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правда ли что отменят пенсии работающим пенсионерам, Loop Diuretics - StatPearls - NCBI Bookshelf, Clinical Pharmacology in Diuretic Use : Clinical Journal of the , Diuretic Therapy for Patients With Heart Failure:, Comparative Effect of Loop Diuretic Prescription on Mortality and Heart , Comparison of continuous loop diuretic versus bolus injection regimens , Diuretic Treatment in Heart Failure | New England Journal of Medicine, Comparison of all types of loop-diuretics for chronic heart failure: A .
Although human mutations in OAT1 have not been described, these pathways may be inhibited by drugs and endogenous toxins, thereby causing diuretic resistance (31). Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit diuretic secretion and alter diuretic responsiveness, and because of their frequent use, are an important cause of heart failure exacerbations (34). Yet other classes of drugs, including antihypertensives, antibiotics, and antivirals, may also interact with these transporters and cause resistance (35). Endogenous metabolites also compete for diuretic secretion, including indoxyl sulfate, carboxy-methyl-propyl-furanpropionate, p-cresol sulfate, and kynurenate, which accumulate in CKD (36). In all of these situations, the natriuretic dose-response curve is shifted to the right ().Pharmacokinetics and pharmacodynamics of diuretic action. (A) Effects of CKD on diuretic actions. Note that in CKD, baseline fractional sodium excretion is high, to maintain absolute rates of sodium excretion equal to intake. There is a shift in the dose-response curve to the right (R), primarily owing to impaired diuretic secretion, but no change in the ceiling effect. (B) The same relationship plotted versus absolute rates of sodium excretion. The same rightward shift is evident, but the ceiling is lower, owing to the GFR reduction (as indicated by D). (C) Comparing effects of loop diuretics and distal convoluted tubule (DCT) diuretics on absolute sodium excretion, given a retained effect on fractional excretion.There are additional reasons that CKD is a loop diuretic–resistant state. Metabolic acidosis, which is frequently observed in uremia, depolarizes the membrane potential of proximal tubule cells (37), which also decreases organic anion secretion, an effect that may explain why diuretic secretion is enhanced by alkalosis (38). In addition to a shift in the dose-response curve, patients with CKD and those taking NSAIDs have a downward shift of the ceiling natriuresis, when expressed as absolute sodium excretion (rather than fractional). The mechanism for resistance attributable to NSAIDs is complex. Loop diuretic inhibition of NaCl reabsorption at the macula densa stimulates both renin secretion and prostaglandin (PG) production, the latter predominantly via cyclooxygenase-2 (39). When this happens, PG E2 feeds back on tubules, contributing to the resulting natriuresis by inhibiting NaCl transport along the thick ascending limb and collecting duct (40,41). NSAIDs block this PG-mediated antinatriuresis. When used chronically, NSAIDs increase the abundance and activity of NKCC2 along the thick ascending limb (42). Additionally, loop diuretics inhibit the second transporter isoform, NKCC1, mentioned above, which is also expressed by vascular smooth muscle cells; loop diuretics contribute to afferent arteriolar vasodilation by blocking this transporter (43), thus helping to maintain GFR despite a lower ECF volume. Again, this compensatory adaptation is largely dependent on PG production and can be blocked by NSAIDs. The clinical consequence of these effects is evident in the association between recent use of NSAIDs and risk for hospitalization in patients with heart failure (34). In fact, the combination of three classes of drugs that affect hemodynamics of the kidney, loop diuretics, angiotensin-converting inhibitors (or receptor blockers), and NSAIDs, is associated with AKI (44)., Loop diuretics are medications used in the management and treatment of fluid overload conditions such as heart failure, nephrotic syndrome or cirrhosis, and hypertension, in addition to edema. This activity reviews the indications, action, and contraindications for loop diuretics as a valuable agent in managing fluid overload and hypertension., (C) Comparing effects of loop diuretics and distal convoluted tubule (DCT) diuretics on absolute sodium excretion, given a retained effect on fractional excretion. There are additional reasons that CKD is a loop diuretic–resistant state..
Loop diuretics have steep dose-response curves, meaning there is little effect until a threshold level is reached, then an upper threshold of effect. Diuretic resistance is a complex clinical problem with poor prognosis and ill-defined treatment options, clearly in need of further study., Few real-world comparative effectiveness studies have examined outcomes across all 3 loop diuretics. The study goal was to compare the effects of loop diuretic prescribing at HF hospitalization discharge on mortality and HF readmission., The studies were selected based on the following criteria: (1) prospective, randomized studies comparing intravenous (IV) continuous infusion of a loop diuretic to IV bolus injection of diuretics treatment in decompensated HF patients; (2) studies with at least in-hospital follow-up duration; (3) studies with the clinical outcomes, such as , Loop diuretics have complex effects on renal and systemic hemodynamics, which are influenced by the dose and route of administration, concomitant disease and treatment, and long-term use., Loop diuretics are the cornerstone to treat congestion and to maintain euvolemia. While furosemide is the most used loop diuretic, other loop diuretics may exhibit theoretical advantages. We aim to compare all types of loop diuretics for patients with CHF., Administration routes, doses, and duration of effectiveness vary from drug to drug. Establish baseline values for complete blood cell count, liver function tests, serum electrolytes, magnesium, blood urea nitrogen, and creatinine levels, and review periodically..