Progressive Decline in Estimated GFR in Patients With Sickle Cell Disease: An Observational Cohort Study
Rationale & Objective: Progression of chronic kidney disease (CKD) in sickle cell disease (SCD) and its risk factors remain poorly defined. We identified characteristics associated with CKD as well as decline in estimated glomerular filtration rate (eGFR) and presence of proteinuria over time in...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Derebail, Vimal K. [verfasserIn] Ciccone, Emily J. [verfasserIn] Zhou, Qingning [verfasserIn] Kilgore, R. Rosina [verfasserIn] Cai, Jianwen [verfasserIn] Ataga, Kenneth I. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2019 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: American journal of kidney diseases - Philadelphia, Pa. : Elsevier Saunders, 1981, 74, Seite 47-55 |
|---|---|
| Übergeordnetes Werk: |
volume:74 ; pages:47-55 |
| DOI / URN: |
10.1053/j.ajkd.2018.12.027 |
|---|
| Katalog-ID: |
ELV002477084 |
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| 245 | 1 | 0 | |a Progressive Decline in Estimated GFR in Patients With Sickle Cell Disease: An Observational Cohort Study |
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| 520 | |a Rationale & Objective: Progression of chronic kidney disease (CKD) in sickle cell disease (SCD) and its risk factors remain poorly defined. We identified characteristics associated with CKD as well as decline in estimated glomerular filtration rate (eGFR) and presence of proteinuria over time in adults with SCD.Study Design: Retrospective observational study.Setting & Participants: Patients with SCD 18 years or older in a single center from 2004 to 2013.Predictors: Baseline clinical and laboratory measures, comorbid conditions, SCD-related complications, relevant treatments, and severity of genotypes defined as severe (homozygous SCD [HbSS]/sickle-β0-thalassemia [HbSβ0]) or mild (hemoglobin SC disease [HbSC]/sickle-β+-thalassemia [HbSβ+]-thalassemia).Outcomes: Presence at baseline of CKD, defined here as eGFR<90mL/min/1.73m2 or proteinuria (≥1+) on urinalysis or current kidney transplant or dialysis therapy; change in eGFR; and presence of proteinuria over time.Analytical Approach: Logistic regression for baseline CKD. Linear mixed-effects model for eGFR decline and generalized linear mixed-effects model for proteinuria during the study period evaluating for interaction with time. Stratified by genotype severity.Results: Among 427 patients, 331 had 2 or more measurements of creatinine. During a median follow-up of 4.01 (interquartile range, 1.66-7.19) years, annual eGFR decline was 2.05mL/min/1.73m2 for severe genotypes (P <0.001) and 1.16mL/min/1.73m2 (P =0.02) for mild genotypes. At baseline, 21.4% of patients with severe genotypes had CKD versus 17.2% of those with mild genotypes. For severe genotypes, angiotensin-converting enzyme–inhibitor/angiotensin receptor blocker use (OR, 6.10; 95% CI, 2.03-18.29; P =0.001) and avascular necrosis (OR, 0.40; 95% CI, 0.16-0.97; P =0.04) were associated with baseline CKD. Among those with mild genotypes, higher hemoglobin level was associated with lower probability of CKD (OR per 1-g/dL greater hemoglobin level, 0.63; 95% CI, 0.43-0.93; P =0.02). Rate of eGFR decline was inversely related to hemoglobin level (β = 0.46 [SE, 0.23]; P =0.04) within the severe genotype subgroup. No factors were identified to be associated with proteinuria over time.Limitations: Retrospective observational study, limited direct measures of albuminuria.Conclusions: Patients with SCD exhibit rapid decline in eGFR over time. Decline in eGFR is associated with markers of disease severity and associated comorbid conditions. | ||
| 650 | 4 | |a Sickle cell disease | |
| 650 | 4 | |a chronic kidney disease (CKD) | |
| 650 | 4 | |a estimated glomerular filtration rate (eGFR) | |
| 650 | 4 | |a eGFR decline | |
| 650 | 4 | |a proteinuria | |
| 650 | 4 | |a sickle hemoglobin | |
| 650 | 4 | |a genotype | |
| 650 | 4 | |a hyperfiltration | |
| 650 | 4 | |a thalassemia | |
| 700 | 1 | |a Ciccone, Emily J. |e verfasserin |4 aut | |
| 700 | 1 | |a Zhou, Qingning |e verfasserin |4 aut | |
| 700 | 1 | |a Kilgore, R. Rosina |e verfasserin |4 aut | |
| 700 | 1 | |a Cai, Jianwen |e verfasserin |4 aut | |
| 700 | 1 | |a Ataga, Kenneth I. |e verfasserin |4 aut | |
