In acute decompensated heart failure (ADHF), intestinal wall edema is common and markedly reduces the oral bioavailability of loop diuretics—particularly furosemide—by impairing absorption and delaying onset of action. For this reason, intravenous administration is preferred during the acute phase to ensure predictable and adequate natriuretic exposure until gut perfusion and absorption normalize (18, 19).

Loop diuretics such as furosemide are highly protein bound and rely on active secretion in the proximal tubule to reach their site of action. Hypoalbuminemia can reduce effective delivery by decreasing protein binding and increasing distribution volume (7, 20). Competition for tubular secretion from uremic toxins, metabolic acidosis in chronic kidney disease (CKD), or concomitant drugs may further limit excretion. Among these, nonsteroidal anti-inflammatory drugs (NSAIDs) are particularly relevant, as they not only compete for secretion but also reduce renal blood flow and blunt prostaglandin-mediated vasodilation.

In advanced HF, additional hemodynamic factors—low cardiac output (CO) and elevated central venous pressure (CVP)—further compromise renal perfusion and drug delivery. The combination of reduced renal blood flow and impaired proximal secretion directly limits the amount of loop diuretic reaching the thick ascending limb, thereby reducing pharmacologic efficacy (7, 9, 21).

Even when drug delivery is adequate, diuretic efficacy is often blunted by compensatory sodium reabsorption downstream. Chronic exposure to loop diuretics induces structural and functional changes in the distal nephron, including hypertrophy and hyperplasia of epithelial cells, upregulation of sodium-chloride cotransporters, and activation of the epithelial sodium channel (ENaC). In the nephrotic syndrome, urinary plasmin directly activates ENaC, explaining the efficacy of amiloride in resistant edema (11, 22).

These compensatory mechanisms contribute to the phenomenon of “long-term braking,” in which the distal nephron increases sodium avidity regardless of loop diuretic dosing, thereby shifting the dose–response relationship downward and to the right (7, 9, 11).

Loss of sodium and water after loop diuretic administration stimulates counter-regulatory activation of the renin–angiotensin–aldosterone system (RAAS) and the sympathetic nervous system (SNS). This response, often referred to as the “braking phenomenon,” enhances proximal sodium reabsorption, reduces glomerular filtration, and blunts the natriuretic effect. Clinically, this is reflected by a shift of the dose–response curve downward and to the right, meaning progressively higher doses are needed to achieve the same effect, until a “ceiling dose” is reached beyond which further escalation is ineffective (9, 11).

While the braking phenomenon is well established in experimental and healthy volunteer studies, its role in ADHF appears to be less prominent. In the Mechanisms of Diuretic Resistance cohort, patients receiving intravenous loop diuretics showed increased sodium excretion not only in the first 6 h after dosing but also at 18 h—without evidence of the expected “post-diuretic” sodium retention. Interestingly, those who had a greater initial natriuretic response tended to maintain higher sodium excretion over time.

These observations suggest that in acute HF (AHF), resistance is less about an immediate counter-regulatory “braking” effect and more about a chronically heightened sodium-retaining state of the kidneys—often termed “basal sodium avidity”. This reflects long-standing neurohormonal activation (RAAS, sympathetic stimulation, vasopressin release) and renal adaptation to volume overload, which together reinforce a sodium-retentive state within the nephron. Consequently, even when loop diuretic delivery is adequate, these patients may exhibit a blunted natriuretic response because the kidney is functionally “primed” to conserve sodium rather than excrete it (7, 20, 21).

Although sodium has traditionally been the focus in HF, recent evidence highlights chloride as a key determinant of diuretic response and prognosis. Hypochloremia, more than hyponatremia, is consistently associated with adverse outcomes and reduced diuretic efficiency. In both chronic and AHF cohorts, lower serum chloride correlates with impaired natriuresis despite adequate loop diuretic dosing, and post hoc analyses of the Renal Optimization Strategies Evaluation (ROSE) trial confirmed its strong prognostic value (23, 24).

Mechanistically, chloride regulates renal salt handling through its interaction with the With-no-Lysine kinases (WNK), intracellular sensors that control sodium transporters along the nephron. Low intracellular chloride activates these kinases, upregulating sodium–chloride reabsorption and counteracting the effects of loop and thiazide diuretics. Loop diuretics themselves can worsen hypochloremia, creating a vicious cycle of falling chloride, persistent neurohormonal activation, and declining therapeutic efficacy (24–27).

