Abstract
Cardiorenal syndrome (CRS) describes the reciprocally detrimental interaction between both acute and chronic cardiac and renal dysfunction. The syndrome is prevalent and carries a high mortality. CRS has five clinical subtypes, which share common pathogenetic mechanisms including neurohumoral and haemodynamic derangements. We describe several serum markers that offer improvements over traditional measurement of serum creatinine for the diagnosis of CRS. The mainstay of therapy of CRS is loop diuretics in the acute setting and ACE-inhibition in the chronic setting, the latter should in most cases continue despite therapy-associated increases in creatinine. Extracorporeal therapies remain second line treatment.
Highlights
Cardiorenal syndrome (CRS) refers to the increasingly recognised reciprocal association between cardiac and renal dysfunction, whereby injury to one organ directly promotes deterioration of the other
We describe several serum markers that offer improvements over traditional measurement of serum creatinine for the diagnosis of CRS
The mainstay of therapy of CRS is loop diuretics in the acute setting and angiotensin converting enzyme (ACE)-inhibition in the chronic setting, the latter should in most cases continue despite therapy-associated increases in creatinine
Summary
Cardiorenal syndrome (CRS) describes the reciprocally detrimental interaction between both acute and chronic cardiac and renal dysfunction. The syndrome is prevalent and carries a high mortality. CRS has five clinical subtypes, which share common pathogenetic mechanisms including neurohumoral and haemodynamic derangements. We describe several serum markers that offer improvements over traditional measurement of serum creatinine for the diagnosis of CRS. The mainstay of therapy of CRS is loop diuretics in the acute setting and ACE-inhibition in the chronic setting, the latter should in most cases continue despite therapy-associated increases in creatinine.
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