Renal & Urinary

Prerenal AKI: volume status assessment and management

Clinical Overview and When to Suspect Prerenal AKI

— Volume loss: vomiting, diarrhea, GI bleed, burns, diuretic overuse, third-spacing (pancreatitis, sepsis, post-op)

— Decreased effective circulating volume: HF (cardiorenal), cirrhosis (hepatorenal physiology), nephrotic syndrome

— Hemodynamic medications: NSAIDs (afferent constriction), ACEi/ARB (efferent dilation), contrast, calcineurin inhibitors, SGLT2 in volume depletion

— Renal artery stenosis with ACEi exposure

— Sepsis (early, before ATN supervenes)

— BUN:Cr >20:1

— FENa <1% (FEUrea <35% if on diuretics)

— Bland urine sediment, hyaline casts

— Rapid improvement (<24–72 h) with volume or hemodynamic correction

Definition: Prerenal AKI is a functional decline in GFR from reduced effective renal perfusion, with intact tubular function and rapid reversibility upon restoration of perfusion. By KDIGO, AKI = ↑Cr ≥0.3 mg/dL in 48 h, ≥1.5× baseline within 7 days, or UOP <0.5 mL/kg/h for ≥6 h.

Pathophysiology: Reduced renal blood flow → afferent arteriolar vasodilation and efferent constriction (angiotensin II) maintain GFR until autoregulation fails (MAP <65–70 or renal perfusion pressure drop >~20%). Tubules avidly reabsorb Na⁺ and water → concentrated, Na-poor urine.

Most common cause of AKI in both inpatient (~40–55%) and outpatient settings.

When to suspect:

Clues that point prerenal:

Step 3 management: When you see an elderly patient on lisinopril + HCTZ + ibuprofen presenting with gastroenteritis and ↑Cr, the diagnosis is almost always prerenal AKI — hold offending meds, give isotonic fluids, recheck Cr in 24 h before ordering an extensive workup.

Board pearl: Prerenal AKI that is not promptly corrected progresses to ischemic ATN; the same patient, same labs, but with muddy brown casts and FENa >2% marks the transition.

Presentation Patterns and Key History

— Hypovolemic elder: 80-year-old with 3 days of vomiting/diarrhea, decreased PO intake, dark concentrated urine, dizziness on standing. On lisinopril, HCTZ, and meloxicam. Cr 2.1 (baseline 0.9).

— Cardiorenal: Decompensated HFrEF, EF 20%, with rising Cr despite ongoing diuresis — low forward flow, not over-diuresis (check JVP).

— Hepatorenal physiology: Cirrhotic with ascites and SBP, Cr rising despite albumin; splanchnic vasodilation → low effective volume.

— Postoperative: Bowel resection patient with third-spacing, NPO, epidural-related hypotension, oliguria on POD#1.

— Sepsis: Hypotensive pneumonia patient with lactate 4, oliguric; prerenal early, ATN if perfusion not restored.

— Fluid losses: vomiting/diarrhea episodes, stoma output, GI bleed (melena, hematemesis), polyuria (DKA, hyperglycemia)

— Intake: PO tolerance, thirst, access to water (nursing home, dementia)

— Weight change (acute drop >2 kg suggests volume loss)

— Orthostatic symptoms, syncope

— Medication reconciliation is the single highest-yield step: NSAIDs (OTC ibuprofen, naproxen), ACEi/ARB, diuretics, SGLT2, contrast within 72 h, tacrolimus/cyclosporine, ARNI

— Cardiac history: orthopnea, PND, edema, recent diuretic up-titration

— Hepatic history: ascites taps, lactulose, recent LVP without albumin

Classic clinical narratives — recognize the archetypes:

Targeted history questions:

Key distinction: Hypovolemia (true low total body water) vs. decreased effective arterial blood volume (HF, cirrhosis, sepsis, nephrosis) — both produce identical urinary indices, but management diverges sharply: fluids help the first, harm the second.

CCS pearl: Always order "medication reconciliation" and review the home med list as one of your first actions in a CCS AKI case — discontinuing the offending NSAID or ACEi often resolves the case before any IV fluid is hung.

Document baseline creatinine from prior records; without a baseline you cannot stage AKI or interpret recovery.

Physical Exam Findings and Hemodynamic Assessment

— Tachycardia, orthostatic hypotension (>20 mmHg SBP drop or >10 DBP drop, or HR rise >30 within 3 min of standing)

— Dry mucous membranes, decreased skin turgor (less reliable in elderly), absent axillary sweat

— Flat JVP (<5 cm H₂O), collapsed IVC on POCUS (<1.5 cm, >50% respiratory variation)

— Cool extremities with delayed capillary refill in late/shock states

— Oliguria (<400 mL/day) or anuria

— Weight loss from documented baseline

— HF: elevated JVP, S3 gallop, bibasilar rales, peripheral edema, hepatojugular reflux, cool extremities (low CO)

— Cirrhosis: ascites, spider angiomata, palmar erythema, caput medusae, asterixis; warm peripheries from splanchnic vasodilation

— Sepsis: fever, warm flushed skin early; mottled cool skin late; bounding pulses initially

— IVC diameter and collapsibility

— Lung B-lines (pulmonary edema → don't bolus)

— Cardiac function (LV/RV size, gross EF)

— Passive leg raise with stroke volume response predicts fluid responsiveness better than CVP

— Pulse pressure variation in mechanically ventilated patients (>13% suggests responsiveness)

Hypovolemic prerenal AKI signs:

Decreased effective volume (euvolemic or hypervolemic prerenal):

POCUS in volume assessment (high Step 3 yield):

Dynamic measures > static measures:

Step 3 management: Before reflexively giving a 30 mL/kg bolus, categorize the patient: hypovolemic → fluids; cardiorenal with congestion → diuresis (yes, even with rising Cr); hepatorenal → albumin + vasoconstrictor, not crystalloid alone.