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10.1053/j.ajkd.2018.12.027 doi (DE-627)ELV002477084 (ELSEVIER)S0272-6386(19)30007-1 DE-627 ger DE-627 rda eng 610 DE-600 44.88 bkl Derebail, Vimal K. verfasserin aut Progressive Decline in Estimated GFR in Patients With Sickle Cell Disease: An Observational Cohort Study 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Rationale & Objective: Progression of chronic kidney disease (CKD) in sickle cell disease (SCD) and its risk factors remain poorly defined. We identified characteristics associated with CKD as well as decline in estimated glomerular filtration rate (eGFR) and presence of proteinuria over time in adults with SCD.Study Design: Retrospective observational study.Setting & Participants: Patients with SCD 18 years or older in a single center from 2004 to 2013.Predictors: Baseline clinical and laboratory measures, comorbid conditions, SCD-related complications, relevant treatments, and severity of genotypes defined as severe (homozygous SCD [HbSS]/sickle-β0-thalassemia [HbSβ0]) or mild (hemoglobin SC disease [HbSC]/sickle-β+-thalassemia [HbSβ+]-thalassemia).Outcomes: Presence at baseline of CKD, defined here as eGFR<90mL/min/1.73m2 or proteinuria (≥1+) on urinalysis or current kidney transplant or dialysis therapy; change in eGFR; and presence of proteinuria over time.Analytical Approach: Logistic regression for baseline CKD. Linear mixed-effects model for eGFR decline and generalized linear mixed-effects model for proteinuria during the study period evaluating for interaction with time. Stratified by genotype severity.Results: Among 427 patients, 331 had 2 or more measurements of creatinine. During a median follow-up of 4.01 (interquartile range, 1.66-7.19) years, annual eGFR decline was 2.05mL/min/1.73m2 for severe genotypes (P <0.001) and 1.16mL/min/1.73m2 (P =0.02) for mild genotypes. At baseline, 21.4% of patients with severe genotypes had CKD versus 17.2% of those with mild genotypes. For severe genotypes, angiotensin-converting enzyme–inhibitor/angiotensin receptor blocker use (OR, 6.10; 95% CI, 2.03-18.29; P =0.001) and avascular necrosis (OR, 0.40; 95% CI, 0.16-0.97; P =0.04) were associated with baseline CKD. Among those with mild genotypes, higher hemoglobin level was associated with lower probability of CKD (OR per 1-g/dL greater hemoglobin level, 0.63; 95% CI, 0.43-0.93; P =0.02). Rate of eGFR decline was inversely related to hemoglobin level (β = 0.46 [SE, 0.23]; P =0.04) within the severe genotype subgroup. No factors were identified to be associated with proteinuria over time.Limitations: Retrospective observational study, limited direct measures of albuminuria.Conclusions: Patients with SCD exhibit rapid decline in eGFR over time. Decline in eGFR is associated with markers of disease severity and associated comorbid conditions. Sickle cell disease chronic kidney disease (CKD) estimated glomerular filtration rate (eGFR) eGFR decline proteinuria sickle hemoglobin genotype hyperfiltration thalassemia Ciccone, Emily J. verfasserin aut Zhou, Qingning verfasserin aut Kilgore, R. Rosina verfasserin aut Cai, Jianwen verfasserin aut Ataga, Kenneth I. verfasserin aut Enthalten in American journal of kidney diseases Philadelphia, Pa. : Elsevier Saunders, 1981 74, Seite 47-55 Online-Ressource (DE-627)320593169 (DE-600)2019205-8 (DE-576)091138760 1523-6838 nnns volume:74 pages:47-55 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_31 GBV_ILN_2011 GBV_ILN_4305 44.88 Urologie Nephrologie AR 74 47-55 |
| spelling |
10.1053/j.ajkd.2018.12.027 doi (DE-627)ELV002477084 (ELSEVIER)S0272-6386(19)30007-1 DE-627 ger DE-627 rda eng 610 DE-600 44.88 bkl Derebail, Vimal K. verfasserin aut Progressive Decline in Estimated GFR in Patients With Sickle Cell Disease: An Observational Cohort Study 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Rationale & Objective: Progression of chronic kidney disease (CKD) in sickle cell disease (SCD) and its risk factors remain poorly defined. We identified characteristics associated with CKD as well as decline in estimated glomerular filtration rate (eGFR) and presence of proteinuria over time in adults with SCD.Study Design: Retrospective observational study.Setting & Participants: Patients with SCD 18 years or older in a single center from 2004 to 2013.Predictors: Baseline clinical and laboratory measures, comorbid conditions, SCD-related complications, relevant treatments, and severity of genotypes defined as severe (homozygous SCD [HbSS]/sickle-β0-thalassemia [HbSβ0]) or mild (hemoglobin SC disease [HbSC]/sickle-β+-thalassemia [HbSβ+]-thalassemia).Outcomes: Presence at baseline of CKD, defined here as eGFR<90mL/min/1.73m2 or proteinuria (≥1+) on urinalysis or current kidney transplant or dialysis therapy; change in eGFR; and presence of proteinuria over time.Analytical Approach: Logistic regression for baseline CKD. Linear mixed-effects model for eGFR decline and generalized linear mixed-effects model for proteinuria during the study period evaluating for interaction with time. Stratified by genotype severity.Results: Among 427 patients, 331 had 2 or more measurements of