Diuretic resistance in patients with kidney disease: Challenges and opportunities

Guo, Lifei; Fu, Baohui; Liu, Yang; Hao, Na; Ji, Yue

doi:10.1016/j.biopha.2022.114058

Cited by 14 publications

(14 citation statements)

References 146 publications

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“…Pharmacodynamics describes how the kidney responds to a diuretic, such as increased tubular sodium reabsorption in the presence of various proteases (plasmin, furin, and plasminogen, etc.) [ 74 , 75 , 76 , 77 , 78 ].…”

Section: Edema Development: the Underfill And Overfill Hypothesesmentioning

confidence: 99%

“…The most frequently reported adverse events are genital mycotic infections and urinary tract infections. Other significant adverse reactions to SGLT2-inhibitors include lower limb amputation, diabetic ketoacidosis, euglycemic diabetic ketoacidosis, AKI, Fournier gangrene, and hyperkalemia, especially when SGLT2-inhibitors are combined with ACE-inhibitors or angiotensin-receptor blockers (ARBs) in patients with renal impairment (Sodium–Glucose Transport Protein 2 (SGLT2)-Inhibitors—inderbir padda) [ 77 , 109 ].…”

Section: Diuretic Treatmentmentioning

confidence: 99%

“…Drugs from a different class may act synergistically with the first by blocking the adaptive processes that limit the efficacy of diuretics, such as the activation of the RAAS and SNS, excessive NaCl consumption and the remodeling of the distal nephron. Distal convoluted tubule hypertrophy and hyperplasia occur due to the workload induced via diuretics [ 72 , 77 , 110 , 115 ].…”

Section: Diuretic Treatmentmentioning

confidence: 99%

“…As previously stated, limitations are encountered in the use of diuretics to address fluid overload due to various factors, including severe hypervolemia, dyselectrolytemia, and kidney dysfunction. In such cases, ultrafiltration remains the lone viable option [ 77 , 79 , 158 ]. Recent attention has been directed toward novel and promising pharmacological interventions.…”

Section: Diuretic Treatmentmentioning

confidence: 99%

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Nephrotic Syndrome: From Pathophysiology to Novel Therapeutic Approaches

Frățilă,

Lupușoru,

Sorohan

et al. 2024

Biomedicines

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Nephrotic edema stands out as one of the most common complications of nephrotic syndrome. The effective management of hypervolemia is paramount in addressing this condition. Initially, “the underfill hypothesis” suggested that proteinuria and hypoalbuminemia led to fluid extravasation into the interstitial space, causing the intravascular hypovolemia and activation of neurohormonal compensatory mechanisms, which increased the retention of salt and water. Consequently, the recommended management involved diuretics and human-albumin infusion. However, recent findings from human and animal studies have unveiled a kidney-limited sodium-reabsorption mechanism, attributed to the presence of various serine proteases in the tubular lumen-activating ENaC channels, thereby causing sodium reabsorption. There is currently no standardized guideline for diuretic therapy. In clinical practice, loop diuretics continue to be the preferred initial choice. It is noteworthy that patients often exhibit diuretic resistance due to various factors such as high-sodium diets, poor drug compliance, changes in pharmacokinetics or pharmacodynamics, kidney dysfunction, decreased renal flow, nephron remodeling and proteasuria. Considering these challenges, combining diuretics may be a rational approach to overcoming diuretic resistance. Despite the limited data available on diuretic treatment in nephrotic syndrome complicated by hypervolemia, ENaC blockers emerge as a potential add-on treatment for nephrotic edema.

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Section: Edema Development: the Underfill And Overfill Hypothesesmentioning

confidence: 99%

Section: Diuretic Treatmentmentioning

confidence: 99%

Section: Diuretic Treatmentmentioning

confidence: 99%

Section: Diuretic Treatmentmentioning

confidence: 99%

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Nephrotic Syndrome: From Pathophysiology to Novel Therapeutic Approaches

Frățilă,

Lupușoru,

Sorohan

et al. 2024

Biomedicines

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“…End-stage renal disease (ESRD) occurs when chronic kidney disease has advanced so far that the kidneys no longer work well enough to filter wastes and fluids from the blood, resulting in dangerous levels of buildup within the body [1]. ESRD is the loss of kidney function with this condition is irreversible.…”

Section: End-stage Renal Disease (Esrd)mentioning

confidence: 99%

Review on the neuron damage parameters in patients with end-stage renal disease

2023

JPTCP

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Many studies have found toxic effects on the body and mental state at near and long-term parameters in end-stage renal disease (ESRD) patients of neuronal integrity. Consequently, studying chemical molecules that cause tissue damage to neurons is essential for understanding the mechanism of toxicity and available treatment prospects. Which includes some parameters of myelin basic protein (MBP), ionized calcium-binding adaptor molecule 1 IBA1, calcium-binding protein B (S100B), Glial fibrillary acidic protein (GFAP), neuroepithelial stem cell protein (Nestin), neurofilament light polypeptide (NFL), neuron-specific enolase, T-tau and claudin proteins. The published papers on changes in neuronal damage final products in ESRD patients were reviewed, and the explanations obtained from previous research were collected. It is concluded from this review that causes an increase in parameters in patients with ESRD lead to neurodegeneration, which leads to severe damage to patients health that requires therapeutic intervention to reduce the harmful effects of parameters on the health of patients.

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