Calcium oxalate (CaOx) (CaOx)

Calcium oxalate is an inorganic salt formed by the combination of calcium and oxalate ions, representing the most common component of human kidney stones [1, 2]. It exists primarily in two hydrate forms in biological systems: whewellite (monohydrate) and weddellite (dihydrate) [1]. While it serves as a defense mechanism in many plant species through the formation of sharp raphide crystals, in humans, it is a metabolic byproduct with no known beneficial biological function [5]. Pathological accumulation occurs when urinary concentrations of calcium and oxalate exceed their solubility product, leading to crystal nucleation, growth, and aggregation in the renal tubules [2, 4]. This process is the hallmark of nephrolithiasis and can lead to severe conditions such as primary hyperoxaluria and systemic oxalosis, which may cause end-stage renal disease [3]. Although calcium oxalate itself is not a traditional therapeutic target like a receptor or enzyme, it is the central focus of treatments aimed at preventing stone formation [2]. Pharmacological interventions include the use of citrate to inhibit crystallization and thiazide diuretics to reduce urinary calcium excretion [4]. Recent advancements have also introduced RNA interference therapies that target upstream enzymes in the oxalate biosynthetic pathway to reduce the overall burden of calcium oxalate in the body [3]. Sources: [1] PubChem. Calcium oxalate (CID 2733787). https://pubchem.ncbi.nlm.nih.gov/compound/Calcium-oxalate [2] StatPearls. Nephrolithiasis. https://www.ncbi.nlm.nih.gov/books/NBK470361/ [3] Mayo Clinic. Hyperoxaluria and oxalosis. https://www.mayoclinic.org/diseases-conditions/hyperoxaluria/symptoms-causes/syc-20352254 [4] NIH/NIDDK. Kidney Stone Causes & Prevention. https://www.niddk.nih.gov/health-information/urologic-diseases/kidney-stones/causes-prevention [5] Coe FL, et al. Kidney stone disease. J Clin Invest. 2005;115(10):2598-2608.

Other names

Calcium ethanedioateWhewelliteWeddelliteOxalic acid calcium salt

Therapeutic strategies involve the inhibition of crystal nucleation, growth, and aggregation through the use of citrate, which chelates calcium ions and increases urinary pH. Thiazide diuretics are employed to reduce urinary calcium excretion, thereby lowering the calcium-oxalate supersaturation index. Additionally, novel RNA interference therapies like lumasiran and nedosiran reduce the production of oxalate by silencing hepatic enzymes such as glycolate oxidase and lactate dehydrogenase, respectively.