User:Mr. Ibrahem/Renal tubular acidosis
| Mr. Ibrahem/Renal tubular acidosis | |
|---|---|
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| Significant bilateral nephrocalcinosis (calcification of the kidneys) on a frontal X-ray (radiopacities (white) in the right upper and left upper quadrant of the image), as seen in distal renal tubular acidosis | |
| Specialty | Nephrology |
| Symptoms | None, dehydration, weakness, confusion[1][2] |
| Complications | Kidney stones, low or high potassium, rickets, osteomalacia, kidney failure[3][4] |
| Types | Type 1, 2, 3, 4[2] |
| Causes | Lupus, multiple myeloma, diabetic kidney disease, certain medications, following a kidney transplant[2] |
| Diagnostic method | Metabolic acidosis with a normal anion gap, high blood chloride, and normal glomerular filtration rate[3] |
| Treatment | Depends on the cause and type[2] |
| Frequency | Uncommon[2] |
Renal tubular acidosis (RTA) is the increase of acid in the body due to failure of the kidneys to appropriately acidify the urine, despite the kidneys otherwise functioning normally.[3][2] Often there are no symptoms, though dehydration, weakness, or confusion may occur.[1][2] Without treatment complications may include kidney stones, low or high potassium, bone abnormalities such as rickets or osteomalacia, and kidney failure.[3][4]
RTA is more commonly acquire later in life and less commonly inherited from a person's parents.[2] Some causes include lupus, multiple myeloma, diabetic kidney disease, certain medications, and following a kidney transplant.[2] There are four types: type 1 (distal) involving failure to release hydrogen ions into the urine, type 2 (proximal) involving failure to reabsorb bicarbonate from the urine, type 3 is a mixed of the first two, and type 4 is due to low or resistance to aldosterone.[2] Diagnosis is based on a metabolic acidosis with a normal anion gap, high blood chloride, and normal glomerular filtration rate.[3]
Treatment partly depends on the underlying cause.[2] Treatment of type I and II may involve taking either sodium bicarbonate or potassium citrate.[2] Phosphate and vitamin D supplements may also be required.[2] Type IV disease may be treated with fludrocortisone or limiting dietary potassium and a diuretic.[2] Renal tubular acidosis is uncommon.[2] The condition was first described in 1935 by Lightwood.[5]
References[edit]
- ^ a b Yaxley J, Pirrone C (2016-12-21). "Review of the Diagnostic Evaluation of Renal Tubular Acidosis". The Ochsner Journal. 16 (4): 525–530. PMC 5158160. PMID 27999512. Archived from the original on 2019-11-03. Retrieved 2019-11-03.
- ^ a b c d e f g h i j k l m n o Mustaqeem, R; Arif, A (January 2020). "Renal Tubular Acidosis". PMID 30085586.
{{cite journal}}: Cite journal requires|journal=(help) - ^ a b c d e Laing CM, Toye AM, Capasso G, Unwin RJ (June 2005). "Renal tubular acidosis: developments in our understanding of the molecular basis". The International Journal of Biochemistry & Cell Biology. 37 (6): 1151–61. doi:10.1016/j.biocel.2005.01.002. PMID 15778079.
- ^ a b "Renal Tubular Acidosis | NIDDK". National Institute of Diabetes and Digestive and Kidney Diseases. Archived from the original on 9 January 2021. Retrieved 23 January 2021.
- ^ Avner, Ellis D.; Harmon, William E.; Niaudet, Patrick; Yoshikawa, Norishige (2009). Pediatric Nephrology. Springer Science & Business Media. p. 979. ISBN 978-3-540-76327-7. Archived from the original on 2021-08-29. Retrieved 2021-01-23.