Renal Function and Healthcare Costs in Patients with Polycystic Kidney Disease

Lentine, Krista L.; Xiao, Huiling; Machnicki, Gerardo; Gheorghian, Adrian; Schnitzler, Mark A.

doi:10.2215/cjn.00780110

Cited by 46 publications

(51 citation statements)

References 26 publications

(18 reference statements)

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“…In Northeast Ohio, efforts are being made to facilitate health information exchange across various institutions that may not only facilitate the data transfer in EHRs for clinical care but may provide additional data for research purposes. Lastly, care for non-dialysis dependent CKD is associated with higher costs (compared to non-CKD population) and such registries could also provide an opportunity to examine costs incurred for various management aspects of CKD [45, 49]. …”

Section: Cleveland Clinic Experiencementioning

confidence: 99%

Electronic health records: a new tool to combat chronic kidney disease?

Navaneethan

Jolly²,

Sharp

et al. 2013

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Electronic health records (EHRs) were first developed in the 1960s as clinical information systems for document storage and retrieval. Adoption of EHRs has increased in the developed world and is increasing in developing countries. Studies have shown that quality of patient care is improved among health centers with EHRs. In this article, we review the structure and function of EHRs along with an examination of its potential application in CKD care and research. Well-designed patient registries using EHRs data allow for improved aggregation of patient data for quality improvement and to facilitate clinical research. Preliminary data from the United States and other countries have demonstrated that CKD care might improve with use of EHRs-based programs. We recently developed a CKD registry derived from EHRs data at our institution and complimented the registry with other patient details from the United States Renal Data System and the Social Security Death Index. This registry allows us to conduct a EHRs-based clinical trial that examines whether empowering patients with a personal health record or patient navigators improves CKD care, along with identifying participants for other clinical trials and conducting health services research. EHRs use have shown promising results in some settings, but not in others, perhaps attributed to the differences in EHRs adoption rates and varying functionality. Thus, future studies should explore the optimal methods of using EHRs to improve CKD care and research at the individual patient level, health system and population levels.

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Section: Cleveland Clinic Experiencementioning

confidence: 99%

Electronic health records: a new tool to combat chronic kidney disease?

Navaneethan

Jolly²,

Sharp

et al. 2013

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“…In patients with ADPKD, dysregulation of the primary cilium causes localized and unregulated expansion of the renal tubule epithelium, resulting in the formation of fluid-filled cysts that grow and ultimately obstruct renal tubules, blood vessels, and lymphatics [9]. In general, progression of the disease, as measured by increasing kidney volume and decreasing kidney function, is inexorable, with an estimated 45–70% of patients developing end-stage renal disease (ESRD) by the age of 65 [10]. Twenty-eight thousand prevalent cases of ESRD were attributable to ADPKD in the United States in 2011, making it the fourth leading cause of ESRD next to diabetes, hypertension, and glomerulonephritis [11].…”

Section: Introductionmentioning

confidence: 99%

Rationale and Design of a Clinical Trial Investigating Tolvaptan Safety and Efficacy in Autosomal Dominant Polycystic Kidney Disease

et al. 2017

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Background: In TEMPO 3:4, the vasopressin V2-receptor antagonist tolvaptan slowed kidney growth and function decline in autosomal dominant polycystic kidney disease (ADPKD) patients with relatively preserved kidney function. Methods: Prospective, phase 3b, multi-center, randomized-withdrawal, placebo-controlled, double-blind trial of tolvaptan in ADPKD patients with late stage 2 to early stage 4 chronic kidney disease (CKD). The primary endpoint was estimated glomerular filtration rate (eGFR) change from pre-treatment baseline to post-treatment follow-up. Secondary endpoints included annualized eGFR slope, incidence of ADPKD complications, and overall and hepatic safety profiles. Participants were 18-55 year-old ADPKD patients with baseline eGFR ≥25 and ≤65 mL/min/1.73 m² or 56-65 year-old with eGFR ≥25 and ≤44 mL/min/1.73 m² and evidence of eGFR decline >2.0 mL/min/1.73 m² per year. Daily split doses of tolvaptan were titrated to tolerance (30/15, 45/15, 60/30, or 90/30 mg) and maintained for 12 months, after an 8-week pre-randomization period to screen out subjects unable to tolerate at least 60/30 mg for 3 weeks. Results: Of 1,495 subjects who entered the tolvaptan titration period, 125 (8.4%) discontinued the study before randomization. One thousand three hundred seventy subjects (684 tolvaptan, 686 placebo) from 213 centers across 21 countries were randomized. Baseline demographics were well balanced across treatment arms. Information collected during the study included eGFR, survey scores (PKD history and outcome), adverse events, vital signs, hematology, urinalysis, and serum chemistry tests. Conclusion: Replicating Evidence of Preserved Renal Function: An Investigation of Tolvaptan Safety and Efficacy (REPRISE) determines whether tolvaptan administered over 1 year exhibits disease-modifying properties in ADPKD patients with late stage 2 to early stage 4 CKD, which provides an important therapeutic advancement for this difficult-to-treat disease.

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“…By the age of 65 years, an estimated 45% to 70% of patients with ADPKD progress to ESRD and require dialysis therapy or transplantation. 4 However, recently, understanding of the underlying mechanisms of cystogenesis in this disease has led to a proliferation of research into targeted therapies for ADPKD itself. Some of the pathways that have been investigated include mediators of cell proliferation (eg, sarcoma [src]-family kinases, mammalian target of rapamycin [mTOR], mitogen-activated protein kinase [MAPK] inhibition 5-7 ), intracellular calcium regulation (eg, calcimimetics and polycystin 2 [PC-2] agonists 8,9 ), and intracellular cyclic adenosine monophosphate (cAMP) regulation (eg, vasopressin V2 receptor and somatostatin analogues 10,11 ).…”

mentioning

confidence: 99%