For years, medicine has followed a simple rule that is easy to understand even without a medical degree. In heart failure, salt is the enemy. It retains water. It increases edema. It worsens shortness of breath. If the heart cannot cope with pumping blood, the body already tends to store fluids—so why add sodium, which is physiologically bound to water in the body? It seems logical. And yet, logic in biology can be surprising.

A team from Wroclaw Medical University, led by Professor Jan Biegus, published a study in 2025 in the European Journal of Heart Failure that demonstrates an interesting and important mechanism related to sodium chloride. In acute heart failure, not only the amount of water is the problem, but also the signals that the kidneys interpret as a threat. Sometimes these signals can be reversed. Put simply, under appropriate conditions, in selected patients, and in a controlled manner, intravenous saline administration may paradoxically help eliminate excess fluid more quickly. It sounds surprising—but only until we understand how the kidneys work and their “survival mechanism.”

Heart failure and fluid dynamics

Acute heart failure is a condition in which a patient is usually admitted to the hospital with dyspnea and edema. Fluid accumulates in the lungs, and the legs become swollen. The body becomes heavier—literally and metaphorically. The most important short-term goal of treatment is to eliminate excess fluid. The standard therapy consists of loop diuretics, most commonly furosemide. These are drugs that force the kidneys to excrete large volumes of urine. And this is where the problem begins.

Diuretics do not act like a magic sponge, squeezing water out of the entire body. The kidneys filter blood and remove fluid mainly from the intravascular space, that is, the blood that circulates within the vessels. If the body does not replenish this volume by shifting fluid from the tissues into the bloodstream, a situation may arise in which the patient remains fluid-overloaded—for example, edema persists—while the vessels become relatively depleted. It is somewhat like drying a flooded house using pumps that work only in one room. If water from other rooms does not flow in quickly enough, the pumps may remove too much from the area where they are operating.

There is, however, a second and even more important mechanism. Loop diuretics remove water by inhibiting sodium reabsorption. This is the key to understanding sodium-based mechanisms. Water in the body does not travel alone—it follows electrolytes. And in this journey, sodium is the main protagonist.

Podcast: The salt paradox in heart failure

Click here to listen to the podcast!

The kidneys do not like losing sodium

When a diuretic begins to work, the patient produces liters of urine. Along with water, sodium and chloride are also excreted. The body may interpret this as an alarm signal. The kidneys then activate sodium-conserving mechanisms to prevent further loss of this electrolyte. In medicine, this state is referred to as “sodium avidity.” This is the moment when treatment begins to resemble a tug-of-war. The physician tries to remove fluid, while the body does everything it can to retain it.

This paradox was the starting point for the team from Wroclaw. As Professor Biegus explains:

-The obtained results may be perceived as surprising, because to some extent they challenge the commonly accepted understanding of how congestion in heart failure should be treated. However, based on previous data, we assumed that such results were possible. For this reason, the study was designed and conducted to verify this hypothesis, using a study of the highest quality—prospective and randomized.

dr hab. n. med., prof. UMW Jan Biegus, Instytut chorób serca, Uniwersytet Medyczny we Wrocławiu

dr hab. n. med., prof. UMW Jan Biegus, Instytut chorób serca, Uniwersytet Medyczny we Wrocławiu

In simple terms, congestion in heart failure—manifesting for the patient as edema and additional kilograms on the scale—is merely the accumulation of water and salt. For years, a common-sense approach dominated: remove excess fluid and sodium with diuretics and restrict salt and fluid intake. Professor Biegus describes it directly:

-In the simplest terms, congestion means the accumulation of water and sodium chloride in the body. The classical therapeutic approach has been based on the assumption that this excess should be removed by using diuretics that increase urinary excretion by the kidneys, as well as by restricting fluid and sodium intake. Consequently, the administration of sodium chloride was by definition considered an inappropriate intervention.

The team, however, posed a surprisingly simple question. What if the problem is not just the water itself, but the signal of sodium loss? What if, at a certain point, the kidney ‘reads’ the therapy as a threat and begins to act defensively?