creatinine. During a median follow-up of 4.01 (interquartile range, 1.66-7.19) years, annual eGFR decline was 2.05mL/min/1.73m2 for severe genotypes (P <0.001) and 1.16mL/min/1.73m2 (P =0.02) for mild genotypes. At baseline, 21.4% of patients with severe genotypes had CKD versus 17.2% of those with mild genotypes. For severe genotypes, angiotensin-converting enzyme–inhibitor/angiotensin receptor blocker use (OR, 6.10; 95% CI, 2.03-18.29; P =0.001) and avascular necrosis (OR, 0.40; 95% CI, 0.16-0.97; P =0.04) were associated with baseline CKD. Among those with mild genotypes, higher hemoglobin level was associated with lower probability of CKD (OR per 1-g/dL greater hemoglobin level, 0.63; 95% CI, 0.43-0.93; P =0.02). Rate of eGFR decline was inversely related to hemoglobin level (β = 0.46 [SE, 0.23]; P =0.04) within the severe genotype subgroup. No factors were identified to be associated with proteinuria over time.Limitations: Retrospective observational study, limited direct measures of albuminuria.Conclusions: Patients with SCD exhibit rapid decline in eGFR over time. Decline in eGFR is associated with markers of disease severity and associated comorbid conditions. Sickle cell disease chronic kidney disease (CKD) estimated glomerular filtration rate (eGFR) eGFR decline proteinuria sickle hemoglobin genotype hyperfiltration thalassemia Ciccone, Emily J. verfasserin aut Zhou, Qingning verfasserin aut Kilgore, R. Rosina verfasserin aut Cai, Jianwen verfasserin aut Ataga, Kenneth I. verfasserin aut Enthalten in American journal of kidney diseases Philadelphia, Pa. : Elsevier Saunders, 1981 74, Seite 47-55 Online-Ressource (DE-627)320593169 (DE-600)2019205-8 (DE-576)091138760 1523-6838 nnns volume:74 pages:47-55 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_31 GBV_ILN_2011 GBV_ILN_4305 44.88 Urologie Nephrologie AR 74 47-55 |
| allfields_unstemmed |
10.1053/j.ajkd.2018.12.027 doi (DE-627)ELV002477084 (ELSEVIER)S0272-6386(19)30007-1 DE-627 ger DE-627 rda eng 610 DE-600 44.88 bkl Derebail, Vimal K. verfasserin aut Progressive Decline in Estimated GFR in Patients With Sickle Cell Disease: An Observational Cohort Study 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Rationale & Objective: Progression of chronic kidney disease (CKD) in sickle cell disease (SCD) and its risk factors remain poorly defined. We identified characteristics associated with CKD as well as decline in estimated glomerular filtration rate (eGFR) and presence of proteinuria over time in adults with SCD.Study Design: Retrospective observational study.Setting & Participants: Patients with SCD 18 years or older in a single center from 2004 to 2013.Predictors: Baseline clinical and laboratory measures, comorbid conditions, SCD-related complications, relevant treatments, and severity of genotypes defined as severe (homozygous SCD [HbSS]/sickle-β0-thalassemia [HbSβ0]) or mild (hemoglobin SC disease [HbSC]/sickle-β+-thalassemia [HbSβ+]-thalassemia).Outcomes: Presence at baseline of CKD, defined here as eGFR<90mL/min/1.73m2 or proteinuria (≥1+) on urinalysis or current kidney transplant or dialysis therapy; change in eGFR; and presence of proteinuria over time.Analytical Approach: Logistic regression for baseline CKD. Linear mixed-effects model for eGFR decline and generalized linear mixed-effects model for proteinuria during the study period evaluating for interaction with time. Stratified by genotype severity.Results: Among 427 patients, 331 had 2 or more measurements of creatinine. During a median follow-up of 4.01 (interquartile range, 1.66-7.19) years, annual eGFR decline was 2.05mL/min/1.73m2 for severe genotypes (P <0.001) and 1.16mL/min/1.73m2 (P =0.02) for mild genotypes. At baseline, 21.4% of patients with severe genotypes had CKD versus 17.2% of those with mild genotypes. For severe genotypes, angiotensin-converting enzyme–inhibitor/angiotensin receptor blocker use (OR, 6.10; 95% CI, 2.03-18.29; P =0.001) and avascular necrosis (OR, 0.40; 95% CI, 0.16-0.97; P =0.04) were associated with baseline CKD. Among those with mild genotypes, higher hemoglobin level was associated with lower probability of CKD (OR per 1-g/dL greater hemoglobin level, 0.63; 95% CI, 0.43-0.93; P =0.02). Rate of eGFR decline was inversely related to hemoglobin level (β = 0.46 [SE, 0.23]; P =0.04) within the severe genotype subgroup. No factors were identified to be associated with proteinuria over time.Limitations: Retrospective observational study, limited direct measures of albuminuria.Conclusions: Patients with SCD exhibit rapid decline in eGFR over time. Decline in eGFR is associated with markers of disease severity and associated comorbid conditions. Sickle cell disease chronic kidney disease (CKD) estimated glomerular filtration rate (eGFR) eGFR decline proteinuria sickle hemoglobin genotype hyperfiltration thalassemia Ciccone, Emily J. verfasserin aut Zhou, Qingning verfasserin aut Kilgore, R. Rosina verfasserin aut Cai, Jianwen verfasserin aut Ataga, Kenneth I. verfasserin aut Enthalten in American journal of kidney diseases Philadelphia, Pa. : Elsevier Saunders, 1981 74, Seite 47-55 Online-Ressource (DE-627)320593169 (DE-600)2019205-8 (DE-576)091138760 1523-6838 nnns volume:74 pages:47-55 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_31 GBV_ILN_2011 GBV_ILN_4305 44.88 Urologie Nephrologie AR 74 47-55 |
