Cardiorenal Acute Kidney Injury

Cardiorenal acute kidney injury is acute kidney injury caused by acute cardiac dysfunction, classically acute decompensated heart failure or cardiogenic shock. It is also termed acute cardiorenal syndrome. It occurs in 20% to 40% of admissions for acute heart failure and independently predicts longer admission, readmission and mortality.

Haemodynamic mechanisms dominate:

• Venous congestion: raised central venous pressure (above 8 to 10 mmHg) transmits to renal veins, raises interstitial and tubular pressures and lowers the net filtration gradient. Congestion is more strongly associated with renal impairment than low cardiac output
• Low cardiac output: reduced renal perfusion pressure and flow in cardiogenic shock
• Neurohormonal activation: sympathetic, renin-angiotensin-aldosterone and vasopressin axes cause vasoconstriction and sodium retention
• Intra-abdominal hypertension from ascites and gut oedema
• Drug effects: ACE inhibitors, angiotensin receptor blockers, NSAIDs, aggressive diuresis, contrast, inotropes

An increase in creatinine during effective decongestion, with falling congestion and stable or improving clinical status, has no adverse prognosis and should not stop treatment. Worsening creatinine with persistent congestion or hypotension carries a poor prognosis.

• Dyspnoea, orthopnoea, oedema, weight gain, reduced exercise tolerance
• Elevated jugular venous pressure, third heart sound, bibasal crackles, hepatomegaly, ascites
• Low output state: cool peripheries, narrow pulse pressure, confusion, oliguria, lactate above 2 mmol/L
• Hyponatraemia, hyperkalaemia and metabolic acidosis in advanced disease
• Triggers: acute coronary syndrome, arrhythmia (atrial fibrillation with rapid rate), uncontrolled hypertension, infection, non-adherence, valvular disease, NSAIDs, anaemia, thyroid disease

Red flags: systolic pressure below 90 mmHg, lactate above 4 mmol/L, oliguria below 0.3 mL/kg/h, potassium above 6.0 mmol/L, pulmonary oedema with hypoxia (saturation below 90%), ventricular arrhythmia.

• Creatinine, urea, electrolytes, bicarbonate, magnesium, lactate, liver tests, troponin
• NT-proBNP above 300 pg/mL or BNP above 100 pg/mL supports heart failure (higher in renal impairment, NT-proBNP above 1000 pg/mL)
• Echocardiography: ejection fraction, valvular disease, right ventricular function, tricuspid regurgitation, inferior vena cava size (above 2.1 cm with less than 50% collapse)
• Chest radiograph or lung ultrasound (B-lines)
• Doppler of intrarenal veins: discontinuous or biphasic flow indicates congestion
• Natriuresis response: spot urine sodium below 50 to 70 mmol/L at 2 hours after a loop diuretic dose, or urine volume below 100 to 150 mL/h over the first 6 hours, indicates inadequate diuretic response
• Renal ultrasound to exclude obstruction and renal artery disease

Differentials: sepsis, hypovolaemia (over diuresis), obstruction, renal artery stenosis with ACE inhibitor, acute tubular injury, hepatorenal syndrome, contrast injury.

Decongestion

• Loop diuretic intravenous bolus: furosemide 40 to 80 mg in diuretic naive patients; for patients on oral diuretics give an intravenous dose equal to 2 to 2.5 times the total daily oral furosemide dose. Assess natriuresis at 2 hours and urine volume at 6 hours; double the dose if inadequate (up to 200 mg in a single bolus).
• Infusion furosemide 5 to 40 mg/h after the bolus for sustained effect, and monitor for ototoxicity when the daily total exceeds 600 mg.
• Sequential nephron blockade for resistance: acetazolamide 500 mg intravenously, metolazone 2.5 to 10 mg orally, or hydrochlorothiazide 25 to 50 mg; spironolactone 25 to 50 mg daily; monitor sodium and potassium every 12 hours.
• Target net negative balance 2 to 3 L daily or weight loss of 0.5 to 1 kg daily, continued until congestion resolves even if creatinine rises.

Haemodynamic support

• Vasodilators when systolic pressure is above 110 mmHg: glyceryl trinitrate infusion 10 to 200 microg/min.
• Low output with hypotension: dobutamine 2.5 to 10 microg/kg/min, noradrenaline for shock, mechanical circulatory support in refractory shock.
• Treat arrhythmia, ischaemia, valvular disease and infection.

Drugs

• Hold ACE inhibitors, angiotensin receptor blockers and mineralocorticoid antagonists during hypotension or potassium above 6.0 mmol/L; restart at the lowest dose once stable.
• Avoid NSAIDs, nephrotoxins and thiazolidinediones.
• Start an SGLT2 inhibitor (dapagliflozin 10 mg daily with eGFR at least 25, or empagliflozin 10 mg daily with eGFR at least 20 mL/min/1.73 m2) once stable.

Renal replacement therapy. Ultrafiltration or haemodialysis for fluid overload refractory to maximal diuretics, hyperkalaemia, acidosis or uraemia; net ultrafiltration rate no more than 10 to 13 mL/kg/h.

Monitoring. Daily weight, hourly urine output in the first 24 hours, electrolytes every 12 hours during diuresis, and creatinine daily.

Refer to cardiology for all patients; to nephrology when creatinine continues to rise despite decongestion or renal replacement is considered.