Renal & Urinary

Acute kidney injury: classification (KDIGO) and CCS-style workup

Clinical Overview and When to Suspect AKI

— Rise in serum creatinine (SCr) ≥ 0.3 mg/dL within 48 h

— Rise in SCr to ≥ 1.5× baseline known or presumed within prior 7 days

— Urine output < 0.5 mL/kg/h for ≥ 6 h

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

— Stage 2: SCr 2.0–2.9× baseline; UOP < 0.5 mL/kg/h × ≥ 12 h

— Stage 3: SCr ≥ 3.0× baseline, or SCr ≥ 4.0 mg/dL, or initiation of RRT, or eGFR < 35 in patients < 18 y; UOP < 0.3 mL/kg/h × ≥ 24 h or anuria × 12 h

— Any hospitalized patient with falling UOP, rising BUN/Cr, or new metabolic acidosis

— Post-contrast study, post-cardiac surgery, post-major bleed/sepsis

— Outpatient on ACEi/ARB + diuretic + NSAID ("triple whammy")

— Elderly with vomiting/diarrhea, CHF exacerbation, cirrhosis with SBP, rhabdomyolysis after fall with "long lie"

Board pearl: A SCr that "looks normal" in a frail 85-year-old (e.g., 1.2 mg/dL) can represent stage 1 AKI if baseline was 0.7 — always anchor to baseline creatinine, not the reference range.

CCS pearl: On any CCS case with sepsis, GI bleed, contrast exposure, or new diuretic/ACEi, order BMP and strict I/Os on day 1 and recheck creatinine in 24 h; missing AKI by failing to trend Cr is a classic point loss.

Definition (KDIGO 2012): Acute kidney injury is diagnosed by any one of:

KDIGO staging:

When to suspect on Step 3:

Epidemiology: Occurs in ~20% of hospitalized adults and >50% of ICU patients; independently increases mortality and risk of progression to CKD.

Conceptual framework: Always classify by pre-renal vs intrinsic vs post-renal — this drives the entire workup tree.

Presentation Patterns and Key History

— Vomiting, diarrhea, poor PO intake, diuretic overuse, burns, hemorrhage

— CHF, cirrhosis with ascites (hepatorenal), nephrotic syndrome, sepsis (early)

— NSAIDs (afferent constriction), ACEi/ARB (efferent dilation) — especially with bilateral RAS

— ATN (most common intrinsic): prolonged ischemia (continued pre-renal insult) or nephrotoxins — aminoglycosides, vancomycin, amphotericin B, cisplatin, IV contrast, myoglobin (rhabdo), hemoglobin, tumor lysis (urate/phosphate)

— AIN: new drug (PPIs, NSAIDs, β-lactams, sulfa, rifampin), fever, rash, eosinophilia

— Glomerulonephritis: hematuria, edema, HTN, recent infection, hemoptysis (pulmonary-renal), purpura

— Vascular: TTP/HUS, scleroderma renal crisis, atheroembolic (post-cath)

— BPH, pelvic malignancy, retroperitoneal fibrosis, bilateral stones, neurogenic bladder, anticholinergic-induced retention

— Anuria alternating with polyuria suggests intermittent obstruction

— Baseline creatinine, recent SCr trend

— Med rec: NSAIDs, ACEi/ARB, diuretics, PPIs, antibiotics, contrast within 72 h

— Volume status changes: weight trend, thirst, orthostasis

— Urinary symptoms: hesitancy, dribbling, gross hematuria, frothy urine

Key distinction: Pre-renal AKI is reversible with volume; if creatinine fails to improve within 24–72 h of adequate resuscitation, suspect transition to ATN.

Board pearl: A patient on lisinopril + HCTZ + ibuprofen presenting with stage 1 AKI is the prototypical "triple whammy" — stop the NSAID and ACEi, hold the diuretic, and recheck Cr in 48 h before assuming intrinsic disease.

Pre-renal pattern (~60% of AKI): Volume loss or effective volume depletion

Intrinsic pattern (~35%):

Post-renal (~5%):

High-yield history checklist:

Physical Exam Findings and Hemodynamic Assessment

— Hypovolemic: dry mucous membranes, flat JVP, orthostatic ↓SBP ≥ 20 or ↑HR ≥ 30, decreased skin turgor, oliguria, cool extremities

— Hypervolemic but effectively underfilled (CHF, cirrhosis): elevated JVP or ascites with cool extremities, narrow pulse pressure, hyponatremia — kidneys "see" low volume despite total-body overload

— Euvolemic/overloaded with intrinsic AKI: crackles, S3, peripheral edema, hypertension (think GN, ATN with fluid given)

— Palpable bladder, suprapubic dullness → obstruction; do bedside post-void residual

— Flank pain, CVA tenderness → obstruction, pyelonephritis, papillary necrosis, renal infarction

— Maculopapular rash + low-grade fever → AIN

— Livedo reticularis, blue toes post-catheterization → cholesterol atheroembolic disease

— Palpable purpura → IgA vasculitis, cryoglobulinemia, ANCA vasculitis

— Periorbital/pedal edema with HTN → nephritic/nephrotic syndrome

— Asterixis, uremic frost, pericardial rub → advanced uremia

— Bedside POCUS: IVC collapsibility, B-lines (pulmonary edema), bladder volume, hydronephrosis

— Passive leg raise + stroke volume change as a dynamic fluid-responsiveness test in ICU

Step 3 management: When volume status is ambiguous in a hospitalized patient with AKI, POCUS of IVC, lungs, and bladder is preferred over an empiric fluid bolus or empiric diuretic — wrong guess in either direction worsens AKI.

