scholarly journals Cinacalcet may suppress kidney enlargement in hemodialysis patients with autosomal dominant polycystic kidney disease

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shinya Nakatani ◽  
Kozo Nishide ◽  
Senji Okuno ◽  
Eiji Ishimura ◽  
Daijiro Kabata ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Autosomal Dominant ◽  
Hemodialysis Patients ◽  
Kidney Volume ◽  
Polycystic Kidney ◽  
Calcium Sensing Receptor ◽  
Total Kidney Volume ◽  
Calcium Sensing ◽  
Autosomal Dominant Polycystic Kidney

AbstractA massively enlarged kidney can impact quality of life of autosomal dominant polycystic kidney disease (ADPKD) patients. A recent in vitro study demonstrated that an allosteric modulator of the calcium sensing receptor decreases adenosine-3′,5′-cyclic monophosphate, an important factor for kidney enlargement in ADPKD. Therefore, the present study was performed to determine whether cinacalcet, a calcium sensing receptor agonist, suppresses kidney enlargement in hemodialysis patients with ADPKD. Alteration of total kidney volume together with clinical parameters was retrospectively examined in 12 hemodialysis patients with ADPKD treated at a single institution in Japan. In the non-cinacalcet group with longer hemodialysis duration (n = 5), total kidney volume had an annual increase of 4.19 ± 1.71% during an overall period of 877 ± 494 days. In contrast, the annual rate of increase in total kidney volume in the cinacalcet group (n = 7) was significantly suppressed after cinacalcet treatment, from 3.26 ± 2.87% during a period of 734 ± 352 days before the start of cinacalcet to − 4.71 ± 6.42% during 918 ± 524 days after initiation of treatment (p = 0.047). The present findings showed that cinacalcet could be a novel therapeutic tool for suppression of kidney enlargement in hemodialysis patients with ADPKD.

scholarly journals Effect of tolvaptan in Japanese patients with autosomal dominant polycystic kidney disease: a post hoc analysis of TEMPO 3:4 and TEMPO Extension Japan

2021 ◽  
Author(s):  
Satoru Muto ◽  
Tadashi Okada ◽  
Yoshiyuki Shibasaki ◽  
Tatsuki Ibuki ◽  
Shigeo Horie
Keyword(s):  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Autosomal Dominant ◽  
Kidney Volume ◽  
Polycystic Kidney ◽  
Efficacy Evaluation ◽  
Total Kidney Volume ◽  
Post Hoc Analysis ◽  
Autosomal Dominant Polycystic Kidney ◽  
Post Hoc

Abstract Background Autosomal dominant polycystic kidney disease (ADPKD) is a progressive condition that eventually leads to end-stage renal disease. A phase 3 trial of tolvaptan (TEMPO 3:4; NCT00428948) and its open-label extension (TEMPO Extension Japan: TEMPO-EXTJ; NCT01280721) were conducted in patients with ADPKD. In this post hoc analysis, effects on renal function and the safety profile of tolvaptan were assessed over a long-term period that included the 3-year TEMPO 3:4 and the approximately 3-year TEMPO-EXTJ trials. Methods Patients from Japanese trial sites who completed TEMPO 3:4 were offered participation in TEMPO-EXTJ. Patients whose efficacy parameters were measured at year 2 in TEMPO-EXTJ for efficacy evaluation were included. The annual slope of the estimated glomerular filtration rate (eGFR) and growth in total kidney volume (TKV) were analyzed. Results In patients who received tolvaptan in TEMPO 3:4 and TEMPO-EXTJ, the annual slope of eGFR (mL/min/1.73 m2) was − 3.480 in TEMPO 3:4 and − 3.417 in TEMPO-EXTJ, with no apparent effect of an approximately 3.6-month off-treatment interval between the two trials. In patients who received a placebo in TEMPO 3:4 before initiating tolvaptan in TEMPO-EXTJ, the slope of eGFR was significantly less steep from TEMPO 3:4 (− 4.287) to TEMPO-EXTJ (− 3.364), a difference of 0.923 (P = 0.0441). Conclusion The TEMPO-EXTJ trial supports a sustained beneficial effect of tolvaptan on eGFR. In patients who received a placebo in TEMPO 3:4, initiation of tolvaptan in TEMPO-EXTJ was associated with a significant slowing of eGFR decline.