| allfieldsGer |
10.1053/j.ajkd.2018.12.027 doi (DE-627)ELV002477084 (ELSEVIER)S0272-6386(19)30007-1 DE-627 ger DE-627 rda eng 610 DE-600 44.88 bkl Derebail, Vimal K. verfasserin aut Progressive Decline in Estimated GFR in Patients With Sickle Cell Disease: An Observational Cohort Study 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Rationale & Objective: Progression of chronic kidney disease (CKD) in sickle cell disease (SCD) and its risk factors remain poorly defined. We identified characteristics associated with CKD as well as decline in estimated glomerular filtration rate (eGFR) and presence of proteinuria over time in adults with SCD.Study Design: Retrospective observational study.Setting & Participants: Patients with SCD 18 years or older in a single center from 2004 to 2013.Predictors: Baseline clinical and laboratory measures, comorbid conditions, SCD-related complications, relevant treatments, and severity of genotypes defined as severe (homozygous SCD [HbSS]/sickle-β0-thalassemia [HbSβ0]) or mild (hemoglobin SC disease [HbSC]/sickle-β+-thalassemia [HbSβ+]-thalassemia).Outcomes: Presence at baseline of CKD, defined here as eGFR<90mL/min/1.73m2 or proteinuria (≥1+) on urinalysis or current kidney transplant or dialysis therapy; change in eGFR; and presence of proteinuria over time.Analytical Approach: Logistic regression for baseline CKD. Linear mixed-effects model for eGFR decline and generalized linear mixed-effects model for proteinuria during the study period evaluating for interaction with time. Stratified by genotype severity.Results: Among 427 patients, 331 had 2 or more measurements of creatinine. During a median follow-up of 4.01 (interquartile range, 1.66-7.19) years, annual eGFR decline was 2.05mL/min/1.73m2 for severe genotypes (P <0.001) and 1.16mL/min/1.73m2 (P =0.02) for mild genotypes. At baseline, 21.4% of patients with severe genotypes had CKD versus 17.2% of those with mild genotypes. For severe genotypes, angiotensin-converting enzyme–inhibitor/angiotensin receptor blocker use (OR, 6.10; 95% CI, 2.03-18.29; P =0.001) and avascular necrosis (OR, 0.40; 95% CI, 0.16-0.97; P =0.04) were associated with baseline CKD. Among those with mild genotypes, higher hemoglobin level was associated with lower probability of CKD (OR per 1-g/dL greater hemoglobin level, 0.63; 95% CI, 0.43-0.93; P =0.02). Rate of eGFR decline was inversely related to hemoglobin level (β = 0.46 [SE, 0.23]; P =0.04) within the severe genotype subgroup. No factors were identified to be associated with proteinuria over time.Limitations: Retrospective observational study, limited direct measures of albuminuria.Conclusions: Patients with SCD exhibit rapid decline in eGFR over time. Decline in eGFR is associated with markers of disease severity and associated comorbid conditions. Sickle cell disease chronic kidney disease (CKD) estimated glomerular filtration rate (eGFR) eGFR decline proteinuria sickle hemoglobin genotype hyperfiltration thalassemia Ciccone, Emily J. verfasserin aut Zhou, Qingning verfasserin aut Kilgore, R. Rosina verfasserin aut Cai, Jianwen verfasserin aut Ataga, Kenneth I. verfasserin aut Enthalten in American journal of kidney diseases Philadelphia, Pa. : Elsevier Saunders, 1981 74, Seite 47-55 Online-Ressource (DE-627)320593169 (DE-600)2019205-8 (DE-576)091138760 1523-6838 nnns volume:74 pages:47-55 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_31 GBV_ILN_2011 GBV_ILN_4305 44.88 Urologie Nephrologie AR 74 47-55 |
| allfieldsSound |
