Clinical effects of calcium channel blockers and renin-angiotensin-aldosterone system inhibitors on changes in the estimated glomerular filtration rate in patients with polycystic kidney disease

2010 ◽  
Vol 14 (6) ◽  
pp. 573-577 ◽  
Author(s):  
Michihiro Mitobe ◽  
Takumi Yoshida ◽  
Hidekazu Sugiura ◽  
Shunji Shiohira ◽  
Katsunori Shimada ◽  
...  
1994 ◽  
Vol 267 (6) ◽  
pp. F965-F970
Author(s):  
G. M. Eisner ◽  
I. Yamaguchi ◽  
R. A. Felder ◽  
L. D. Asico ◽  
P. A. Jose

The direct tubular natriuretic effect of calcium channel blockers (CCBs) may be due to an interaction between CCBs and a renal tubular dopamine receptor. We therefore studied the effects of two chemically unrelated CCBs, diltiazem and isradipine, infused into the right renal artery of 5% saline-loaded anesthetized rats alone or in the presence of a D1 antagonist, SKF-83742. Isradipine (0.03 microgram.kg-1.min-1) or diltiazem (20 but not 10 micrograms.kg-1.min-1) alone produced an increase in urine flow and an approximate doubling of absolute and fractional sodium excretion, which was not seen in the left kidney or in the control animals (analysis of variance, Scheffe's test, P < 0.05). SKF-83742 alone given systemically or into the right renal artery did not affect these parameters but did block the actions of diltiazem or isradipine. There was no change in mean arterial pressure, renal blood flow, or glomerular filtration rate in any of the experiments. In additional studies, we found that a combined infusion of dopamine (0.1 microgram.kg-1.min-1) and diltiazem (10 micrograms.kg-1.min-1) (doses that by themselves did not alter renal function) produced a twofold or greater increase in urine flow and absolute and fractional sodium excretion; glomerular filtration rate was not significantly changed. Intrarenal arterial CCBs, without a change in renal hemodynamics, produce a natriuresis that is blocked by a D1 antagonist. Concomitant administration of diltiazem and dopamine (each in subeffective doses when used alone) produces a synergistic effect.(ABSTRACT TRUNCATED AT 250 WORDS)


2014 ◽  
Vol 307 (10) ◽  
pp. H1504-H1511 ◽  
Author(s):  
Miki Imazu ◽  
Hiroyuki Takahama ◽  
Hiroshi Asanuma ◽  
Akira Funada ◽  
Yasuo Sugano ◽  
...  

Although the important role of fibroblast growth factor (FGF)23 on cardiac remodeling has been suggested in advanced chronic kidney disease (CKD), little is known about serum (s)FGF23 levels in patients with heart failure (HF) due to nonischemic cardiac disease (NICD) and early CKD. The present study aimed to investigate sFGF23 levels in NICD patients and identify the responsible factors for the elevation of sFGF23 levels. We prospectively measured sFGF23 levels in consecutive hospitalized NICD patients with early CKD (estimated glomerular filtration rate ≥ 40 ml·min−1·1.73 m−2) and analyzed the data of both echocardiography and right heart catheterization. Of the 156 NICD patients (estimated glomerular filtration rate range: 41–128 ml·min−1·1.73 m−2), the most severe HF symptom (New York Heart Association class III-IV, 53% vs. 33%, P = 0.015) was found in the above median sFGF23 (39.1 pg/ml) group compared with the below median sFGF23 group. sFGF23 levels were higher in patients with HF hospitalization history compared with those without HF [median: 46.8 (interquartile range: 38.8–62.7) vs. 34.7 (interquartile range: 29.6–42.4) pg/ml, P < 0.0001]. In the multivariate analysis, HF hospitalization was independently related to elevated sFGF23 levels ( P = 0.022). Both systolic dysfunction and high plasma aldosterone concentration were identified as predictors of high sFGF23 levels ( P < 0.05). Among the neurohormonal parameters, elevated sFGF23 levels were the only factor to predict a declining left ventricular ejection fraction ( P = 0.001). These findings suggest that the progression of HF per se contributes to the elevation of sFGF23 levels even in the early stages of CKD, which leads to further myocardial dysfunction, potentially creating a vicious cycle.


2015 ◽  
Vol 61 (10) ◽  
pp. 1265-1272 ◽  
Author(s):  
Jeffrey W Meeusen ◽  
Andrew D Rule ◽  
Nikolay Voskoboev ◽  
Nikola A Baumann ◽  
John C Lieske

