In nine normal subjects, four men and five women between 23 and 49 years of age, 800mg calcium was orally administered as active absorbable algal calcium (AAA Ca) (A) and calcium carbonate (CaCO3) (B), to compare with non-calcium-containing placebo (C) in a crossover design. Calcium, oxalate, osmolality, creatinine, and pH were measured in the first three morning urine samples and Ca/osmolality, Ca/osmolality/body weight, Ca/creatinine, and oxalate/ osmolality were calculated to correct for urine dilution. Ca x oxalate product was also calculated, and Ca oxalate crystal in the sediment was microscopically examined, semiquantitatively estimated as -, +, ++, or , and numerically expressed as 0, 1, 2, or 3, respectively. Urinary Ca excretion was similar in groups A and B, but significantly larger than in group C, regardless of the method of correction for dilution. Urinary oxalate excretion with correction for osmolality, however, was significantly lower in A than in B and C, which gave similar values. Urine pH was similar among all three groups. Ca x oxalate product was significantly higher in C than in A, but A and B were not significantly different. AAA Ca appeared to decrease urinary oxalate excretion and Ca x oxalate product more efficiently than CaCO3, suggesting the possibility of inhibiting the formation of Ca x oxalate kidney stones.
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http://dx.doi.org/10.1007/pl00010643 | DOI Listing |
Pediatr Nephrol
January 2025
Novo Nordisk A/S, Lexington, MA, USA.
Background: Primary hyperoxaluria type 1 (PH1) is an autosomal recessive disorder with dysregulated glyoxylate metabolism in the liver. Oxalate over-production leads to renal stones, progressive kidney damage and renal failure, with potentially life-threatening systemic oxalosis. Nedosiran is a synthetic RNA interference therapy, designed to reduce hepatic lactate dehydrogenase (LDH) to decrease oxalate burden in PH.
View Article and Find Full Text PDFGut Microbes
December 2025
Department of Urology, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.
Hyperoxaluria, including primary and secondary hyperoxaluria, is a disorder characterized by increased urinary oxalate excretion and could lead to recurrent calcium oxalate kidney stones, nephrocalcinosis and eventually end stage renal disease. For secondary hyperoxaluria, high dietary oxalate (HDOx) or its precursors intake is a key reason. Recently, accumulated studies highlight the important role of gut microbiota in the regulation of oxalate homeostasis.
View Article and Find Full Text PDFPediatr Nephrol
January 2025
University Medical Center Hamburg-Eppendorf, University Children's Hospital, Martinistrasse 52, Hamburg, 20246, Germany.
Background: Primary hyperoxaluria type 1 (PH 1) is a rare genetic condition due to mutations in the AGXT gene. This leads to an overproduction of oxalate in the liver. Hyperoxaluria often causes kidney stones, nephrocalcinosis, and chronic kidney disease.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
Department of Urology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, 430060, P. R. China.
The initiation of calcium oxalate (CaOx) kidney stone formation is highly likely to stem from injury to the renal tubular epithelial cells (RTECs) induced by stimulation from an aberrant urinary environment. CHAC1 plays a critical role in stress response mechanisms by regulating glutathione metabolism. Endoplasmic reticulum (ER) stress and ferroptosis are demonstrated to be involved in stone formation.
View Article and Find Full Text PDFNefrologia (Engl Ed)
January 2025
Servicio de Nefrología, Hospital Universitario de la Princesa, Madrid, Spain. Electronic address:
Secondary hyperoxaluria is a metabolic disorder characterized by an increase in urinary oxalate excretion. The etiology may arise from an increase in the intake of oxalate or its precursors, decreased elimination at the digestive level, or heightened renal excretion. Recently, the role of the SLC26A6 transporter in the etiopathogenesis of this disease has been identified.
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