scholarly journals Effect of Statins on Renal Function and Total Kidney Volume in Autosomal Dominant Polycystic Kidney Disease

2020 ◽  
Vol 6 (6) ◽  
pp. 407-413
Author(s):  
Cheng Xue ◽  
Li-Ming Zhang ◽  
Chenchen Zhou ◽  
Chang-Lin Mei ◽  
Sheng-Qiang Yu
Keyword(s):  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Autosomal Dominant ◽  
Lipid Lowering ◽  
Control Group ◽  
Kidney Volume ◽  
Polycystic Kidney ◽  
Total Kidney Volume ◽  
Yearly Change ◽  
Autosomal Dominant Polycystic Kidney

<b><i>Background:</i></b> Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary nephropathy with few treatments to slow renal progression. The evidence on the effect of lipid-lowering agents (statins) on ADPKD progression remains inconclusive. <b><i>Methods:</i></b> We performed a systematic review and meta-analysis by searching the PubMed, Embase, Web of Science, and Cochrane databases (up to November 2019). Changes in estimated glomerular filtration rate (eGFR) and total kidney volume (TKV) were the primary outcomes. Mean differences (MDs) for continuous outcomes and 95% confidence intervals (CIs) were calculated by a random-effects model. <b><i>Results:</i></b> Five clinical studies with 648 participants were included. Statins did not show significant benefits in the yearly change in eGFR (4 studies, MD = −0.13 mL/min/m<sup>2</sup>, 95% CI: −0.78 to 0.52, <i>p</i> = 0.70) and the yearly change in TKV (3 studies, MD = −1.17%, 95% CI: −3.40 to 1.05, <i>p</i> = 0.30) compared with the control group. However, statins significantly decreased urinary protein excretion (−0.10 g/day, 95% CI: −0.16 to -0.03, <i>p</i> = 0.004) and serum low-density lipoprotein level (−0.34 mmol/L, 95% CI: −0.58 to −0.10, <i>p</i> = 0.006). <b><i>Conclusion:</i></b> Despite these proteinuria and lipid-lowering benefits, the effect of statins on ADPKD progression was uncertain.

scholarly journals Recent Advances in the Management of Autosomal Dominant Polycystic Kidney Disease

2018 ◽  
Vol 13 (11) ◽  
pp. 1765-1776 ◽  
Author(s):  
Fouad T. Chebib ◽  
Vicente E. Torres
Keyword(s):  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Autosomal Dominant ◽  
Somatostatin Analogs ◽  
Kidney Volume ◽  
Polycystic Kidney ◽  
Total Kidney Volume ◽  
Disease Modifying ◽  
Autosomal Dominant Polycystic Kidney ◽  
Disease Stratification

Autosomal dominant polycystic kidney disease (ADPKD), the most common monogenic cause of ESKD, is characterized by relentless development of kidney cysts, hypertension, and destruction of the kidney parenchyma. Over the past few years, major advancements in diagnosing, prognosticating, and understanding the pathogenesis and natural course of the disease have been made. Currently, no kidney disease is more suitable for nephron-protective strategies. Early nephrology referral and implementation of these strategies may have a substantial effect. Total kidney volume is a good prognostication marker and allows stratification of patients into slow or rapid progressing disease, with implications for their management. Measurement of total kidney volume, disease stratification, and prognostication are possible using readily available tools. Although some patients require only monitoring and basic optimized kidney protective measures, such as rigorous BP control and various lifestyle and dietary changes, others will benefit from disease-modifying treatments. Vasopressin V2 receptor antagonists, a likely disease-modifying treatment, has been approved in several countries and recently by the US Food and Drug Administration; other therapies, such as somatostatin analogs and other novel agents, are currently in clinical trials. The purpose of this article is to present our views on the optimal management to delay kidney disease progression in ADPKD.

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