10.1053/j.ajkd.2018.12.027 doi (DE-627)ELV002477084 (ELSEVIER)S0272-6386(19)30007-1 DE-627 ger DE-627 rda eng 610 DE-600 44.88 bkl Derebail, Vimal K. verfasserin aut Progressive Decline in Estimated GFR in Patients With Sickle Cell Disease: An Observational Cohort Study 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Rationale & Objective: Progression of chronic kidney disease (CKD) in sickle cell disease (SCD) and its risk factors remain poorly defined. We identified characteristics associated with CKD as well as decline in estimated glomerular filtration rate (eGFR) and presence of proteinuria over time in adults with SCD.Study Design: Retrospective observational study.Setting & Participants: Patients with SCD 18 years or older in a single center from 2004 to 2013.Predictors: Baseline clinical and laboratory measures, comorbid conditions, SCD-related complications, relevant treatments, and severity of genotypes defined as severe (homozygous SCD [HbSS]/sickle-β0-thalassemia [HbSβ0]) or mild (hemoglobin SC disease [HbSC]/sickle-β+-thalassemia [HbSβ+]-thalassemia).Outcomes: Presence at baseline of CKD, defined here as eGFR<90mL/min/1.73m2 or proteinuria (≥1+) on urinalysis or current kidney transplant or dialysis therapy; change in eGFR; and presence of proteinuria over time.Analytical Approach: Logistic regression for baseline CKD. Linear mixed-effects model for eGFR decline and generalized linear mixed-effects model for proteinuria during the study period evaluating for interaction with time. Stratified by genotype severity.Results: Among 427 patients, 331 had 2 or more measurements of creatinine. During a median follow-up of 4.01 (interquartile range, 1.66-7.19) years, annual eGFR decline was 2.05mL/min/1.73m2 for severe genotypes (P <0.001) and 1.16mL/min/1.73m2 (P =0.02) for mild genotypes. At baseline, 21.4% of patients with severe genotypes had CKD versus 17.2% of those with mild genotypes. For severe genotypes, angiotensin-converting enzyme–inhibitor/angiotensin receptor blocker use (OR, 6.10; 95% CI, 2.03-18.29; P =0.001) and avascular necrosis (OR, 0.40; 95% CI, 0.16-0.97; P =0.04) were associated with baseline CKD. Among those with mild genotypes, higher hemoglobin level was associated with lower probability of CKD (OR per 1-g/dL greater hemoglobin level, 0.63; 95% CI, 0.43-0.93; P =0.02). Rate of eGFR decline was inversely related to hemoglobin level (β = 0.46 [SE, 0.23]; P =0.04) within the severe genotype subgroup. No factors were identified to be associated with proteinuria over time.Limitations: Retrospective observational study, limited direct measures of albuminuria.Conclusions: Patients with SCD exhibit rapid decline in eGFR over time. Decline in eGFR is associated with markers of disease severity and associated comorbid conditions. Sickle cell disease chronic kidney disease (CKD) estimated glomerular filtration rate (eGFR) eGFR decline proteinuria sickle hemoglobin genotype hyperfiltration thalassemia Ciccone, Emily J. verfasserin aut Zhou, Qingning verfasserin aut Kilgore, R. Rosina verfasserin aut Cai, Jianwen verfasserin aut Ataga, Kenneth I. verfasserin aut Enthalten in American journal of kidney diseases Philadelphia, Pa. : Elsevier Saunders, 1981 74, Seite 47-55 Online-Ressource (DE-627)320593169 (DE-600)2019205-8 (DE-576)091138760 1523-6838 nnns volume:74 pages:47-55 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_31 GBV_ILN_2011 GBV_ILN_4305 44.88 Urologie Nephrologie AR 74 47-55 |
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We identified characteristics associated with CKD as well as decline in estimated glomerular filtration rate (eGFR) and presence of proteinuria over time in adults with SCD.Study Design: Retrospective observational study.Setting & Participants: Patients with SCD 18 years or older in a single center from 2004 to 2013.Predictors: Baseline clinical and laboratory measures, comorbid conditions, SCD-related complications, relevant treatments, and severity of genotypes defined as severe (homozygous SCD [HbSS]/sickle-β0-thalassemia [HbSβ0]) or mild (hemoglobin SC disease [HbSC]/sickle-β+-thalassemia [HbSβ+]-thalassemia).Outcomes: Presence at baseline of CKD, defined here as eGFR<90mL/min/1.73m2 or proteinuria (≥1+) on urinalysis or current kidney transplant or dialysis therapy; change in eGFR; and presence of proteinuria over time.Analytical Approach: Logistic regression for baseline CKD. Linear mixed-effects model for eGFR decline and generalized linear mixed-effects model for proteinuria during the study period evaluating for interaction with time. Stratified by genotype severity.Results: Among 427 patients, 331 had 2 or more measurements of creatinine. During a median follow-up of 4.01 (interquartile range, 1.66-7.19) years, annual eGFR decline was 2.05mL/min/1.73m2 for severe genotypes (P <0.001) and 1.16mL/min/1.73m2 (P =0.02) for mild genotypes. At baseline, 21.4% of patients with severe genotypes had CKD versus 17.2% of those with mild genotypes. For severe genotypes, angiotensin-converting enzyme–inhibitor/angiotensin receptor blocker use (OR, 6.10; 95% CI, 2.03-18.29; P =0.001) and avascular necrosis (OR, 0.40; 95% CI, 0.16-0.97; P =0.04) were associated with baseline CKD. Among those with mild genotypes, higher hemoglobin level was associated with lower probability of CKD (OR per 1-g/dL greater hemoglobin level, 0.63; 95% CI, 0.43-0.93; P =0.02). Rate of eGFR decline was inversely related to hemoglobin level (β = 0.46 [SE, 0.23]; P =0.04) within the severe genotype subgroup. No factors were identified to be associated with proteinuria over time.Limitations: Retrospective observational study, limited direct measures of albuminuria.Conclusions: Patients with SCD exhibit rapid decline in eGFR over time. 