Renal, Fluids, Electrolytes & Acid-Base · Topic 1 of 22
Acute Kidney Injury
Renal · kidney injury & replacement
Acute Kidney Injury
Creatinine up 0.3 mg/dL in 48 hours or oliguria for 6 hours: rule out prerenal and obstructive causes, and stop the nephrotoxins.
Key numbers
Creatinine up 0.3 in 48 hoursSCr ↑ ≥ 0.3 mg/dL / 48 h
KDIGO stages 1–3 by creatinine riseStage 3: ≥ 3× or ≥ 4.0
FENa below 1% suggests prerenal AKIFENa < 1%
Bladder scan: PVR over 100 mL is retentionPVR > 100 mL
On diuretics, use FEUrea below 35%FEUrea < 35%
01 · Defined byCreatinine up 0.3 in 48 hours
KDIGO AKI = serum creatinine rise ≥ 0.3 mg/dL within 48 hours, or to ≥ 1.5 times baseline within the prior 7 days, or urine output < 0.5 mL/kg/h for 6 hours.
02 · The numberFENa below 1% suggests prerenal AKI
In oliguric AKI, FENa < 1% suggests prerenal azotemia and > 1% suggests acute tubular injury; urinary indices are unreliable in nonoliguric AKI.
03 · Defined byKDIGO stages 1–3 by creatinine rise
KDIGO stage by the worst criterion — stage 1: creatinine 1.5–1.9× baseline or +0.3 mg/dL; stage 2: 2.0–2.9×; stage 3: ≥ 3×, creatinine ≥ 4.0 mg/dL, or RRT started.
01
Causes & risk factors
Why it happensATN: ischemia, nephrotoxins, contrast, myoglobinAcute tubular necrosis is most often ischemic (prolonged prerenal state); nephrotoxic ATN follows vancomycin, aminoglycosides, iodinated contrast and pigments (myoglobin in rhabdomyolysis, hemoglobin in hemolysis).
Drug-induced interstitial nephritis: beta-lactams, PPIs, NSAIDsAcute interstitial nephritis is usually a drug reaction (beta-lactams, PPIs, NSAIDs, sulfonamides, immune checkpoint inhibitors), sometimes with rash; urine eosinophils have limited diagnostic accuracy. Stop the drug.
02
Diagnosis & monitoring
Work-upOn diuretics, use FEUrea below 35%Diuretics raise FENa above 1% even in prerenal states; fractional excretion of urea < 35% still indicates a prerenal cause because urea is reabsorbed proximally.
BUN/creatinine over 20 suggests prerenal AKIBUN/creatinine ratio > 20 suggests prerenal AKI and < 10 tubular injury, but BUN also rises with GI bleeding, corticosteroids, trauma, surgery and parenteral nutrition.
Recheck kidney function 3 months after AKIEvaluate every patient 3 months after AKI for resolution, new CKD or worsened CKD; even after recovery, AKI survivors stay at higher risk of CKD and kidney failure.
Urine-output stages: 6, 12, 24 hoursBy urine output: stage 1 = < 0.5 mL/kg/h for 6–12 h; stage 2 = < 0.5 for ≥ 12 h; stage 3 = < 0.3 for ≥ 24 h or anuria ≥ 12 h.
03
Do right now
In this orderFirst moves
1
→Treat hyperkalemia and pulmonary edema immediately
2
→Exclude prerenal and postrenal causes first
3
→Stop nephrotoxins and renally dose every drug
4
Bladder scan: PVR over 100 mL is retentionPVR > 100 mL
Why each step
Treat hyperkalemia and pulmonary edema immediatelyTreat life-threatening hyperkalemia (calcium gluconate 10 mL of 10% IV, then regular insulin 5–10 units IV with 50 mL of 50% dextrose [25 g]) and pulmonary edema first; these temporize — refractory cases need dialysis.
Exclude prerenal and postrenal causes firstFirst exclude the immediately reversible causes: correct volume depletion or low cardiac output (improvement confirms prerenal AKI) and look for obstruction with a postvoid bladder scan and renal ultrasound.
Stop nephrotoxins and renally dose every drugStop all potentially nephrotoxic drugs (NSAIDs, aminoglycosides, IV contrast where avoidable; hold ACE inhibitors/ARBs in hypoperfusion) and adjust every renally cleared drug, using serum levels for drugs such as digoxin and vancomycin.
