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Combination of | |
---|---|
Potassium citrate | Mineral supplement |
Potassium hydrogencarbonate | Mineral supplement |
Clinical data | |
Trade names | Sibnayal |
Other names | ADV7103 |
License data | |
ATC code | |
Legal status | |
Legal status |
Potassium citrate/potassium hydrogencarbonate is a fixed-dose combination medication intended for the treatment of distal renal tubular acidosis. [1] It contains potassium citrate and potassium hydrogencarbonate. [1]
Potassium citrate/potassium hydrogencarbonate was approved for medical use in the European Union in April 2021. [1]
Potassium citrate/potassium hydrogencarbonate is indicated for the treatment of distal renal tubular acidosis (dRTA) in people aged one year and older. [1]
On 10 December 2020, the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA) adopted a positive opinion, recommending the granting of a marketing authorization for the medicinal product Sibnayal. [1] The applicant for this medicinal product is Advicenne S.A. [1] Potassium citrate/potassium hydrogencarbonate was approved for medical use in the European Union in April 2021. [1]
Potassium citrate/potassium hydrogencarbonate is recommended for approval in the United Kingdom. [3]
Potassium citrate/potassium hydrogencarbonate is undergoing Phase III trials in preparation for evaluation by the U.S. Food and Drug Administration (FDA). [4]
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. 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. The metabolic acidosis that results from RTA may be caused either by insufficient secretion of hydrogen ions into the latter portions of the nephron or by failure to reabsorb sufficient bicarbonate ions from the filtrate in the early portion of the nephron. Although a metabolic acidosis also occurs in those with chronic kidney disease, the term RTA is reserved for individuals with poor urinary acidification in otherwise well-functioning kidneys. Several different types of RTA exist, which all have different syndromes and different causes. RTA is usually an incidental finding based on routine blood draws that show abnormal results. Clinically, patients may present with vague symptoms such as dehydration, mental status changes, or delayed growth in adolescents.
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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. This failure of acid secretion may be due to a number of causes. It leads to relatively alkaline urine, due to the kidney's inability to acidify the urine to a pH of less than 5.3.
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 dRTA and the urine can acidify to a pH of less than 5.3. pRTA also has several causes, and may occasionally be present as a solitary defect, but is usually associated with a more generalised dysfunction of the proximal tubular cells called Fanconi syndrome where there is also phosphaturia, glycosuria, aminoaciduria, uricosuria and tubular proteinuria.
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