Board pearl: A cirrhotic patient with ascites and AKI looks volume-overloaded but has low effective arterial volume — give 25% albumin 1 g/kg/day as the diagnostic-therapeutic challenge for hepatorenal syndrome.

Document vitals trends (not just one set), urine output hourly when oliguric, and daily weights — these drive your CCS clock advances.

Diagnostic Workup — Initial Labs and Urine Studies

— Cr trend with prior baseline (essential — order old records)

— BUN:Cr ratio >20:1 suggests prerenal (urea reabsorbed with Na in low-flow states); also elevated by GI bleed, steroids, high-protein intake, catabolism

— Bicarbonate (metabolic acidosis if severe), K⁺ (often elevated with ACEi/ARB), Na⁺ (hypo- or hypernatremia clues hydration)

— Glucose (osmotic diuresis), Ca/Mg/Phos

— Specific gravity >1.020, urine osm >500 mOsm/kg (concentrated)

— Bland sediment, occasional hyaline casts

— No proteinuria, no hematuria, no WBC, no cellular casts

— Granular/muddy brown casts → ATN (perfusion failure has progressed)

— RBC casts → glomerulonephritis; WBC casts → AIN/pyelonephritis; eosinophils → AIN

— Urine Na <20 mEq/L, FENa <1% = prerenal

— FENa = (UNa × PCr)/(PNa × UCr) × 100

— FEUrea <35% preferred if patient is on diuretics (which falsely raise FENa)

— Exceptions where prerenal physiology gives FENa >1%: diuretics, CKD baseline, glucosuria, bicarbonaturia

— Exceptions where FENa <1% despite intrinsic disease: contrast nephropathy, pigment nephropathy (rhabdo, hemolysis), early GN, hepatorenal

Basic chemistry panel:

Urinalysis — the single most cost-effective test:

Urine electrolytes:

CBC: hemoconcentration (↑Hct/Hb) in dehydration; anemia in GI bleed or CKD

Lactate, VBG: sepsis/shock screen

Pregnancy test in reproductive-age women before imaging/meds

Key distinction: FENa <1% + bland urine + BUN:Cr >20 + responds to fluids = prerenal. FENa >2% + muddy brown casts + no response to fluids = ATN. The clinical course over 24–48 h often makes the call.

Board pearl: Contrast nephropathy and hepatorenal syndrome both have FENa <1% despite being intrinsic/structural — don't be fooled by the urinary indices alone; context matters.

Diagnostic Workup — Advanced and Confirmatory Studies

— Indicated when obstruction is plausible (older male with BPH, anuria, single kidney, pelvic malignancy, retroperitoneal process, anticoagulation with possible retroperitoneal bleed)

— Findings supporting prerenal: normal-sized kidneys, no hydronephrosis, no stones

— Small echogenic kidneys → underlying CKD (and worse prognosis)

— Asymmetric kidney sizes (>1.5 cm difference) → renal artery stenosis

— NGAL, KIM-1, [TIMP-2]×[IGFBP7] elevate in tubular injury (ATN), help distinguish from sustained prerenal

— Not yet standard of care for routine use

— 500 mL–1 L isotonic crystalloid bolus (if not contraindicated) and reassess Cr/UOP in 6–24 h

— Improvement within 24–72 h supports prerenal physiology

— Persistent AKI after adequate resuscitation → suspect ATN or another intrinsic process

Renal ultrasound — when and why:

Bladder scan / post-void residual: quick bedside test to exclude obstruction; PVR >150–200 mL warrants catheter placement

Renal artery imaging: Duplex ultrasound, CTA, or MRA when bilateral RAS suspected (flash pulmonary edema, Cr ↑↑ after ACEi, refractory HTN, abdominal bruit)

Echocardiogram: when cardiorenal physiology suspected — quantify EF, RV function, valvular disease, pericardial effusion/tamponade, IVC

Biomarkers (emerging, low yield on Step 3 but appearing):

Fluid challenge as diagnostic test:

Invasive hemodynamic monitoring: Rarely needed; PA catheter reserved for mixed/uncertain cardiorenal cases in ICU

Step 3 management: In an oliguric patient with unclear etiology, the appropriate sequence is (1) bladder scan/Foley, (2) urinalysis + FENa, (3) renal US if obstruction possible, (4) fluid challenge if no congestion — not a CT or biopsy first.

CCS pearl: Renal biopsy is not indicated for suspected prerenal AKI; reserve for unexplained intrinsic AKI, suspected GN/vasculitis, or AKI lasting >2–3 weeks without explanation. Ordering one early on a CCS case loses points.

Risk Stratification and First-Line Management Logic

— Stage 1: Cr 1.5–1.9× baseline OR ↑≥0.3 mg/dL; UOP <0.5 mL/kg/h × 6–12 h

— Stage 2: Cr 2.0–2.9× baseline; UOP <0.5 × ≥12 h

— Stage 3: Cr ≥3.0× baseline OR Cr ≥4.0 OR RRT initiated OR UOP <0.3 × ≥24 h OR anuria ≥12 h

— Hold nephrotoxins: NSAIDs, ACEi/ARB, ARNI, SGLT2i, diuretics (if hypovolemic), aminoglycosides, vancomycin (consider), contrast

— Dose-adjust renally cleared drugs (gabapentin, LMWH, DOACs, metformin)

— Treat reversible causes: restore perfusion, relieve obstruction, treat sepsis source

