scholarly journals Urine Osmolarity and Risk of Dialysis Initiation in a CKD Cohort

2015 ◽  
Vol 66 (Suppl. 3) ◽  
pp. 14-17 ◽  
Author(s):  
Lise Bankir ◽  
Max Plischke ◽  
Nadine Bouby ◽  
Martin Haas
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Association Studies ◽  
Experimental Studies ◽  
Dialysis Initiation ◽  
Hazards Model ◽  
Baseline Creatinine ◽  
Stage Renal Disease ◽  
End Stage ◽  
Disease Stages

Background: Several experimental studies in rats and a few association studies in humans suggest that the antidiuretic action of vasopressin may accelerate the progression of chronic kidney disease. We undertook a retrospective analysis in a monocentric cohort of 273 patients with chronic kidney disease stages 1-4, focusing on a strong variable of interest, urinary osmolarity, and a strong endpoint, dialysis initiation. Data was analyzed in a multivariate proportional sub-distribution hazards model for competing risk data with appropriate co-variates. Main Results: Over a median follow-up period of 92 months, dialysis was initiated in 105 patients. After adjustments for baseline creatinine clearance, and other confounding factors, a higher risk for initiation of dialysis was found in patients with higher urinary osmolarity. After 72 months, the estimated adjusted cumulative incidence probability for dialysis initiation was 15, 24, and 34% in patients with baseline urinary osmolarity of 315, 510, and 775 mosm/l, respectively (p = 0.033). Key Messages: In this retrospective, longitudinal study, a higher baseline urinary osmolarity was strongly associated with a higher risk of end-stage renal disease (after appropriate adjustments). Further, prospective studies are required to evaluate the possible benefit of interventions aiming at reducing urinary osmolarity as a potential treatment for slowing chronic kidney disease progression.

scholarly journals Comparing the Effect of Folic Acid and Pentoxifylline on Delaying Dialysis Initiation in Patients with Advanced Chronic Kidney Disease

Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 2192
Author(s):  
Hsun Yang ◽  
Shiun-Yang Juang ◽  
Kuan-Fu Liao ◽  
Yi-Hsin Chen
Keyword(s):  
Chronic Kidney Disease ◽  
Folic Acid ◽  
Kidney Disease ◽  
Index Date ◽  
Dialysis Initiation ◽  
Nutrient Loss ◽  
Research Database ◽  
Advanced Chronic Kidney Disease ◽  
Stage Renal Disease ◽  
End Stage

Background: We hypothesized that the nutrient loss and chronic inflammation status may stimulate progression in advanced chronic kidney disease. Therefore, we aimed to generate a study to state the influence of combined nutritional and anti-inflammatory interventions. Methods: The registry from the National Health Insurance Research Database in Taiwan was searched for 20–90 years individuals who had certified end-stage renal disease. From January 2005 through December 2010, the diagnosis code ICD-9 585 (chronic kidney disease, CKD) plus erythropoiesis-stimulating agent (ESA) use was defined as entering advanced chronic kidney disease. The ESA starting date was defined as the first index date, whereas the initiation day of maintenance dialysis was defined as the second index date. The duration between the index dates was analyzed in different medical treatments. Results: There were 10,954 patients analyzed. The combination therapy resulted in the longest duration (n = 2184, median 145 days, p < 0.001) before the dialysis initiation compared with folic acid (n = 5073, median 111 days), pentoxifylline (n = 1119, median 102 days, p = 0.654), and no drug group (control, n = 2578, median 89 days, p < 0.001). Lacking eGFR data and the retrospective nature are important limitations. Conclusions: In patients with advanced CKD on the ESA treatment, the combination of folic acid and pentoxifylline was associated with delayed initiation of hemodialysis.

Markers of Arterial Stiffness Are Risk Factors for Progression to End-Stage Renal Disease among Patients with Chronic Kidney Disease Stages 4 and 5

2007 ◽  
Vol 107 (4) ◽  
pp. c177-c181 ◽  
Author(s):  
Maarten W. Taal ◽  
Mhairi K. Sigrist ◽  
Apostolos Fakis ◽  
Richard J. Fluck ◽  
Christopher W. McIntyre
Keyword(s):  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Arterial Stiffness ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Stage Renal Disease ◽  
End Stage ◽  
Disease Stages

scholarly journals Mineral Metabolites, Angiotensin II Inhibition and Outcomes in Advanced Chronic Kidney Disease

2015 ◽  
Vol 42 (5) ◽  
pp. 361-368 ◽  
Author(s):  
Anna J. Jovanovich ◽  
Michel B. Chonchol ◽  
Atousa Sobhi ◽  
Jessica B. Kendrick ◽  
Alfred K. Cheung ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
End Stage Renal Disease ◽  
Mineral Metabolism ◽  
Dialysis Initiation ◽  
Advanced Chronic Kidney Disease ◽  
All Cause Mortality ◽  
Stage Renal Disease ◽  
End Stage ◽  
Lower Hazard

