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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 ...
Hypoaldosteronism may result in high blood potassium and is the cause of 'type 4 renal tubular acidosis', sometimes referred to as hyperkalemic RTA or tubular hyperkalemia. However, the acidosis, if present, is often mild. It can also cause urinary sodium wasting, leading to volume depletion and hypotension.
In patients with low levels of citrate in the urine (hypocitraturia) and incomplete distal renal tubular acidosis, treatment with potassium citrate helps prevent the formation of new kidney stones. [8] Urinary tract infections, when they occur, should also be treated. [8]
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.
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]
Secondary hyperaldosteronism (also hyperreninism, or hyperreninemic hyperaldosteronism) is due to overactivity of the renin–angiotensin–aldosterone system (RAAS).. The causes of secondary hyperaldosteronism are accessory renal veins, fibromuscular dysplasia, reninoma, renal tubular acidosis, nutcracker syndrome, ectopic tumors, massive ascites, left ventricular failure, and cor pulmonale.