When to intubate in GCS?

GCS ≤ 8 requires intubation for airway protection. The patient cannot protect their own airway at this level of consciousness. Motor score is the most prognostically important component.

What is the best initial fluid for sepsis resuscitation?

Lactated Ringer's (LR) is the preferred resuscitation fluid. The SMART trial (2018) showed balanced crystalloids reduced death, new renal failure, and persistent renal dysfunction compared to normal saline.

When to start vasopressors in septic shock?

Start norepinephrine (first-line vasopressor) if MAP remains < 65 mmHg after initial 30 mL/kg crystalloid resuscitation, or earlier if patient is profoundly hypotensive. Do not delay pressors to complete full fluid resuscitation.

Why can serum uric acid be normal during acute gout?

During acute inflammation, IL-6 increases renal urate excretion and redistributes urate from plasma to tissues. Up to 40% of acute gout flares have normal serum uric acid. Joint aspiration with polarized microscopy is needed for definitive diagnosis.

How do you distinguish lupus flare from infection in SLE?

Key clues: CRP is low/normal in flare but elevated in infection. Complement (C3/C4) drops in flare but is normal/elevated in infection. Procalcitonin is elevated in bacterial infection but normal in flare. Anti-dsDNA rises in flare, stable in infection.

What is the difference between DKA and HHS?

DKA features acidosis (pH 600), hyperosmolality (> 320), and minimal ketosis -typically in Type 2 DM. DKA requires insulin drip; HHS requires aggressive fluid resuscitation first.

When to give tPA in acute ischemic stroke?

IV alteplase (tPA) can be given within 4.5 hours of last known well time in eligible patients. CT head must rule out hemorrhage first. For large vessel occlusion, mechanical thrombectomy can be performed up to 24 hours with favorable imaging.

What antibiotics for community-acquired pneumonia?

Inpatient non-ICU: ceftriaxone + azithromycin. ICU: ceftriaxone + azithromycin (add vancomycin if MRSA risk). Outpatient healthy: amoxicillin. Outpatient with comorbidities: augmentin + azithromycin or respiratory fluoroquinolone. Duration: 5 days if clinically stable for 48 hours.

How to interpret iron studies?

Iron deficiency: low ferritin (< 30), high TIBC, low iron, low transferrin saturation (< 20%). Anemia of chronic disease: normal/high ferritin (acute phase reactant), low TIBC, low iron. A ferritin of 50-100 in an inflamed patient may still represent iron deficiency.

What is the correction rate for hyponatremia?

Correct sodium no more than 8 mEq/L in 24 hours to avoid osmotic demyelination syndrome (ODS). For symptomatic severe hyponatremia with seizures, give 3% hypertonic saline 100-150 mL bolus over 10-20 minutes. If overcorrected, use D5W + DDAVP rescue protocol.

When to start antibiotics in meningitis?

Within 30-60 minutes. Do NOT delay antibiotics for LP or CT. Draw blood cultures, start empiric antibiotics (vancomycin + ceftriaxone ± ampicillin if > 50 or immunocompromised), then perform LP when possible. Dexamethasone should be given before or with the first antibiotic dose.

DOACs vs warfarin in antiphospholipid syndrome?

DOACs are contraindicated in APS. The TRAPS trial (2018) showed rivaroxaban was inferior to warfarin with more thrombotic events in triple-positive APS patients. Warfarin with INR target 2-3 is the standard for APS, indefinitely.

How to manage scleroderma renal crisis?

ACE inhibitors (captopril) are life-saving -start immediately and titrate aggressively. Do NOT hold for rising creatinine. Steroids > 15 mg prednisone per day precipitate scleroderma renal crisis. ARBs are NOT a substitute -evidence is only for ACEi.

What are the 4 pillars of heart failure treatment?

Guideline-directed medical therapy (GDMT) for HFrEF: (1) ARNI or ACEi/ARB, (2) beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) MRA (spironolactone or eplerenone), (4) SGLT2 inhibitor (dapagliflozin or empagliflozin). All four should be initiated and titrated to target doses.

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NephrologyCommon

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

🚨 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

First Move

Bladder scan + renal U/S to rule out obstruction. Then UA with micro + FENa to localize.

Pre-Renal

FENa < 1%, BUN:Cr > 20. Treat with fluids, hold nephrotoxins. Creatinine improves in 24–48h.

ATN

FENa > 2%, muddy brown casts. Supportive care. No diuretics force recovery. Avoid all nephrotoxins.

Post-Renal

Hydronephrosis on U/S. Foley or urology consult. Watch for post-obstructive diuresis.

Dialysis Triggers

AEIOU: Acidosis, Electrolytes, Ingestion, Overload, Uremia

Biggest Pitfall

Missing contrast nephropathy, or giving fluids to an ATN patient expecting pre-renal response -causes volume overload.

📄 One Pager

Nephrology · One Pager

Acute Kidney Injury

Pre-renal, intrinsic, or post-renal. Bladder scan + renal U/S first. FENa localises 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).

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