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Indapamide is contraindicated in known hypersensitivity to sulfonamides, severe kidney failure, hepatic encephalopathy or severe liver failure, and a low blood potassium level. [citation needed] There is insufficient safety data to recommend indapamide use in pregnancy or breastfeeding. [citation needed]
Unsuppressed ADH causes a physiologically inappropriate increase in solute-free water being reabsorbed by the tubules of the kidney to the venous circulation leading to hypotonic hyponatremia (a low plasma osmolality and low sodium levels). [2] The causes of SIADH are commonly grouped into categories including: central nervous system diseases ...
Conditions that can lead to falsely low sodium measurements include high blood protein levels such as in multiple myeloma, high blood fat levels, and high blood sugar. [5] [6] Treatment is based on the underlying cause. [4] Correcting hyponatremia too quickly can lead to complications. [5]
Doing so lessens the chance of increaseing the serum sodium level too rapidly as blood volume rises and ADH levels fall. [citation needed] In people who are volume depleted (e.g., their blood volume is too low), ADH secretion is increased since volume depletion is a potent stimulus for ADH secretion.
Sodium reabsorption also causes water retention. [8] [9] When the kidneys detect low blood pressure, the renin–angiotensin–aldosterone system (RAAS) is activated and eventually, aldosterone is secreted. Aldosterone binds to aldosterone receptors (mineralocorticoid receptors) increasing sodium reabsorption in an effort to increase blood ...
The thiazides cause a net decrease in calcium lost in urine. [7] The potassium-sparing diuretics cause a net increase in calcium lost in urine, but the increase is much smaller than the increase associated with other diuretic classes. [7] By contrast, loop diuretics promote a significant increase in calcium excretion. [8]
The most obvious cause is a kidney or systemic disorder, including amyloidosis, [2] polycystic kidney disease, [3] electrolyte imbalance, [4] [5] or some other kidney defect. [2] The major causes of acquired nephrogenic diabetes insipidus that produce clinical symptoms (e.g., polyuria) in the adult are lithium toxicity and high blood calcium.
Using a fixed combination of an ACE inhibitor and a chlorosulfamoyl diuretic leads to additive synergy of the antihypertensive effects of the two constituents. Its pharmacological properties are derived from those of each of the components taken separately, in addition to those due to the additive synergistic action of the two constituents, when combined, on vascular endothelium ...