— Avoid further insults: no contrast, no NSAIDs, cautious with ACEi reintroduction

— Hypovolemic → isotonic crystalloid (LR or NS); 500 mL–1 L bolus, reassess; avoid chloride-rich NS in large volumes (hyperchloremic acidosis)

— Cardiorenal congested → IV loop diuretic (furosemide 1–2.5× home dose IV), consider inotropes if low CO; diuresis often improves Cr in true cardiorenal

— Hepatorenal → albumin 1 g/kg day 1 (max 100 g), then 20–40 g/day + terlipressin (preferred, FDA-approved 2022) or midodrine + octreotide + albumin if terlipressin unavailable

— Septic → early antibiotics + balanced crystalloid 30 mL/kg, add norepinephrine if MAP <65 after initial resuscitation

KDIGO AKI staging (drives disposition):

Universal first steps (the "AKI bundle"):

Volume management decision tree:

Fluid choice: Balanced crystalloids (LR, Plasmalyte) preferred over NS in most AKI (SMART, BaSICS trials suggest modest benefit, especially in sepsis). Avoid hydroxyethyl starches.

Board pearl: In HFrEF with rising Cr during diuresis, do not stop the diuretic if the patient remains congested — "permissive" Cr rise up to ~30% is acceptable; decongestion improves long-term renal outcomes (CARRESS-HF, DOSE).

Step 3 management: Reassess volume status and Cr every 6–12 h after intervention; titrate, don't set-and-forget.

Pharmacotherapy and Specific Drug Management

— NSAIDs (all, including COX-2, ketorolac, OTC ibuprofen/naproxen) — afferent vasoconstriction

— ACEi/ARB/ARNI — efferent vasodilation removes GFR-preserving constriction in low-flow states

— SGLT2 inhibitors — hold during acute illness/volume depletion ("sick day rules")

— Diuretics — if hypovolemic; continue if congested cardiorenal

— Aminoglycosides, IV contrast, amphotericin B, calcineurin inhibitors — additive toxicity

— Metformin — hold when eGFR <30 or during acute illness (lactic acidosis risk)

— LMWH → unfractionated heparin if CrCl <30

— DOACs: apixaban dose-adjust; dabigatran avoid in severe AKI

— Gabapentin, pregabalin, baclofen — reduce dose to avoid CNS toxicity

— Antibiotics: vancomycin (trough/AUC monitoring), piperacillin-tazobactam (controversial nephrotoxicity, especially with vanc)

— Norepinephrine = first-line vasopressor in septic shock; restores renal perfusion pressure

— Vasopressin as second agent, especially with norepinephrine-sparing intent

— Terlipressin for HRS-AKI: 1 mg IV q6h, titrate to 2 mg q6h; monitor for ischemic and respiratory complications

— Midodrine 7.5–12.5 mg TID + octreotide 100–200 mcg SC TID + albumin as outpatient/alternative HRS regimen

— Antiemetics (ondansetron — watch QT), antidiarrheals (loperamide only if no infectious cause)

— PPI/octreotide + endoscopy for GI bleed; transfuse if Hgb <7 (or <8 with cardiac disease)

— Antibiotics for sepsis within 1 hour of recognition

— Restart ACEi/ARB once Cr stable and back toward baseline, usually within days–weeks; important for long-term CV/renal protection in HF, DM, proteinuric CKD

— SGLT2i restart once volume status normalized

Drugs to STOP immediately in prerenal AKI:

Drugs to ADJUST (renal dosing):

Vasoactive agents (when fluids insufficient):

Treat underlying drivers:

When to RESUME held meds:

Board pearl: Holding an ACEi during AKI is not the same as discontinuing it forever — failure to restart in HFrEF/proteinuric CKD post-discharge is a quality gap and a common Step 3 follow-up question.

Advanced Management and Renal Replacement Therapy

— Reassess: is this still prerenal, or has ATN supervened? Recheck UA for muddy brown casts, recheck FENa

— Consider hemodynamic monitoring (POCUS, arterial line, occasionally PA catheter in mixed shock)

— Add vasopressors to maintain MAP ≥65 mmHg (higher target ~80–85 may benefit chronic HTN patients — SEPSISPAM)

— Acidosis — refractory metabolic, pH <7.1

— Electrolytes — refractory hyperkalemia (K >6.5 with ECG changes despite medical therapy)

— Ingestions — dialyzable toxins (methanol, ethylene glycol, salicylates, lithium, metformin-associated lactic acidosis)

— Overload — diuretic-refractory volume overload with pulmonary edema

— Uremia — pericarditis, encephalopathy, bleeding from platelet dysfunction

— AKIKI, IDEAL-ICU, STARRT-AKI: no benefit to early "preemptive" RRT over standard indication-based initiation

— Initiate when clinical indication present, not based on Cr threshold alone

— Intermittent HD for hemodynamically stable patients

— CRRT (CVVHDF) for hemodynamically unstable ICU patients — gentler fluid removal

— SLED as a hybrid option

— Peritoneal dialysis rare in acute adult AKI

— HRS-AKI awaiting transplant: RRT as bridge; medical therapy first

— Cardiorenal refractory to diuresis: ultrafiltration is an option but CARRESS-HF showed no benefit over stepped diuretic therapy and more adverse events

When fluid responsiveness fails — escalation pathway:

Indications for renal replacement therapy (AEIOU):

Timing controversy:

Modality:

Specific scenarios:

Vascular access: Temporary non-tunneled IJ catheter; avoid subclavian (stenosis risk for future fistula); femoral acceptable short-term

CCS pearl: On a CCS case with K 7.2 and peaked T waves, your immediate orders are: IV calcium gluconate (stabilize membrane) → insulin + D50 → albuterol → loop diuretic or kayexalate/patiromer → then consult nephrology for emergent HD if refractory or anuric.