In addition, chloride depletion contributes to the development of metabolic alkalosis, historically termed “contraction alkalosis” but more accurately described as chloride-depletion alkalosis. In the absence of adequate luminal chloride, pendrin-mediated chloride–bicarbonate exchange in the collecting duct is impaired, perpetuating alkalemia and further reducing natriuretic responsiveness. Together, these mechanisms highlight chloride as both a mediator of resistance and a potential therapeutic target in HF (24, 26, 28).

RHF is characterized by the inability of the right ventricle to maintain adequate forward flow, resulting in systemic venous hypertension and congestion. In this phenotype, DR is particularly common and reflects a complex interplay of impaired renal perfusion, chronic loop diuretic exposure, venous hypertension, low cardiac output, hypotension, and acute kidney injury (36).

Elevated right-sided filling pressures compromise renal prefusion by increasing renal venous pressure, reducing the transrenal perfusion gradient and promoting renal and intestinal congestion that limits loop diuretic delivery. In advanced stages, impaired right-to-left ventricular coupling can cause left-sided underfilling and ultimately cardiogenic shock. Congestion is the predominant clinical feature and a principal driver of renal deterioration and multiorgan dysfunction (37–39). Hemodynamically, these patients exhibit marked preload dependence and afterload sensitivity of the right ventricle (RV). Adequate preload is necessary to preserve stroke volume through the Frank–Starling mechanism; however, excessive filling pressures rapidly translate into systemic venous hypertension, hepatic congestion, and renal stasis. Conversely, over-aggressive decongestion or ultrafiltration can lower RV output and LV filling, leading to systemic hypotension and renal hypoperfusion. Increases in pulmonary vascular resistance—due to hypoxia, acidosis, or vasoconstrictor use—further elevate RV afterload and impair forward flow. This delicate balance between maintaining adequate preload and avoiding excessive afterload defines the therapeutic challenge in managing decompensated RHF (37, 38, 40, 41).

The primary goal is to relieve congestion since elevated central venous pressure (CVP) remains a key finding and a major factor in CRS (42, 43). Loop diuretics are the cornerstone of treatment, but higher doses are often necessary, and using sequential nephron blockade with thiazides, metolazone, or acetazolamide may be beneficial (36, 40, 41). SGLT2i can also offer additional natriuresis and kidney protection, without significant hemodynamic effects (44). Decongestion should be prioritized even in the presence of borderline blood pressure, provided there is no evidence of hypoperfusion—such as cool extremities, rising lactate, altered mental status or a narrow pulse pressure. In such cases, inotropes/vasopressors can be used to maintain systemic perfusion and enable effective diuresis; these agents support decongestion but should not replace it (1, 3, 36, 40).

Because patients with RHF are highly preload dependent, therapy should aim to reduce venous congestion while preserving right ventricular preload to maintain forward flow. Excessive volume removal may precipitate hypotension, reduced cardiac output and “true” worsening renal function (WRF). Continuous monitoring of volume status, urine sodium and hemodynamics is essential to tailor therapy and prevent these complications (36, 38).

When impaired contractility is a major contributor, inotropic support can improve right ventricle–pulmonary artery coupling. The choice of agent depends on blood pressure, concomitant therapies, and renal function (36).

Dobutamine remains the most commonly used first-line inotrope. It has a rapid onset, a short half-life, and modest vasodilatory properties, making it suitable for patients with RV dysfunction and borderline hemodynamics. However, it can provoke tachyarrhythmias at higher doses and tolerance may develop during prolonged infusions. Milrinone, by contrast, exerts stronger pulmonary and systemic vasodilation, leading to greater reductions in filling pressures. It is often preferred in patients receiving chronic β-blocker therapy, as its mechanism bypasses adrenergic signaling. Tachycardia is less frequent than dobutamine, and tolerance is uncommon. On the downside, milrinone carries a higher risk of hypotension—especially with bolus dosing—owing to its long half-life and vasodilator effects. In such cases, concurrent vasopressor support may be necessary. Because it is partly renally cleared, dosing must be adjusted for kidney function (36, 40, 45). When pulmonary vasoconstriction predominates, therapy should prioritize afterload reduction—optimizing oxygenation and ventilation, correcting acidosis, and avoiding pure α-agonists that raise pulmonary vascular resistance (46, 47).

