Search

Objective Cardiovascular disease (CVD) is accelerated in patients with systemic lupus erythematosus and lupus nephritis (LN). Despite the literature suggesting that renal arteriosclerosis predicts CVD in other glomerulonephritis diseases, arteriosclerosis grading and reporting might be particularly overlooked in LN biopsies. Our objective was to examine the burden of renal arteriosclerosis in LN and to assess whether arteriosclerosis is underreported in LN biopsies. Methods We identified all patients with LN undergoing kidney biopsy between 1994 and 2017 at an academic center. We interpreted LN biopsy reports to classify the Banff categories of absent, mild, moderate, or severe renal arteriosclerosis. The prevalence of renal arteriosclerosis was compared with the prevalence published for age-matched healthy peers, and predictors of arteriosclerosis were examined. We overread biopsies for Banff renal arteriosclerosis grading and compared to pathology reports. Results Among 189 incident patients with LN, renal arteriosclerosis prevalence was 2 decades earlier compared to their healthy peers, affecting 40% of patients ages 31-39 years with LN compared to 44% of healthy peers ages 50-59 years. A multivariable analysis showed a 3-fold higher odds of renal arteriosclerosis in patients ages ≥30 years with LN. LN chronicity on biopsy results predicted a 4-fold higher odds of renal arteriosclerosis. The overreads determined that 50% of standard LN biopsy reports missed reporting the presence or absence of renal arteriosclerosis. Conclusion Renal arteriosclerosis is accelerated by 2 decades in patients with LN compared to their healthy peers and is overlooked by pathologists in half of the routine biopsy reports. We propose incorporating Banff renal arteriosclerosis grading in all LN biopsy reports.

Hypercalcemia most often results from primary hyperparathyroidism and malignancy. Adynamic bone disease (ABD) is a form of renal osteodystrophy characterized by reduced bone turnover, which can limit the ability of bone to release or store calcium, potentially leading to low, normal, or high serum calcium levels. We describe a 51‐year‐old dialysis‐dependent female with hypercalcemia after parathyroidectomy. A demeclocycline‐labeled bone biopsy confirmed adynamic bone disease. Teriparatide, a recombinant form of parathyroid hormone (PTH) used to treat postmenopausal osteoporosis, was prescribed for 12 months and normalized serum calcium levels. Although previous case reports and series have described favorable changes in spine bone mineral density when teriparatide was prescribed for ABD, ours is the first documented case in which teriparatide resolved hypercalcemia due to ABD. © 2019 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.

Temporal and spatial variations in bone marrow adipose tissue (MAT) can be indicative of several pathologies and confound current methods of assessing immediate changes in bone mineral remodeling. We present a novel dual-energy computed tomography (DECT) method to monitor MAT and marrow-corrected volumetric BMD (mcvBMD) throughout the body. Twenty-three cancellous skeletal sites in 20 adult female cadavers aged 40–80 years old were measured using DECT (80 and 140 kVp). vBMD was simultaneous recorded using QCT. MAT was further sampled using MRI. Thirteen lumbar vertebrae were then excised from the MRI-imaged donors and examined by microCT. After MAT correction throughout the skeleton, significant differences (p

Proton pump inhibitors (PPIs) increase osteoporotic fracture risk presumably via hypochlorhydria and consequent reduced fractional calcium absorption (FCA). Existing studies provide conflicting information regarding the direct effects of PPIs on FCA. We evaluated the effect of PPI therapy on FCA. We recruited women at least 5 years past menopause who were not taking acid suppressants. Participants underwent three 24-hour inpatient FCA studies using the dual stable isotope method. Two FCA studies were performed 1 month apart to establish baseline calcium absorption. The third study occurred after taking omeprazole (40 mg/day) for 30 days. Each participant consumed the same foods during all FCA studies; study meals replicated subjects' dietary habits based on 7-day diet diaries. Twenty-one postmenopausal women ages 58 ± 7 years (mean ± SD) completed all study visits. Seventeen women were white, and 2 each were black and Hispanic. FCA (mean ± SD) was 20% ± 10% at visit 1, 18% ± 10% at visit 2, and 23% ± 10% following 30 ± 3 days of daily omeprazole (p = .07, ANOVA). Multiple linear regression revealed that age, gastric pH, serum omeprazole levels, adherence to omeprazole, and 25-hydroxyvitamin D levels were unrelated to changes in FCA between study visits 2 and 3. The 1,25-dihydroxyvitamin D3 level at visit 2 was the only variable (p = .049) associated with the change in FCA between visits 2 and 3. PPI-associated hypochlorhydria does not decrease FCA following 30 days of continuous use. Future studies should focus on identifying mechanisms by which PPIs increase the risk of osteoporotic fracture. © 2010 American Society for Bone and Mineral Research.

