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Current Pharmaceutical Design 2023Heart failure is a major problem in developed countries, leading to a high number of hospitalizations and healthcare costs. The most common symptom of heart failure is... (Review)
Review
Heart failure is a major problem in developed countries, leading to a high number of hospitalizations and healthcare costs. The most common symptom of heart failure is congestion, which is also the primary reason for hospitalization. Diuretics, particularly loop diuretics, are the cornerstone of the treatment of congestion. Likewise, there are other types of diuretics with different pathways of action, bioavailability profiles, adverse reactions, and effects on the cardiovascular and renal systems. Moreover, in recent years, new therapeutic alternatives have been proposed for challenging cases of diuretic resistance, such as ultrafiltration through peripheral access or peritoneal dialysis. The main objective of this article is to provide a step-guided approach to the management of congestion in patients with heart failure in order to guide the medical practice. Despite the significant amount of research published in recent years, there are no clear algorithms for managing acute heart failure. Diuretics remain the primary treatment of acute heart failure, and nephron blockade is key, but new therapies are emerging, and ongoing research is needed to develop better strategies for managing this condition.
Topics: Humans; Diuretics; Heart Failure; Ultrafiltration
PubMed: 37455461
DOI: 10.2174/1381612829666230714153404 -
Current Heart Failure Reports Oct 2022Progressive intravascular, interstitial, and alveolar fluid overload underlies the transition from compensated to acutely decompensated heart failure and loop diuretics... (Review)
Review
PURPOSE OF THE REVIEW
Progressive intravascular, interstitial, and alveolar fluid overload underlies the transition from compensated to acutely decompensated heart failure and loop diuretics are the mainstay of treatment. Adverse effects and resistance to loop diuretics received much attention while the contribution of a depressed cardiac output to diuretic resistance was downplayed.
RECENT FINDINGS
Analysis of experience with positive inotropic agents, especially dobutamine, indicates that enhancement of cardiac output is not consistently associated with increased renal blood flow. However, urinary output and renal sodium excretion increase likely due to dobutamine-mediated decrease in renal and systemic reduced activation of sympathetic nervous- and renin-angiotensin-aldosterone system. Mechanical circulatory support with left ventricular assist devices ascertained the contribution of low cardiac output to diuretic resistance and the pathogenesis and progression of kidney disease in acutely decompensated heart failure. Diuretic resistance commonly occurs in acutely decompensated heart failure. However, failure to resolve fluid overload despite high doses of loop diuretics should alert to the presence of a low cardiac output state.
Topics: Cardiac Output, Low; Diuretics; Dobutamine; Heart Failure; Humans; Sodium; Sodium Potassium Chloride Symporter Inhibitors; Water-Electrolyte Imbalance
PubMed: 36045314
DOI: 10.1007/s11897-022-00573-y -
Mini Reviews in Medicinal Chemistry 2021Over the years, the development of bioactive heterocycles has aroused the interest of the scientific community, because in general, these heterocycles are strategic in... (Review)
Review
Over the years, the development of bioactive heterocycles has aroused the interest of the scientific community, because in general, these heterocycles are strategic in maintaining life. Research into bioactive heterocycles is associated with the development of methods of synthesis and the biological evaluation of different nuclei. In consequence, there has been a growing interest in the nucleus of fused pyrimidine, which has diversified pharmacological activities, including diuretic, antimicrobial, antifolate, tyrosine kinase, anti-inflammatory, anticancer, anthelminthic, and antiviral activities. This review focuses on describing a diverse set of structures derived from pyrimido[4,5-d]pyrimidines and contemplates the main bioactivities of these nuclei.
