Acute Kidney Injury (AKI)
Rise in creatinine ≥ 0.3 mg/dL in 48h or ≥ 1.5× baseline in 7 days. Step 1: is it pre-renal, intrinsic, or post-renal? The answer drives everything.
🔍 Overview
2024–2026 Practice Updates
What's changed since the original 2012 KDIGO guideline:
- Terlipressin is first-line for HRS-AKI in the US (FDA approved 2022), replaces midodrine + octreotide as the preferred regimen when available. CONFIRM, 2021
- Contrast-associated AKI is overestimated. N-acetylcysteine and bicarbonate are not recommended; isotonic saline only for eGFR <30. PRESERVE, 2018 · AMACING, 2017 Don't withhold needed imaging for moderate CKD.
- SGLT2 inhibitors: Hold during acute illness / volume depletion, but resume after recovery, they are renoprotective long-term. EMPA-KIDNEY, 2022
- Early vs delayed RRT: Watchful waiting is preferred for stage 2/3 AKI without emergent indications. STARRT-AKI, 2020 · AKIKI, 2016
- Furosemide stress test (1–1.5 mg/kg IV; UOP <200 mL/2h predicts progression) is now an accepted bedside risk-stratification tool.
- Biomarkers (TIMP-2 × IGFBP-7 / NephroCheck): FDA-cleared for early AKI prediction in ICU patients, adoption variable, not yet standard of care.
- Patiromer / SZC have replaced SPS (Kayexalate) for non-emergent hyperkalemia, faster onset, lower risk of intestinal necrosis.
KDIGO Staging
| Stage | Creatinine Criteria | Urine Output |
|---|---|---|
| 1 | ↑ ≥ 0.3 in 48h OR 1.5–1.9× baseline | < 0.5 mL/kg/hr × 6–12h |
| 2 | 2.0–2.9× baseline | < 0.5 mL/kg/hr × ≥ 12h |
| 3 | ≥ 3× baseline OR ≥ 4.0 mg/dL OR RRT initiated | < 0.3 mL/kg/hr × ≥ 24h or anuria × 12h |
Causes -The Classic 3-Category Framework
Pre-Renal (most common -60–70%)
- Volume depletion: vomiting, diarrhea, poor intake, diuresis
- Low CO states: heart failure, cardiogenic shock
- Renal hypoperfusion: ACEi/ARB in bilateral RAS, NSAIDs, hepatorenal syndrome
Intrinsic Renal (20–30%)
- ATN (most common intrinsic): ischemia, nephrotoxins (aminoglycosides, contrast, myoglobin, vancomycin)
- Glomerulonephritis: RBCs + protein + RBC casts on UA
- AIN (interstitial nephritis): drug-induced (PCN, NSAIDs, PPIs), eosinophiluria
- Vascular: renal artery thrombosis, TTP, HUS
Post-Renal (5–10%)
- Bilateral ureteral obstruction, BPH, bladder outlet obstruction
- Check with renal ultrasound + bladder scan
🧪 Workup & Diagnosis
Workup Algorithm
First Move: Bladder scan + renal ultrasound (rule out obstruction) -quick, cheap, and you'll miss post-renal without it.
- UA with microscopy -RBC casts (GN), waxy/granular casts (ATN), eosinophils (AIN), protein
- FENa = (UNa × PCr) / (PNa × UCr) × 100
< 1% = pre-renal or early contrast nephropathy
> 2% = ATN (intrinsic)
Note: FEUrea more reliable in patients on diuretics (< 35% = pre-renal)
🔄 Updated Practice: Old teaching: FENa <1% = pre-renal, FENa >2% = intrinsic (ATN). This is unreliable if the patient is on diuretics (which increase FENa regardless of etiology). Use FEUrea instead -it is NOT affected by diuretics. FEUrea <35% = pre-renal, FEUrea >50% = intrinsic. Also: "pre-renal" and "ATN" exist on a spectrum -prolonged pre-renal azotemia leads to ATN. Early volume resuscitation prevents progression.