Board pearl: Hepatorenal syndrome patients look "wet" (ascites, edema) but are physiologically pre-renal — give albumin, not diuretics.

Volume status — the central exam task in AKI:

Targeted exam clues by etiology:

Hemodynamic adjuncts:

Diagnostic Workup — Initial Labs, Urinalysis, Imaging

— BMP (Na, K, HCO3, BUN, Cr, glucose), CBC, Mg, Phos, Ca

— Urinalysis with microscopy (the single highest-yield test)

— Urine electrolytes: urine Na, Cr, urea (calculate FENa, FEUrea)

— Bladder scan / post-void residual; place Foley if obstruction suspected or strict I/Os needed

— Renal ultrasound if obstruction possible, AKI without obvious cause, or AKI > 48 h

— VBG if acidosis suspected; EKG if K ≥ 5.5 or stage 2–3 AKI

— > 20:1 suggests pre-renal (or GI bleed)

— 10–15:1 suggests intrinsic

— < 1% → pre-renal or contrast nephropathy, early rhabdo, hepatorenal

— > 2% → ATN

— FEUrea < 35% → pre-renal even if patient is on diuretics

— Bland sediment, hyaline casts → pre-renal

— Muddy brown granular casts, renal tubular epithelial cells → ATN

— WBC casts, eosinophils (low sens) → AIN or pyelonephritis

— RBC casts, dysmorphic RBCs, proteinuria → glomerulonephritis

— Heme-positive dip with no RBCs → myoglobin (rhabdo) or hemoglobin

— Crystals → uric acid (TLS), oxalate (ethylene glycol), drug crystals (acyclovir, sulfa, methotrexate)

Board pearl: Muddy brown granular casts + FENa > 2% is the classic ATN signature; hyaline casts + FENa < 1% is pre-renal.

CCS pearl: Order renal ultrasound in any AKI without an obvious pre-renal cause — missing bilateral hydronephrosis is a high-yield CCS error because relief of obstruction reverses AKI.

Initial CCS order set (within first hour):

BUN:Cr ratio:

FENa (off diuretics):

Urinalysis patterns:

Diagnostic Workup — Advanced and Confirmatory Studies

— Urine protein-to-creatinine ratio (spot): nephrotic-range > 3.5 g/g suggests primary glomerular disease, diabetic nephropathy, amyloid, MM

— Serum and urine protein electrophoresis + free light chains if age > 50, anemia, hypercalcemia, bone pain — rule out multiple myeloma / cast nephropathy

— Serologies for GN workup:

— ANA, anti-dsDNA (lupus nephritis)

— ANCA (granulomatosis with polyangiitis, MPA)

— Anti-GBM (Goodpasture)

— C3, C4 (low in lupus, post-strep, MPGN, cryoglobulinemia)

— ASO, anti-DNase B (post-strep GN)

— Hep B, Hep C, HIV (PAN, MPGN, HIVAN)

— Cryoglobulins

— Intrinsic AKI of unclear cause after non-invasive workup

— Suspected rapidly progressive GN (RPGN) — biopsy urgently

— Nephrotic syndrome in adults, suspected AIN not improving off drug, lupus nephritis class assignment

Key distinction: RPGN (rapidly rising Cr + active urinary sediment + crescents) is a renal emergency — do not wait for serologies; obtain biopsy and start empiric high-dose steroids ± cyclophosphamide/rituximab/plasmapheresis based on suspected etiology.

Board pearl: In an older patient with unexplained AKI, always send SPEP/UPEP and free light chains — myeloma cast nephropathy is a classic missed diagnosis on Step 3.

When initial workup is non-diagnostic, layer on:

CK and myoglobin if rhabdomyolysis suspected (heme-positive UA without RBCs, immobilization, statin use, seizure)

LDH, haptoglobin, peripheral smear for schistocytes → TMA (TTP/HUS, scleroderma renal crisis, malignant HTN, HELLP)

Renal biopsy indications:

Imaging beyond US: CT abdomen (non-contrast) for stones, mass, retroperitoneal fibrosis; MRA or duplex for renovascular disease; nuclear renogram rarely in AKI

Risk Stratification and First-Line Management Logic

— Is there a life-threatening complication requiring emergent dialysis? (AEIOU)

— Acidosis (pH < 7.1 refractory), Electrolytes (K > 6.5 or rising despite therapy), Ingestion (methanol, ethylene glycol, salicylate, lithium), Overload (refractory pulmonary edema), Uremia (pericarditis, encephalopathy, bleeding)

— Is there obstruction? Relieve with Foley, percutaneous nephrostomy, or stent

— Is the patient volume-depleted, euvolemic, or overloaded?