Topics: Anti-Infective Agents; Anti-Inflammatory Agents; Antineoplastic Agents; Diuretics; Folic Acid Antagonists; Humans; Protein-Tyrosine Kinases; Pyrimidines
PubMed: 33605856
DOI: 10.2174/1389557521666210219160115 -
Hospital Practice (1995) Apr 2022The objectives of the study are to investigate the causes of diuretic resistance in patients with advanced congestive heart failure (CHF), since diuretics are the... (Review)
Review
OBJECTIVES
The objectives of the study are to investigate the causes of diuretic resistance in patients with advanced congestive heart failure (CHF), since diuretics are the cornerstone of treatment of these patients. Several studies have shown that diuretic resistance in patients with advanced CHF is common, ranging from 25% to 50% in hospitalized patients.
METHODS
In order to get a current perspective as to the magnitude of diuretic resistance in such patients, a focused Medline search of the English language literature was conducted between 2015 and 2020 using the search terms, CHF, diuretics, treatment, resistance, frequency, and 30 papers with pertinent information were selected.
RESULTS
The analysis of data from the selected papers demonstrated that diuretic resistance is common in hospitalized patients with advanced CHF and frequently associated with renal failure, which is secondary to CHF.
CONCLUSIONS
Diuretic resistance appears to be common in patients with advanced CHF and it is mostly due to decreased cardiac output, low blood pressure, decreased glomerular filtration rate, decreased filtration of sodium, and increased tubular reabsorption of sodium. Diuretic resistance in such patients can be overcome with the combination of loop diuretics with thiazide and thiazide-like diuretics, aldosterone antagonists, as well as other agents. The data from these studies in combination with collateral literature will be discussed in this review.
Topics: Diuretics; Heart Failure; Humans; Sodium; Thiazides
PubMed: 33596757
DOI: 10.1080/21548331.2021.1893065 -
Critical Care Nursing Quarterly 2017Most patients with acute decompensated heart failure (ADHF) present with signs and symptoms of volume overload, and those with a significant history of diuretic exposure... (Review)
Review
Most patients with acute decompensated heart failure (ADHF) present with signs and symptoms of volume overload, and those with a significant history of diuretic exposure may demonstrate varying degrees of diuretic resistance. Although this phenomenon is commonly reported, no consensus definition exists and recommendations regarding an optimal therapeutic approach remain limited. Optimizing the use of intravenous (IV) loop diuretic therapy is the most common initial approach, and therapy may be augmented by the addition of a thiazide-type diuretic or an IV vasodilator. Patients whose resistance to diuretic therapy is due to low cardiac output may require inotropic therapy, and other options (eg, ultrafiltration and vasopressin antagonists) may be considered in select populations. The purpose of this review is to describe diuretic resistance and its underlying mechanisms in ADHF, as well as the most commonly employed strategies for overcoming it. A stepwise approach to managing volume overload in patients with ADHF and diuretic resistance is also provided.
Topics: Acute Disease; Diuretics; Heart Failure; Humans; Sodium Potassium Chloride Symporter Inhibitors
PubMed: 28834858
DOI: 10.1097/CNQ.0000000000000173 -
Biomedicine & Pharmacotherapy =... Jan 2023Edema caused by kidney disease is called renal edema. Edema is a common symptom of many human kidney diseases. Patients with renal edema often need to take... (Review)
Review
Edema caused by kidney disease is called renal edema. Edema is a common symptom of many human kidney diseases. Patients with renal edema often need to take diuretics.However, After taking diuretics, patients with kidney diseases are prone to kidney congestion, decreased renal perfusion, decreased diuretics secreted by renal tubules, neuroendocrine system abnormalities, abnormal ion transporter transport, drug interaction, electrolyte disorder, and hypoproteinemia, which lead to ineffective or weakened diuretic use and increase readmission rate and mortality. The main causes and coping strategies of diuretic resistance in patients with kidney diseases were described in detail in this report. The common causes of DR included poor diet (electrolyte disturbance and hypoproteinemia due to patients' failure to limit diet according to correct sodium, chlorine, potassium, and protein level) and poor drug compliance (the patient did not take adequate doses of diuretics. true resistance occurs only if the patient takes adequate doses of diuretics, but they are not effective), changes in pharmacokinetics and pharmacodynamics, electrolyte disorders, changes in renal adaptation, functional nephron reduction, and decreased renal blood flow. Common treatment measures include increasing in the diuretic dose and/or frequency, sequential nephron blockade,using new diuretics, ultrafiltration treatment, etc. In clinical work, measures should be taken to prevent or delay the occurrence and development of DR in patients with kidney diseases according to the actual situation of patients and the mechanism of various causes. Currently, there are many studies on DR in patients with heart diseases. Although the phenomenon of DR in patients with kidney diseases is common, there is a relatively little overview of the mechanism and treatment strategy of DR in patients with kidney diseases. Therefore, this paper hopes to show the information on DR in patients with kidney diseases to clinicians and researchers and broaden the research direction and ideas to a certain extent.