This brings us to the core of the matter. Gracjan Iwanek, MD, a co-author of the publication, explains the mechanism as follows:

-Paradoxically, it turns out that proper kidney function requires the presence of sodium—it is precisely sodium that enables effective urine production and excretion, and thus efficient elimination of NaCl. In a state of sodium deficiency, the kidney, through mechanisms that are not fully understood, interprets this as a threat to homeostasis, which leads to inhibition of diuresis and the production of low-quality urine.

That is why the study employed a solution that, at first glance, seems counterintuitive. During intensive decongestion, patients received a controlled intravenous saline infusion. As Professor Biegus summarizes:

-In our study, while ‘forcing’ the kidney to produce urine, we administered sodium chloride as a catalyst of this process. Contrary to previous beliefs, this approach proved highly beneficial. The kidney produced larger volumes of high-quality urine.

Salt versus glucose

The study was mechanistic, meaning that the investigators were interested not only in whether patients produced more urine, but also in why this occurred.

Fifty patients with acute heart failure and marked fluid overload were enrolled in the study: edema extending at least to the knees and high NT-proBNP levels. All patients were treated with furosemide according to a standardized protocol.

Patients were randomly assigned to two groups that received the same volume of fluid intravenously at a constant rate of 2 liters per day for 48 hours.

The difference was as follows:

one group received 0.9% NaCl (standard saline),
the other group received 5% glucose (isotonic, but without sodium).

This was a clever comparison, because both solutions are isotonic. From the perspective of volume alone, the body receives a similar stimulus. The only key differentiating factors are sodium and chloride.

After 48 hours, the differences were clear. Patients receiving NaCl produced more urine.

First day: approximately 4.8 liters versus 3.5 liters
Second day: approximately 4.4 liters versus 3.6 liters
Total over 48 hours: approximately 9.5 liters versus 7.4 liters

This means that the NaCl group achieved about 2 liters of additional diuresis over two days. What is even more interesting is that this result was achieved with a lower dose of furosemide.

What happens in the kidneys

The authors did not stop at counting urine volume. They also examined how the kidneys handled sodium at different segments of the renal tubule. This is a technical aspect that can be translated into a simpler image.

The nephron in the kidney functions like a system of filters and conveyor belts that determine what remains in the body and what is excreted. The largest proportion of sodium is reabsorbed at the beginning of this system, in the proximal tubule. The Wroclaw team used an index based on lithium excretion (fractional excretion of lithium, FeLi) to assess the amount of sodium reabsorbed in this first segment.

The results showed that in the chloride group, the kidneys reabsorbed less sodium in the proximal tubule. This meant that more sodium passed downstream and was ultimately excreted.

Importantly, the distal segments of the nephron did not fully compensate for this effect; they did not activate compensatory mechanisms to a degree sufficient to negate it. This is exactly what would be expected if sodium administration reduces the alarm signal of sodium loss and weakens sodium-retaining mechanisms.

The authors also measured neurohormones. One result stood out in particular: aldosterone levels were lower in the NaCl group after 48 hours. Aldosterone is a hormone that promotes sodium retention and, with it, water retention. When aldosterone levels are high, the body becomes conservative. When they fall, it is easier to eliminate sodium and fluid. This is another piece of the same puzzle. The sodium chloride solution did not act like pouring water into an already full bathtub, but rather like adjusting the regulator that signals to the kidneys that they no longer need to panic.

Does this mean that patients with heart failure should be given salt?

No. And the authors state this explicitly. This was a small, single-center, mechanistic study. The protocol involving 2 liters of infusion per day was designed for scientific purposes, not as a ready-to-use recipe for everyday clinical practice. Not every patient with heart failure tolerates such fluid volumes. In real-world practice, physicians individualize both the rate and the amount of therapy.

-Of course, caution is required in patients with extreme serum sodium—and likely chloride—levels. Uncontrolled administration of sodium chloride is not indicated in such situations, although it should be emphasized that in our study, we administered 0.9% NaCl in a very controlled manner, - Professor Biegus stresses.

The point is not that salt is good or bad. The point is that in acute heart failure, the body is in a state in which the kidneys behave differently than intuition would suggest. There are likely patients who may benefit from NaCl supplementation, but there are also patient profiles for whom it may not help or may even be harmful.