— Stop nephrotoxins: NSAIDs, ACEi/ARB (temporarily), aminoglycosides, vancomycin if alternative exists, IV contrast unless essential, PPI if AIN suspected

— Renal dose-adjust all medications (especially LMWH, gabapentin, opioids, antibiotics, DOACs)

— Avoid contrast when possible; if essential, use isotonic saline pre/post and lowest-volume iso-osmolar contrast

— Target MAP ≥ 65 mmHg (higher, ~80–85, in chronic HTN)

— Strict I/Os, daily weights, daily BMP

— Hypovolemic → isotonic crystalloid (balanced solutions like LR preferred over NS in large volumes to avoid hyperchloremic acidosis)

— Overloaded → loop diuretics (does not change AKI outcome but manages volume)

— Cardiorenal → diurese + optimize forward flow; albumin in cirrhosis/SBP/HRS

Step 3 management: Loop diuretics do not prevent or treat AKI — use them for volume management only. Choosing "high-dose furosemide to convert oliguric to non-oliguric AKI for renal protection" is a board trap.

CCS pearl: On any AKI case, your day-1 advance-clock orders should include strict I/Os, daily weight, daily BMP, hold nephrotoxins — these score reliably across scenarios.

Immediate triage questions:

General first-line bundle:

Volume strategy:

Pharmacotherapy — First-Line Regimens by Etiology

— Isotonic crystalloid bolus 500–1000 mL, reassess; LR or Plasma-Lyte preferred over NS for large-volume resuscitation

— Sepsis: 30 mL/kg over first 3 h, then dynamic reassessment; norepinephrine first-line vasopressor

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

Board pearl: Dopamine ("renal-dose"), fenoldopam, mannitol, and "renal-protective" diuretics are not recommended for AKI prevention or treatment — recognizing these as wrong answers is high-yield.

Step 3 management: In hepatorenal syndrome, albumin + terlipressin is now first-line in the US (CONFIRM trial); definitive therapy is liver transplantation.

Pre-renal / hypovolemic AKI:

ATN: Supportive — no drug reverses ATN; avoid further insults, manage electrolytes and volume, anticipate diuretic (recovery) phase with marked polyuria and K/Mg/Phos wasting

AIN: Discontinue offending drug (most important step); if Cr fails to improve in 3–7 days or biopsy confirms, prednisone 1 mg/kg/day tapered over 4–6 weeks

Rhabdomyolysis: Aggressive IV NS or LR at 200–500 mL/h targeting UOP 200–300 mL/h; routine bicarb/mannitol not recommended

Tumor lysis syndrome: IVF + rasburicase (high risk) or allopurinol (low/intermediate risk); avoid alkalinization (precipitates Ca-phos)

Contrast-associated AKI prevention: Isotonic IV fluids before and after contrast; N-acetylcysteine and bicarbonate are not recommended (PRESERVE trial)

GN / vasculitis: High-dose steroids ± cyclophosphamide, rituximab, plasmapheresis (anti-GBM, severe ANCA with pulmonary hemorrhage or Cr > 5.7)

Renal Replacement Therapy and Procedural Management

— Acidosis: severe metabolic acidosis (pH < 7.1) refractory to bicarbonate

— Electrolytes: hyperkalemia ≥ 6.5 or with EKG changes refractory to medical therapy

— Ingestions: dialyzable toxins — methanol, ethylene glycol, salicylates, lithium, valproate, metformin (severe lactic acidosis), theophylline

— Overload: pulmonary edema unresponsive to diuretics

— Uremia: pericarditis, encephalopathy, uremic bleeding

— IHD (intermittent hemodialysis): hemodynamically stable, rapid solute clearance, toxin removal

— CRRT (continuous renal replacement therapy): ICU patients with hemodynamic instability, cerebral edema, severe fluid overload requiring slow correction

— SLED (sustained low-efficiency dialysis): hybrid for borderline hemodynamics

— Peritoneal dialysis: rarely first-line in acute setting in US adults

— Foley catheter for any suspected outflow obstruction or strict UOP monitoring

— Percutaneous nephrostomy or ureteral stent for upper-tract obstruction (stones, malignancy, retroperitoneal fibrosis)

— Renal biopsy for unexplained intrinsic AKI or suspected RPGN

CCS pearl: On a CCS case with K = 7.2 and peaked T-waves, the correct sequence is IV calcium gluconate → insulin + D50 → albuterol → loop diuretic or kayexalate/patiromer → emergent dialysis if refractory; ordering dialysis without first stabilizing the membrane loses points.

Board pearl: Avoid the left subclavian for temporary dialysis access — central stenosis there sabotages future AV fistula on that arm.

