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 Table of Contents    
Year : 2016  |  Volume : 48  |  Issue : 3  |  Page : 340-341

Antiurolithiatic effect of lithocare against ethylene glycol-induced urolithiasis in Wistar rats

Department of Urology, Christian Medical College, Vellore, Tamil Nadu, India

Date of Web Publication23-May-2016

Correspondence Address:
Dr. Ranil Johann Boaz
Department of Urology, Christian Medical College, Vellore, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0253-7613.182897

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How to cite this article:
Boaz RJ, Dangi AD, John NT. Antiurolithiatic effect of lithocare against ethylene glycol-induced urolithiasis in Wistar rats. Indian J Pharmacol 2016;48:340-1

How to cite this URL:
Boaz RJ, Dangi AD, John NT. Antiurolithiatic effect of lithocare against ethylene glycol-induced urolithiasis in Wistar rats. Indian J Pharmacol [serial online] 2016 [cited 2023 Dec 3];48:340-1. Available from: https://www.ijp-online.com/text.asp?2016/48/3/340/182897


This letter is in context to the article published in your journal titled, “Antiurolithiatic effect of lithocare (LC) against ethylene glycol (EG)-induced urolithiasis in Wistar rats.”[1] This was a well-designed interventional study with clearly defined intervention and availability of control and comparator (Cystone). However, there are some limitations which deserve mention.

In terms of methodology, the EG rat model is not without limitations. To decrease crystal formation after EG ingestion, intervention may work at any level in the metabolism of the EG or beyond. The question as to whether the new agent under study decreases crystallization and deposition of calcium oxalate or whether it acts on EG metabolism itself is unanswered. The rate limiting step in EG metabolism catalyzed by alcohol dehydrogenase is the site of action of the conventional antidotes to human EG poisoning; ethanol and 4-methylpyrazone (fomepizole). Both these agents increase the half-life of EG allowing the liver time to metabolize EG and excrete it via the kidneys.[2] Monitoring the serum concentration of EG would have differentiated between drug action affecting the metabolism of EG to oxalic acid as opposed to primarily creating conditions unfavorable for deposition of calcium oxalate crystals in the tubules.

Ethanol increases the fraction of EG excreted unchanged in the urine before toxic metabolites are formed. If any of the herbal ingredients were obtained as an ethanolic extract, this would present a confounder (detail unavailable in materials and methods). Similarly, if the preparation contained the vitamins thiamine or pyridoxine, it could facilitate metabolic detoxification of EG since these allow bypass of the regular EG metabolic pathway toward the formation of less toxic products (α-amino-β-ketoadipic acid and glycine, respectively).[3],[4]

Regarding choice of comparator; two out of three constitutive herbal ingredients of LC were listed to have diuretic effects. Urine output was significantly higher in rats receiving LC as compared to controls. Diuretic action alone would have been expected to decrease crystal accumulation by virtue of preventing supersaturation and retarding the process of crystallization. This is especially pertinent since the rats were given a free access to drinking water. Indeed, administration of a thiazide diuretic would have also resulted in hypocalciuria, hypooxaluria, decreased serum creatinine, serum urea, and blood urea nitrogen.[5] To examine for this effect, an arm treated with EG and diuretic such as a thiazide might have allowed a more valuable comparison than one with Cystone.

Further research will be required to elucidate the active principles and identify the sites of action. The conclusion that the new agent prevents EG-induced urolithiasis and reduced the growth of urinary stones would not be accurate as the experiment dealt with crystalluria and not lithogenesis per se. This assertion is an extrapolation of previous research showing that calcium oxalate crystals form aggregates in the collecting ducts that act as nidi for stone formation.[6]

On the basis of evidence provided, it would be better to conclude that the new agent reduces EG-induced crystalluria in rats and may prove to render benefit in reducing calcium oxalate stone formation in human subjects. There is scope for investigation as a novel therapy for EG poisoning by virtue of decreasing calcium oxalate monohydrate crystalluria in addition to the benefit of evident antioxidant properties.

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There are no conflicts of interest.

  References Top

Lulat SI, Yadav YC, Balaraman R, Maheshwari R. Antiurolithiatic effect of lithocare against ethylene glycol-induced urolithiasis in Wistar rats. Indian J Pharmacol 2016;48:78-82.  Back to cited text no. 1
[PUBMED]  Medknow Journal  
Beatty L, Green R, Magee K, Zed P. A systematic review of ethanol and fomepizole use in toxic alcohol ingestions. Emerg Med Int 2013;2013:638057.  Back to cited text no. 2
Lheureux P, Penaloza A, Gris M. Pyridoxine in clinical toxicology: A review. Eur J Emerg Med 2005;12:78-85.  Back to cited text no. 3
Hall TL. Fomepizole in the treatment of ethylene glycol poisoning. CJEM 2002;4:199-204.  Back to cited text no. 4
Woelfel A, Kaplan RA, Pak CY. Effect of hydrochlorothiazide therapy on the crystallization of calcium oxalate in urine. Metabolism 1977;26:201-5.  Back to cited text no. 5
Khan SR, Thamilselvan S. Nephrolithiasis: A consequence of renal epithelial cell exposure to oxalate and calcium oxalate crystals. Mol Urol 2000;4:305-12.  Back to cited text no. 6

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