Levosimendan, a calcium sensitizer with additional vasodilatory effects, offers an attractive alternative to conventional adrenergic inotropes. Unlike catecholamines, it enhances contractility without increasing intracellular calcium or oxygen demand. In clinical studies, it has been associated with improved RV systolic performance, reduced pulmonary artery pressures, and greater diuretic responsiveness. Observational data suggest a neutral safety profile regarding mortality, in contrast to the signal of harm seen with chronic adrenergic inotrope use. Levosimendan can be used alone, but in hypotensive patients it is often combined with norepinephrine to maintain perfusion pressure. Some centers also employ it prophylactically in patients at high risk of RV dysfunction after left ventricular assist device (LVAD) implantation (48–50).

When hypotension dominates (mean arterial pressure <65 mmHg or systolic blood pressure <80–90 mmHg with hypoperfusion), the focus shifts to vasopressors. Norepinephrine is generally preferred, as it restores systemic pressure with limited chronotropic stimulation and can improve the pulmonary/systemic vascular resistance ratio. Vasopressin may be added when catecholamine-sparing support is desired, as it augments mean arterial pressure without substantially worsening pulmonary pressures. Epinephrine can be considered in refractory cases, while pure α-agonists such as phenylephrine are usually avoided because they increase RV afterload. In practice, contractile failure and venous congestion often coexist. Decongestion should continue even in patients requiring inotropes or vasopressors, with hemodynamic support serving to maintain perfusion and allow effective volume removal, since relief of venous hypertension often restores renal perfusion and may even lead to improvement in systemic blood pressure (51, 52).

Continuous monitoring includes rhythm surveillance, urine output measurement, serial UNa assessment, and lactate measurements every 4–6 h in shock states, together with bedside echocardiographic assessment of filling pressures and RV function. Therapy should be reassessed frequently—typically every 6–12 h—to guide de-escalation. Once mean arterial pressure (MAP) is stabilized and effective diuresis achieved, adrenergic agents should be tapered first, as minimizing their duration reduces arrhythmic and ischemic risks (Table 3) (12, 36, 40, 53).

For patients who remain congested despite maximum pharmacological therapy, renal replacement strategies may be necessary. Ultrafiltration has yielded mixed results, whereas peritoneal dialysis (PD) provides gradual, hemodynamically stable fluid removal and can sometimes be continued outside the hospital setting. In cases progressing to severe contraction failure or cardiogenic shock, escalation to mechanical circulatory support (MCS)—such as extracorporeal membrane oxygenation (ECMO) or percutaneous RV assist devices—may be essential as a bridge to recovery or transplantation (40, 54).

In summary, RHF is a distinct phenotype of CRS defined by systemic venous hypertension and impaired RV–pulmonary artery (PA) coupling, in which congestion is both the cause and consequence of DR. Management is not strictly sequential but often requires simultaneous decongestion and circulatory support, combined with close monitoring and escalation to advanced therapies when standard measures fail (Figure 2, Table 4) (36, 38, 40).

Patients with advanced CKD who present with ADHF represent one of the most challenging clinical scenarios in diuretic management. Congestion is not only more frequent and severe in this population, but also more tightly linked to outcomes, with lung congestion emerging as a stronger predictor of mortality than traditional risk factors such as diabetes or hypertension. This phenotype is characterized by profoundly altered pharmacokinetics, impaired tubular function, and heightened neurohormonal activation, making DR more prevalent and more difficult to reverse than in other CRS profiles (55–57).

The first step in approaching these patients is to address modifiable contributors. Excessive sodium restriction, long considered fundamental, is now being questioned, as very low salt intake has been associated with worse outcomes, hyponatremia, and hypochloremia—all of which may blunt diuretic efficacy. A moderate restriction—no more than 5 g of salt per day in patients with HF—is therefore preferable (58).

Equally important is the correction of hypochloremic alkalosis, as restoring chloride levels with potassium chloride or other chloride salts can help re-establish distal tubular sodium delivery and improve loop diuretic responsiveness. Potassium chloride remains the preferred option when hypokalemia coexists, whereas in normokalemic or hyperkalemic patients, chloride supplementation can be achieved using chloride–arginine or lysine chloride preparations. Experimental and early clinical studies have shown that chloride repletion (e.g., lysine chloride 115 mmol/day) increases serum chloride concentrations and favorably modulates neurohormonal and volume-related parameters, suggesting that hypochloremia in HF is not merely a marker of disease severity but a potentially modifiable therapeutic target (27, 59).