- BMP -creatinine trend, K⁺, bicarb, BUN:Cr ratio (> 20:1 suggests pre-renal)
- CBC, LFTs
- Complement, ANA, ANCA, anti-GBM -if GN suspected
- Renal ultrasound -hydronephrosis, echogenicity, kidney size
- Review all medications -nephrotoxins, ACEi/ARBs, NSAIDs (full renal dosing reference)
🚨 Management
Management by Category
Pre-Renal AKI
- Volume resuscitation with IV crystalloid (LR preferred SMART, 2018)
- Hold ACEi/ARBs, NSAIDs, diuretics until creatinine stabilizes
- Treat underlying cause (heart failure, hepatorenal syndrome, hemorrhage)
- Expect creatinine to improve within 24–48h if truly pre-renal
ATN (Intrinsic)
- Supportive care -no specific treatment accelerates recovery
- Strict I&Os, careful fluid management (avoid overload)
- Aggressive electrolyte management (K⁺, bicarb, phosphate)
- Avoid contrast, nephrotoxins
Post-Renal AKI
- Foley catheter if BPH/bladder outlet obstruction → expect post-obstructive diuresis
- Urology consult for ureteral obstruction (stenting vs percutaneous nephrostomy)
- Monitor for post-obstructive diuresis (replace 50–75% UOP with IV fluids)
Indications for Emergent Dialysis -AEIOU
Mnemonic: AEIOU -If any of these are refractory to medical management, call nephrology for emergent dialysis.
| Letter | Indication | Details |
|---|---|---|
| A | Acidosis | Severe metabolic acidosis (pH < 7.1) refractory to bicarb infusion |
| E | Electrolytes | Refractory hyperkalemia (K⁺ > 6.5 with ECG changes despite medical Rx -insulin/glucose, calcium, patiromer/Lokelma) |
| I | Ingestions | Toxic alcohols (methanol, ethylene glycol), lithium, salicylates -dialyzable toxins |
| O | Overload | Volume overload causing pulmonary edema/respiratory failure refractory to diuretics |
| U | Uremia | Uremic encephalopathy (asterixis, AMS, seizures), uremic pericarditis (friction rub -pericardial effusion risk) |
Timing of Dialysis -Don't Rush. Early initiation of RRT does NOT improve mortality vs a delayed/watchful strategy STARRT-AKI, 2020 AKIKI, 2016. Only dialyze when you have a clear AEIOU indication.
| Trial | Year | Finding |
|---|---|---|
| AKIKI | 2016 | Early RRT (within 6h of KDIGO 3) vs delayed (watchful waiting for AEIOU indication) in critically ill AKI -no mortality difference. 49% of delayed group never needed dialysis at all. |
| IDEAL-ICU | 2018 | Early vs delayed RRT in septic shock with AKI -no benefit. Stopped early for futility. 38% of delayed group avoided RRT entirely. |
| STARRT-AKI | 2020 | Largest trial (n=2,927). Accelerated vs standard RRT initiation -no 90-day mortality benefit. Accelerated group had more catheter-related bloodstream infections and hypotension during dialysis. |
Bottom line: Wait for a hard AEIOU indication before initiating RRT. Many critically ill AKI patients recover renal function and never require dialysis if given time. Early initiation exposes patients to catheter complications and hemodynamic instability without survival benefit.
🔄 Updated Practice: Old teaching: start dialysis early in AKI to prevent complications. AKIKI 2016 and STARRT-AKI 2020 both showed that delayed/watchful waiting strategy is safe and avoids unnecessary dialysis in ~50% of patients. Only start RRT for absolute indications: refractory hyperkalemia, severe metabolic acidosis, refractory fluid overload, or uremic complications (encephalopathy, pericarditis, bleeding). "The best dialysis is the one you never need to start."
