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Kidney Disease May Accelerate With Higher Rheumatoid Arthritis Disease Activity
TOPLINE:
Higher rheumatoid arthritis (RA) disease activity is associated with an accelerated kidney function decline and increased risk for chronic kidney disease (CKD) stages G3a and G3b.
METHODOLOGY:
- Researchers analyzed data from the CorEvitas RA registry, a prospective observational cohort in the United States, between 2001 and 2022, to evaluate the longitudinal association between RA disease activity and changes in kidney function.
- They included 31,129 patients with RA (median age, 58 years; 76.3% women) who had a baseline estimated glomerular filtration rate (eGFR) ≥ 60 mL/min per 1.73 m2 and received treatment with disease-modifying antirheumatic drugs (DMARDs).
- The participants were categorized into those in remission (n = 6647) and those with low (n = 10,028), moderate (n = 8548), and high (n = 5906) disease activity based on the time-averaged Clinical Disease Activity Index and followed for a median duration of 3.5 years.
- The primary outcome was a longitudinal change in eGFR, and the secondary outcomes were the development of CKD stage G3a (eGFR < 60 mL/min/1.73 m2) and stage G3b (eGFR < 45 mL/min/1.73 m2).
TAKEAWAY:
- Higher RA disease activity was associated with a faster decline in eGFR, with those having moderate and high RA disease activity experiencing an additional mean annual decline of 0.17 mL/min per 1.73 m2 and 0.18 mL/min per 1.73 m2, respectively, compared with those in remission.
- The decline in annual eGFR was even more accelerated when patients had consistently high disease activity since the time of enrollment (−0.43 mL/min per 1.73 m2).
- Patients with high RA disease activity had a 1.27 times (adjusted hazard ratio, 1.27; 95% CI, 1.05-1.52) higher risk of developing CKD stage G3a and a 1.93 times (aHR, 1.93; 95% CI, 1.16-3.20) higher risk for CKD stage G3b, compared with those in remission.
IN PRACTICE:
“This study suggests that controlling disease activity may potentially contribute to preserving kidney function in patients with RA,” the authors wrote.
SOURCE:
This study was led by Sho Fukui, MD, Division of Rheumatology, Inflammation, and Immunity, Brigham and Women’s Hospital and Harvard Medical School, both in Boston, Massachusetts, and was published online in Annals of the Rheumatic Diseases.
LIMITATIONS:
This study relied on serum creatinine and not cystatin C to estimate kidney function. It also did not collect information on the severity of comorbidities, which may have introduced residual confounding. Further studies are warranted to check the effect of DMARD therapy on renal function.
DISCLOSURES:
The study was funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Some authors reported serving as scientific advisers or consultants, receiving consulting fees or salary support, or having other ties with pharmaceutical companies.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
Higher rheumatoid arthritis (RA) disease activity is associated with an accelerated kidney function decline and increased risk for chronic kidney disease (CKD) stages G3a and G3b.
METHODOLOGY:
- Researchers analyzed data from the CorEvitas RA registry, a prospective observational cohort in the United States, between 2001 and 2022, to evaluate the longitudinal association between RA disease activity and changes in kidney function.
- They included 31,129 patients with RA (median age, 58 years; 76.3% women) who had a baseline estimated glomerular filtration rate (eGFR) ≥ 60 mL/min per 1.73 m2 and received treatment with disease-modifying antirheumatic drugs (DMARDs).
- The participants were categorized into those in remission (n = 6647) and those with low (n = 10,028), moderate (n = 8548), and high (n = 5906) disease activity based on the time-averaged Clinical Disease Activity Index and followed for a median duration of 3.5 years.
- The primary outcome was a longitudinal change in eGFR, and the secondary outcomes were the development of CKD stage G3a (eGFR < 60 mL/min/1.73 m2) and stage G3b (eGFR < 45 mL/min/1.73 m2).
TAKEAWAY:
- Higher RA disease activity was associated with a faster decline in eGFR, with those having moderate and high RA disease activity experiencing an additional mean annual decline of 0.17 mL/min per 1.73 m2 and 0.18 mL/min per 1.73 m2, respectively, compared with those in remission.
- The decline in annual eGFR was even more accelerated when patients had consistently high disease activity since the time of enrollment (−0.43 mL/min per 1.73 m2).
- Patients with high RA disease activity had a 1.27 times (adjusted hazard ratio, 1.27; 95% CI, 1.05-1.52) higher risk of developing CKD stage G3a and a 1.93 times (aHR, 1.93; 95% CI, 1.16-3.20) higher risk for CKD stage G3b, compared with those in remission.
IN PRACTICE:
“This study suggests that controlling disease activity may potentially contribute to preserving kidney function in patients with RA,” the authors wrote.
SOURCE:
This study was led by Sho Fukui, MD, Division of Rheumatology, Inflammation, and Immunity, Brigham and Women’s Hospital and Harvard Medical School, both in Boston, Massachusetts, and was published online in Annals of the Rheumatic Diseases.
