Renal: Congestive heart failure and diuretics

Congestive heart failure (CHF) is caused by the inability of the heart to pump blood and maintain proper blood flow throughout the body. As a result of poor pumping action, blood can pool in various areas of the body, and excess extracellular fluid (ECF) accumulates in the areas where the blood pools. The accumulation of excess ECF can occur in various parts of the body, depending on which chambers of the heart are not pumping effectively.

Treatment of generalized edema primarily relies on the administration of natriuretic agents, or diuretics, that diminish sodium reabsorption at different sites in the nephron, thereby increasing urinary sodium and water losses. However, the effectiveness of diuretics can be compromised by chronic renal failure (CRF), which is a distinct medical condition but can often be linked to CHF through a complex interplay of hemodynamic changes and shared risk factors.

The following experiments were conducted to examine the effectiveness of diuretics in patients with CHF plus or minus comorbid CRF.

Researchers measured the effectiveness of various modes of delivery of furosemide, a loop diuretic that blocks the Na–K–2Cl symporter in the loop of Henle, preventing the active transport of these ions into the interstitium. They compared a group of patients receiving continuous intravenous doses of furosemide to patients receiving intermittent oral doses of furosemide. For each patient, researchers measured the amount of Na+ in the urine per hour.

Figure 1 Urinary sodium measurement in patients receiving continuous (intravenous) vs. intermittent (oral) doses of furosemide

Researchers examined sodium excretion versus the diuretic concentration in normal patients as well as patients with CHF or CRF. They constructed dose–response curves for loop diuretics illustrating the fractional Na excretion (FENa) as a function of loop diuretic urine concentration for all patient groups.

Figure 2 Dose–response curves for three patient groups