Potassium disturbances should also be addressed, and new potassium binders such as patiromer or sodium zirconium cyclosilicate allow the safe continuation of renin–angiotensin–aldosterone system inhibitors, which remain beneficial in HF and CKD despite concerns about hyperkalemia (55, 56, 60, 61).

Loop diuretics remain the cornerstone of treatment, but higher doses are often required due to impaired tubular delivery and competition at organic anion transporters. Strategies to optimize loop therapy include splitting the daily dose to reduce drug-free intervals, switching to agents with more predictable bioavailability (torsemide or bumetanide over furosemide), and using the intravenous route in decompensated patients or in the presence of gut edema. Continuous infusion may provide more stable exposure and limit rebound sodium retention, but randomized data have not demonstrated clear superiority over intermittent bolus administration, so the choice should be individualized (11, 55, 56, 60).

When congestion persists, sequential nephron blockade is the most effective pharmacological strategy. Recent evidence helps refine this approach. In the Acetazolamide in Acute Decompensated Heart Failure with Volume Overload (ADVOR) trial, acetazolamide added to loop diuretics significantly improved early decongestion, particularly in patients with higher baseline bicarbonate levels, but its effect was attenuated among those chronically exposed to high loop diuretic doses. Conversely, in the CLOROTIC trial, thiazide-like diuretics showed greater efficacy in patients receiving higher baseline loop doses, suggesting that chronic loop exposure induces distal tubular adaptation that limits the impact of proximal blockade. Therefore, acetazolamide appears most useful in patients with limited prior diuretic exposure or metabolic alkalosis, whereas thiazide-type agents may be preferable in those already on high-dose chronic loop therapy (3, 10, 56, 62–67).

Beyond natriuresis, acetazolamide may also blunt neurohormonal activation by reducing proximal sodium reabsorption, particularly in patients not treated with renin–angiotensin system inhibitors. In ADVOR, patients with metabolic alkalosis (serum bicarbonate ≥27 mmol/L) experienced higher diuretic and natriuretic responses and shorter hospital stays compared with those with normal bicarbonate levels. These findings support early acetazolamide use to prevent loop diuretic–induced metabolic alkalosis and mitigate secondary resistance. However, its role in eGFR <20 mL/min/1.73 m² remains uncertain, as such patients were excluded from pivotal trials (62, 64, 68, 69).

Thiazide-based regimens, as demonstrated in the CLOROTIC study were associated with higher rates of hypokalemia, consistent with the expected physiological consequences of distal sodium delivery and aldosterone-mediated potassium loss. Neither ADVOR nor CLOROTIC demonstrated differences in readmission or mortality, suggesting that while sequential nephron blockade enhances short-term decongestion, it does not translate into long-term prognostic benefit. This highlights the importance of structured outpatient follow-up and specialized cardiorenal programs to sustain euvolemia and optimize chronic therapy once congestion is resolved (64, 65, 69, 70).

Mineralocorticoid receptor antagonists (MRAs) or epithelial sodium channel blockers may be considered in selected cases, particularly when hypokalemia or metabolic alkalosis complicate treatment, though the risk of hyperkalemia in CKD requires vigilance. SGLT2i also play a role; although their natriuretic effect diminishes at low estimated glomerular filtration rates, they remain safe to initiate above guideline thresholds and provide long-term renal and cardiovascular protection (55, 56, 71–74).

Adjunct strategies have been proposed for truly refractory cases. Combining hypertonic saline with loop diuretics can acutely enhance natriuresis and shift the dose–response curve, particularly in patients with profound hyponatremia or hypochloremia, though results are heterogeneous and the risk of acute kidney injury with high chloride loads limits widespread adoption. Vasopressin antagonists such as tolvaptan reliably correct hyponatremia and increase free water clearance, but they have failed to improve long-term outcomes and are therefore reserved for patients with symptomatic hyponatremia. Limited data also suggest a potential role for urea as a low-cost osmotic agent to promote free water clearance and correct dilutional hyponatremia in selected patients with refractory HF. Small studies indicate that urea may improve serum sodium and facilitate decongestion without adversely affecting renal function, although evidence remains scarce and its use has not yet been validated in large randomized trials (75, 76). Modest rises in serum Cr during aggressive diuresis should not prompt premature therapy de-escalation, as they often reflect hemoconcentration rather than structural kidney injury. Preserving renal function is important, but adequate volume removal remains the cornerstone for improving symptoms and outcomes (60, 77, 78).