Indications for urgent dialysis (AEIOU):

Modality selection:

Timing controversy: STARRT-AKI and AKIKI trials show no mortality benefit to early/preemptive RRT in absence of urgent indications — wait for clear indication

Vascular access: Non-tunneled internal jugular catheter preferred for emergent access; ultrasound-guided; right IJ > left IJ > femoral > subclavian (avoid subclavian to preserve future fistula site)

Adjunct procedures:

Special Populations — Elderly and Hepatic Impairment

— Baseline GFR declines ~1 mL/min/year after age 40; "normal" creatinine of 1.0–1.3 may represent eGFR < 45

— Use CKD-EPI 2021 equation (race-free) for eGFR estimation; cystatin C–based eGFR helpful when muscle mass is low

— Sarcopenic patients under-estimate AKI severity by SCr alone — anchor to UOP and trends

— Polypharmacy: review for NSAIDs, ACEi/ARB, diuretics, gabapentin, metformin, SGLT2 inhibitors, herbal supplements

— Higher risk of contrast-associated AKI, drug-induced AIN (PPIs), and obstruction (BPH, pelvic malignancy)

— Use caution with bowel preps (oral sodium phosphate → acute phosphate nephropathy)

— Baseline SCr underestimates dysfunction (low muscle mass, reduced creatine generation)

— Hepatorenal syndrome (HRS-AKI) criteria: cirrhosis with ascites, ≥ 0.3 mg/dL rise in SCr in 48 h or ≥ 50% from baseline, no improvement after 2 days of diuretic withdrawal + albumin 1 g/kg/day, absence of shock, no nephrotoxins, no structural disease

— Always rule out SBP with diagnostic paracentesis (PMN ≥ 250) in any cirrhotic with AKI

— Treat SBP with cefotaxime + albumin 1.5 g/kg day 1, 1 g/kg day 3 to prevent HRS

— Avoid NSAIDs, aminoglycosides, ACEi/ARB, large-volume paracentesis without albumin replacement

— Acute-on-chronic AKI common; even small ↑ Cr can represent large GFR drop

— Higher threshold for contrast, gadolinium (NSF risk if eGFR < 30 with older agents)

Step 3 management: Any cirrhotic admitted with AKI gets diagnostic paracentesis before antibiotics if SBP is on the differential — missing SBP is a Step 3 favorite.

Board pearl: Albumin + terlipressin is now first-line for HRS-AKI; TIPS is second-line bridge to transplant in selected patients.

Elderly:

Hepatic impairment / cirrhosis:

Renal impairment (pre-existing CKD):

Special Populations — Pregnancy and Pediatrics

— Early pregnancy: hyperemesis gravidarum (pre-renal), septic abortion

— Late pregnancy/postpartum: preeclampsia/HELLP, acute fatty liver of pregnancy, TTP, atypical HUS, postpartum hemorrhage

— Normal pregnancy: GFR ↑ 50%, SCr falls to 0.4–0.5 mg/dL; a SCr of 0.9 in pregnancy is abnormal

— Preeclampsia with severe features: BP ≥ 160/110, proteinuria, Cr > 1.1 or doubling, LFTs 2× ULN, plt < 100k, pulmonary edema, neuro symptoms → magnesium for seizure prophylaxis, antihypertensives (labetalol, hydralazine, nifedipine), delivery is definitive

— HELLP: hemolysis, elevated LFTs, low platelets; deliver

— AFLP: hypoglycemia, coagulopathy, encephalopathy — deliver urgently

— Avoid ACEi/ARB, SGLT2i, NSAIDs (after 20 weeks)

— Use pediatric KDIGO with eGFR < 35 mL/min/1.73 m² as a stage 3 criterion (in addition to adult criteria)

— Common etiologies:

— Neonates: perinatal asphyxia, sepsis, congenital anomalies (CAKUT), umbilical artery catheter thrombosis

— Children: dehydration (gastroenteritis), HUS (Shiga toxin–producing E. coli O157:H7), post-strep GN, IgA nephropathy, drug-induced AIN, TLS in leukemia

— HUS triad: MAHA, thrombocytopenia, AKI; avoid antibiotics and antimotility agents in suspected STEC HUS; supportive care; consider eculizumab for atypical HUS

Key distinction: Preeclampsia with severe features triggers delivery regardless of gestational age if ≥ 34 weeks; < 34 weeks may temporize with magnesium, antihypertensives, and steroids for fetal lung maturity unless maternal/fetal deterioration.

Board pearl: Bloody diarrhea in a child + AKI + thrombocytopenia = STEC-HUS — do not give antibiotics (increases toxin release).

Pregnancy-associated AKI:

Pediatric AKI:

Reproductive counseling: Women with CKD/AKI history should have preconception counseling; pregnancy worsens proteinuric kidney disease.

Complications and Adverse Outcomes

— Hyperkalemia: EKG changes (peaked T → wide QRS → sine wave → asystole); treat with Ca gluconate, insulin/glucose, albuterol, loop diuretic, K-binders (patiromer, sodium zirconium cyclosilicate), dialysis if refractory

— Metabolic acidosis (high anion gap from retained organic acids): bicarbonate if pH < 7.2 or HCO3 < 12; correct underlying cause

— Hyperphosphatemia, hypocalcemia, hyperuricemia: common in TLS and severe AKI

— Hyponatremia from impaired water excretion; restrict free water

— Hypermagnesemia in severe AKI — avoid Mg-containing antacids/laxatives

— Progression to CKD: AKI doubles the risk of CKD and triples the risk of ESRD

— Increased cardiovascular mortality even after recovery

— Risk of recurrent AKI within 1 year ~30%

Board pearl: Uremic bleeding from platelet dysfunction → DDAVP is first-line; the platelet count is normal but function is impaired. Dialysis also corrects it.