Swipe for more examples
📋 Case 1, AKI Workup Interpretation
Patient: 72M admitted for pneumonia, Cr rising 1.0 → 2.4 over 48h (KDIGO Stage 2)
Step 1 -Pre-renal vs Intrinsic vs Post-renal:
- BUN/Cr ratio: 42 (> 20:1 → suggests pre-renal)
- FENa: 0.4% (< 1% → pre-renal)
- Urine Na: 8 mEq/L (< 20 → avid Na retention = pre-renal)
- UA: No casts, no protein (argues against ATN or glomerulonephritis)
- Renal US: No hydronephrosis (rules out post-renal obstruction)
Assessment: Pre-renal AKI from volume depletion. Management: IV LR boluses, hold ACEi. Cr improved to 1.8 at 24h → confirms pre-renal.
📋 Case 2, Contrast-Induced AKI
Patient: 68M with CKD Stage 3 (baseline Cr 1.8), underwent cardiac catheterization with contrast 48h ago. Cr now 3.2. UOP declining.
Workup:
- FENa: 2.8% → intrinsic (ATN pattern)
- UA: Muddy brown granular casts → classic for ATN
- Timeline: Cr rise 24–72h post-contrast = classic contrast nephropathy
Management:
- IV isotonic fluids, NS or LR at 1 mL/kg/hr. Avoid volume overload (monitor lung exam, JVP).
- Hold all nephrotoxins, metformin, ACEi, NSAIDs, aminoglycosides.
- No more contrast for at least 48–72h. If urgent need → minimize volume + use iso-osmolar contrast.
- Expect peak Cr at 3–5 days, recovery over 7–14 days. If no recovery by day 14 → may need nephrology consult.
Key lesson: CKD + contrast = high risk. Pre-hydration with IV NS reduces risk. NAC (N-acetylcysteine) has been debunked, no benefit (PRESERVE trial, 2018).
📋 Case 3, Rhabdomyolysis-Induced AKI
Patient: 34M found down after drug overdose (unknown duration). Cr 4.6 (baseline normal). CK 85,000. Dark tea-colored urine. K⁺ 6.2 with peaked T-waves on ECG.
Pathophysiology: Muscle breakdown → myoglobin released → precipitates in renal tubules → ATN. Also causes massive K⁺ and phosphate release and Ca²⁺ sequestration.
Treatment:
- Aggressive IV fluids: NS at 200–300 mL/hr initially. Target UOP > 200–300 mL/hr to flush myoglobin. May need 10–15 L/day.
- Hyperkalemia: Calcium gluconate 1g IV (cardioprotection), insulin + D50, kayexalate. Continuous telemetry.
- Monitor CK q6–12h until trending down. Monitor compartment pressures if limb swelling.
- Avoid calcium repletion even if Ca²⁺ is low, it deposits in damaged muscle. Only give calcium for symptomatic hypocalcemia or ECG changes.
- Dialysis if refractory hyperkalemia, acidosis, or fluid overload despite aggressive IVF.
Key lesson: CK > 5,000 = rhabdo risk for AKI. Flood with fluids early, the best treatment is prevention of tubular precipitation. Always check CK in any "found down" patient.
⚡ Summary
Summary
Define and Stage It
A creatinine rise of 0.3 mg/dL or more within 48 h, or 1.5 times baseline within 7 days, or urine output below 0.5 mL/kg/h for 6 h. KDIGO stages 1 to 3 by creatinine multiple and urine output. The urine output criterion is met before the creatinine moves, so an oliguric patient with a normal creatinine already has AKI.
The Three-Bucket Question Drives Everything
Pre-renal, intrinsic or post-renal. Pre-renal and post-renal are common and reversible, so exclude them first. Intrinsic then splits by compartment: tubular (ATN), interstitial (AIN), glomerular (GN) and vascular.