When pharmacologic strategies fail, extracorporeal fluid removal must be considered. Ultrafiltration provides predictable sodium and water removal, but randomized trials such as CARRESS-HF have shown worse renal outcomes and higher adverse event rates compared with stepped pharmacologic therapy. For carefully selected patients with true diuretic resistance, ultrafiltration remains an option, but its resource intensity and complication profile restrict its use. Peritoneal dialysis offers a gentler, continuous means of decongestion with fewer hemodynamic shifts, and observational studies suggest improvements in symptoms, hospitalizations, and quality of life, though robust randomized evidence is lacking. In unstable patients with concomitant acute kidney injury, continuous renal replacement therapy may be the only feasible option (55, 60, 79).

In summary, advanced CKD represents a distinct CRS phenotype in which impaired tubular handling, reduced diuretic delivery, and chronic neurohormonal activation converge to limit natriuretic response. Moderate sodium restriction, correction of electrolyte and acid–base abnormalities, optimization of loop diuretics, and sequential nephron blockade form the cornerstone of management. Adjunctive measures such as hypertonic saline or vasopressin antagonists may be considered selectively, while extracorporeal therapies should be reserved for refractory cases. The key principle is to prioritize effective decongestion while recognizing that small rises in Cr are often acceptable in the pursuit of improved symptoms and outcomes (10, 55, 60) (Table 5).

Obesity represents a growing and particularly complex phenotype in acute and chronic HF, with implications extending from diagnosis to treatment response. In the acute setting, the evaluation of congestion is considerably more challenging than in other patient groups. Excess adiposity decreases the accuracy of both the physical examination and noninvasive imaging modalities. Traditional clinical signs—such as jugular venous distension, pulmonary rales, or peripheral edema—are often obscured, while echocardiographic indices and natriuretic peptide levels systematically underestimate the degree of circulatory congestion. As a result, hemodynamic congestion can remain clinically silent until it becomes advanced, complicating both the diagnosis and the titration of decongestive therapy. This phenotype is unique because volume overload often masks itself clinically, while neurohormonal activation and renal congestion develop early—driving DR even before overt edema or weight gain appear (80–82).

From a pathophysiological perspective, adipose tissue is not merely an inert reservoir but an active endocrine organ. It produces a variety of pro-inflammatory cytokines, adipokines, and mineralocorticoid-like factors that promote sodium retention, vascular stiffness, and sympathetic activation. Sympathetic overactivity is particularly pronounced when obesity coexists with obstructive sleep apnea, further enhancing neurohormonal activation and sodium avidity. These mechanisms contribute to plasma volume expansion, renal congestion, and right ventricular overload, particularly in patients with HFpEF (83–86). Consequently, obesity is associated with higher rates of volume overload, a greater need for diuretics, and a poorer diuretic response. The coexistence of obesity-related kidney dysfunction further compounds these effects. Increased intra-abdominal pressure reduces renal perfusion, while ectopic fat deposition within the kidney promotes inflammation, oxidative stress, and tubulointerstitial fibrosis. Together, these factors blunt natriuretic efficiency and reinforce DR (84, 87–89).

In clinical practice, patients with obesity frequently require higher doses of loop diuretics to achieve an adequate response, reflecting both altered pharmacokinetics and increased volume of distribution, while chronic high-dose loop exposure further amplifies neurohormonal activation and sodium avidity, perpetuating DR (87, 89). Weight-based dosing may partially mitigate underdosing, but clinicians must balance this with the risk of hypotension and renal dysfunction, particularly in those with comorbid CKD (1, 11, 14). When standard loop diuretic therapy fails, the same stepwise approach used in other resistant states applies: sequential nephron blockade with thiazide or thiazide-like agents, and in selected cases, the addition of acetazolamide to counteract metabolic alkalosis or proximal sodium reabsorption. SGLT2i may further enhance natriuresis and improve renal hemodynamics, although their diuretic effect is modest compared with classical agents (20, 89).