Recently, several studies have shown that the simplistic thinking ‘the less salt, the better’ is simply wrong and may actually harm patients. I think attitudes toward NaCl will change in the near future,” comments Professor Biegus.

Under certain conditions, a diuretic can itself create a problem that limits its effectiveness: a relative sodium deficiency that signals sodium conservation. And then, paradoxically, controlled sodium supplementation may facilitate further decongestion.

The results proved stimulating enough to spark lively and substantive scientific discussion, as evidenced by four letters published in the journal.

A change in guidelines

What is most interesting in science is that sometimes it does not provide new drugs, but a new way of thinking.

The study from Wroclaw Medical University shows that treating acute heart failure is not a simple equation in which less fluid always leads to better outcomes. It is rather a game with a regulatory system that defends the body against resource loss.

-I think our study is another element that fits into a very coherent and logical whole, and that taking into account all available data will lead to an evolution in our understanding of the role of NaCl in heart failure,- summarizes the researcher from the Institute of Heart Diseases at the University Clinical Hospital in Wroclaw.

If we want to remove excess fluid effectively, we must understand when the kidneys cooperate and when they resist.

In a sense, the Wroclaw team reminded us that there are no simple prohibitions or commandments in the human body. There are mechanisms designed to ensure survival, and sometimes they must be bypassed not by force, but by ingenuity. Sometimes, to remove excess fluid more effectively, one must do something that at first glance looks like a mistake—add a small amount of salt. Not to retain water, but to stop the kidneys from protecting it in panic.

D. Sikora

Photo by Nick Fewings on Unsplash

FAQ: Paradoks soli w niewydolności serca

What was the main objective of the SOLVRED-AHF study?

The main objective of this prospective, randomized study was to challenge the long-standing paradigm that sodium and chloride restriction are essential for effective decongestion in acute heart failure (AHF). The investigators aimed to determine whether NaCl supplementation during diuretic therapy would improve the effectiveness of excess fluid removal compared with volume infusion without sodium.

Which specific solutions were compared in the study?

The study compared two isotonic infusion strategies administered at a constant rate of 83.3 ml/h (a total of 2 liters per day) for 48 hours: 0.9% NaCl solution (providing intravascular volume expansion and sodium and chloride) and 5% glucose solution (providing volume expansion only). Both interventions were added to a standardized furosemide treatment protocol.

Which group of patients achieved better urine output?

Patients in the NaCl group achieved significantly higher diuresis than patients in the glucose group. The median cumulative urine volume after 48 hours was 9,500 ml in the NaCl group compared with 7,395 ml in the glucose group (p = 0.001).

How did NaCl supplementation affect the need for diuretics (furosemide)?

The improved decongestive effect in the NaCl group was achieved with significantly lower furosemide doses. The median cumulative dose after 48 hours was 220 mg in the NaCl group, compared with 280 mg in the glucose group (p = 0.02).

What physiological mechanism explains the greater effectiveness of the NaCl infusion?

The key mechanism was inhibition of sodium reabsorption in the proximal renal tubule, as evidenced by higher lithium fractional excretion in the NaCl group. In addition, saline infusion prevented a decline in serum sodium concentration, which may have suppressed “sodium hunger” signals (sodium avidity) that normally limit diuretic effectiveness.

Were differences observed in hormone levels affecting water and sodium balance?

Yes. The NaCl group had significantly lower serum aldosterone levels after 48 hours of treatment than the glucose group (6.2 vs 14.1 pg/mL). This suggests that sodium administration helps suppress hormonal mechanisms responsible for sodium retention.

Did the study results translate into a shorter hospital stay?

Yes. Clinical analysis showed that hospital length of stay was significantly shorter in the NaCl group. The median hospitalization duration was 11 days in the NaCl group, compared with 15 days in the glucose group (p = 0.038).

What are the most important conclusions of the study for the traditional approach to heart failure treatment?

The SOLVRED-AHF study challenges the dogma of strict sodium restriction in patients with congestive heart failure. The results suggest that, paradoxically, sodium administration may facilitate its excretion and increase urine output by preventing activation of renal defense mechanisms against dehydration and salt loss.

Powerd by NotebookLM