Bladder scan: PVR over 100 mL is retentionScan the bladder right after voiding (or place a catheter): a postvoid residual > 100 mL means inadequate emptying, as in prostatic outlet obstruction or neurogenic bladder.
04
Management
OrdersIsotonic crystalloids, not colloids; add vasopressorsExpand volume with isotonic crystalloids rather than albumin or starches (absent hemorrhagic shock), and give vasopressors with fluids in vasodilatory shock to restore renal perfusion.
Dialyze for refractory potassium, fluid, acid, uremiaStart dialysis when hyperkalemia (eg, K⁺ > 6 mmol/L), pulmonary edema or metabolic acidosis is refractory to medical therapy, or uremic complications appear (pericarditis, encephalopathy, seizures) — not for a BUN value alone.
Bicarbonate for pH ≤ 7.2 with AKI: less dialysisFor severe metabolic acidemia (pH ≤ 7.2) with moderate–severe AKI, IV sodium bicarbonate reduces the need for kidney replacement therapy but has not been shown to lower mortality; titrate to serial labs.
05
Red flags & don'ts
Avoid harmPostobstructive diuresis: replace with 0.45% saline complicationAfter obstruction is relieved, brisk diuresis can cause hypokalemia, hypo- or hypernatremia, hypomagnesemia and volume depletion; replace about 75% of urine output with 0.45% saline and follow electrolytes closely.
06
The rules
Know theseNo diuretics or dopamine to treat AKIDo not use diuretics to prevent or treat AKI except for volume overload, and do not use low-dose dopamine or fenoldopam — none improves kidney outcomes.
07
Prerenal AKI or acute tubular injury?
Commonly confused| FENa | < 1% |
|---|---|
| Urine sodium | < 10 mmol/L |
| BUN/creatinine ratio | > 20 |
| Urine/plasma osmolality | > 1.5 |
| Sediment | Bland |
08
More detail
ReferenceShow 7 reference facts
Avoid aminoglycosides when a less nephrotoxic alternative exists; if used, give once daily (normal steady-state kidney function) and monitor levels after 24 h of multiple-daily or 48 h of once-daily dosing.
Creatinine-based eGFR and creatinine-clearance formulas are invalid while creatinine is rising, because creatinine lags behind the fall in GFR.
Oliguria is urine output < 500 mL/day; nonoliguric AKI carries lower mortality and less need for dialysis, and the postoliguric phase may bring sodium wasting and massive polyuria.
Give 20–30 kcal/kg/day, preferably enterally, and do not restrict protein to delay dialysis: 0.8–1.0 g/kg/day without dialysis, 1.0–1.5 on RRT, up to 1.7 g/kg/day on CRRT or when hypercatabolic.
Normal or enlarged kidneys on ultrasound favor reversible AKI; small kidneys suggest CKD, except in diabetic nephropathy, polycystic kidney disease, HIV nephropathy and infiltrative disease, which keep kidneys large.
Avoid gadolinium when eGFR is below 30 mL/min/1.73 m² because of nephrogenic systemic fibrosis; if essential, use a group II agent.
Other oliguric urinary indices: prerenal AKI has urine sodium < 10 mmol/L and urine/plasma osmolality > 1.5; tubular injury has urine sodium > 40 mmol/L and U/P osmolality 1–1.5.
Prerenal, renal, postrenal: check the volume, scan the bladder, then read the urine.
Sources · Merck Manual Professional — Acute Kidney Injury (AKI) (Feb 2026) · KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl 2012;2:1–138 · KDIGO — Acute Kidney Injury (AKI) and Acute Kidney Disease (AKD) guideline page (2026 update in public review) · Hamadah A, Gharaibeh K. Fractional Excretion of Sodium and Urea are Useful Tools in the Evaluation of AKI: PRO. Kidney360 2023 · Merck Manual Professional — Hyperkalemia (insulin 5–10 units with 50 mL of 50% dextrose) · Surviving Sepsis Campaign adult guidelines (SCCM, 2026) · BICARICU-2 trial (JAMA 2025): sodium bicarbonate for severe metabolic acidemia with AKI · Starter sheet built from the verified AGACNP fact map (facts reviewed 2026-10-15).