Background: Evidence suggests that the renin-angiotensin-aldosterone system (RAAS) interacts with the vitamin D-fibroblast growth factor 23-Klotho axis. We investigated whether circulating mineral metabolism markers modify outcomes in response to RAAS inhibition in subjects with advanced chronic kidney disease (CKD). Methods: In this retrospective cohort study, we analyzed the association of angiotensin-converting enzyme inhibitor (ACEI) and angiotensin receptor blocker (ARB) use with all-cause mortality and dialysis initiation among 1,753 subjects (1,099 CKD, estimated glomerular filtration rate 18 ± 6 ml/min/1.73 m2 and 654 end-stage renal disease [ESRD]) from the Homocysteine in Kidney and End Stage Renal Disease (HOST) study. A propensity score analysis accounted for indication bias and Cox regression models adjusted for mineral metabolism markers. Results: Mean follow-up was 3.2 years; 714 (41%) subjects died and 615 (56%) initiated dialysis. In adjusted analyses, all subjects treated with ACEI/ARB had a significantly lower hazard of death (hazards ratio (HR) 0.81, 95% CI 0.70-0.95, p = 0.007). Those with CKD not on dialysis and treated with ACEI/ARB trended toward a lower hazard of dialysis initiation (HR 0.86, 95% CI 0.73-1.01, p = 0.06). The association with mortality did not differ by level of mineral metabolism marker (p for interaction >0.16); however, the relationship with dialysis initiation differed according to the median serum phosphorus level (p for interaction <0.001). Conclusions: RAAS inhibition was associated with decreased all-cause mortality independent of disordered mineral metabolism among mostly male HOST subjects with advanced CKD and ESRD. However, among those with CKD not requiring dialysis, the renoprotection associated with RAAS inhibition was attenuated by higher serum phosphorus levels. Further studies are needed to confirm this association.

scholarly journals Renoprotective Effects of ETA Receptor Antagonists Therapy in Experimental Non-Diabetic Chronic Kidney Disease: Is There Still Hope for the Future?

2018 ◽  
pp. S55-S67 ◽  
Author(s):  
I. VANĚČKOVÁ ◽  
S. HOJNÁ ◽  
M. KADLECOVÁ ◽  
Z. VERNEROVÁ ◽  
L. KOPKAN ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Cell Injury ◽  
Interstitial Fibrosis ◽  
Experimental Studies ◽  
Tubular Atrophy ◽  
Eta Receptor ◽  
Life Threatening ◽  
Stage Renal Disease ◽  
End Stage

Chronic kidney disease (CKD) is a life-threatening disease arising as a frequent complication of diabetes, obesity and hypertension. Since it is typically undetected for long periods, it often progresses to end-stage renal disease. CKD is characterized by the development of progressive glomerulosclerosis, interstitial fibrosis and tubular atrophy along with a decreased glomerular filtration rate. This is associated with podocyte injury and a progressive rise in proteinuria. As endothelin-1 (ET-1) through the activation of endothelin receptor type A (ETA) promotes renal cell injury, inflammation, and fibrosis which finally lead to proteinuria, it is not surprising that ETA receptors antagonists have been proven to have beneficial renoprotective effects in both experimental and clinical studies in diabetic and non-diabetic CKD. Unfortunately, fluid retention encountered in large clinical trials in diabetic CKD led to the termination of these studies. Therefore, several advances, including the synthesis of new antagonists with enhanced pharmacological activity, the use of lower doses of ET antagonists, the addition of diuretics, plus simply searching for distinct pathological states to be treated, are promising targets for future experimental studies. In support of these approaches, our group demonstrated in adult subtotally nephrectomized Ren-2 transgenic rats that the addition of a diuretic on top of renin-angiotensin and ETA blockade led to a further decrease of proteinuria. This effect was independent of blood pressure which was normalized in all treated groups. Recent data in non-diabetic CKD, therefore, indicate a new potential for ETA antagonists, at least under certain pathological conditions.

Buffering chronic kidney disease with sodium bicarbonate

2018 ◽  
Vol 132 (17) ◽  
pp. 1999-2001 ◽  
Author(s):  
Emily N. Williams ◽  
Keisa W. Mathis
Keyword(s):  
Chronic Kidney Disease ◽  
Renal Function ◽  
Kidney Disease ◽  
End Stage Renal Disease ◽  
Filtration Rate ◽  
Experimental Studies ◽  
Progressive Loss ◽  
Research Findings ◽  
Stage Renal Disease ◽  
End Stage

The roles of the kidney are well defined, if there is a progressive loss in renal function, the kidney is no longer able to perform the listed tasks and chronic kidney disease (CKD) persists. In both clinical and experimental studies, NaHCO3 supplementation has been shown to improve glomerular filtration rate (GFR) as well as halt the progression toward end-stage renal disease (ESRD). In an article recently published in Clinical Science (vol 132 (11) 1179-1197), Ray et al. presented an intriguing and timely study, which investigates the mechanisms involved in the protection that follows oral NaHCO3 ingestion. Here we comment on their research findings.

