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From the Research
Ethanol Ingestion and Oxalate Crystal Formation
- Ethanol ingestion can lead to the formation of oxalate crystals in urine, although the exact mechanism is not directly stated in the provided studies 1, 2, 3.
- However, it is known that oxalate is a metabolite that promotes the formation of calcium oxalate crystals in urine, and hyperoxaluria is a feature of genetic diseases that can lead to chronic kidney disease 1.
- Ethylene glycol poisoning, which is related to ethanol ingestion, induces the crystallization of calcium oxalate crystals in renal tubules, promoting acute renal failure 1, 2.
- The formation of oxalate crystals in urine is also related to the metabolism of glyoxylate to oxalate in the liver, due to lactate dehydrogenase (LDH) activity, especially the LDH-5 isoenzyme 1.
Mechanism of Oxalate Crystal Formation
- The metabolism of ethylene glycol leads to the formation of oxalic acid, which precipitates in the kidney in the form of calcium oxalate crystals, causing physical damage to the renal tubules 2.
- The internalization of calcium oxalate monohydrate (COM) crystals by proximal tubule cells is a critical step in the resulting cytotoxicity, and COM crystals are internalized by cells in a time- and concentration-dependent manner 3.
- The binding and internalization of COM crystals by cells play critical roles in cytotoxicity, and explain why rat cells are more sensitive to COM crystals than human cells 3.
Clinical Relevance
- The use of stiripentol, a drug that inhibits neuronal LDH-5 isoenzyme activity, has been shown to decrease urine oxalate excretion in rats and protect kidney tissue and function against ethylene glycol intoxication and hydroxyproline-induced calcium oxalate crystalline nephropathy 1.
- Further clinical studies are needed to determine the effectiveness of stiripentol in reducing urine oxalate excretion in humans 1.