Abstract BACKGROUND The Kidney Disease Improving Global Outcomes (KDIGO) guideline recommends use of a cystatin C–based estimated glomerular filtration rate (eGFR) to confirm creatinine-based eGFR between 45 and 59 mL · min−1 · (1.73 m2)−1. Prior studies have demonstrated that comorbidities such as solid-organ transplant strongly influence the relationship between measured GFR, creatinine, and cystatin C. Our objective was to evaluate the performance of cystatin C–based eGFR equations compared with creatinine-based eGFR and measured GFR across different clinical presentations. METHODS We compared the performance of the CKD-EPI 2009 creatinine-based estimated GFR equation (eGFRCr) and the newer CKD-EPI 2012 cystatin C–based equations (eGFRCys and eGFRCr-Cys) with measured GFR (iothalamate renal clearance) across defined patient populations. Patients (n = 1652) were categorized as transplant recipients (n = 568 kidney; n = 319 other organ), known chronic kidney disease (CKD) patients (n = 618), or potential kidney donors (n = 147). RESULTS eGFRCr-Cys showed the most consistent performance across different clinical populations. Among potential kidney donors without CKD [stage 2 or higher; eGFR &gt;60 mL · min−1 · (1.73 m2)−1], eGFRCys and eGFRCr-Cys demonstrated significantly less bias than eGFRCr; however, all 3 equations substantially underestimated GFR when eGFR was &lt;60 mL · min−1 · (1.73 m2)−1. Among transplant recipients with CKD stage 3B or greater [eGFR &lt;45 mL · min−1 · (1.73 m2)−1], eGFRCys was significantly more biased than eGFRCr. No clear differences in eGFR bias between equations were observed among known CKD patients regardless of eGFR range or in any patient group with a GFR between 45 and 59 mL · min−1 · (1.73 m2)−1. CONCLUSIONS The performance of eGFR equations depends on patient characteristics that are readily apparent on presentation. Among the 3 CKD-EPI equations, eGFRCr-Cys performed most consistently across the studied patient populations.


2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Boby Pratama Putra ◽  
Felix Nugraha Putra

Abstract Background and Aims Recent evidences showed an association between NAFLD and extrahepatic manifestations such as chronic kidney disease (CKD) although the result is still inconclusive. This study aims to measure the association of microalbuminuria and estimated glomerular filtration rate (eGFR) decline as CKD risks in NAFLD patients. Method Comprehensive searching using predefined queries was done through online databases Pubmed, EMBASE, ScienceDirect, and The Cochrane Library to include all relevant literature until November 2020. We included all cohort studies of NAFLD patients diagnosed by ultrasonography (USG), commutated tomography (CT), or scoring system fatty liver index (FLI) that reports microalbuminuria and eGFR decline below 60 ml/min/1.73m2. Bias risk was assessed by The Newcastle-Ottawa Scale for cohort studies. Analysis of this study was performed to provide pooled hazard ratio (HR) with 95% confidence interval (CI) using random-effect heterogeneity test. Results We included 10 cohort studies met our criteria. Analysis of 6 NAFLD cohort studies diagnosed by USG is significantly associated with eGFR decline (pooled HR = 1.54, 95% CI 1.13 to 2.11, p=0.006, I2=88%), while NAFLD patients diagnosed by FLI also showed significant association with eGFR decline (pooled HR = 1.58, 95% CI 1.52 to 1.64, p&lt;0.0001, I2=0%), thus overall analysis combined with CT diagnostic modalities showed significant association between NAFLD and eGFR decline (pooled HR=1.53 95%CI 1.29-1.80 p&lt;0.00001 I2=82%). Microalbuminuria risk is significantly increased in NAFLD patients (pooled HR = 1.93, 95% CI 1.39 to 2.67, p&lt;0.0001, I2=0%). Surprisingly, NAFLD patients whose increased gamma-glutamyltransferase (GGT) has higher eGFR decline risk (pooled HR = 1.73, 95% CI 1.02 to 2.92, p=0.04, I2=78%). Conclusion Microalbuminuria and eGFR decline are associated as CKD risks in NAFLD patients. However, further studies are still needed to establish the causality.


2021 ◽  
Vol 10 (22) ◽  
pp. 5309
Author(s):  
Yusuke Kameda ◽  
Tadashiro Saeki ◽  
Ko Hanai ◽  
Yuta Suzuki ◽  
Yasuko Uchigata ◽  
...  

Chronic kidney disease (CKD) is a well-known risk factor for postoperative complications in several surgical fields. However, although prevalent among diabetic candidates for vitrectomy, the effect of CKD on vitrectomy outcomes remains unclear. This study aimed at clarifying the relationship between CKD and the occurrence of vitrectomy-related complications in patients with proliferative diabetic retinopathy (PDR). The 6-month incidences of vitreous hemorrhage (VH) and neovascular glaucoma (NVG) following vitrectomy for PDR were compared among the following groups: stages 1–2 CKD (60 patients), stages 3–5 CKD (70 patients not on hemodialysis), and hemodialysis (HD; 30 patients). We also determined whether the deterioration of the estimated glomerular filtration rate (eGFR) was associated with post-vitrectomy events. The incidence of VH was significantly higher in the stages 3–5 CKD group (43%) than in the stages 1–2 CKD (10%) and HD (10%) groups. NVG was more common in the stages 3–5 CKD group (17%) than in the stages 1–2 CKD (2%) and HD (0%) groups. The reduced estimated glomerular filtration rate (eGFR) was the only significant variable associated with post-vitrectomy VH and NVG. Patients with PDR and CKD, particularly those with lower eGFR, might be at risk for post-vitrectomy VH and NVG.


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