LIMITATIONS:
This study relied on serum creatinine and not cystatin C to estimate kidney function. It also did not collect information on the severity of comorbidities, which may have introduced residual confounding. Further studies are warranted to check the effect of DMARD therapy on renal function.
DISCLOSURES:
The study was funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Some authors reported serving as scientific advisers or consultants, receiving consulting fees or salary support, or having other ties with pharmaceutical companies.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
Higher rheumatoid arthritis (RA) disease activity is associated with an accelerated kidney function decline and increased risk for chronic kidney disease (CKD) stages G3a and G3b.
METHODOLOGY:
- Researchers analyzed data from the CorEvitas RA registry, a prospective observational cohort in the United States, between 2001 and 2022, to evaluate the longitudinal association between RA disease activity and changes in kidney function.
- They included 31,129 patients with RA (median age, 58 years; 76.3% women) who had a baseline estimated glomerular filtration rate (eGFR) ≥ 60 mL/min per 1.73 m2 and received treatment with disease-modifying antirheumatic drugs (DMARDs).
- The participants were categorized into those in remission (n = 6647) and those with low (n = 10,028), moderate (n = 8548), and high (n = 5906) disease activity based on the time-averaged Clinical Disease Activity Index and followed for a median duration of 3.5 years.
- The primary outcome was a longitudinal change in eGFR, and the secondary outcomes were the development of CKD stage G3a (eGFR < 60 mL/min/1.73 m2) and stage G3b (eGFR < 45 mL/min/1.73 m2).
TAKEAWAY:
- Higher RA disease activity was associated with a faster decline in eGFR, with those having moderate and high RA disease activity experiencing an additional mean annual decline of 0.17 mL/min per 1.73 m2 and 0.18 mL/min per 1.73 m2, respectively, compared with those in remission.
- The decline in annual eGFR was even more accelerated when patients had consistently high disease activity since the time of enrollment (−0.43 mL/min per 1.73 m2).
- Patients with high RA disease activity had a 1.27 times (adjusted hazard ratio, 1.27; 95% CI, 1.05-1.52) higher risk of developing CKD stage G3a and a 1.93 times (aHR, 1.93; 95% CI, 1.16-3.20) higher risk for CKD stage G3b, compared with those in remission.
IN PRACTICE:
“This study suggests that controlling disease activity may potentially contribute to preserving kidney function in patients with RA,” the authors wrote.
SOURCE:
This study was led by Sho Fukui, MD, Division of Rheumatology, Inflammation, and Immunity, Brigham and Women’s Hospital and Harvard Medical School, both in Boston, Massachusetts, and was published online in Annals of the Rheumatic Diseases.
LIMITATIONS:
This study relied on serum creatinine and not cystatin C to estimate kidney function. It also did not collect information on the severity of comorbidities, which may have introduced residual confounding. Further studies are warranted to check the effect of DMARD therapy on renal function.
DISCLOSURES:
The study was funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Some authors reported serving as scientific advisers or consultants, receiving consulting fees or salary support, or having other ties with pharmaceutical companies.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
Risk for Giant Cell Arteritis Rises With Air Pollution Levels
TOPLINE:
Exposure to environmental particulate matter ≤ 10 μm in diameter (PM10) is associated with an increased risk for giant cell arteritis, particularly in older individuals aged ≥ 70 years and those with prolonged exposure to high levels of air pollution.
METHODOLOGY:
- Researchers conducted a retrospective case-crossover study to examine the association between exposure to airborne PM10 and the risk for giant cell arteritis and its ischemic complications.
- They included 232 patients with giant cell arteritis (median age at diagnosis, 73 years; 69% women) from three hospitals in northern Italy between June 2013 to December 2021.
- The hourly and daily average concentrations of PM10 were collected from the Italian monitoring network; patients’ exposure to PM10 was calculated using a space-time statistical model, incorporating meteorological variables, elevation, and proximity to main roads.
- The mean follow-up time of this cohort was 38 months.
TAKEAWAY:
- Every 10 μg/m3 increase in PM10 exposure in the preceding 60 days increased the incremental risk (IR) for giant cell arteritis by 27.1% (95% CI, 5.8-52.6).
- This association was more pronounced (IR, 38.8%; 95% CI, 9.2-76.3) in the subgroup of patients aged ≥ 70 years.
- The positive association between incident giant cell arteritis and concentrations of PM10 was seen only when patients were exposed to high concentrations of PM10 (26.9 ± 13.8 μg/m3) but not low concentrations (11.9 ± 7.9 μg/m3).
- This study did not show any significant association between exposure to PM10 and ischemic complications.
IN PRACTICE:
“Exposure to PM10 in the 60 days preceding [giant cell arteritis] symptoms onset seems to be associated with an increased risk of developing the disease, especially in older individuals with prolonged exposure to high levels of air pollution,” the authors wrote.
SOURCE:
The study was led by Milena Bond, MD, Hospital of Bruneck, Teaching Hospital of the Paracelsus Medical University, Brunico, Italy, and was published online in Arthritis Care & Research.