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Rosina</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Cai, Jianwen</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ataga, Kenneth I.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">American journal of kidney diseases</subfield><subfield code="d">Philadelphia, Pa. : Elsevier Saunders, 1981</subfield><subfield code="g">74, Seite 47-55</subfield><subfield code="h">Online-Ressource</subfield><subfield code="w">(DE-627)320593169</subfield><subfield code="w">(DE-600)2019205-8</subfield><subfield code="w">(DE-576)091138760</subfield><subfield code="x">1523-6838</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:74</subfield><subfield code="g">pages:47-55</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_31</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2011</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.88</subfield><subfield code="j">Urologie</subfield><subfield code="j">Nephrologie</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">74</subfield><subfield code="h">47-55</subfield></datafield></record></collection>
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Derebail, Vimal K. |
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Derebail, Vimal K. ddc 610 bkl 44.88 misc Sickle cell disease misc chronic kidney disease (CKD) misc estimated glomerular filtration rate (eGFR) misc eGFR decline misc proteinuria misc sickle hemoglobin misc genotype misc hyperfiltration misc thalassemia Progressive Decline in Estimated GFR in Patients With Sickle Cell Disease: An Observational Cohort Study |
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610 DE-600 44.88 bkl Progressive Decline in Estimated GFR in Patients With Sickle Cell Disease: An Observational Cohort Study Sickle cell disease chronic kidney disease (CKD) estimated glomerular filtration rate (eGFR) eGFR decline proteinuria sickle hemoglobin genotype hyperfiltration thalassemia |
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ddc 610 bkl 44.88 misc Sickle cell disease misc chronic kidney disease (CKD) misc estimated glomerular filtration rate (eGFR) misc eGFR decline misc proteinuria misc sickle hemoglobin misc genotype misc hyperfiltration misc thalassemia |
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Progressive Decline in Estimated GFR in Patients With Sickle Cell Disease: An Observational Cohort Study |
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progressive decline in estimated gfr in patients with sickle cell disease: an observational cohort study |
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Progressive Decline in Estimated GFR in Patients With Sickle Cell Disease: An Observational Cohort Study |
| abstract |
Rationale & Objective: Progression of chronic kidney disease (CKD) in sickle cell disease (SCD) and its risk factors remain poorly defined. We identified characteristics associated with CKD as well as decline in estimated glomerular filtration rate (eGFR) and presence of proteinuria over time in adults with SCD.Study Design: Retrospective observational study.Setting & Participants: Patients with SCD 18 years or older in a single center from 2004 to 2013.Predictors: Baseline clinical and laboratory measures, comorbid conditions, SCD-related complications, relevant treatments, and severity of genotypes defined as severe (homozygous SCD [HbSS]/sickle-β0-thalassemia [HbSβ0]) or mild (hemoglobin SC disease [HbSC]/sickle-β+-thalassemia [HbSβ+]-thalassemia).Outcomes: Presence at baseline of CKD, defined here as eGFR<90mL/min/1.73m2 or proteinuria (≥1+) on urinalysis or current kidney transplant or dialysis therapy; change in eGFR; and presence of proteinuria over time.Analytical Approach: Logistic regression for baseline CKD. Linear mixed-effects model for eGFR decline and generalized linear mixed-effects model for proteinuria during the study period evaluating for interaction with time. Stratified by genotype severity.Results: Among 427 patients, 331 had 2 or more measurements of creatinine. During a median follow-up of 4.01 (interquartile range, 1.66-7.19) years, annual eGFR decline was 2.05mL/min/1.73m2 for severe genotypes (P <0.001) and 1.16mL/min/1.73m2 (P =0.02) for mild genotypes. At baseline, 21.4% of patients with severe genotypes had CKD versus 17.2% of those with mild genotypes. For