Beyond decongestion, addressing obesity itself has emerged as a cornerstone of long-term management. Weight reduction improves symptoms, exercise capacity, and overall quality of life in patients with HFpEF, while modest weight loss may also benefit those with reduced ejection fraction. Recent trials have highlighted the potential of metabolic therapies to modify both congestion and diuretic needs. In the SUMMIT trial, treatment with tirzepatide in obese HFpEF patients improved functional status and reduced estimated blood volume. Similarly, pooled analyses from the STEP-HFpEF and STEP-HFpEF-DM trials demonstrated that semaglutide not only improved HF outcomes but also decreased the requirement for loop diuretics by up to 17%, compared with an increase in the placebo group. Patients receiving semaglutide were three times more likely to have their loop diuretic dose reduced and three times less likely to require escalation. These findings position metabolic therapies not only as weight-loss agents but also as modulators of congestion oand DR through improvements in endothelial function, renal hemodynamics and inflammatory pathways (82, 87, 90).

In the chronic setting, comprehensive management of obesity should combine caloric restriction, increased physical activity, and, when indicated, pharmacologic or surgical interventions. Beyond symptomatic relief, sustained weight loss can slow the progression of renal dysfunction, reduce proteinuria, and improve glomerular filtration rate in obese patients with concomitant CKD. Bariatric surgery, when feasible, has been shown to prevent renal decline and reduce cardiovascular morbidity. The introduction of glucagon-like peptide-1 (GLP-1) and dual glucose-dependent insulinotropic peptide (GIP)/GLP-1 receptor agonists has transformed the therapeutic landscape, offering robust weight reduction with additional cardiovascular and renal protection (82, 87, 91, 92).

In summary, obesity amplifies the risk of congestion and DR through overlapping hemodynamic, neurohormonal, and renal mechanisms, while also complicating the clinical recognition of volume overload. Management requires higher or combination diuretic dosing in the acute setting and targeted weight reduction strategies in the chronic phase. The growing evidence supporting GLP-1–based therapies provides new hope for improving both symptom control and long-term outcomes in this difficult-to-treat population (Table 6) (84, 87–89).

Elderly and frail HF patients represent a growing and particularly complex population, in whom diuretic resistance often develops in the context of multiple coexisting conditions and diminished physiological reserve. Frailty, a dynamic state of reduced resilience to stressors, amplifies vulnerability to volume shifts, electrolyte imbalances, and adverse drug reactions. Most older HF patients also suffer from multimorbidity—atrial fibrillation, chronic kidney disease, hypertension, dementia, or valvular disease—requiring cautious polytherapy and close interdisciplinary coordination. This phenotype is distinct because age-related changes in drug handling, neurohormonal activation, and sarcopenia reduce both diuretic delivery and tolerance to aggressive volume removal, making the balance between decongestion and preservation uniquely challenging (93, 94).

The pharmacokinetics and pharmacodynamics of diuretics are substantially altered in advanced age. Reduced renal plasma flow and tubular secretion, lower serum albumin, and changes in body composition attenuate loop diuretic delivery and potency. As a result, older adults frequently require higher or combination diuretic doses to achieve decongestion, but they are equally prone to overdiuresis, hypotension, and acute kidney injury. Clinical evaluation is further complicated by unreliable physical findings: edema may stem from hypoalbuminemia rather than congestion, and jugular venous distension or weight change may be misleading in sarcopenic individuals. Therefore, treatment must be guided by comprehensive assessment—urine output, daily weight trends, and, when available, urinary sodium or non-invasive hemodynamic monitoring (93–95).

In this setting, gradual decongestion with careful monitoring is preferred over rapid fluid removal. Thiazide-like agents or acetazolamide can be added temporarily for sequential nephron blockade, but only under close electrolyte and renal function surveillance. Guideline-directed medical therapy (GDMT) remains beneficial and should not be withheld solely due to age or frailty (93, 94). Although GDMT is often under-prescribed in advanced age, evidence indicates that use of at least one GDMT class—ACE inhibitors/ARNI, β-blockers, MRAs, or SGLT2i—reduces hospitalizations and mortality even in advanced age. Among these, SGLT2i appear well tolerated in the frailest categories, though vigilance for dehydration, genitourinary infections, or hypotension remains essential (93, 94, 96–99).

Ultimately, diuretic management in frail elderly patients is a delicate balancing act between decongestion and preservation. The therapeutic goal is not maximal diuresis but sustained euvolemia, maintenance of renal function, and preservation of autonomy and quality of life through individualized, closely supervised care (Table 7) (93, 94).