Topics: Humans; Diuretics; Heart Failure; Kidney Diseases; Kidney; Sodium; Water-Electrolyte Imbalance; Edema; Drug Resistance
PubMed: 36473405
DOI: 10.1016/j.biopha.2022.114058 -
Kidney & Blood Pressure Research 2019Diuretic resistance is among the most challenging problems that the cardio-nephrologist must address in daily clinical practice, with a considerable burden on hospital... (Review)
Review
BACKGROUND
Diuretic resistance is among the most challenging problems that the cardio-nephrologist must address in daily clinical practice, with a considerable burden on hospital admissions and health care costs. Indeed, loop diuretics are the first-line therapy to overcome fluid overload in heart failure patients. The pathophysiological mechanisms of fluid and sodium retention are complex and depend on several neuro-hormonal signals mainly acting on sodium reabsorption along the renal tubule. Consequently, doses and administration modalities of diuretics must be carefully tailored to patients in order to overcome under- or overtreatment. The frequent and tricky development of diuretic resistance depends in part on post-diuretic sodium retention, reduced tubular secretion of the drug, and reduced sodium/chloride sensing. Sodium and chloride depletions have been recently shown to be major factors mediating these processes. Aquaretics and high-saline infusions have been recently suggested in cases of hyponatremic conditions. This review discusses the limitations and strengths of these approaches.
SUMMARY
Long-term diuretic use may lead to diuretic resistance in cardio-renal syndromes. To overcome this complication intravenous administration of loop diuretics and a combination of different diuretic classes have been proposed. In the presence of hyponatremia, high-saline solutions in addition to loop diuretics might be beneficial, whereas aquaretics require caution to avoid overcorrection. Key Messages: Diuretic resistance is a central theme for cardio-renal syndromes. Hyponatremia and hypochloremia may be part of the mechanisms for diuretic resistance. Aquaretics and high-saline solutions have been proposed as possible new therapeutic solutions.
Topics: Cardio-Renal Syndrome; Diuretics; Heart Failure; Humans; Kidney; Nephrology
PubMed: 31437845
DOI: 10.1159/000502648 -
Current Pharmaceutical Design 2017Heart failure, hypertension, cirrhosis and nephritic syndrome are among conditions that alter volume and composition of body fluids and are modulated by diuretics.... (Review)
Review
Heart failure, hypertension, cirrhosis and nephritic syndrome are among conditions that alter volume and composition of body fluids and are modulated by diuretics. Natural products are important source of diuretics and have been considered remarkable alternative with greater effectiveness and fewer side effects. However, many of these plants used in traditional medicine must be scientifically assessed about their efficacy and toxicity. Despite the large number of published articles claiming that plants or plant-derived components may act as diuretic agents, few studies have addressed the mechanism of action of medicinal plants. Thus, the aim of this review was to provide an overview of the current knowledge about the major cellular and molecular mechanisms of diuretic plants and/or their main compounds. Many well-established mechanisms (water channels, renal carriers, nitric oxide-cGMP and prostaglandin-cAMP pathways, renin-angiotensin and kinin-kallikrein systems, carbonic anhydrase, and osmotic effects), along with other newly identified targets, are connected to the diuretic activity of many natural products. However, the central path responsible for the activity of these agents remains unclear. Further studies may help clarifying the central role of each of these pathways in the pleiotropic response of these agents.
