Switching to an L/N-Type Calcium Channel Blocker Shows Renoprotective Effects in Patients with Chronic Kidney Disease: The Kyoto Cilnidipine Study

Hatta, Tsuguru; Takeda, Kazuo; Shiotsu, Yayoi; Sugishita, Chikako; Adachi, Takaomi; Kimura, Takayasu; Sonomura, Kazuhiro; Kusaba, Tetsuro; Kishimioto, N; Narumiya, Hisao; Tanda, Shuji; Tamagaki, Keiichi; Yamada, Kazutaka; Kameyama, Hisako; Kido, Hidenori; Harada, S.; Bito, Yasuyuki; Moriguchi, Jiro; Morimoto, Satoshi; Okigaki, Mitsuhiko; Itoh, Hideki; Mori, Yuichi; Nakata, Tetsuo; Maki, Kei; Sasaki, Sachiko; Sawada, Kenichi; Matsubara, Hiroaki

doi:10.1177/147323001204000420

Cited by 15 publications

(17 citation statements)

References 42 publications

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“…One such example is cilnidipine (Uneyama et al, 1997;Kato et al, 2002), which has analgesic properties in rats (Koganei et al, 2009) in addition to being kidney protective and antihypertensive in human patients (Hatta et al, 2012;Kario et al, 2013). These beneficial effects may be attributable to the actions of this compound on N-type channels in the sympathetic nervous system (Takahara, 2009).…”

Section: Ca V 2 Channel Pathophysiologymentioning

confidence: 99%

The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential

Zamponi¹,

Striessnig²,

Koschak³

et al. 2015

Pharmacol Rev

871

992

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Section: Ca V 2 Channel Pathophysiologymentioning

confidence: 99%

The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential

Zamponi¹,

Striessnig²,

Koschak³

et al. 2015

Pharmacol Rev

871

992

View full text Add to dashboard Cite

“…[22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38] Blockers of the RAAS were prescribed in both the intervention and control groups in all included studies. Characteristics of the individual trials are displayed in Table 1.…”

Section: Characteristics and Quality Of The Studiesmentioning

confidence: 99%

“…Nine studies enrolled patients with preserved kidney function (GFR460 ml min − 1 1.73 m − 2 ) 22,24,26,[28][29][30]32,33,36 and eight studies enrolled patients with low GFR (o60 ml min − 1 1.73 m − 2 ). 23,25,27,31,34,35,37,38 At enrollment, hypertension was well controlled in only 3 studies 22,28,34 and poorly controlled in the remaining 14 studies. The GFR was assessed in 15 studies.…”

Section: Characteristics and Quality Of The Studiesmentioning

confidence: 99%

Effect of N- and T-type calcium channel blocker on proteinuria, blood pressure and kidney function in hypertensive patients: a meta-analysis

et al. 2015

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The combination of a calcium channel blocker (CCB) and a blocker of the renin-angiotensin-aldosterone system (RAAS) is recommended in clinical practice guidelines. L/N- and L/T-type CCBs might provide an additional effect on lowering proteinuria. Therefore, we conducted a meta-analysis to assess the efficacy of L/N- and L/T-type CCBs in hypertensive patients with proteinuria. We searched MEDLINE, Scopus, Cochrane Central Register of Controlled Trials and ClinicalTrials.gov for single-arm studies and randomized controlled trials (RCTs) that examined the effect of L/N- and L/T-type CCBs as add-on therapy compared with standard antihypertensive regimen for proteinuria on hemodynamic and kidney-related parameters in hypertensive patients with proteinuria. Random-effect model meta-analyses were used to compute changes in the outcomes of interest. We identified 17 RCTs, representing 1905 patients. By meta-analysis, L/N- and L/T-type CCB add-on therapy did not yield significant changes in systolic and diastolic blood pressure compared with standard treatment, but there was a significant lowering of the pulse rate. However, L/N- and L/T-type CCBs resulted in a significant standardized net decrease in albuminuria and proteinuria (-1.01; 95% confidence interval (CI), -1.78 to -0.23; P=0.01), and a standardized net improvement in the estimated glomerular filtration rate and serum creatinine (0.23; 95% CI, 0.11 to 0.35, P<0.001; and -0.25; 95% CI, -0.46 to -0.03; P=0.02, respectively). Despite no additional lowering effect on blood pressure, L/N- and L/T-type CCBs combined with a blocker of the RAAS provided a decrease in proteinuria and improvement in kidney function. Further studies are required to establish the long-term kidney benefits of this combination therapy.

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“…The high efficacy and tolerability of calcium channel blockers make them as one of the first line monotherapy for the treatment of hypertension [1]. The mechanism by which amlodipine lowers the blood pressure includes, reduction in peripheral resistance thereby leading to vasodilation.…”

Section: Discussionmentioning

confidence: 99%

Amlodipine Induced Severe Pedal Edema: A Case Report from a Tertiary Care Hospital

Sanghavi¹,

Someshwari²,

Ganesan³

et al. 2017

J Pharmacovigil

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Amlodipine is a fourth generation dihydropyridine derivative calcium channel blocker, mainly used in the treatment of hypertension, angina and certain other cardiac disorders. It is an L-type Ca2+ channel blocker, which leads to inhibitory action on the sympathetic N-type Ca2+ channels. The oral bioavailability of amlodipine is between 64% and 90%. The longer duration of action of amlodipine is due to a combination of high bioavailability, slow clearance and long half-life where by plasma concentration of the drug is above minimum effective concentration for a long time and show sustained efficacy. The most frequently occurring adverse effect with amlodipine therapy includes palpitation, flushing, ankle edema, hypotension, headache and nausea. PedaPl edema is a common adverse effect of calcium channel blocker (Amlodipine, Nifedipine, Diltiazem, Felodpine, Isradipine). We report a patient who developed pitting type pedal edema after treating with amlodipine for hypertension.Keywords: Amlodipine; Glimepride; Pedal edema Case DescriptionA 43 yrs old male patient was admitted to general medicine ward with complaints of swelling of the legs. On further interviewing, he was a known case of diabetes mellitus, under oral hypoglycemic agent of glimepride 2 mg and metformin 500 mg for past 1 yr. Before 3 months the patient was also diagnosed with hypertension and was under irregular medication.By examining the vital sign, blood pressure was found to be 160/90 mmHg, pulse rate 78 beats per minute and all other laboratory investigations such as complete blood count, liver function test urine analysis, chest X ray, electrocardiograph seems to be normal. The diabetic profile shows Random blood glucose -262 mg/dl, HbA1C-7%. From the subjective, laboratory examination and past history of the patient he was diagnosed with type II diabetes mellitus and hypertension. The patient was treated with glimepride 2 mg, metformin 500 mg and amlodipine 2.5 mg orally once daily. On the 4th day after initiation of amlodipine therapy, the patient was presented with pedal edema (pitting type). The physician interprets that the pedal edema was caused by amlodipine. On cessation of amlodipine the patient was recovered from edema and an alternative anti-hypertensive agent, telmisartan 40 mg and hydrochlorothiazide 12.5 mg once daily was prescribed.

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Switching to an L/N-Type Calcium Channel Blocker Shows Renoprotective Effects in Patients with Chronic Kidney Disease: The Kyoto Cilnidipine Study

Cited by 15 publications

References 42 publications

The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential

The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential

Effect of N- and T-type calcium channel blocker on proteinuria, blood pressure and kidney function in hypertensive patients: a meta-analysis

Amlodipine Induced Severe Pedal Edema: A Case Report from a Tertiary Care Hospital

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