Key distinction: "AKI resolved" on labs ≠ "kidneys recovered" — eGFR and proteinuria should be reassessed at 3 months to define CKD status.

Acute metabolic complications:

Volume complications: Pulmonary edema, hypertension, congestive heart failure

Uremic complications: Encephalopathy, asterixis, uremic pericarditis (friction rub, low-voltage EKG, effusion), platelet dysfunction → bleeding (treat with DDAVP, cryoprecipitate, dialysis)

Drug toxicity: Accumulation of renally cleared drugs — digoxin, gabapentin, opioids (especially morphine, meperidine), LMWH, DOACs, metformin (lactic acidosis), baclofen

Infection: Catheter-associated UTI, bacteremia from dialysis access, increased susceptibility to nosocomial infections

Long-term sequelae:

Diuretic (recovery) phase of ATN: Massive polyuria (3–5 L/day) with K, Mg, Phos wasting — monitor and replace aggressively

When to Escalate Care — ICU, Consult, Triage

— Hemodynamic instability requiring vasopressors

— Severe acidosis (pH < 7.2) or refractory hyperkalemia

— Need for CRRT or hourly hemodynamic monitoring

— Pulmonary edema requiring NIV/intubation

— Massive rhabdomyolysis (CK > 50,000) or severe TLS

— Suspected fulminant RPGN with hypoxia (pulmonary-renal syndrome)

— Stage 2–3 AKI, AKI requiring or anticipated to require RRT

— Unclear etiology after initial workup, suspected GN/vasculitis/TMA

— Refractory electrolyte or acid-base abnormalities

— Hepatorenal syndrome, scleroderma renal crisis, suspected myeloma kidney

— Need for biopsy

— Obstructive uropathy needing stent or nephrostomy

— Massive hematuria, suspected bladder/renal tumor

— Percutaneous nephrostomy when ureteral stenting fails or upper-tract obstruction

— Suspected lupus nephritis, vasculitis, TTP, atypical HUS

— Floor → ICU when patient meets criteria above

— ED → floor when hemodynamically stable, K controlled, oxygenating well, has clear etiology

— Discharge only when SCr is stable or improving × 24–48 h, electrolytes normalized, off nephrotoxins, follow-up arranged

CCS pearl: Calling nephrology consult early in stage 2–3 AKI consistently scores well; delayed consultation is associated with worse outcomes in observational data and is a common CCS deduction.

Step 3 management: Don't forget medication reconciliation at every transition — re-introducing the ACEi or NSAID that caused AKI upon discharge is a classic patient-safety question.

ICU admission criteria:

Nephrology consultation:

Urology consultation:

Interventional radiology:

Rheumatology/hematology:

CCS-style transitions:

Key Differentials — Within AKI Categories

— True hypovolemia: GI losses, hemorrhage, burns, renal losses (diuretics, DI, osmotic), third-spacing

— Decreased cardiac output: HF, cardiogenic shock, tamponade, massive PE

— Decreased effective arterial volume: cirrhosis with HRS, sepsis (early), nephrotic syndrome

— Drug-induced afferent vasoconstriction: NSAIDs, contrast, calcineurin inhibitors (cyclosporine, tacrolimus)

— Drug-induced efferent vasodilation: ACEi/ARB (especially in bilateral RAS or single kidney with RAS)

— Tubular (ATN): ischemic (prolonged pre-renal), nephrotoxic (aminoglycosides, vancomycin, amphotericin, cisplatin, contrast), pigment (myoglobin, hemoglobin), crystals (uric acid, oxalate, drug)

— Interstitial (AIN): drugs (PPI, NSAID, β-lactam, sulfa, rifampin, allopurinol), infections (pyelonephritis, leptospirosis, Legionella), autoimmune (sarcoid, Sjögren, TINU, IgG4)

— Glomerular (GN):

— Nephritic: post-strep, IgA, lupus, ANCA-associated, anti-GBM, MPGN, cryoglobulinemia

— Nephrotic with AKI: collapsing FSGS, severe MN, diabetic nephropathy with superimposed insult

— Vascular: TTP, HUS, scleroderma renal crisis, malignant HTN, renal artery/vein thrombosis, atheroembolic disease, polyarteritis nodosa

— Lower tract: BPH, prostate cancer, bladder cancer, urethral stricture, neurogenic bladder, blocked Foley

— Upper tract (must be bilateral or unilateral in solitary kidney): stones, malignancy (cervical, colorectal, lymphoma), retroperitoneal fibrosis, papillary necrosis

Key distinction: Post-renal AKI from upper-tract obstruction requires bilateral involvement (or unilateral in a solitary functioning kidney); unilateral hydronephrosis with a normal contralateral kidney rarely causes AKI.