First Move Is a Bladder Scan and an Ultrasound
Cheap, quick, and you will miss obstruction without it. Post-renal AKI reverses completely if it is relieved early and causes permanent damage if it is not, and a distended bladder in a confused elderly man is easy to overlook on examination.
Use FEUrea, Not FENa, in a Diuresed Patient
The classic FENa below 1% for pre-renal and above 2% for ATN is unreliable on diuretics, which raise FENa regardless of cause. FEUrea is not affected by diuretics: below 35% is pre-renal, above 50% is intrinsic. Always look at the sediment too: muddy brown casts for ATN, white cell casts and eosinophiluria for AIN, red cell casts for glomerulonephritis, bland for pre-renal.
Stop the Insults and Fix the Perfusion
Hold NSAIDs, aminoglycosides, contrast and other nephrotoxins, and renally dose everything else. ACE inhibitors and ARBs are held in the acute setting, though they are not the villain in a well-perfused patient. Give fluid for genuine hypovolemia and stop when the patient is euvolemic: fluid is a treatment for pre-renal AKI, not a treatment for oliguria, and volume overload in established ATN worsens outcomes.
Do Not Rush Dialysis
Early initiation does not improve mortality compared with a watchful strategy (AKIKI, STARRT-AKI), and a delayed strategy avoids dialysis altogether in roughly half of patients. Dialyze for an indication, not for a number.
AEIOU Is the Indication List
Acidosis refractory to medical therapy, Electrolytes (refractory hyperkalemia), Intoxications (methanol, ethylene glycol, lithium, salicylates), Overload refractory to diuretics, Uremia (pericarditis, encephalopathy, bleeding). Refractory is the operative word: each of these means dialysis only after medical management has failed.
Two Practice Changes Worth Knowing
Terlipressin is now first line for hepatorenal syndrome AKI in the US (FDA approved 2022), replacing midodrine plus octreotide where it is available. Contrast-associated AKI has been substantially overestimated, so an indicated scan should not be withheld. Diuretics do not treat AKI: they treat volume overload, and converting oliguric to non-oliguric AKI does not improve survival. Document and follow up, because AKI raises long-term CKD and cardiovascular risk even when the creatinine returns to baseline.
📄 One Pager
Text version
Nephrology · One Pager
Acute Kidney Injury
Pre-renal, intrinsic, or post-renal. Bladder scan + renal U/S first. FENa localizes the rest. Stop the nephrotoxins.
Pre-Renal (60–70%)
- FENa < 1% / BUN:Cr > 20
- Volume depletion, low CO
- NSAIDs, ACEi/ARB
- Rx: IV fluids, hold nephrotoxins
- Cr improves in 24–48h
Intrinsic (20–30%)
- FENa > 2% / muddy brown casts
- ATN: ischemia, contrast, aminoglycosides
- AIN: drugs (PPIs, NSAIDs, PCN)
- GN: RBC casts + proteinuria
- Rx: Supportive, avoid nephrotoxins
Post-Renal (5–10%)
- Hydronephrosis on U/S
- BPH, bladder outlet obstruction
- Ureteral obstruction
- Rx: Foley or urology consult
- Watch for post-obstructive diuresis
FENa Calculation
- (UNa × PCr) ÷ (PNa × UCr) × 100
- < 1% = Pre-renal
- > 2% = ATN (intrinsic)
- Use FEUrea if on diuretics (< 35% = pre-renal)
Dialysis Indications -AEIOU
- A -Acidosis (pH < 7.1)
- E -Electrolytes (refractory K⁺)
- I -Ingestion (toxic)
- O -Overload (refractory)
- U -Uremia (pericarditis, encephalopathy)
📋 On Rounds
Pimp Questions
What is the difference between FENa and FEUrea, and when do you use each?
