Kardiyorenal Sendrom

 

Among patients with HF who have an elevated serum creatinine and/or a reduced estimated GFR, it is important to distinguish between underlying kidney disease and impaired kidney function due to the cardiorenal syndrome (CRS). This distinction may be difficult and some patients have both underlying chronic kidney disease and CRS.

Findings suggestive of underlying kidney disease include significant proteinuria (usually more than 1000 mg/day), an active urine sediment with hematuria with or without pyuria or cellular casts, and/or small kidneys on radiologic evaluation. However, a normal urinalysis, which is typically present in CRS without underlying kidney disease, can also be seen in variety of renal diseases including nephrosclerosis and obstructive nephropathy.

HF is a cause of prerenal azotemia, although evidence suggests that worsening renal function due to HF is not solely related to reduced cardiac output and frequently occurs in the setting of volume overload

 

Measurement of the urine sodium concentration (UNa) may also be helpful. UNa is easily measurable and readily available. A UNa below 25 meq/L would be expected with HF, since renal perfusion is reduced with associated activation of the renin-angiotensin-aldosterone and sympathetic nervous systems, both of which promote sodium retention. However, higher UNa values may be seen with concurrent diuretic therapy if the measurement is made while the diuretic is still acting.

İdrar Sodyumu ve diüretik cevabı değerlendirilmesi

There is a mounting evidence suggesting that UNa profiling can predict short-term responsiveness to IV loop diuretics in patients with acute HF [24,25]. Low UNa concentration from spot and continuous urine collection samples are associated with diminished diuretic response, as well as increased risk of HF readmission and cardiovascular mortality [25-30]. Natriuretic response from a single dose of loop diuretic can be predicted rapidly from a spot urine sample collected one to two hours after dose of loop diuretic is administered [25]. Spot urinary sodium may thus allow clinicians to more rapidly interpret diuretic responsiveness, providing an opportunity to intervene if sodium content is low, prompting aggressive diuretic titration [24,31]. A position statement on use of diuretics in HF from the European Society of Cardiology (ESC) proposes a spot urine sodium content of <50 to 70 mEq/L after two hours, or an hourly urine output <100 to 150mL during the first six hours to identify a patient with insufficient diuretic response

Diuretics — Diuretics, typically beginning with a loop diuretic, are first-line therapy for managing volume overload in patients with HF as manifested by peripheral and/or pulmonary edema.

Among patients with decompensated HF, the best outcomes may occur with aggressive fluid removal even if associated with mild to moderate worsening of renal function. 

These findings provide support for the recommendation included in the 2013 American College of Cardiology/American Heart Association HF guidelines that the goal of diuretic therapy is to eliminate clinical evidence of fluid retention such as an elevated jugular venous pressure and peripheral edema [49]. The rapidity of diuresis can be slowed if the patient develops hypotension or worsening renal function. However, the goal of diuretic therapy is to eliminate fluid retention even if this leads to asymptomatic mild to moderate reductions in blood pressure or renal function.

Renin-angiotensin system antagonists

General effects — Angiotensin inhibition with an angiotensin converting enzyme (ACE) inhibitor, angiotensin receptor-neprilysin inhibitor (ARNI), or an angiotensin II receptor blocker (ARB) is a standard part of the therapy of HF with reduced ejection fraction, being associated with symptomatic improvement, reduced hospitalization for HF, and enhanced survival.

 

Sodium-glucose co-transporter 2 inhibitors — In patients with HFrEF, but not in patients with HFpEF, sodium-glucose co-transporter 2 (SGLT2) inhibitors reduce the risk of cardiovascular and kidney outcomes

Vasodilators — Intravenous vasodilators used in the treatment of acute decompensated HF include nitroglycerin and nitroprusside.

Inotropic drugs — Intravenous administration of inotropic (calcitropic) drugs, such as dobutamine, dopamine, and milrinone, has a role in the treatment of cardiogenic shock in a subset of patients with acute decompensated HF.

Ultrafiltration — Ultrafiltration refers to the removal of isotonic fluid from the venous compartment via filtration of plasma across a semipermeable membrane. In HF patients, ultrafiltration is most often considered in patients with acute decompensated HF and diuretic resistance and/or impaired renal function.