Hospital Medicine Unplugged

Cardiorenal Syndrome in the Hospitalized Patient: Targeting Venous Congestion and Pseudo-AKI with the VeXUS Protocol


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In this episode of Hospital Medicine Unplugged, we blitz cardiorenal syndrome (CRS)—define fast, subtype smart, decongest early, protect kidneys, and tighten the cardio–nephro handshake.

We start with the frame: CRS = bidirectional heart–kidney dysfunction where trouble in one organ triggers or worsens the other. Know the five plays: Type 1 (acute cardiorenal), Type 2 (chronic cardiorenal), Type 3 (acute renocardiac), Type 4 (chronic renocardiac), Type 5 (secondary/systemic). Classification isn’t trivia—it drives workup and therapy.

Pathophys in one breath: venous congestion > low forward flow; RAAS/SNS surge, vasopressin, inflammation & endothelial dysfunction; sodium avidity → diuretic resistance. CKD stacks the deck toward higher mortality and rehospitalization.

Bedside diagnosis—do-firsts and don’t-miss:

• History + trend the eGFR, meds, and prior decompensations.
• UA + urine sediment to rule intrinsic renal disease; check albuminuria/proteinuria.
• BNP/NT-proBNP, Cystatin C for risk; watch electrolytes, BUN/Cr.
• TTE for LV/RV function and filling pressures; consider renal US/Doppler and VeXUS POCUS for systemic congestion; CMR selectively.
• True AKI vs pseudo-AKI: a small creatinine rise during effective diuresis can reflect hemoconcentration, not injury—don’t abort decongestion if the patient is clinically improving.

Risk & admit cues: refractory hypoxemia, rising JVP/edema, oliguria, shock/low MAP, refractory hyperK/acidosis, suspected Type 1 or 3 CRS, or diagnostic uncertainty.

Treatment—make decongestion the north star:

• First-line: IV loop diuretic (adequate dose & frequency) with daily weights, I/O, urine Na, and electrolyte/renal panels. Aim for complete decongestion.
• If resistance hits: sequential nephron blockade (add thiazide-type), consider MRA when safe, and natriuresis-guided up-titration.
• Vasodilators/afterload reduction for high filling pressures with preserved BP; inotropes for low-output states or shock—short and targeted.
• SGLT2 inhibitors & RAAS blockade: recommended in HF; initiate/continue with renal vigilance and pause only for hypotension, hyperK, or true AKI.
• Refractory congestion: ultrafiltration, peritoneal dialysis, or acute RRT—select carefully and match removal rate to plasma refill.
• Devices: consider CRT for dyssynchrony and mechanical circulatory support in advanced cases—heart help can be kidney help.

Monitoring that matters:

• Trend congestion (exam, weights, VeXUS, echo signs), urine output/Na, and CR/BUN/electrolytes.
• Expect and accept permissive creatinine bumps if hemodynamics and volume status are improving.
• Reassess daily: diuretic plan, RAAS/SGLT2 status, K/Mg, and hemodynamics (noninvasive first; invasive if shock/ambiguity).

Etiology threads—treat the cause:

• Sepsis (Type 5): source control + hemodynamics.
• Renal-first hits (Type 3/4): correct nephrotoxins, ischemia, or GN; manage afterload/arrhythmias.
• Cardiac-first (Type 1/2): guideline-directed HF therapy with congestion-first strategy.

Pitfalls to dodge: underdosing loops, stopping diuresis for mild Cr rise, ignoring RV failure/venous hypertension, delayed escalation to combo diuretics/UF, and premature RAAS/SGLT2 withdrawal without a clear reason.

We close with the hospital CRS bundle that sticks:

  1. Classify type (1–5) and rule intrinsic kidney disease (UA/sediment, albuminuria, renal US).

  2. Default to loop + natriuresis-guided titration; add thiazide-type early for resistance; consider MRA.

  3. Track congestion multimodally (exam + weights + VeXUS ± TTE).

  4. Guard rails: daily labs, K/Mg repletion, renal & hemodynamic checks.

  5. RAAS/SGLT2 smart use—continue/initiate when safe; hold for hypotension, hyperK, true AKI.

  6. Escalation pathway: UF/RRT for refractory overload or life-threatening derangements; CRT/MCS in select HF.

  7. Team sport: cardiology + nephrology + ICU/pharmacy from day one; discharge with diuretic plan, labs, and early follow-up.

    Bottom line: Congestion kills kidneys—decongest completely, use RAAS/SGLT2 wisely, monitor like a hawk, and move fast together.

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    Hospital Medicine UnpluggedBy Roger Musa, MD