Cardiorenal Syndrome

Cardiorenal syndrome (CRS) is a spectrum of disorders in which acute or chronic dysfunction of the heart or kidney induces dysfunction in the other.

• Type 1 (acute cardiorenal): acute heart failure or cardiogenic shock causing AKI (occurs in 25 to 33% of acute decompensated heart failure).
• Type 2 (chronic cardiorenal): chronic heart failure causing progressive CKD.
• Type 3 (acute renocardiac): AKI causing acute cardiac dysfunction (volume overload, hyperkalaemia, acidosis).
• Type 4 (chronic renocardiac): CKD causing cardiovascular disease and heart failure.
• Type 5 (secondary): systemic disease (sepsis, diabetes, amyloidosis, lupus) affecting both organs.
• Mechanisms: venous congestion and raised central venous pressure (the dominant driver), low cardiac output, neurohormonal activation, inflammation, anaemia, diuretic resistance.
• Worsening renal function is associated with higher mortality and hospitalisation.

• Dyspnoea, orthopnoea, peripheral oedema, weight gain, raised jugular venous pressure, ascites, hepatic congestion.
• Declining urine output, rising creatinine, hyperkalaemia, hyponatraemia, diuretic resistance.
• Cold extremities and hypotension in low output states.
• Oedema with proteinuria in intrinsic kidney disease.

• Creatinine, eGFR, urea, electrolytes, NT proBNP (interpret with reduced clearance), troponin, urine albumin/creatinine, liver tests, lactate.
• Echocardiography: ejection fraction, filling pressures, right ventricular function, IVC distension, valvular disease.
• Venous congestion assessment: jugular venous pressure, hepatic and portal vein Doppler, VExUS score, lung ultrasound.
• Right heart catheterisation in uncertain haemodynamics: elevated central venous pressure (over 10 to 15 mmHg), low cardiac index.
• Urine sodium 2 hours after furosemide (below 50 to 70 mmol/L indicates diuretic resistance); urine output.
• Exclude obstruction, intrinsic renal disease, contrast and drug effects.

• Decongestion is the priority:
  • Loop diuretics: furosemide 40 to 80 mg IV (or twice the oral daily dose), boluses or infusion 10 to 40 mg/h; torsemide or bumetanide with better bioavailability.
  • Sequential nephron blockade for resistance: add metolazone 2.5 to 10 mg, chlorthalidone 12.5 to 50 mg, or acetazolamide 250 to 500 mg IV; SGLT2 inhibitor (empagliflozin 10 mg, dapagliflozin 10 mg) enhances natriuresis; spironolactone 25 to 50 mg.
  • Ultrafiltration for refractory congestion; hypertonic saline with furosemide in selected patients.
• Low-output states: inotropes (dobutamine 2.5 to 10 micrograms/kg/min, milrinone 0.25 to 0.5), vasodilators if blood pressure allows, mechanical support.
• Continue guideline-directed therapy where feasible: ACE inhibitor/ARNI, beta blocker, MRA, SGLT2 inhibitor; a creatinine rise up to 30% during decongestion is acceptable and not an indication to stop therapy, but hold for hypotension, hyperkalaemia over 5.5, or severe AKI.
• Avoid nephrotoxins and NSAIDs; correct anaemia and iron deficiency (IV ferric carboxymaltose 500 to 1000 mg).
• Renal replacement therapy for refractory overload, acidosis, hyperkalaemia, uraemia.
• Manage hyperkalaemia with potassium binders to enable RAAS inhibition (patiromer 8.4 g, sodium zirconium cyclosilicate 10 g).
• Treat arrhythmia, valvular disease, revascularise ischaemia, and consider device therapy (CRT, ICD).
• Advanced disease: LVAD, transplantation, combined heart-kidney transplantation, palliative care.