Board pearl: "Blue toes after cardiac cath" + eosinophilia + low complement + stepwise rise in Cr = cholesterol atheroembolic disease; supportive treatment only.

Pre-renal differentials (volume "real" vs "effective"):

Intrinsic AKI subcategories:

Post-renal differentials:

Key Differentials — Mimics and Other-Category Pitfalls

— Trimethoprim, cimetidine, dolutegravir, cobicistat block tubular creatinine secretion → SCr rises ~0.1–0.4 without GFR change

— Increased creatine intake (creatine supplements, large meat meal)

— Rhabdomyolysis early on can cause modest spurious rise

— Cefoxitin and flucytosine falsely elevate SCr by Jaffe assay interference

— Ketones (DKA) interfere with Jaffe-based creatinine assay

— High protein intake, GI bleeding, corticosteroids, tetracycline raise BUN disproportionately

— Acute glomerulonephritis with rapid Cr rise can look like ATN — urine sediment distinguishes

— Thrombotic microangiopathy (TTP/HUS) with MAHA + thrombocytopenia + AKI — peripheral smear is key

— Hypercalcemia causes nephrogenic DI and pre-renal AKI; check Ca

— Acute decompensated heart failure ("cardiorenal syndrome") — Cr rises with diuresis but is hemodynamically driven; gentle continued diuresis often improves rather than worsens renal function

— Abdominal compartment syndrome: intra-abdominal pressure > 20 mmHg causes oligo-anuric AKI; check bladder pressure in post-op or massively resuscitated patients

— Small, echogenic kidneys on US, anemia, hyperphosphatemia with hypocalcemia + secondary hyperparathyroidism → CKD

— Look for prior labs

Key distinction: A patient on bactrim for UTI with a 0.3 mg/dL bump in Cr and a normal urinalysis likely has benign tubular secretion blockade, not AKI — recheck off the drug.

Board pearl: Abdominal compartment syndrome is a reversible cause of oligo-anuric AKI in ICU patients with massive resuscitation, ascites, or abdominal trauma — measure bladder pressure and consider decompression.

"Pseudo-AKI" — creatinine rises without true GFR fall:

Other causes of azotemia without AKI:

Conditions mimicking AKI presentations:

Chronic kidney disease vs AKI:

Secondary Prevention, Discharge, and Long-Term Plan

— SCr trending down or stable × 24–48 h

— Electrolytes (especially K) normalized

— Volume status stable, off IV fluids, oral intake adequate

— Nephrotoxins discontinued or alternatives selected

— Clear etiology and plan in discharge summary

— Hold or stop: NSAIDs, nephrotoxic antibiotics, IV contrast exposure planning

— Reintroduce cautiously: ACEi/ARB (often restart at discharge or 1–2 weeks post if BP/cardiac indication exists and Cr stable), diuretics at lower dose, SGLT2 inhibitors (hold during acute illness, restart when stable — they have long-term renoprotective benefit in DM/CKD/HF)

— Dose-adjust: metformin (hold if eGFR < 30), gabapentin, DOACs, opioids, statins, allopurinol, antibiotics

— Recheck SCr and urinalysis at 3 months post-AKI to assess for CKD development and proteinuria

— Annual monitoring thereafter in patients with persistent eGFR reduction or proteinuria

— BP control < 130/80 (ACEi/ARB if proteinuric, once stable)

— Glycemic control in diabetics; SGLT2 inhibitors (empagliflozin, dapagliflozin) for renoprotection if eGFR ≥ 20

— Smoking cessation, weight management, avoid NSAIDs lifelong if recurrent AKI risk

— "Sick day rules": hold ACEi/ARB, diuretics, SGLT2i, metformin, NSAIDs during vomiting, diarrhea, fever, or poor PO intake

— Avoid OTC NSAIDs and herbal supplements

— Hydration awareness before contrast studies

Step 3 management: Schedule a follow-up SCr and UA at 3 months post-AKI — failure to do so is the most common missed opportunity to detect post-AKI CKD; document on the discharge plan.

Board pearl: SGLT2 inhibitors cause a small initial Cr bump but provide long-term renal and cardiovascular protection — don't permanently discontinue them after AKI recovery in eligible patients.

Discharge readiness criteria:

Medication reconciliation:

Long-term renal monitoring (KDIGO recommends):

Cardiovascular and lifestyle prevention:

Patient education:

Follow-Up, Monitoring, and Counseling

— Primary care or nephrology visit within 7–14 days of discharge

— BMP and UA at the post-discharge visit

— Nephrology referral if persistent stage ≥ 2 AKI, eGFR < 60 sustained, proteinuria ACR > 30 mg/g, or unresolved etiology

— Repeat full assessment (SCr, eGFR, UA, urine ACR, BP) at 3 months to define CKD status per KDIGO

— Trends in SCr and eGFR (use CKD-EPI 2021)

— Urine albumin/creatinine ratio (proteinuria is the strongest predictor of CKD progression)

— Blood pressure (home BP log preferred for accuracy)