FENa (fractional excretion of sodium) differentiates pre-renal (< 1%) from intrinsic (> 2%) AKI. However, FENa is unreliable if the patient is on diuretics -diuretics increase sodium excretion even in pre-renal states, giving a falsely elevated FENa. In this case, use FEUrea -urea reabsorption is not affected by diuretics. FEUrea < 35% = pre-renal, > 50% = intrinsic. Rule of thumb: use FENa if no diuretics, use FEUrea if on diuretics.
A patient's creatinine is rising but urine output is normal. Is this still AKI?
Yes -non-oliguric AKI is more common than oliguric AKI. Creatinine reflects GFR, not urine output. The kidneys can still produce urine (especially dilute urine) even when filtration is impaired. In fact, non-oliguric AKI generally has a better prognosis than oliguric AKI because it suggests less severe tubular damage. KDIGO stages AKI by Cr rise OR UOP decrease -you only need one criterion.
What are the indications for emergent dialysis in AKI? Use the mnemonic.
AEIOU: A cidosis (pH < 7.1, refractory to bicarb) · E lectrolytes (hyperkalemia > 6.5 refractory to medical management, or with ECG changes) · I ngestion (toxic alcohols: methanol, ethylene glycol -dialyzable; lithium, salicylate toxicity) · O verload (volume overload refractory to diuretics, especially with pulmonary edema) · U remia (uremic pericarditis, uremic encephalopathy, uremic bleeding). Key: these are indications for emergent dialysis.
How do you differentiate ATN from pre-renal AKI when the patient is on diuretics?
FENa is unreliable on diuretics (falsely elevated -diuretics increase sodium excretion). Use FEUrea instead -urea reabsorption is NOT affected by diuretics. FEUrea < 35% = pre-renal, > 50% = intrinsic (ATN). Other clues: Urine microscopy is the most underused tool -muddy brown granular casts = ATN (renal tubular cell debris). Pre-renal has bland sediment or hyaline casts.
Clinical Examples
📋 Case 1, Pre-renal AKI from Volume Depletion
Patient: 82 y/o F with HTN and DM2, admitted for gastroenteritis with 3 days of vomiting/diarrhea. Home meds: lisinopril, ibuprofen PRN.
Key findings: HR 104, BP 92/58, dry mucous membranes. Cr 3.1 (baseline 1.0), BUN/Cr 32, FENa 0.3%, urine osm 620, bland sediment.
Management:
- Hold nephrotoxins: stop lisinopril and ibuprofen (ACEi + NSAID + dehydration = classic triple hit)
- Volume resuscitation with LR, reassess Cr at 24-48h
- Monitor UOP ≥ 0.5 mL/kg/hr
- Cr improved 3.1 → 2.2 → 1.4 over 72h confirming pre-renal recovery
Teaching point: FENa < 1% with concentrated urine (osm > 500) confirms avid sodium retention. The ACEi + NSAID + dehydration combination is the most common iatrogenic cause of pre-renal AKI.
📋 Case 2, ATN with Muddy Brown Casts
Patient: 70 y/o M with CKD3 (baseline Cr 1.8) and DM2, Cr rises to 3.4 at 48h post-contrast CT. On furosemide chronically.
Key findings: UOP 25 mL/hr, FEUrea 58% (FENa unreliable on diuretics), urine microscopy: muddy brown granular casts. KDIGO stage 2.
Management:
- Supportive care, no specific treatment reverses established ATN
- Avoid further nephrotoxins, dose-adjust renally cleared medications
- Maintain euvolemia (ATN does not respond to volume loading)
- Monitor for dialysis indications (AEIOU mnemonic)
Teaching point: Use FEUrea when patients are on diuretics. Muddy brown granular casts are pathognomonic for ATN. NAC for contrast prophylaxis was debunked by PRESERVE, 2018.
📋 Case 3, Obstructive AKI Requiring Emergent Intervention
Patient: 65 y/o M with BPH and prostate cancer, presents with anuria x24h, nausea, and confusion. K⁺ 7.1 with peaked T waves.
