Hemodynamically, the kidney is at the heart of cardiorenal syndrome

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In heart failure, the heart and the kidneys share a rocky relationship. Cardiac dysfunction can heighten renal dysfunction and vice versa—appropriately dubbed “cardiorenal syndrome.”

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Although classically defined by a reduction in the glomerular filtration rate (GFR), 1 cardiorenal syndrome also encompasses complex neurohormonal, pharmacologic, and metabolic interactions affecting or affected by both glomerular and tubular function. Unfortunately, all of these maladaptive processes occur in heart failure and perpetuate a vicious circle of continued dual-organ dysfunction.

The central insult here is hemodynamic disarray from acute or chronic cardiac dysfunction, which can directly influence glomerular function. However, to understand the hemodynamic ramifications for glomerular function, we focus on the determinants of glomerular filtration.


The GFR is the rate of fluid flow between the glomerular capillaries and the Bowman capsule and is classically represented by the following equations 2:

GFR = K f × (P G – P B – π G + π B)

Kf = N × L p × S

Kf is the filtration constant, N the number of functional nephrons, L p the hydraulic conductivity of the glomerular capillary, S the filtration area, P G the hydrostatic pressure in the glomerular capillaries, P B the hydrostatic pressure in the Bowman capsule, and π G and π B the colloid osmotic pressures within the glomerular capillaries and Bowman space, respectively.

Based on this relationship, the GFR is reduced when P G is reduced in the setting of hypovolemia, hypotension, or renin-angiotensin system antagonist use or when P B is increased in the setting of elevated central venous pressure or elevated abdominal pressure—all common in heart failure. With this understanding, one would assume that strategies to increase P G (improve perfusion) and reduce P B (reduce congestion) might ameliorate ongoing renal dysfunction and improve the GFR in heart failure.

In this issue, Thind et al 3 highlight the impact of hemodynamic derangements in heart failure with acute cardiorenal syndrome and provide an overview of its treatment. They review the complex relationship between progressive cardiac failure translating into accelerated neurohormonal responses (increases in sympathetic nervous system and renin-angiotensin-aldosterone system activation) and the impact of increased central venous pressure on progressive renal dysfunction. They also provide an overview of efforts to mitigate cardiorenal syndrome, after careful appraisal of volume status, through diuretic-mediated decongestion with aggressive use of loop diuretics (either in isolation or in the form of sequential nephron blockade with a thiazide or acetazolamide), and they highlight the lingering uncertainty regarding inotrope use.


Returning to the GFR equation, it is clear that an imbalance in P G and P B can worsen glomerular function. Because cardiac dysfunction can lead to both venous congestion and decreased cardiac output, this leads to the question, “Of these, which is the more important driver of this imbalance and its effects on renal function?”

A compelling argument can be made for each side. On one hand, experiments over a half-century old in human models of venous congestion highlighted the profound impact of elevated venous pressure, which decreases electrolyte excretion (sodium included) and diminishes urine flow. 4,5 This has been replicated in more-contemporary decompensated heart failure cohorts in which worsening renal function was more closely associated with elevated central venous pressure rather than cardiac output. 6,7 On the other hand, early landmark experiments and more recent cohorts with heart failure have also shown that reductions in effective arterial blood volume, renal blood flow, and cardiac output are also associated with reductions in GFR. 5,8,9

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