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Renal tubular acidosis (RTA) is a medical condition that involves an accumulation of acid in the body due to a failure of the kidneys to appropriately acidify the urine. [1] In renal physiology, when blood is filtered by the kidney, the filtrate passes through the tubules of the nephron, allowing for exchange of salts, acid equivalents, and other solutes before it drains into the bladder as urine.
Proximal renal tubular acidosis (pRTA) or type 2 renal tubular acidosis (RTA) is a type of RTA caused by a failure of the proximal tubular cells to reabsorb filtered bicarbonate from the urine, leading to urinary bicarbonate wasting and subsequent acidemia. The distal intercalated cells function normally, so the acidemia is less severe than ...
Distal renal tubular acidosis (dRTA) is the classical form of RTA, being the first described. Distal RTA is characterized by a failure of acid secretion by the alpha intercalated cells of the distal tubule and cortical collecting duct of the distal nephron . [ 1 ]
Renal salt wasting and high concentrations of sodium in sweat, stool, and saliva. The disorder often involves multiple organ systems and can be life threatening in the neonatal period. Patients usually present with hyponatremia, hyperkalemia, and increased plasma renin activity with high serum aldosterone concentrations.
Proximal renal tubular acidosis; Distal renal tubular acidosis; Hyperalimentation; Addison disease; Acetazolamide; Spironolactone; Saline infusion; To distinguish between the main types of metabolic acidosis, a clinical tool called the anion gap is very useful. The anion gap is calculated by subtracting the sum of the serum concentrations of ...
Fanconi syndrome or Fanconi's syndrome (English: / f ɑː n ˈ k oʊ n i /, / f æ n-/) is a syndrome of inadequate reabsorption in the proximal renal tubules [1] of the kidney.The syndrome can be caused by various underlying congenital or acquired diseases, by toxicity (for example, from toxic heavy metals), or by adverse drug reactions. [2]
Lightwood–Albright syndrome is a neonatal form of renal tubular acidosis. [1] It is characterized by distal renal tubular acidosis that occurs as a result of bicarbonate wasting and the inability to excrete hydrogen ions. [2] [3] By definition, it is a transient process and has no particular disease course.
It is used to aid in the differential diagnosis of metabolic acidosis. [2] The term "anion gap" without qualification usually implies serum anion gap. The "urine anion gap" is a different measure, principally used to determine whether the kidneys are capable of appropriately acidifying urine.