Human Immunodeficiency Virus (HIV) infected individuals have increased susceptibility to and greater morbidity and mortality due to tuberculosis (TB).1–5 These observations may in part be related to hypovitaminosis D, as low vitamin D levels are associated with decreased macrophage production of the peptide cathelicidin6 that exerts antimicrobial properties. Cathelicidin, part of the innate immune system, plays a critical role in the fight against TB. Mycobacterium tuberculosis binds to toll-like receptors (TLR 2/1) on macrophages, leading to upregulation of 1α-hydroxylase gene expression to promote greater conversion of 25(OH)D to 1,25(OH)2D.6 Intracellular 1,25(OH)2D binds to the vitamin D receptor and induces production of the antimicrobial peptide cathelicidin.6 Cathelicidin localizes to monocytes infected with M. tuberculosis, where it has a direct antimicrobial effect.7 Low vitamin D levels could potentially blunt cathelicidin production, limiting the host's ability to fight TB.2 It was observed that serum containing lower 25(OH)D3 levels demonstrated lower production of c athelicidin mRNA than serum with higher 25(OH)D levels.6 When serum with low 25(OH)D3 was supplemented with 25(OH)D3, cathelicidin mRNA production increased. These findings suggest that vitamin D therapy among individuals with suboptimal levels might induce production of cathelicidin mRNA and improve the immune response to TB infection. Vitamin D could therefore be used as inexpensive adjunctive therapy among HIV patients, especially in settings where TB is highly prevalent, to reduce TB-related morbidity and mortality. In the present study, we describe the serum vitamin D, calcium and albumin levels in HIV-infected Ugandans with and without TB.

If the optimal serum 25(OH)D level for skeletal health is 30 ng/mL or greater, then vitamin D insufficiency is widespread, affecting about 75% of adults based on a recent survey of more than 20,000 Americans. However, after a comprehensive analysis of existing research studies, the Institute of Medicine recently concluded that nearly all individuals are vitamin D replete when their 25(OH)D levels are 20 ng/mL or greater. Furthermore, two recent publications challenge the belief that 25(OH)D levels greater than 30 ng/mL are optimal for bone health. In a randomized, placebo-controlled trial, high-dose, once-yearly vitamin D therapy increased the incidence of fractures and falls. The second study reported that high-dose vitamin D did not reduce levels of parathyroid hormone or bone resorption among adults with 25(OH)D levels less than 32 ng/mL at baseline. It is time to question whether serum 25(OH)D levels of 30 ng/mL or greater are necessary for all individuals.

Introduction Diabetes mellitus is a key predictor of mortality in rheumatoid arthritis (RA) patients. Both RA and diabetes increase the risk of cardiovascular disease (CVD), yet understanding of how comorbid RA impacts the receipt of guideline-based diabetes care is limited. The purpose of this study was to examine how the presence of RA affected hemoglobin A1C (A1c) and lipid measurement in older adults with diabetes. Methods Using a retrospective cohort approach, we identified beneficiaries ≥65 years old with diabetes from a 5% random national sample of 2004 to 2005 Medicare patients (N = 256,331), then examined whether these patients had comorbid RA and whether they received guideline recommended A1c and lipid testing in 2006. Multivariate logistic regression was used to examine the effect of RA on receiving guideline recommended testing, adjusting for baseline sociodemographics, comorbidities and health care utilization. Results Two percent of diabetes patients had comorbid RA (N = 5,572). Diabetes patients with comorbid RA were more likely than those without RA to have baseline cardiovascular disease (such as 17% more congestive heart failure), diabetes-related complications including kidney disease (19% higher), lower extremity ulcers (77% higher) and peripheral vascular disease (32% higher). In adjusted models, diabetes patients with RA were less likely to receive recommended A1c testing (odds ratio (OR) 0.84, CI 0.80 to 0.89) than those without RA, but were slightly more likely to receive lipid testing (OR 1.08, CI 1.01 to 1.16). Conclusions In older adults with diabetes, the presence of comorbid RA predicted lower rates of A1c testing but slightly improved lipid testing. Future research should examine strategies to improve A1c testing in patients with diabetes and RA, in light of increased CVD and microvascular risks in patients with both conditions.