Step 3 management: Document a clear goal MAP, UOP target (0.5 mL/kg/h), and reassessment interval — vague "supportive care" orders lose points.

Special Populations — Elderly and Renal/Hepatic Impairment

— Baseline eGFR is lower even with "normal" Cr because of reduced muscle mass — a Cr of 1.2 in an 85-year-old woman may represent eGFR ~40

— Use CKD-EPI 2021 (race-free) eGFR; cystatin C–based estimate more accurate when sarcopenic

— Blunted thirst response → silent dehydration in nursing home residents

— Polypharmacy: ACEi + diuretic + NSAID = "triple whammy" — single biggest preventable cause of community-acquired AKI

— Orthostatic hypotension may be from autonomic dysfunction, antihypertensives, or volume depletion — sort it out

— Lower fluid resuscitation thresholds: 250–500 mL boluses with reassessment to avoid pulmonary edema

— "Acute-on-chronic" — Cr trajectory matters more than absolute value

— Higher risk of progression to ESRD with each AKI episode

— Reintroduce ACEi/ARB carefully; tolerate Cr rise up to ~30% if K manageable

— Avoid contrast when possible; if essential, use minimum volume iso-osmolar agent with IV isotonic hydration; N-acetylcysteine and bicarbonate not recommended (PRESERVE trial)

— Cr underestimates renal dysfunction due to low muscle mass and impaired hepatic creatine synthesis

— HRS-AKI criteria: cirrhosis + ascites, ↑Cr per AKI definition, no improvement after 2 days of diuretic withdrawal + albumin challenge, no shock, no nephrotoxins, no structural kidney disease

— Treat with albumin + terlipressin (CONFIRM trial); definitive therapy is liver transplant

— Avoid NSAIDs absolutely; avoid aminoglycosides; cautious with diuretics (large-volume paracentesis without albumin precipitates HRS)

— Tolerate Cr rise during decongestion; do not abandon GDMT prematurely

— Restart ACEi/ARNI, β-blocker, MRA, SGLT2i once euvolemic — these are mortality-reducing and Step 3 expects you to know not to drop them long-term

Elderly patients (the prototypical Step 3 AKI patient):

Underlying CKD:

Cirrhosis (hepatorenal physiology):

Heart failure:

Board pearl: The "triple whammy" (ACEi/ARB + diuretic + NSAID) in an elderly patient with an intercurrent illness is the single most testable prerenal AKI scenario on Step 3.

Special Populations — Pregnancy, Pediatrics, and Other Subgroups

— Hyperemesis gravidarum (first trimester) → classic volume-depletion prerenal AKI; treat with IV fluids, antiemetics (pyridoxine + doxylamine first-line, then ondansetron, metoclopramide)

— Preeclampsia/HELLP → AKI from renal vasoconstriction, endothelial injury; deliver baby as definitive

— Postpartum hemorrhage → hypovolemic shock → prerenal then ATN if not corrected

— Avoid ACEi/ARB in pregnancy (teratogenic); use labetalol, nifedipine, methyldopa for HTN

— Normal pregnancy lowers Cr (hyperfiltration) — a Cr of 1.0 in pregnancy is abnormal

— Gastroenteritis with dehydration is the dominant cause

— Use Holliday-Segar maintenance + bolus 20 mL/kg isotonic for resuscitation, reassess

— Watch for hemolytic uremic syndrome (Shiga toxin E. coli O157:H7) → intrinsic not prerenal; bloody diarrhea + thrombocytopenia + MAHA

— Pediatric AKI staging by pRIFLE/KDIGO pediatric criteria

— Third-spacing, blood loss, epidural-induced hypotension, prolonged NPO

— Watch for abdominal compartment syndrome (bladder pressure >20 mmHg with new organ dysfunction) — looks prerenal but is obstructive/venous congestion physiology; treated with decompression

— Tumor lysis syndrome (intrinsic, but volume depletion contributes)

— Hypercalcemia of malignancy → nephrogenic DI → volume depletion → prerenal

— Immune checkpoint inhibitors → AIN (intrinsic, watch out for misdiagnosis)

— Calcineurin inhibitors (tacrolimus, cyclosporine) cause afferent vasoconstriction — prerenal physiology; check trough levels

Pregnancy-associated prerenal AKI:

Pediatrics:

Post-surgical patients:

Oncology patients:

Transplant recipients:

Burn patients: massive insensible losses; use Parkland formula (4 mL × kg × %TBSA, half in first 8 h) but titrate to UOP 0.5 mL/kg/h

Key distinction: In pregnancy, don't reflexively give ACEi-equivalent renoprotection — choose pregnancy-safe agents. In post-paracentesis cirrhosis, always give albumin (6–8 g per liter removed) if >5 L drained to prevent post-paracentesis circulatory dysfunction and HRS.

