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Drug-induced renal tubular acidosis in a patient receiving trimethoprim-sulfamethoxazole.
BMJ Case Rep
January 2025
General Surgery, Changi General Hospital, Singapore.
An Asian woman in her 70s was started on trimethoprim-sulfamethoxazole (TMP-SMX) for treatment of her left fourth toe osteomyelitis. During the course of her therapy, she developed renal tubular acidosis despite being immunocompetent with no known renal disease. Cessation of TMP-SMX and supportive care resulted in resolution of her condition.
View Article and Find Full Text PDFOn the substrate turnover rate of NBCe1 and AE1 SLC4 transporters: structure-function considerations.
Front Physiol
January 2025
Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
A transport protein's turnover rate (TOR) is the maximum rate of substrate translocation under saturating conditions. This parameter represents the number of transporting events per transporter molecule (assuming a single transport site) per second (s). From this standpoint, a transporter's TOR is similar to an enzyme's catalytic constant.
View Article and Find Full Text PDFA Rare Clinical Confluence: Metachromatic Leukodystrophy and Distal Renal Tubular Acidosis.
Indian J Nephrol
August 2024
Department of Pediatrics, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India.
Exocrine pancreatic insufficiency as an unusual extrarenal manifestation of proximal renal tubular acidosis associated with a novel SLC4A4 mutation.
Pediatr Nephrol
January 2025
Department of Pediatric Nephrology, Istanbul University- Cerrahpasa, Cerrahpasa Faculty of Medicine, 34098, Istanbul, Turkey.
Autosomal recessive proximal renal tubular acidosis (AR-pRTA) with ocular abnormalities is a rare syndrome caused by variants in the SLC4A4 gene, which encodes Na/HCO3 cotransporter (NBCe1). The syndrome primarily affects the kidneys, but also causes extra-renal manifestations. Pancreatic type NBCe1 is located at the basolateral membrane of the pancreatic ductal cells and together with CFTR chloride channel, it is involved in bicarbonate secretion.
View Article and Find Full Text PDFRenal Tubular Acidosis: Core Curriculum 2025.
Am J Kidney Dis
January 2025
Division of Nephrology and Hypertension, Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Renal tubular acidoses (RTAs) are a subset of non-anion gap metabolic acidoses that result from complex disturbances in renal acid excretion. Net acid excretion is primarily accomplished through the reclamation of sodium bicarbonate and the buffering of secreted protons with ammonia or dibasic phosphate, all of which require a series of highly complex and coordinated processes along the renal tubule. Flaws in any of these components lead to the development of metabolic acidosis and/or a failure to compensate fully for other systemic acidoses.
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