severe genotypes, angiotensin-converting enzyme–inhibitor/angiotensin receptor blocker use (OR, 6.10; 95% CI, 2.03-18.29; P =0.001) and avascular necrosis (OR, 0.40; 95% CI, 0.16-0.97; P =0.04) were associated with baseline CKD. Among those with mild genotypes, higher hemoglobin level was associated with lower probability of CKD (OR per 1-g/dL greater hemoglobin level, 0.63; 95% CI, 0.43-0.93; P =0.02). Rate of eGFR decline was inversely related to hemoglobin level (β = 0.46 [SE, 0.23]; P =0.04) within the severe genotype subgroup. No factors were identified to be associated with proteinuria over time.Limitations: Retrospective observational study, limited direct measures of albuminuria.Conclusions: Patients with SCD exhibit rapid decline in eGFR over time. Decline in eGFR is associated with markers of disease severity and associated comorbid conditions. |
| abstractGer |
Rationale & Objective: Progression of chronic kidney disease (CKD) in sickle cell disease (SCD) and its risk factors remain poorly defined. We identified characteristics associated with CKD as well as decline in estimated glomerular filtration rate (eGFR) and presence of proteinuria over time in adults with SCD.Study Design: Retrospective observational study.Setting & Participants: Patients with SCD 18 years or older in a single center from 2004 to 2013.Predictors: Baseline clinical and laboratory measures, comorbid conditions, SCD-related complications, relevant treatments, and severity of genotypes defined as severe (homozygous SCD [HbSS]/sickle-β0-thalassemia [HbSβ0]) or mild (hemoglobin SC disease [HbSC]/sickle-β+-thalassemia [HbSβ+]-thalassemia).Outcomes: Presence at baseline of CKD, defined here as eGFR<90mL/min/1.73m2 or proteinuria (≥1+) on urinalysis or current kidney transplant or dialysis therapy; change in eGFR; and presence of proteinuria over time.Analytical Approach: Logistic regression for baseline CKD. Linear mixed-effects model for eGFR decline and generalized linear mixed-effects model for proteinuria during the study period evaluating for interaction with time. Stratified by genotype severity.Results: Among 427 patients, 331 had 2 or more measurements of creatinine. During a median follow-up of 4.01 (interquartile range, 1.66-7.19) years, annual eGFR decline was 2.05mL/min/1.73m2 for severe genotypes (P <0.001) and 1.16mL/min/1.73m2 (P =0.02) for mild genotypes. At baseline, 21.4% of patients with severe genotypes had CKD versus 17.2% of those with mild genotypes. For severe genotypes, angiotensin-converting enzyme–inhibitor/angiotensin receptor blocker use (OR, 6.10; 95% CI, 2.03-18.29; P =0.001) and avascular necrosis (OR, 0.40; 95% CI, 0.16-0.97; P =0.04) were associated with baseline CKD. Among those with mild genotypes, higher hemoglobin level was associated with lower probability of CKD (OR per 1-g/dL greater hemoglobin level, 0.63; 95% CI, 0.43-0.93; P =0.02). Rate of eGFR decline was inversely related to hemoglobin level (β = 0.46 [SE, 0.23]; P =0.04) within the severe genotype subgroup. No factors were identified to be associated with proteinuria over time.Limitations: Retrospective observational study, limited direct measures of albuminuria.Conclusions: Patients with SCD exhibit rapid decline in eGFR over time. Decline in eGFR is associated with markers of disease severity and associated comorbid conditions. |
| abstract_unstemmed |
Rationale & Objective: Progression of chronic kidney disease (CKD) in sickle cell disease (SCD) and its risk factors remain poorly defined. We identified characteristics associated with CKD as well as decline in estimated glomerular filtration rate (eGFR) and presence of proteinuria over time in adults with SCD.Study Design: Retrospective observational study.Setting & Participants: Patients with SCD 18 years or older in a single center from 2004 to 2013.Predictors: Baseline clinical and laboratory measures, comorbid conditions, SCD-related complications, relevant treatments, and severity of genotypes defined as severe (homozygous SCD [HbSS]/sickle-β0-thalassemia [HbSβ0]) or mild (hemoglobin SC disease [HbSC]/sickle-β+-thalassemia [HbSβ+]-thalassemia).Outcomes: Presence at baseline of CKD, defined here as eGFR<90mL/min/1.73m2 or proteinuria (≥1+) on urinalysis or current kidney transplant or dialysis therapy; change in eGFR; and presence of proteinuria over time.Analytical Approach: Logistic regression for baseline CKD. Linear mixed-effects model for eGFR decline and generalized linear mixed-effects model for proteinuria during the study period evaluating for interaction with time. Stratified by genotype severity.Results: Among 427 patients, 331 had 2 or more measurements of creatinine. During a median follow-up of 4.01 (interquartile range, 