Key findings: Cr 8.2 (baseline 1.1), pH 7.18, bicarb 12. Renal US: bilateral hydronephrosis. Bladder scan 1,200 mL.
Management:
- Calcium gluconate 1g IV stat for cardiac membrane stabilization
- Foley catheter, 1,400 mL immediate drainage; anticipate post-obstructive diuresis
- Insulin 10U + D50 + albuterol 10 mg neb for K⁺ shifting
- Urology for nephrostomy tubes if needed; dialysis if refractory hyperkalemia/acidosis
Teaching point: Always get renal ultrasound in AKI to rule out obstruction, the most readily treatable cause. Post-obstructive diuresis causes massive electrolyte losses; monitor BMP q6h and replace IVF at 50-75% of UOP.
📣 Sample Presentation
One-Liner
"Mrs. Adams is a 70-year-old with DM and HTN admitted for pneumonia, found to have Cr rise from baseline 1.0 to 2.8 (KDIGO stage 2). FENa 0.4%, bland urine sediment. Likely pre-renal from volume depletion."
Key Points to Cover on Rounds
Baseline Cr 1.0, now 2.8 (KDIGO stage 2). FENa 0.4% (pre-renal). UA: no casts, no protein. Renal US: no hydronephrosis. Nephrotoxins held: lisinopril, ibuprofen stopped on admission. Volume resuscitation with LR ongoing. UOP improving 20→55 mL/hr. Cr trending 2.8→2.4. Plan: continue fluids, recheck BMP PM, restart ACEi only after Cr returns to baseline.
AKI Monitoring Parameters
| Parameter | Frequency | Target / Action |
|---|---|---|
| Vitals | q4h floor, q1–2h ICU | HR, BP, RR, SpO₂, Temp -notify for significant deviations |
| Labs (BMP, CBC) | Daily AM or as indicated | Trend Cr, K⁺, WBC, Hgb -adjust treatment based on trajectory |
| Disease-specific markers | Per clinical context | See Overview and Management tabs for condition-specific targets |
| I&Os | Strict if volume-sensitive | UOP ≥ 0.5 mL/kg/hr. Net fluid balance guides diuresis or resuscitation. |
| Telemetry | Continuous if indicated | Arrhythmia detection. Discontinue when no longer indicated (reduces alarm fatigue). |
| Clinical response | Each assessment | Symptom improvement, functional status, appetite, mental status -the exam matters more than labs |
Don't just order labs -act on them. Every lab should have a clear clinical question. If you wouldn't change management based on the result, don't order it.
💊 Medications
AKI Medications, Frequency Ordered
Most AKI is managed by stopping nephrotoxins, restoring perfusion, and treating the underlying cause, not by adding drugs. The drugs below are for specific complications, not for "treating AKI" itself. Always renal-dose and review the med list daily.
Hyperkalemia Bundle (most common AKI emergency)
| Drug | Dose | Onset / Notes |
|---|---|---|
| Calcium gluconate 10% | 1–2 g IV over 2–5 min (or CaCl₂ via central line) | 1–3 min · membrane stabilization · K>6.5 or any ECG change |
| Insulin regular + D50 | 10 u IV + 25 g dextrose (check glc, recheck q1h ×4) | 15–30 min · drops K ~0.6–1.0 · hypoglycemia common, especially in AKI |
| Albuterol nebulizer | 10–20 mg neb (4–8× the asthma dose) | 15–30 min · drops K ~0.5–1.0 · additive to insulin |
| Sodium bicarbonate | 50–150 mEq IV (only if acidemic, pH <7.2) | Slow · best when AKI + metabolic acidosis · avoid in volume overload |
| Loop diuretic | Furosemide 40–80 mg IV (higher if known CKD) | Only if making urine · potassium-wasting |
| Patiromer / SZC | Patiromer 8.4 g PO daily · SZC 10 g PO TID ×48h then daily | Hours · for non-emergent K removal · bridge to definitive therapy |
| Hemodialysis | Emergent | Definitive · refractory hyperK, ESRD, or AEIOU criteria |
Avoid SPS (Kayexalate) in AKI, slow onset, intestinal necrosis risk, and patiromer/SZC are safer and faster.