LIMITATIONS:
The retrospective nature of the study may have introduced recall bias. The study did not include data for other particulate matter fractions or gaseous pollutants, which may have impacted the findings. The use of residential addresses at the time of diagnosis precluded assessment of potential recent relocations.
DISCLOSURES:
This study did not disclose any funding source. Some authors reported having financial relationships with multiple pharmaceutical companies.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
TOPLINE:
Exposure to environmental particulate matter ≤ 10 μm in diameter (PM10) is associated with an increased risk for giant cell arteritis, particularly in older individuals aged ≥ 70 years and those with prolonged exposure to high levels of air pollution.
METHODOLOGY:
- Researchers conducted a retrospective case-crossover study to examine the association between exposure to airborne PM10 and the risk for giant cell arteritis and its ischemic complications.
- They included 232 patients with giant cell arteritis (median age at diagnosis, 73 years; 69% women) from three hospitals in northern Italy between June 2013 to December 2021.
- The hourly and daily average concentrations of PM10 were collected from the Italian monitoring network; patients’ exposure to PM10 was calculated using a space-time statistical model, incorporating meteorological variables, elevation, and proximity to main roads.
- The mean follow-up time of this cohort was 38 months.
TAKEAWAY:
- Every 10 μg/m3 increase in PM10 exposure in the preceding 60 days increased the incremental risk (IR) for giant cell arteritis by 27.1% (95% CI, 5.8-52.6).
- This association was more pronounced (IR, 38.8%; 95% CI, 9.2-76.3) in the subgroup of patients aged ≥ 70 years.
- The positive association between incident giant cell arteritis and concentrations of PM10 was seen only when patients were exposed to high concentrations of PM10 (26.9 ± 13.8 μg/m3) but not low concentrations (11.9 ± 7.9 μg/m3).
- This study did not show any significant association between exposure to PM10 and ischemic complications.
IN PRACTICE:
“Exposure to PM10 in the 60 days preceding [giant cell arteritis] symptoms onset seems to be associated with an increased risk of developing the disease, especially in older individuals with prolonged exposure to high levels of air pollution,” the authors wrote.
SOURCE:
The study was led by Milena Bond, MD, Hospital of Bruneck, Teaching Hospital of the Paracelsus Medical University, Brunico, Italy, and was published online in Arthritis Care & Research.
LIMITATIONS:
The retrospective nature of the study may have introduced recall bias. The study did not include data for other particulate matter fractions or gaseous pollutants, which may have impacted the findings. The use of residential addresses at the time of diagnosis precluded assessment of potential recent relocations.
DISCLOSURES:
This study did not disclose any funding source. Some authors reported having financial relationships with multiple pharmaceutical companies.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
TOPLINE:
Exposure to environmental particulate matter ≤ 10 μm in diameter (PM10) is associated with an increased risk for giant cell arteritis, particularly in older individuals aged ≥ 70 years and those with prolonged exposure to high levels of air pollution.
METHODOLOGY:
- Researchers conducted a retrospective case-crossover study to examine the association between exposure to airborne PM10 and the risk for giant cell arteritis and its ischemic complications.
- They included 232 patients with giant cell arteritis (median age at diagnosis, 73 years; 69% women) from three hospitals in northern Italy between June 2013 to December 2021.
- The hourly and daily average concentrations of PM10 were collected from the Italian monitoring network; patients’ exposure to PM10 was calculated using a space-time statistical model, incorporating meteorological variables, elevation, and proximity to main roads.
- The mean follow-up time of this cohort was 38 months.
TAKEAWAY:
- Every 10 μg/m3 increase in PM10 exposure in the preceding 60 days increased the incremental risk (IR) for giant cell arteritis by 27.1% (95% CI, 5.8-52.6).
- This association was more pronounced (IR, 38.8%; 95% CI, 9.2-76.3) in the subgroup of patients aged ≥ 70 years.
- The positive association between incident giant cell arteritis and concentrations of PM10 was seen only when patients were exposed to high concentrations of PM10 (26.9 ± 13.8 μg/m3) but not low concentrations (11.9 ± 7.9 μg/m3).
- This study did not show any significant association between exposure to PM10 and ischemic complications.
IN PRACTICE:
“Exposure to PM10 in the 60 days preceding [giant cell arteritis] symptoms onset seems to be associated with an increased risk of developing the disease, especially in older individuals with prolonged exposure to high levels of air pollution,” the authors wrote.
SOURCE:
The study was led by Milena Bond, MD, Hospital of Bruneck, Teaching Hospital of the Paracelsus Medical University, Brunico, Italy, and was published online in Arthritis Care & Research.
LIMITATIONS:
The retrospective nature of the study may have introduced recall bias. The study did not include data for other particulate matter fractions or gaseous pollutants, which may have impacted the findings. The use of residential addresses at the time of diagnosis precluded assessment of potential recent relocations.
DISCLOSURES:
This study did not disclose any funding source. Some authors reported having financial relationships with multiple pharmaceutical companies.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.