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Worsening symptoms and fluid overload are the hallmarks of heart failure (HF) decompensation, and fluid removal is central to improvement. Despite high-dose loop diuretics, patients with decompensated HF may develop suboptimal diuresis/diuretic resistance. Sequential nephron blockade with a combination of loop and thiazide/thiazide-like diuretics m...
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Context 1
... our clinical observation stems from our experience with a single case, controlled studies are needed to establish the clinical utility of acetazolamide. Drawing from available literature and anecdotal experiences, we propose an algorithmic approach to diuresis in patients (Figures 1, 2). BID indicates twice a day; IV, intravenous; PO, oral. ...
Context 2
... our clinical observation stems from our experience with a single case, controlled studies are needed to establish the clinical utility of acetazolamide. Drawing from available literature and anecdotal experiences, we propose an algorithmic approach to diuresis in patients (Figures 1, 2). BID indicates twice a day; IV, intravenous; PO, oral. ...
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Diuretics are the cornerstone therapy for acute heart failure (HF) and congestion. Patients chronically exposed to loop diuretics may develop diuretic resistance as a consequence of nephron remodelling, and the combination of diuretics will be necessary to improve diuretic response and achieve decongestion. This review integrates data from recent r...
Citations
... The effect is achieved both due to sequential blockade of the nephron and mutual potentiation of diuretic activity [21,29]. For example, acetazolamide increases sensitivity to loop diuretics by correcting metabolic alkalosis [71,72] and to thiazide diuretics by reducing the expression of pendrin [40]. Parallel therapy: 1) continue optimal therapy of the underlying disease and CHF; 2) consider early administration of MCRA in case of hypokalemia; 3) limit salt and water intake; 4) if nec-essary, intravenous administration of K + and Mg 2+ medications Parallel diagnostics: before prescribing a diuretic, determine body weight; standard non-in-vasive monitoring of heart rate, respiration rate, blood oxygen saturation and blood pressure; check for signs of hypoperfusion and, if present, consider invasive monitoring of hemodynamic parameters; ...
The authors analyzed the problem of diuretic resistance (DR) in patients with chronic heart failure (CHF). Most of the symptoms and signs of CHF are associated with hypervolemia and vascular congestion in the systemic and pulmonary circulation. The severity of the latter is the main factor which negatively affects the overall assessment of life satisfaction in patients with CHF. Since the patient, even at the incurable stage of CHF, primarily expects a rapid decrease in the severity of manifestations of decompensation from the prescribed therapy, achieving euvolemia is the essence of its short-term objective. Without diuretics, these immediate effects, according to which most CHF patients judge the qualifications of the doctor, are almost impossible to achieve. Unfortunately, apparently, not a single clinician was able to avoid disappointment in the effectiveness of CHF therapy associated with DR in their practice. As a rule, DR reflects the progressive course of CHF and is often associated with a poor prognosis. The review consistently covers the issues of terminology, diagnosis, pathogenesis, and prevention of DR, which aggravates CHF, and discusses measures aimed at restoring sensitivity to diuretics.
... Contrarily, if the urine output in the next 2 h is less than 150-200 ml, then a new bolus of the same dose should be immediately administered. If diuresis continues to be less than 150-200 ml in 2 h, then the patient is considered non-responsive to intravenous furosemide and could benefit from a sequential diuretic blockade approach (Gill et al., 2021). ...
... In addition, acetazolamide has been associated with renal vasodilation due to the increased sodium that reaches the macula densa, similar to the effect seen with SGLT2 inhibitors, which could be nephroprotective. Moreover, it can also improve apnea-hypopnea symptoms associated with central sleep apnea, a common disorder found in HF patients (Gill et al., 2021). ...
Refractory congestion is common in acute and chronic heart failure, and it significantly impacts functional class, renal function, hospital admissions, and survival. In this paper, the pathophysiological mechanisms involved in cardiorenal syndrome and the interplay between heart failure and chronic kidney disease are reviewed. Although the physical exam remains key in identifying congestion, new tools such as biomarkers or lung, vascular, and renal ultrasound are currently being used to detect subclinical forms and can potentially impact its management. Thus, an integrated multimodal diagnostic algorithm is proposed. There are several strategies for treating congestion, although data on their efficacy are scarce and have not been validated. Herein, we review the optimal use and monitorization of different diuretic types, administration route, dose titration using urinary volume and natriuresis, and a sequential diuretic scheme to achieve a multitargeted nephron blockade, common adverse events, and how to manage them. In addition, we discuss alternative strategies such as subcutaneous furosemide, hypertonic saline, and albumin infusions and the available evidence of their role in congestion management. We also discuss the use of extracorporeal therapies, such as ultrafiltration, peritoneal dialysis, or conventional hemodialysis, in patients with normal or impaired renal function. This review results from a multidisciplinary view involving both nephrologists and cardiologists.
Recent evidence suggests that acetazolamide may be beneficial as an adjunctive diuretic therapy in patients with acute decompensated heart failure (HF). We aim to pool all the studies conducted until now and provide updated evidence regarding the role of acetazolamide as adjunctive diuretic in patients with acute decompensated HF.
PubMed/Medline, Cochrane Library, and Scopus were searched from inception until July 2023, for randomized and nonrandomized studies evaluating acetazolamide as add-on diuretic in patients with acute decompensated HF. Data about natriuresis, urine output, decongestion, and the clinical signs of congestion were extracted, pooled, and analyzed. Data were pooled using a random effects model. Results were presented as risk ratios (RRs), odds ratios (ORs), or weighted mean differences (WMD) with 95% confidence intervals (95% CIs). Certainty of evidence was assessed using the grading of recommendation, assessment, development, and evaluation (GRADE) approach. A P value of < 0.05 was considered significant in all cases.
A total of 5 studies (n = 684 patients) were included with a median follow-up time of 3 months. Pooled analysis demonstrated significantly increased natriuresis (MD 55.07, 95% CI 35.1–77.04, P < 0.00001; I2 = 54%; moderate certainty), urine output (MD 1.04, 95% CI 0.10–1.97, P = 0.03; I2 = 79%; moderate certainty) and decongestion [odds ratio (OR) 1.62, 95% CI 1.14–2.31, P = 0.007; I2 = 0%; high certainty] in the acetazolamide group, as compared with controls. There was no significant difference in ascites (RR 0.56, 95% CI 0.23–1.36, P = 0.20; I2 = 0%; low certainty), edema (RR 1.02, 95% CI 0.52–2.0, P = 0.95; I2 = 45%; very low certainty), raised jugular venous pressure (JVP) (RR 0.86, 95% CI 0.63–1.17, P = 0.35; I2 = 0%; low certainty), and pulmonary rales (RR 0.82, 95% CI 0.44–1.51, P = 0.52; I2 = 25%; low certainty) between the two groups.
Acetazolamide as an adjunctive diuretic significantly improves global surrogate endpoints for decongestion therapy but not all individual signs and symptoms of volume overload.
This systematic review was prospectively registered on the PROSPERO (https://www.crd.york.ac.uk/PROSPERO/), registration number CRD498330.
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.