1.66-7.19) years, annual eGFR decline was 2.05mL/min/1.73m2 for severe genotypes (P <0.001) and 1.16mL/min/1.73m2 (P =0.02) for mild genotypes. At baseline, 21.4% of patients with severe genotypes had CKD versus 17.2% of those with mild genotypes. For severe genotypes, angiotensin-converting enzyme–inhibitor/angiotensin receptor blocker use (OR, 6.10; 95% CI, 2.03-18.29; P =0.001) and avascular necrosis (OR, 0.40; 95% CI, 0.16-0.97; P =0.04) were associated with baseline CKD. Among those with mild genotypes, higher hemoglobin level was associated with lower probability of CKD (OR per 1-g/dL greater hemoglobin level, 0.63; 95% CI, 0.43-0.93; P =0.02). Rate of eGFR decline was inversely related to hemoglobin level (β = 0.46 [SE, 0.23]; P =0.04) within the severe genotype subgroup. No factors were identified to be associated with proteinuria over time.Limitations: Retrospective observational study, limited direct measures of albuminuria.Conclusions: Patients with SCD exhibit rapid decline in eGFR over time. Decline in eGFR is associated with markers of disease severity and associated comorbid conditions. |
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Progressive Decline in Estimated GFR in Patients With Sickle Cell Disease: An Observational Cohort Study |
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We identified characteristics associated with CKD as well as decline in estimated glomerular filtration rate (eGFR) and presence of proteinuria over time in adults with SCD.Study Design: Retrospective observational study.Setting & Participants: Patients with SCD 18 years or older in a single center from 2004 to 2013.Predictors: Baseline clinical and laboratory measures, comorbid conditions, SCD-related complications, relevant treatments, and severity of genotypes defined as severe (homozygous SCD [HbSS]/sickle-β0-thalassemia [HbSβ0]) or mild (hemoglobin SC disease [HbSC]/sickle-β+-thalassemia [HbSβ+]-thalassemia).Outcomes: Presence at baseline of CKD, defined here as eGFR<90mL/min/1.73m2 or proteinuria (≥1+) on urinalysis or current kidney transplant or dialysis therapy; change in eGFR; and presence of proteinuria over time.Analytical Approach: Logistic regression for baseline CKD. Linear mixed-effects model for eGFR decline and generalized linear mixed-effects model for proteinuria during the study period evaluating for interaction with time. Stratified by genotype severity.Results: Among 427 patients, 331 had 2 or more measurements of creatinine. During a median follow-up of 4.01 (interquartile range, 1.66-7.19) years, annual eGFR decline was 2.05mL/min/1.73m2 for severe genotypes (P <0.001) and 1.16mL/min/1.73m2 (P =0.02) for mild genotypes. At baseline, 21.4% of patients with severe genotypes had CKD versus 17.2% of those with mild genotypes. For severe genotypes, angiotensin-converting enzyme–inhibitor/angiotensin receptor blocker use (OR, 6.10; 95% CI, 2.03-18.29; P =0.001) and avascular necrosis (OR, 0.40; 95% CI, 0.16-0.97; P =0.04) were associated with baseline CKD. Among those with mild genotypes, higher hemoglobin level was associated with lower probability of CKD (OR per 1-g/dL greater hemoglobin level, 0.63; 95% CI, 0.43-0.93; P =0.02). Rate of eGFR decline was inversely related to hemoglobin level (β = 0.46 [SE, 0.23]; P =0.04) within the severe genotype subgroup. No factors were identified to be associated with proteinuria over time.Limitations: Retrospective observational study, limited direct measures of albuminuria.Conclusions: Patients with SCD exhibit rapid decline in eGFR over time. 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Rosina</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Cai, Jianwen</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ataga, Kenneth I.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">American journal of kidney diseases</subfield><subfield code="d">Philadelphia, Pa. : Elsevier Saunders, 1981</subfield><subfield code="g">74, Seite 47-55</subfield><subfield code="h">Online-Ressource</subfield><subfield code="w">(DE-627)320593169</subfield><subfield code="w">(DE-600)2019205-8</subfield><subfield code="w">(DE-576)091138760</subfield><subfield code="x">1523-6838</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:74</subfield><subfield code="g">pages:47-55</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_31</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2011</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.88</subfield><subfield code="j">Urologie</subfield><subfield code="j">Nephrologie</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">74</subfield><subfield code="h">47-55</subfield></datafield></record></collection>
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