Diuretics in AKI
| Drug | Dose | Use |
|---|---|---|
| Furosemide | 40–80 mg IV bolus, double q2h to max 200 mg; or drip 5–20 mg/h | Volume overload only · does NOT prevent or treat AKI itself KDIGO |
| Bumetanide | 1–2 mg IV (≈40 mg furosemide) | Alternative if furosemide allergy or poor response |
| Metolazone | 2.5–10 mg PO 30 min before loop | Diuretic resistance · sequential nephron blockade · monitor K, Mg |
"Furosemide stress test" (1–1.5 mg/kg IV): urine output <200 mL over 2 h predicts progression to stage 3 AKI / RRT need.
Hepatorenal Syndrome – AKI (HRS-AKI)
| Drug | Dose | Notes |
|---|---|---|
| Terlipressin CONFIRM, 2021 | 0.5–2 mg IV q4–6h (or continuous infusion) | First-line in US since FDA approval 2022. Hold for hypoxemia (SpO₂ <90%), black-box respiratory failure risk |
| Albumin 25% | 1 g/kg day 1 (max 100 g), then 20–40 g/day | Always paired with terlipressin / midodrine + octreotide |
| Midodrine + Octreotide | Mido 7.5–12.5 mg PO TID + Oct 100–200 mcg SC TID | Alternative if terlipressin unavailable / contraindicated |
| Norepinephrine | 0.5–3 mg/h IV | ICU alternative · titrate to MAP increase ≥10 mmHg |
Common Drugs to STOP or Renal-Dose
- Stop immediately: NSAIDs, ACEi/ARB (during active AKI), aminoglycosides, IV contrast (when avoidable), SGLT2i (hold during acute illness), metformin (lactic acidosis risk if eGFR <30)
- Dose-adjust: Vancomycin (trough or AUC-guided), pip-tazo (extended infusion), cefepime (neurotoxicity at high levels in AKI), LMWH (switch to UFH if CrCl <30), DOACs, gabapentin/pregabalin, opioids (avoid morphine, codeine)
- Hold and reassess: Diuretics if pre-renal · spironolactone/eplerenone (hyperkalemia) · trimethoprim, tacrolimus (creatinine bumps)
- Resume after recovery: ACEi/ARB and SGLT2i once Cr stable and patient euvolemic, both are renoprotective long-term
Contrast-Associated AKI Prophylaxis
2024 reframing: True contrast nephropathy is far rarer than once thought. AMACING 2017 / PRESERVE 2018 Don't withhold needed contrast for moderate CKD.
- Isotonic saline 1–1.5 mL/kg/h ×6–12h before and after, only for eGFR <30 or AKI
- N-acetylcysteine: NOT recommended (PRESERVE), abandon this reflex order
- Bicarbonate infusion: NOT recommended over saline
- SGLT2i / metformin: Hold the day of contrast, resume 48 h later if Cr stable
Adjuncts & Specific Scenarios
- Sodium bicarbonate for severe metabolic acidosis (pH <7.2), BICAR-ICU, 2018
- Rasburicase 0.2 mg/kg IV ×1 for tumor lysis syndrome with uric acid >8 (screen for G6PD)
- Plasma exchange for TTP, anti-GBM, ANCA vasculitis with rapidly progressive GN
- High-dose steroids for biopsy-proven AIN (after stopping the offending drug), prednisone 1 mg/kg taper
- Calcitriol / phosphate binders: Reserve for prolonged AKI with CKD-MBD features, not routine
Renal Dosing Quick Reference
For specific CrCl-based dosing of antibiotics, anticoagulants, and analgesics, see Antibiotic Guide · Drug Interactions · Calculators (CrCl).