scholarly journals Polymorphism in the GATM Locus Associated with Dialysis-Independent Chronic Kidney Disease but Not Dialysis-Dependent Kidney Failure

Genes ◽  
2021 ◽  
Vol 12 (6) ◽  
pp. 834
Author(s):  
Špela Šalamon ◽  
Sebastjan Bevc ◽  
Robert Ekart ◽  
Radovan Hojs ◽  
Uroš Potočnik
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Kidney Failure ◽  
Association Studies ◽  
Genetic Difference ◽  
Genome Wide Association Studies ◽  
Healthy Controls ◽  
Genome Wide ◽  
Stage Renal Disease ◽  
End Stage

The ten most statistically significant estimated glomerular filtration rate (eGFRcrea)-associated loci from genome-wide association studies (GWAs) are tested for associations with chronic kidney disease (CKD) in 208 patients, including dialysis-independent CKD and dialysis-dependent end-stage renal disease (kidney failure). The allele A of intergenic SNP rs2453533 (near GATM) is more frequent in dialysis-independent CKD patients (n = 135, adjusted p = 0.020) but not dialysis-dependent kidney failure patients (n = 73) compared to healthy controls (n = 309). The allele C of intronic SNP rs4293393 (UMOD) is more frequent in healthy controls (adjusted p = 0.042) than in CKD patients. The Allele T of intronic SNP rs9895661 (BCAS3) is associated with decreased eGFRcys (adjusted p = 0.001) and eGFRcrea (adjusted p = 0.017). Our results provide further evidence of a genetic difference between dialysis-dialysis-independent CKD and dialysis-dependent kidney failure, and add the GATM gene locus to the list of loci associated only with dialysis-independent CKD. GATM risk allele carriers in the dialysis-independent group may have a genetic susceptibility to higher creatinine production rather than increased serum creatinine due to kidney malfunction, and therefore, do not progress to dialysis-dependent kidney failure. When using eGFRcrea for CKD diagnosis, physicians might benefit from information about creatinine-increasing loci.

Healthcare resource use and costs associated with chronic kidney disease in US private insurance patients with multiple myeloma

2018 ◽  
Vol 25 (4) ◽  
pp. 855-864 ◽  
Author(s):  
Debajyoti Bhowmik ◽  
Xue Song ◽  
Michele Intorcia ◽  
Shia T Kent ◽  
Nianwen Shi
Keyword(s):  
Chronic Kidney Disease ◽  
Multiple Myeloma ◽  
Kidney Disease ◽  
End Stage Renal Disease ◽  
Index Date ◽  
Healthcare Resource ◽  
Stage Renal Disease ◽  
End Stage ◽  
Disease Stages

Objectives Within a median 1.2 years after patients have an initial diagnosis with multiple myeloma, up to 61% were diagnosed with renal impairment and 50% were diagnosed with chronic kidney disease. This study estimated economic burden associated with chronic kidney disease in multiple myeloma patients in the US. Methods In this retrospective cohort study, patients ≥18 years old with ≥1 inpatient or ≥ 2 outpatient multiple myeloma diagnoses between 1 January 2008 and 31 March 2015 were identified from MarketScan® Commercial and Medicare Supplemental Databases. Chronic kidney disease patients had ≥1 diagnosis of chronic kidney disease Stages 1–5 (first chronic kidney disease diagnosis date = index date) on or after the first multiple myeloma diagnosis, and were propensity score matched 1:1 to multiple myeloma patients without chronic kidney disease, end-stage renal disease, dialysis, or other type of chronically impaired renal function. All patients had ≥six-month continuous enrollment prior to index date and were followed for ≥one month from index date until the earliest of inpatient death, end of continuous enrollment, or end of the study period (30 September 2015). The per-patient per-year healthcare resource utilization and costs were measured during follow-up. Costs were total reimbursed amount in 2016 US dollars. Results A total of 2541 multiple myeloma patients with chronic kidney disease stages 1–5 and 2541 matched controls met the study criteria and were respectively 69.3 and 69.6 years, 54.5% and 55.3% men, and had 572.2 and 533.4 mean days of follow up. Compared to controls, chronic kidney disease patients had significantly (all P < 0.001) higher proportions (57.1% vs. 32.1%) and frequency (1.2 vs. 0.5) of inpatient admissions, frequency of emergency room visits (5.1 vs. 3.3), and total costs ($106,634 vs. $71,880). Sensitivity analyses found that patients with chronic kidney disease, end-stage renal disease, or dialysis had $78,455 ( P < 0.001) higher costs (per-patient per-year) than matched controls. Conclusions The economic burden associated with chronic kidney disease in patients with multiple myeloma was estimated to be between $34,754 and $78,455 per-patient per-year. Given its substantial clinical and economic impact, preservation of renal function is important in multiple myeloma patient care.

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