellow overnight
| Emergency | Threshold | Temporize while they walk over |
|---|---|---|
| Acidosis | pH <7.1, or <7.2 with severe AKI, without a rapidly reversible cause (i.e. not DKA) | Bicarb pushes and isotonic bicarb drip. Intubate and hyperventilate if they cannot blow off CO2. |
| Hyperkalemia | ECG changes / arrhythmia, or K >6.5 (>5.5 if rising rapidly from rhabdo / GI bleed) | Calcium gluconate, diuretics, insulin/D50, albuterol. iHD clears K faster than CVVH — prefer iHD in stable patients who can tolerate it. |
| Hyponatremia | Na <120, symptomatic (AMS with low GCS, seizures), or needing 3% saline ± DDAVP clamp | See Sodium disorders. Do not free-water-restrict a seizing patient. |
| Anuria with ADHF | No urine, wet, and the heart is the reason | Foley. Monitor UOP / MvO2 / labs (LFTs, Cr, lactate, CI). Raising cardiac output (diuresis or HD, ± inotropes) raises GFR. |
| Ingestions | Lithium; ethylene glycol / methanol (osmolar gap → anion gap); metformin with end-organ damage (renal failure, vision loss) | AEIOU. Call toxicology with renal. |
| RPGN | Active sediment, rising Cr over days–weeks, systemic vasculitis clues | Urgent consult for pulse steroids ± plasmapheresis. See Glomerular disease. |
| Scleroderma renal crisis | Abrupt severe HTN then oliguric renal failure in diffuse scleroderma | ACE inhibitor (captopril) at the maximum tolerated dose, starting 6.25 or 12.5 mg, titrating q4h. Avoid steroids. |
Cause-specific treatment
- AIN: stop the offender. Consider prednisone 40–60 mg daily for 1–2 weeks if biopsy-confirmed or high pretest probability — evidence is not great ().
- HRS: see Hepatorenal Syndrome.
- Post-renal: Foley, α-blockers; 5α-reductase inhibitor (effect is not immediate); urology / IR if a perc nephrostomy is needed.
Cardiorenal syndrome (type 1)
Five phenotypes link heart and kidney; type 1 is HF causing AKI (; ). Decreased renal perfusion from ↑ venous congestion ± ↓CO yields a low trans-renal perfusion pressure. This is more “under-draining” (congestion) than “under-filling” (perfusion).
- Treat by relieving renal venous congestion. Trend Cr against total-body balance and daily weights; expect a lag.
- Loop diuretics first-line ± a thiazide (metolazone / chlorothiazide). See Advanced diuresis.
- No benefit of low-dose dopamine or nesiritide to improve forward flow (, ).
- Ultrafiltration: similar weight loss and CHF symptoms, worse renal function vs stepped loop/thiazide therapy (, ).
Contrast-associated AKI
Definition: ↑Cr ≥0.5 or 25% within 48–72 h of contrast; CA-AKI means the AKI is causally related to the contrast (; ; ACR 2025;35). Starts 24–48 h, peaks 3–5 days, resolves ~10 days; usually non-oliguric. Recent data: risk is lower than older estimates and hard to separate from background Cr noise (Ann Em Med 2017;69:577). Mechanism: vasospasm vs osmotic tubular injury.
- Risk factors: higher contrast load, hyperosmolar contrast, intra-arterial injection (cardiac cath), DM, proteinuria, concomitant AKI.
- Prophylaxis for high-risk patients (GFR <30, or 30–45 plus DM) receiving arterial/IV contrast: consider IV NS per protocol. If treating volume overload, hold diuretics the day of contrast with no extra IVF.
- No added benefit of IV bicarb or NAC (, ), or of pre/post/intra HD in anuric patients ().
- Balance CA-AKI risk against the harm of delaying a diagnosis that would change treatment.
Crystals, casts, muscle
- Crystalline nephropathy: stop the drug. Fomepizole / HD for ethylene glycol. Rasburicase / HD for TLS. IVF and diuresis for acyclovir (goal UOP >150 mL/h).
- Myeloma kidney (cast nephropathy): total protein/Cr, SPEP/UPEP/SFLC; kidney biopsy if the diagnosis is unclear. IV hydration to UOP >3 L/day to limit precipitation (volume overload can be diuresed); chemotherapy to cut light-chain production. Plasmapheresis has unclear benefit given rebound production.
- Rhabdomyolysis: AKI is unlikely unless CK >20,000. Aggressive NS for UOP >250 mL/h. Consider isotonic sodium bicarb if marked acidosis () and no hypocalcemia — no convincing evidence HCO3 is superior to NS. Watch hyperK and hypoCa. Continue aggressive IVF until CK <5,000; once volume-replete, keep IVF going with close monitoring and diuresis as needed.