Complications and Adverse Outcomes

— Watch for muddy brown casts, rising FENa, failure to respond to volume

— Common, especially with ACEi/ARB/MRA/K-sparing diuretics, β-blockers, trimethoprim, heparin

— ECG changes: peaked T waves → PR prolongation → wide QRS → sine wave → asystole

— Emergent treatment sequence: calcium gluconate (membrane stabilization) → insulin + dextrose → albuterol → loop diuretic if making urine → kayexalate/patiromer/zirconium for total body removal → HD if refractory

— Anion gap if uremic/lactic; non-gap with bicarb wasting

— Bicarbonate replacement if pH <7.1 or HCO₃ <12

— Pulmonary edema, hypoxemia, prolonged ventilation, ICU stay

— Positive fluid balance is independently associated with mortality in AKI

— Deresuscitate (diuresis) once perfusion restored

— Pericarditis, encephalopathy, platelet dysfunction with bleeding, anorexia, nausea

— Digoxin toxicity, lithium toxicity, gabapentin sedation, LMWH bleeding, metformin-associated lactic acidosis

— AKI is not "fully reversible" — each episode increases CKD risk by ~2–3×

— Increased risk of future AKI, cardiovascular events, mortality

— Post-AKI care bundle (KDIGO): nephrology follow-up within 3 months if stage 2–3, BP control, ACEi/ARB reinstitution when appropriate, avoid future nephrotoxins

Progression to ATN: Sustained prerenal physiology causes ischemic tubular injury — the patient now has intrinsic AKI requiring weeks for recovery rather than days

Hyperkalemia:

Metabolic acidosis:

Volume overload from overzealous resuscitation:

Uremic complications (less common in pure prerenal, more if progresses):

Drug toxicity from failure to dose-adjust:

Long-term sequelae (often underappreciated):

Mortality: In-hospital AKI mortality 20–25%; ICU AKI requiring RRT mortality 40–60%

Board pearl: AKI patients who "recover" their Cr to baseline are still at elevated CKD risk — Step 3 expects you to schedule nephrology follow-up and BP/Cr monitoring at 3 months, not declare them cured at discharge.

CCS pearl: Daily weights, strict I/O, and serial BMP are the bread-and-butter monitoring orders that score points.

When to Escalate Care — ICU, Consult, Inpatient Triage

— Stage 1 AKI, mild, reversible cause identified (e.g., NSAID + dehydration)

— Patient hemodynamically stable, tolerating PO, no electrolyte emergencies

— Reliable follow-up within 48–72 h with repeat BMP

— Hold offending meds, encourage oral hydration, close-interval recheck

— Stage 2 AKI, or stage 1 with poor PO tolerance, unclear etiology

— Electrolyte derangements requiring IV correction

— Comorbid HF, cirrhosis, or CKD with cardiorenal/hepatorenal physiology

— Need for IV fluids with monitoring or IV diuretics for cardiorenal

— Hemodynamic instability requiring vasopressors

— Stage 3 AKI with anuria or rapidly rising Cr

— Severe hyperkalemia (>6.5 with ECG changes) refractory to medical therapy

— Severe metabolic acidosis (pH <7.2)

— Need for emergent RRT

— Pulmonary edema requiring ventilatory support

— Multi-organ failure (sepsis, HRS with hepatic encephalopathy)

— Stage 2–3 AKI of unclear etiology

— Suspected intrinsic renal disease (cellular casts, proteinuria, hematuria)

— Need for or anticipation of RRT

— HRS, cardiorenal type 1, contrast nephropathy that is not improving

— Post-AKI follow-up: KDIGO recommends nephrology referral within 3 months for stage 2–3

— Cardiology for cardiorenal syndrome with refractory congestion

— Hepatology for HRS-AKI

— Urology for obstructive uropathy

— Surgery for abdominal compartment syndrome or retroperitoneal bleed

— Need for RRT not available locally

— Liver transplant evaluation for HRS-AKI

— Higher level of cardiac care for advanced HF/MCS evaluation

Outpatient management appropriate:

Inpatient general medicine admission:

ICU admission criteria:

Nephrology consultation:

Other consults:

Transfer indications:

Step 3 management: Document a clear disposition decision with explicit criteria for escalation — "ICU transfer if SBP <90 despite 2 L crystalloid, K >6.0, or pH <7.2." Vague plans cost points and patients.

Key distinction: Consult nephrology early for stage 2–3 AKI; delayed consultation is associated with worse outcomes and is a Step 3 quality marker.

Key Differentials — Within AKI Categories

— True hypovolemia: documented losses, dry exam, responds to crystalloid

— Cardiorenal syndrome (Type 1): acute HF → low CO + venous congestion → AKI; congested exam, elevated JVP, BNP elevated; treat with diuresis, not fluids

— Hepatorenal syndrome (HRS-AKI): cirrhosis with portal HTN; splanchnic vasodilation; treat with albumin + terlipressin

— Abdominal compartment syndrome: post-op, massive ascites, or trauma; bladder pressure >20 mmHg; treat with decompression

— Renal artery stenosis with ACEi: bilateral RAS or unilateral in solitary kidney; ACEi removes efferent constriction, GFR collapses; reverses with ACEi withdrawal

— Hypercalcemia: nephrogenic DI + vasoconstriction; treat with fluids + bisphosphonate

— ATN follows unresolved prerenal insult, sepsis, or direct toxin (contrast, aminoglycosides, myoglobin, hemoglobin)

— Muddy brown granular casts, FENa >2%, urine osm <350, urine Na >40

— Three phases: initiation → maintenance (1–3 weeks oliguria) → recovery (polyuric phase, watch for hypoK, hypoMg)

— Does not respond to fluid challenge

— AIN: drug-induced (PPIs, NSAIDs, β-lactams, sulfa, allopurinol, checkpoint inhibitors); fever, rash, eosinophilia, WBC casts, eosinophiluria; treat with drug withdrawal ± steroids

— GN: RBC casts, dysmorphic RBCs, proteinuria; rapidly progressive GN needs urgent workup (ANCA, anti-GBM, complement, biopsy)

— Vascular: atheroembolic disease (post-cath, livedo, eosinophilia, low complement), TTP/HUS (MAHA, thrombocytopenia)

— BPH, malignancy, retroperitoneal fibrosis, bilateral stones, neurogenic bladder

— Confirm with bladder scan, US, CT; relieve with catheter or ureteral stent/nephrostomy

Prerenal AKI mimics — other prerenal subtypes to distinguish:

Differentiating from intrinsic AKI (ATN — the close cousin):

Other intrinsic AKI to consider:

Postrenal/obstructive:

Key distinction: Prerenal + cardiorenal + hepatorenal all share FENa <1% — distinguish by volume status exam, not labs. Fluids for the first, diuresis for the second, albumin+vasoconstrictor for the third.