Topics: Biological Products; Diuretics; Fibrosis; Heart Failure; Humans; Hypertension; Nephrotic Syndrome; Plants, Medicinal
PubMed: 27758702
DOI: 10.2174/1381612822666161014114437 -
The American Journal of Medicine Jan 2024Apparent resistant hypertension, defined as uncontrolled office blood pressure despite ≥ 3 antihypertensive medications including a diuretic or use of ≥ 4... (Review)
Review
Apparent resistant hypertension, defined as uncontrolled office blood pressure despite ≥ 3 antihypertensive medications including a diuretic or use of ≥ 4 medications regardless of blood pressure, occurs in ≤ 15% of treated hypertensives. Apparent refractory hypertension, defined as uncontrolled office pressure despite use of 5 or more medications including a diuretic, occurs in ≤ 10% of resistant cases. Both are associated with increased comorbidity and enhanced cardiovascular risk. To rule out pseudo-resistant or pseudo-refractory hypertension, employ guideline-based methodology for obtaining pressure, maximize the regimen, rule out white-coat effect, and assess adherence. True resistant hypertension is characterized by volume overload and aldosterone excess, refractory by enhanced sympathetic tone. Spironolactone is the preferred agent for resistance, with lower doses. Spironolactone, potassium binders, or both, are preferred if the estimated glomerular filtration rate is below 45. If significant albuminuria, finerenone is indicated. The optimal treatment of refractory hypertension is unclear, but sympathetic inhibition (α-β blockade, centrally acting sympathoinhibitors, or both) seems reasonable. Renal denervation has shown minimal benefit for resistance, but its role in refractory hypertension remains to be defined.
Topics: Humans; Spironolactone; Hypertension; Antihypertensive Agents; Blood Pressure; Diuretics; Blood Pressure Monitoring, Ambulatory
PubMed: 37832756
DOI: 10.1016/j.amjmed.2023.09.015 -
Journal of Cardiac Failure Apr 2021Identifying patients at risk of poor diuretic response in acute heart failure (AHF) is critical to make prompt adjustments in therapy. The objective of this study was to... (Randomized Controlled Trial)
Randomized Controlled Trial
BACKGROUND
Identifying patients at risk of poor diuretic response in acute heart failure (AHF) is critical to make prompt adjustments in therapy. The objective of this study was to investigate whether the circulating levels of soluble ST2 predict the cumulative diuretic efficiency (DE) at 24 and 72 hours in patients with AHF and concomitant renal dysfunction.
METHODS AND RESULTS
This is a post hoc analysis of the IMPROVE-HF trial, in which we enrolled 160 patients with AHF and renal dysfunction (estimated glomerular filtrate rate of <60 mL/min/1.73 m). DE was calculated as the net fluid output produced per 40 mg of furosemide equivalents. The association between sST2 and DE was evaluated by using multivariate linear regression analysis. The median cumulative DE at 24 and 72 hour was 747 mL (interquartile range 490-1167 mL) and 1844 mL (interquartile range 1142-2625 mL), respectively. The median sST2 and mean estimated glomerular filtrate rate were 72 ng/mL (interquartile range 47-117 ng/mL), and 34.0 ± 8.5 mL/min/1.73 m, respectively. In a multivariable setting, higher sST2 were significant and nonlinearly related to lower DE both at 24 and 72 hours (P = .002 and P = .019, respectively).
CONCLUSIONS
In patients with AHF and renal dysfunction at presentation, circulating levels of sST2 were independently and negatively associated with a poor diuretic response, both at 24 and 72 hours.
Topics: Acute Disease; Diuretics; Furosemide; Heart Failure; Humans; Kidney Diseases
PubMed: 33038531
DOI: 10.1016/j.cardfail.2020.10.002