— Electrolytes if on RAAS blockade, diuretic, or with reduced eGFR

— Hemoglobin, calcium, phosphate, PTH, bicarbonate if CKD develops

— Hydration: maintain adequate intake but avoid excessive volume in heart failure

— Avoid NSAIDs indefinitely; acetaminophen is preferred for analgesia

— Limit iodinated contrast; if essential, IV hydration before/after

— Diet: moderate protein (0.8 g/kg/day if CKD), low sodium (< 2 g/day), DASH-style; restrict potassium and phosphate only if labs warrant

— Vaccinations: influenza, pneumococcal, hepatitis B (especially if RRT anticipated)

— Post-ICU AKI patients often have deconditioning, sarcopenia — early mobilization, PT/OT, nutrition consult

— Address frailty and falls risk in elderly

CCS pearl: Always order follow-up appointment with PCP in 1–2 weeks and labs (BMP, UA) on the discharge order set after AKI — both score reliably on CCS.

Board pearl: Proteinuria after AKI is the single strongest predictor of progression to CKD — quantify with spot urine ACR, not just dipstick.

Outpatient follow-up cadence after AKI:

What to monitor:

Counseling points:

Rehabilitation considerations:

Ethical, Legal, and Patient Safety Considerations

— Discuss benefits, risks, alternatives, including conservative kidney management (no dialysis) for frail/end-of-life patients

— Surrogate decision-makers needed for incapacitated patients; respect advance directives

— Especially in elderly with multimorbidity, evidence shows dialysis may not improve survival or quality of life vs supportive care

— Document goals of care; consider palliative care consult for prognosis discussion

— Legally and ethically equivalent to withholding any other life-sustaining treatment

— Requires capacity assessment, surrogate input, and clear documentation

— Suspected elder abuse/neglect in a dehydrated nursing home patient with AKI → report to Adult Protective Services

— Toxic exposures (ethylene glycol, methanol) may require poison control notification; occupational exposures may require OSHA reporting

— Medication safety: AKI is the most common drug-related adverse event in hospitalized patients — pharmacist-driven renal dose-adjustment programs reduce harm

— Contrast safety: Pre-procedure eGFR checks, hydration protocols

— Transitions-of-care safety: Up to 30% of patients are inadvertently restarted on the culprit nephrotoxin after discharge — a structured medication reconciliation at every transition is the highest-yield intervention

— Handoff communication: Use I-PASS or SBAR to flag AKI status, baseline Cr, and held medications

— Use race-free CKD-EPI 2021 equation for eGFR (removed Black race coefficient to address inequities in transplant listing and drug dosing)

— Address access to nephrology care, dialysis modalities, transplantation

Step 3 management: When a CCS or vignette describes a patient discharged on NSAIDs or ACEi without follow-up labs after AKI, the patient-safety best answer is implementing a structured medication reconciliation with the discharging team and pharmacy, not simply educating the patient.

Board pearl: Withdrawing dialysis in a patient with capacity who declines further treatment is ethically and legally permitted and is not physician-assisted suicide.

Informed consent for renal procedures and dialysis:

Shared decision-making in dialysis initiation:

Withholding/withdrawing dialysis:

Mandatory reporting:

Patient safety bundles:

Health equity considerations:

High-Yield Associations and Rapid-Fire Facts

Board pearl: Scleroderma renal crisis is the only AKI in which ACE inhibitors are the treatment of choice during active disease — captopril titrated to BP control.

Key distinction: Anti-GBM disease without pulmonary involvement = "renal-limited anti-GBM"; with pulmonary hemorrhage = Goodpasture syndrome.

Muddy brown granular casts + FENa > 2% → ATN

WBC casts + eosinophiluria + rash/fever → AIN (think recent PPI, β-lactam, NSAID)

RBC casts + dysmorphic RBCs + proteinuria → glomerulonephritis

Heme-positive dip + no RBCs on micro → myoglobinuria or hemoglobinuria

Calcium oxalate crystals (envelope-shaped) → ethylene glycol poisoning; high osmolar gap, high anion gap

Uric acid crystals + AKI in lymphoma/leukemia patient post-chemo → TLS

Bilateral hydronephrosis on US → post-renal AKI

Renal artery stenosis: AKI after starting ACEi → bilateral RAS until proven otherwise

Livedo + blue toes + eosinophilia post-cath → cholesterol atheroembolic disease

MAHA + thrombocytopenia + AKI → TMA (TTP, HUS, malignant HTN, scleroderma renal crisis)

Scleroderma renal crisis → ACEi (captopril) is treatment of choice (unique exception where ACEi is given in active AKI)

Hep C + cryoglobulinemia → MPGN with low C4

Anti-GBM (Goodpasture) → linear IgG deposits, pulmonary hemorrhage + GN → plasmapheresis + steroids + cyclophosphamide

ANCA-associated vasculitis → pauci-immune crescentic GN

Post-strep GN → low C3, normal C4, latent period 1–3 weeks after pharyngitis, 3–6 weeks after impetigo

Multiple myeloma → cast nephropathy, hypercalcemia, anemia, bone pain — send SPEP/UPEP/FLC

Contrast-associated AKI → peaks day 3–5, usually resolves in 7–10 days

Aminoglycoside nephrotoxicity → non-oliguric ATN, peaks 5–10 days after start

Lithium toxicity → nephrogenic DI, chronic interstitial nephritis; dialyzable in severe acute toxicity

Metformin + AKI → severe lactic acidosis; hemodialysis indicated

Board Question Stem Patterns

Board pearl: When a question gives a single lab value rise of 0.3 mg/dL in Cr over 48 h, that alone meets KDIGO stage 1 AKI — don't dismiss it as "borderline."