Board pearl: A patient post-cath with livedo reticularis, eosinophilia, and AKI 1–4 weeks later has atheroembolic disease, not contrast nephropathy (which peaks at 48–72 h and resolves by 7 days).

Key Differentials — Other Categories and Mimics

— Trimethoprim, cimetidine, cobicistat, dolutegravir — inhibit tubular Cr secretion; Cr rises 0.1–0.4 mg/dL without ↓GFR; cystatin C is normal

— Fenofibrate — increases Cr production; reversible

— Increased dietary creatine/cooked meat acutely raises Cr

— Rhabdomyolysis releases creatine → ↑Cr (but rhabdo also causes true AKI from myoglobin)

— Physiologic post-op oliguria from ADH surge — UOP <0.5 mL/kg/h for hours is normal in healthy post-op patient with stable Cr

— Heat-related insensible losses

— GI bleed → ↑BUN from protein absorption + prerenal; BUN:Cr often >30:1

— Steroid use, high-protein nutrition → isolated BUN elevation

— Catabolic states (fever, sepsis, burns) → ↑BUN

— Bodybuilders, high muscle mass — high baseline Cr

— CKD with stable Cr — not AKI unless trajectory changes

— Volume depletion from DKA (osmotic diuresis) — prerenal but the headline is the DKA

— SIADH causes hyponatremia and oliguria but normal Cr

— Diabetes insipidus causes polyuria not oliguria but can cause prerenal AKI with restricted water access

— Lab error / specimen contamination (rare)

— Wrong patient / wrong baseline assumption

— Look at prior values, kidney size on US, presence of CKD markers (anemia, hyperphosphatemia, secondary hyperPTH, renal osteodystrophy)

— Small echogenic kidneys + chronic labs = CKD, not AKI

— "Acute-on-chronic" common — treat the acute insult, recognize chronic baseline

Pseudo-AKI (Cr rises without true GFR change):

Conditions presenting with oliguria but not AKI:

Conditions presenting with AKI-like labs:

Conditions with elevated Cr at baseline:

Important non-renal causes of symptoms mimicking AKI:

Other things on the differential of "high Cr in the ED":

Important: distinguish AKI from CKD:

Board pearl: Bactrim raises Cr by ~0.4 without harming GFR — don't stop a needed antibiotic reflexively; check cystatin C or eGFR trend in context.

Step 3 management: Always confirm a baseline Cr from prior records before staging AKI — a "Cr of 2.0" in a known CKD3 patient may not be AKI at all.

Secondary Prevention, Discharge Plan, and Long-Term Care

— Resume ACEi/ARB in HFrEF, proteinuric CKD, post-MI, diabetic kidney disease once Cr stable and K manageable (usually within days–weeks); don't leave these off long-term

— Resume SGLT2i in HFrEF, CKD with proteinuria, T2DM with CV/renal risk once euvolemic — these are renoprotective and mortality-reducing

— Permanently discontinue chronic NSAIDs if alternative analgesia available; document the indication and educate the patient on OTC ibuprofen/naproxen risks

— Educate on "sick day rules": hold ACEi/ARB, SGLT2i, diuretics, metformin during acute illness with vomiting/diarrhea/decreased PO

— Hydration during heat, exercise, illness

— Recognizing symptoms of recurrent AKI (decreased urine output, fatigue, dizziness)

— Avoiding OTC NSAIDs, herbal supplements (aristolochic acid, "kidney cleanses")

— Reporting any new prescription to PCP for renal-dose review

— Target <130/80 in CKD with albuminuria, post-AKI

— ACEi/ARB preferred in proteinuric patients

— A1c goal individualized; SGLT2i preferred for renoprotection

— Avoid metformin if eGFR <30

— Statin for ASCVD risk reduction (CKD is a risk-enhancing factor)

— Annual influenza, pneumococcal (PCV20 or PCV15+PPSV23), COVID-19, RSV (≥60), zoster, hepatitis B (especially if CKD progression toward dialysis)

— Smoking cessation, weight management, Mediterranean/DASH diet, moderate sodium (<2.3 g/day)

— Avoid high-dose protein and creatine supplements

Medication reconciliation at discharge — the highest-yield Step 3 task:

Counseling points:

BP control:

Diabetes management:

Lipid management:

Vaccinations:

Lifestyle:

Step 3 management: The discharge summary should explicitly list held meds and the plan/timing for restart, with a follow-up appointment scheduled — this is a transition-of-care quality metric and a frequently tested Step 3 competency.

Board pearl: Failure to restart guideline-directed ACEi/ARB after AKI resolution in HFrEF patients is associated with increased mortality — Step 3 frequently tests "what do you do at the 1-week follow-up" with a normalized Cr.

