Literature DB >> 17165082

Effect of verapamil on urinary stone-forming risk factors.

Kemal Sarica1, Sakip Erturhan, Bulent Altay.   

Abstract

Prevention of recurrent stone formation will only be possible with careful metabolic evaluation and appropriate management. In this present prospective study, a total of 95 patients with calcium oxalate (CaOx) stone disease were evaluated with respect to the effects of a calcium channel blocking agent (verapamil) therapy on stone-forming risk factors. A total of 95 patients with CaOx urolithiasis were well evaluated for the possible specific effects of verapamil administration on stone-forming risk factors during long-term follow-up. All patients had calcium-containing stones with normal renal morphology and function without any urinary tract infection. The follow-up period ranged from 12 to 36.6 months, with a mean value of 24.4 months. The age of the patients (54 male and 41 female; M/F: 1.31) ranged from 20 to 46 years (mean 34.3 years). On metabolic evaluation all patients had some kind of risk factors and patients were independently randomized into two groups, namely group 1 (n = 49): patients receiving calcium entry blocker, verapamil hydrochloride (isoptin 240 mg KKH tablets, oral t.i.d.); group 2 (n = 46): patients receiving no specific therapy (control patients) that were matched for sex and age. Follow-up results (at least 1 year) with respect to the changes in urinary stone-forming risk factors were recorded in both groups. During long-term follow-up patients undergoing no specific therapy did not show a significant change with respect to the urinary levels of stone-forming risk factors when compared with the others receiving verapamil on a regular basis. In the light of our results as well as the literature data, we believe that the pathophysiological mechanisms underlying the effect of verapamil on stone formation (as a result of enhanced crystal deposition) and on the excretion of the urinary stone-forming risk factors have to be well evaluated in further experimental as well as clinical studies. Although the exact mechanism of action is not clear; we may claim that the limitation of internal calcium shift by these agents may also well effect the tubular process related to oxalate handling which ultimately limits its excretion in urine.

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Year:  2006        PMID: 17165082     DOI: 10.1007/s00240-006-0075-z

Source DB:  PubMed          Journal:  Urol Res        ISSN: 0300-5623


  25 in total

Review 1.  Prevention of nephrolithiasis.

Authors:  M S Pearle
Journal:  Curr Opin Nephrol Hypertens       Date:  2001-03       Impact factor: 2.894

2.  Disparate effects of calcium antagonists on renal microcirculation.

Authors:  K Hayashi; T Nagahama; K Oka; M Epstein; T Saruta
Journal:  Hypertens Res       Date:  1996-03       Impact factor: 3.872

3.  [Comparative quantitative clinico-chemical analysis of the characteristics of 24-hour urine and morning urine].

Authors:  M Krieg; K J Gunsser; E Steinhagen-Thiessen; H Becker
Journal:  J Clin Chem Clin Biochem       Date:  1986-11

4.  Are calcium antagonists potential antilithiasic drugs?

Authors:  G Gambaro; E Cicerello; F Marchini; C Paleari; A Borsatti; B Baggio
Journal:  Contrib Nephrol       Date:  1987       Impact factor: 1.580

5.  Effect of potassium citrate therapy on stone recurrence and regrowth after extracorporeal shockwave lithotripsy in children.

Authors:  Kemal Sarica; Sakip Erturhan; Cihanser Yurtseven; Faruk Yagci
Journal:  J Endourol       Date:  2006-11       Impact factor: 2.942

Review 6.  Current status of calcium channel blockers.

Authors:  W H Frishman
Journal:  Curr Probl Cardiol       Date:  1994-11       Impact factor: 5.200

7.  Effect of T-type selective calcium antagonist on renal microcirculation: studies in the isolated perfused hydronephrotic kidney.

Authors:  Y Ozawa; K Hayashi; T Nagahama; K Fujiwara; T Saruta
Journal:  Hypertension       Date:  2001-09       Impact factor: 10.190

8.  Blockade of calcium influx through L-type calcium channels attenuates mitochondrial injury and apoptosis in hypoxic renal tubular cells.

Authors:  Tetsuhiro Tanaka; Masaomi Nangaku; Toshio Miyata; Reiko Inagi; Takamoto Ohse; Julie R Ingelfinger; Toshiro Fujita
Journal:  J Am Soc Nephrol       Date:  2004-09       Impact factor: 10.121

9.  [Effect of verapamil on urinary calcium and oxalate excretion in renal stone formers].

Authors:  M Iguchi; M Ikegami; H Kiwamoto; T Umekawa; Y Ishikawa; K Kohri; T Kurita
Journal:  Hinyokika Kiyo       Date:  1993-05

10.  Oral potassium citrate treatment for idiopathic hypocitruria in children with calcium urolithiasis.

Authors:  Ali Tekin; Serdar Tekgul; Necmettin Atsu; Mehmet Bakkaloglu; Sezer Kendi
Journal:  J Urol       Date:  2002-12       Impact factor: 7.450

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  3 in total

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Authors:  Kemal Sarica; Alper Kafkasli; Fehmi Narter; Oguz Ozturk; Ozgur Yazici; Bilal Hamarat; Cahit Sahin; Bilal Eryildirim
Journal:  Urolithiasis       Date:  2016-06-09       Impact factor: 3.436

2.  Externalization of phosphatidylserine via multidrug resistance 1 (MDR1)/P-glycoprotein in oxalate-treated renal epithelial cells: implications for calcium oxalate urolithiasis.

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Journal:  Int Urol Nephrol       Date:  2015-11-11       Impact factor: 2.370

3.  Calcium Pyrophosphate And Monosodium Urate Activate The NLRP3 Inflammasome Within Bladder Urothelium Via Reactive Oxygen Species And TXNIP.

Authors:  Shelby N Harper; Patrick D Leidig; Francis M Hughes; Huixia Jin; J Todd Purves
Journal:  Res Rep Urol       Date:  2019-11-20
  3 in total

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