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Andrew Higgins, W H Wilson Tang, Carbohydrate antigen 125 in heart failure: congestive kidneys or beyond?, European Heart Journal. Acute Cardiovascular Care, Volume 10, Issue 5, May 2021, Pages 484–486, https://doi.org/10.1093/ehjacc/zuab027
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Despite improvement in primary and secondary prevention, heart failure (HF) admissions continue to increase internationally.1,2 Though congestive symptoms are the most common cause for hospitalization, many patients are discharged with residual evidence of congestion, which has been associated with both higher readmission and mortality rates.3,4 Unfortunately, though the recent introduction of multiple promising new therapeutic modalities for HF including soluble guanylate cyclase and sodium-glucose cotransporter 2 inhibition continues to expand our therapeutic armamentarium, our diagnostic tools for identifying high-risk congestive phenotypes or residual congestion have made little progress in the past several decades: like prior generations, we rely on a combination of physical examination, clinical gestalt, and trial-and-error diuretic therapy coupled with serial monitoring of weight and renal function.5,6 Systemic congestion with congestive nephropathy presents a particular challenge, as providers often walk a fine line between ensuring adequate decongestion and precipitating over-diuresis with ensuant worsening renal dysfunction.
Identifying and quantitating renal congestion has historically relied on markers of systemic venous pressure via bedside evaluation of the jugular venous pressure or by inferring right atrial pressure based on the inferior vena caval diameter and its respirophasic variations.7 These techniques have well-known limitations, including challenges posed by body habitus or confounding by significant tricuspid regurgitation. Though originally described in patients with primary urologic issues, more recent work has demonstrated the utility of pulsed wave Doppler assessment of parenchymal intrarenal venous flow (IRVF) in identifying renal congestion.8 Physiologic IRVF should be in continuous flow (see Figure 1); Iida et al. demonstrated the emergence of discontinuous venous flow patterns in patients with a higher right atrial pressure, with the highest right atrial pressures being associated with a monophasic flow pattern. Patients with discontinuous flow patterns suggestive of congestion were found to have higher rates of cardiovascular death and HF hospitalizations.9 Notably, abnormal IRVF appears to be reversible with decongestive therapy.10
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