Follow-Up, Monitoring, and Counseling

— Mild AKI (stage 1, resolved): BMP in 1–2 weeks, PCP visit in 1–2 weeks

— Moderate AKI (stage 2): BMP in 3–7 days, PCP visit in 1–2 weeks

— Severe AKI (stage 3, or not fully resolved): Nephrology referral within 3 months, BMP every 1–2 weeks until stable, then every 3 months

— All post-AKI patients: BP, weight, Cr, UA with albumin:Cr ratio at 3 months

— Serum Cr trend toward baseline; if not back to baseline by 3 months → acute kidney disease (AKD) → CKD trajectory

— Electrolytes: K, HCO₃, Mg, Phos

— Urinalysis: persistent proteinuria or hematuria warrants further workup

— BP at each visit; home BP monitoring encouraged

— Daily weight (especially HF patients)

— 1 week post-discharge: review held meds, restart as appropriate

— 1 month: full BMP, reassess for restart of remaining meds

— 3 months: KDIGO post-AKI assessment — eGFR, UACR, BP — categorize as full recovery, AKD, or CKD

— "Your kidneys had an injury and need follow-up even if labs look normal now"

— "Avoid ibuprofen, naproxen, aleve — use acetaminophen for pain"

— "Stay hydrated during illness; if you can't drink fluids, contact us — some meds need to be paused"

— "Bring a complete list of medications to every appointment, including OTC"

— Functional status often declines after hospitalization with AKI — consider PT/OT

— Nutritional consultation if appetite poor or sarcopenic

— Discharge summary with explicit medication changes, follow-up plan, and AKI etiology

— Direct handoff for complex cases

Outpatient follow-up cadence:

Monitoring parameters:

When to recheck and adjust meds:

Patient counseling key messages:

Rehab considerations:

Communication with PCP:

CCS pearl: Schedule the PCP follow-up appointment before discharge in your CCS case and order the labs for that visit — orders like "BMP in 1 week" with a clinic visit scheduled score consistently on transition-of-care competencies.

Key distinction: Full recovery = Cr back to baseline within 7 days; AKD = persistent AKI 7–90 days; CKD = persistent ≥90 days. Each tier escalates surveillance intensity and nephrology involvement.

Ethical, Legal, and Patient Safety Considerations

— Hemodialysis catheter placement requires informed consent including risks (bleeding, pneumothorax, infection, vascular injury) and benefits

— Contrast administration in AKI requires shared decision-making — weigh diagnostic benefit vs. nephrotoxicity; document the discussion

— In emergent situations (hyperkalemia with arrhythmia, pulmonary edema), implied consent for life-saving RRT is appropriate; document urgency

— In elderly, frail, or terminal patients with AKI, initiation of RRT is a major decision — explore patient values, prognosis, quality of life

— Time-limited trials of RRT (e.g., 1–2 weeks) with clear endpoints are ethically appropriate

— In severe dementia or advanced cancer with poor prognosis, conservative kidney management without dialysis may be the patient's preference — engage palliative care

— Held nephrotoxic meds at discharge must be clearly documented with restart plan — failure to restart life-saving meds (ACEi/ARB, SGLT2i) is a known patient safety gap

— Conversely, failure to communicate that NSAIDs should be permanently avoided leads to readmission

— Use medication reconciliation at every transition — admission, transfer, discharge, follow-up

— Pending labs at discharge must be tracked and addressed

— Contrast-induced AKI from elective procedure without proper screening — root cause analysis

— Med error: ACEi continued during AKI with rising K → hyperkalemic arrest

— Missed obstructive uropathy in elderly male — bladder scan should be reflexive

— Suspected elder neglect (dehydration in a nursing home with poor oral care) → Adult Protective Services report

— Heat-related illness clusters → public health notification

— Provide medication lists in patient's language; confirm understanding of "sick day rules" with teach-back

— Ensure follow-up labs are accessible (insurance, transportation)

— Baseline Cr, KDIGO stage, suspected etiology, interventions, response, disposition plan — these support quality reporting and protect against liability

Informed consent for procedures:

Goals of care discussions:

Transitions of care safety (high-yield Step 3):

Patient safety events to recognize and report:

Mandatory reporting / public health:

Health literacy and access:

Documentation:

Step 3 management: When a patient lacks decision-making capacity and needs urgent RRT, use the legally recognized surrogate hierarchy (spouse → adult children → parents → siblings) per state law; document capacity assessment and surrogate's decision rationale.

Board pearl: The single most preventable AKI safety event is the "triple whammy" prescribing pattern in elderly — Step 3 may ask about EHR alerts, deprescribing, and pharmacist-led medication reviews as system-level interventions.

High-Yield Associations and Rapid-Fire Clinical Facts

— Triple whammy = ACEi/ARB + diuretic + NSAID → community-acquired AKI

— Cardiorenal type 1 = acute HF + AKI; congested + low forward flow

— HRS-AKI = cirrhosis + ascites + AKI without other cause; treated with albumin + terlipressin

— Hepatorenal precipitants: SBP, large-volume paracentesis without albumin, GI bleed, diuretic overuse

— Prerenal: UNa <20, FENa <1%, FEUrea <35%, urine osm >500, BUN:Cr >20

— ATN: UNa >40, FENa >2%, urine osm <350, muddy brown casts

— Postrenal: variable; depends on duration and partial vs. complete

— NSAIDs → afferent constriction (block PGE2)

— ACEi/ARB → efferent dilation (block angiotensin II)

— SGLT2i → afferent constriction via tubuloglomerular feedback (initial Cr bump is expected and benign, ~0.1–0.3)

— Calcineurin inhibitors → afferent constriction

— Contrast → vasoconstriction + direct tubular toxicity

— Sepsis, DKA, hypercalcemia → balanced crystalloid (LR/Plasmalyte)

— HRS → albumin (volume expander of choice)