CCS pearl: On a CCS case, always re-check creatinine and urinalysis after key interventions (fluid bolus, Foley placement, drug discontinuation) — the case rewards iterative monitoring.

Stem 1 — Triple whammy: 78-year-old on lisinopril, HCTZ, and ibuprofen presents with fatigue; SCr 2.1 (baseline 0.9), BUN 48, FENa 0.5%. → Pre-renal AKI; stop NSAID and ACEi, give isotonic fluids.

Stem 2 — Post-contrast: 65-year-old diabetic with CKD undergoes coronary angiography; SCr rises from 1.6 to 2.4 on day 3. → Contrast-associated AKI; supportive care, hold metformin, hydrate.

Stem 3 — Sepsis with ATN: Patient with urosepsis resuscitated with fluids; UOP drops, SCr rises, urinalysis shows muddy brown casts. → ATN; supportive care, avoid further nephrotoxins.

Stem 4 — AIN: Patient on omeprazole for 6 weeks develops rash, fever, eosinophilia, SCr 2.5. → Drug-induced AIN; stop PPI; consider steroids if no improvement.

Stem 5 — Rhabdomyolysis: Found down after drug overdose, CK 45,000, heme-positive UA without RBCs, K 6.0. → Rhabdo AKI; aggressive IV fluids, monitor K, treat hyperkalemia.

Stem 6 — TLS: Patient with Burkitt lymphoma 24 h post-chemo: K 6.5, phos 8, Ca 6.5, uric acid 15, Cr 3.0. → TLS; rasburicase, IVF, monitor for dialysis.

Stem 7 — Obstruction: Elderly man with BPH, anuria, suprapubic fullness, SCr rising. → Post-renal AKI; Foley catheter, watch for post-obstructive diuresis.

Stem 8 — HRS: Cirrhotic with ascites, SCr 2.5 unchanged after albumin and diuretic withdrawal, bland UA, FENa < 1%. → HRS-AKI; albumin + terlipressin; refer for transplant.

Stem 9 — RPGN: 60-year-old with hemoptysis, AKI, dysmorphic RBCs, positive p-ANCA. → MPA / ANCA vasculitis; urgent biopsy, high-dose steroids + cyclophosphamide or rituximab; plasmapheresis if severe.

Stem 10 — Hyperkalemia code: AKI patient with K 7.0 and peaked T-waves. → IV calcium gluconate first, then insulin/D50, albuterol, loop diuretic; emergent dialysis if refractory.

One-Line Recap

AKI is defined by KDIGO as a ≥ 0.3 mg/dL rise in creatinine within 48 h, a ≥ 1.5× rise from baseline within 7 days, or UOP < 0.5 mL/kg/h ≥ 6 h — and every workup must systematically distinguish pre-renal, intrinsic, and post-renal etiologies through volume assessment, urinalysis with microscopy, urine electrolytes, and renal ultrasound, while emergent dialysis is reserved for the AEIOU indications.

Board pearl: AKI doubles the risk of CKD and triples the risk of ESRD — recovery from the index event does not erase long-term cardiovascular and renal risk.

Step 3 management: Discharge orders for any AKI patient should always include a medication reconciliation, scheduled BMP within 1–2 weeks, follow-up appointment, and 3-month renal reassessment.

KDIGO staging in one breath: Stage 1 = 1.5–1.9× or +0.3 mg/dL; Stage 2 = 2.0–2.9×; Stage 3 = ≥ 3× or SCr ≥ 4.0 or RRT initiation.

The three-bucket workup: Volume status + UA with sediment + FENa/FEUrea + renal US covers > 90% of cases; layer on serologies, SPEP/UPEP, and biopsy when intrinsic etiology is unclear.

Five non-negotiable bundle items on every AKI patient: Stop nephrotoxins, renal-dose all meds, strict I/Os with daily weights, daily BMP, and reassess volume status with each intervention.

AEIOU dialysis triggers: Acidosis refractory, Electrolytes (K) refractory, Ingestions (MEAL-MMT: methanol, ethylene glycol, ASA, lithium, metformin/MgSO4, theophylline), Overload refractory, Uremia symptomatic.

Post-AKI long game: Recheck SCr + UA + urine ACR at 3 months, restart RAAS blockade and SGLT2 inhibitors cautiously when stable, counsel "sick day rules," avoid NSAIDs lifelong, and arrange nephrology follow-up if eGFR stays < 60 or proteinuria persists.