Congestive nephropathy: a neglected entity? Proposal for diagnostic criteria and future perspectives

Abstract

Venous congestion has emerged as an important cause of renal dysfunction in patients with cardiorenal syndrome. However, only limited progress has been made in differentiating this haemodynamic phenotype of renal dysfunction, because of a significant overlap with pre-existing renal impairment due to long-term hypertension, diabetes, and renovascular disease. We propose congestive nephropathy (CN) as this neglected clinical entity. CN is a potentially reversible subtype of renal dysfunction associated with declining renal venous outflow and progressively increasing renal interstitial pressure. Venous congestion may lead to a vicious cycle of hormonal activation, increased intra-abdominal pressure, excessive renal tubular sodium reabsorption, and volume overload, leading to further right ventricular (RV) stress. Ultimately, renal replacement therapy may be required to relieve diuretic-resistant congestion. Effective decongestion could preserve or improve renal function. Congestive acute kidney injury may not be associated with cellular damage, and complete renal function restoration may be a confirmatory diagnostic criterion. In contrast, a persistently low renal perfusion pressure might induce renal dysfunction and histopathological lesions with time. Thus, urinary markers may differ. CN is mostly seen in biventricular heart failure but may also occur secondary to pulmonary arterial hypertension and elevated intra-abdominal pressure. An increase in central venous pressure to >6 mmHg is associated with a steep decrease in glomerular filtration rate. However, the central venous pressure range that can provide an optimal balance of RV and renal function remains to be determined. We propose criteria to identify cardiorenal syndrome subgroups likely to benefit from decongestive or pulmonary hypertension-specific therapies and suggest areas for future research.

Keywords: Cardiorenal syndromes; Heart failure; Intra-abdominal hypertension; Pulmonary hypertension; Venous congestion.

Figure 1

Congestive nephropathy in pulmonary arterial hypertension and heart failure. Various factors and co‐morbidities related to renal dysfunction appear frequently in patients with PAH and HF. HFpEF, heart failure with preserved ejection fraction; HFrEF, heart failure with reduced ejection fraction; LV, left ventricular; PAH, pulmonary arterial hypertension; PH, pulmonary hypertension; RRI, renal resistance index; RV, right ventricular.

Figure 2

Venous congestion and glomerular haemodynamics. Renal venous congestion caused by intravascular congestion or an increase in intra‐abdominal pressure can lead to a build‐up of renal interstitial hydrostatic pressure through peritubular capillary congestion and development of interstitial oedema. This presumably leads to increased efferent arteriolar pressure, which may initially result in glomerular hyperfiltration; however, further increases in renal venous pressure with decreases in renal perfusion pressure ultimately reduce glomerular filtration rate.