— Hemorrhagic shock → blood products, balanced

— Burns → Parkland formula with LR

— Need for RRT, multi-organ failure, sepsis, age, baseline CKD

— KDIGO stage 1 Cr ↑0.3 mg/dL in 48 h or 1.5× in 7 days

— UOP <0.5 mL/kg/h × 6 h = stage 1

— Sepsis bundle: antibiotics in 1 h, 30 mL/kg crystalloid

— Hyperkalemia: K >6.5 with ECG changes = emergency

— Post-paracentesis albumin: 6–8 g/L removed if >5 L

— MAP goal ≥65 (≥80–85 in chronic HTN per SEPSISPAM)

— SMART, BaSICS: balanced crystalloid ≥ NS in critically ill

— STARRT-AKI, AKIKI: no benefit to early RRT initiation

— CONFIRM: terlipressin improves HRS reversal

— PRESERVE: N-acetylcysteine + bicarb no benefit for contrast prevention

— DOSE, CARRESS-HF: high-dose loop diuretic ≥ ultrafiltration for cardiorenal

Classic triads and patterns:

Urinary indices cheat sheet:

Drug-physiology pairings:

Fluid type pairings:

Quick mortality risk markers:

Numbers to memorize:

Trial pearls:

Board pearl: SGLT2i initial Cr bump is expected and benign — do not stop the drug; it is renoprotective long-term (CREDENCE, DAPA-CKD, EMPA-KIDNEY).

Board Question Stem Patterns

— "An 82-year-old woman with HTN, HF, and OA on lisinopril, furosemide, and ibuprofen presents after 3 days of viral gastroenteritis with Cr 2.4 (baseline 0.9), BUN 68, K 5.4. Next best step?"

— Answer: Hold lisinopril, furosemide, and ibuprofen; give isotonic IV fluids; recheck BMP in 24 h

— "Patient with HFrEF, EF 20%, admitted with dyspnea, JVP 15, bibasilar rales, 3+ edema; Cr rising from 1.2 to 1.8 over 48 h on IV furosemide. Next step?"

— Answer: Continue/intensify diuresis (do NOT stop); consider thiazide adjunct, monitor for response; "permissive" Cr rise acceptable

— "Cirrhotic with ascites, Cr 2.6 (baseline 1.0), no response to albumin challenge + diuretic withdrawal × 48 h, bland UA, FENa 0.2%, no shock. Best next therapy?"

— Answer: Albumin + terlipressin (or midodrine/octreotide/albumin if terlipressin unavailable)

— AKI 24–72 h post-cath, transient, FENa <1%, returns to baseline in a week → contrast nephropathy

— AKI 1–4 weeks post-cath, livedo, eosinophilia, hypocomplementemia, progressive → atheroembolic

— "Patient started on Bactrim for UTI; Cr rises from 1.0 to 1.4 over 5 days; UOP normal, asymptomatic. Next step?"

— Answer: Check cystatin C / reassure; trimethoprim blocks tubular Cr secretion without affecting GFR

— Elderly man with BPH, anuria, suprapubic distention → bladder scan, Foley catheter before anything else

— DM2 patient started on empagliflozin, Cr rises from 1.1 to 1.3 in 2 weeks, asymptomatic. Action?

— Answer: Continue empagliflozin; initial Cr bump is expected and renoprotective

— "Patient hospitalized for AKI, lisinopril held. At 2-week follow-up, Cr 1.0 (baseline), K 4.2, BP 142/86. Action?"

— Answer: Resume lisinopril for HF/CKD protection

— Frail 92-year-old with stage 3 AKI, dementia, advance directive declining dialysis. Action?

— Answer: Honor advance directive, palliative/conservative management, engage palliative care

Pattern 1 — The classic triple whammy:

Pattern 2 — Cardiorenal trap:

Pattern 3 — HRS-AKI:

Pattern 4 — Contrast vs. atheroembolic:

Pattern 5 — Pseudo-AKI:

Pattern 6 — Obstruction missed:

Pattern 7 — SGLT2i Cr bump:

Pattern 8 — Post-discharge management:

Pattern 9 — Ethical:

Step 3 management: Read the stem for vital signs, exam, JVP, edema, and medication list — these distinguish hypovolemic from congested prerenal physiology, which determines whether you give fluids or diuretics.

One-Line Recap

Prerenal AKI is a reversible functional decline in GFR from reduced effective renal perfusion — identify the perfusion deficit, restore it appropriately (fluids for hypovolemia, diuresis for cardiorenal, albumin + vasoconstrictor for hepatorenal), remove nephrotoxins, and prevent progression to ATN.

Diagnose: BUN:Cr >20, FENa <1% (FEUrea <35% if on diuretics), bland UA with hyaline casts, urine osm >500, response to perfusion correction within 24–72 h confirms the diagnosis

Treat by phenotype: True hypovolemia → balanced isotonic crystalloid; congested cardiorenal → IV loop diuretic (tolerate Cr rise up to ~30%); HRS-AKI → albumin 1 g/kg day 1 + terlipressin; septic shock → fluids + norepinephrine to MAP ≥65; obstruction → catheter/stent

Universal AKI bundle: Hold NSAIDs, ACEi/ARB, SGLT2i (in volume depletion), diuretics if hypovolemic, contrast, aminoglycosides; renal-dose all remaining meds; treat hyperkalemia/acidosis; consider RRT for AEIOU indications

Long-term Step 3 thinking: AKI doubles future CKD/CV/mortality risk — schedule nephrology follow-up within 3 months for stage 2–3, restart guideline-directed ACEi/ARB and SGLT2i once stable, educate patients on "sick day rules" and lifelong NSAID avoidance, and document a clear medication reconciliation plan at every care transition

Board pearl: The triple whammy (ACEi/ARB + diuretic + NSAID) in an elderly patient with an acute illness is the prototypical Step 3 prerenal AKI vignette — and the most preventable AKI in clinical practice. Recognize it, deprescribe it, and counsel against it at every transition of care.