The appropriate management of vitamin D deficiency and hyperparathyroidism is essential to prevent metabolic bone disorder (MBD) and cardiovascular diseases in chronic kidney disease (CKD). Recently, the 24,25-dihydroxyvitamin D [24,25(OH)₂D] and vitamin D metabolite ratio (VMR), i.e., the ratio of 24,25(OH)₂D to 25-hydroxyvitamin D [25(OH)D], have emerged as biomarkers of vitamin D level. We analyzed the usefulness of vitamin D biomarkers for the evaluation of MBD in patients with CKD. We analyzed blood and urine samples from 208 outpatients with CKD stage G2–G5. 25(OH)D showed a poor correlation with the estimated glomerular filtration rate (eGFR). Conversely, the 24,25(OH)₂D level and VMR were significantly correlated with eGFR and the intact parathyroid hormone level. In conclusion, 24,25(OH)₂D and VMR have the potential to be vitamin D biomarkers for the detection of MBD in CKD patients.

Ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury (AKI) and progression to chronic kidney disease (CKD). However, no effective therapeutic intervention has been established for ischemic AKI. Endothelial progenitor cells (EPCs) have major roles in the maintenance of vascular integrity and the repair of endothelial damage; they also serve as therapeutic agents in various kidney diseases. Thus, we examined whether EPCs have a renoprotective effect in an IRI mouse model. Mice were assigned to sham, EPC, IRI-only, and EPC-treated IRI groups. EPCs originating from human peripheral blood were cultured. The EPCs were administered 5 min before reperfusion, and all mice were killed 72 h after IRI. Blood urea nitrogen, serum creatinine, and tissue injury were significantly increased in IRI mice; EPCs significantly improved the manifestations of IRI. Apoptotic cell death and oxidative stress were significantly reduced in EPC-treated IRI mice. Administration of EPCs decreased the expression levels of NLRP3, cleaved caspase-1, p-NF-κB, and p-p38. Furthermore, the expression levels of F4/80, ICAM-1, RORγt, and IL-17RA were significantly reduced in EPC-treated IRI mice. Finally, the levels of EMT-associated factors (TGF-β, α-SMA, Snail, and Twist) were significantly reduced in EPC-treated IRI mice. This study shows that inflammasome-mediated inflammation accompanied by immune modulation and fibrosis is a potential target of EPCs as a treatment for IRI-induced AKI and the prevention of progression to CKD.

Background: Further study is warranted to determine the association between estimated glomerular filtration rate (eGFR) or albuminuria and the risk of death from diverse causes. Methods: We screened >10 million general health screening examinees who received health examinations conducted in 2009 using the claims database of Korea. After the exclusion of those previously diagnosed with renal failure and those with missing data, 9,917,838 individuals with available baseline kidney function measurements were included. The primary outcome was mortality and cause-specific death between 2009 and 2019 identified through death certificates based on the diagnostic codes of International Classification of Diseases, 10th revision. Multivariable Cox regression analysis adjusted for various clinicodemographic and social characteristics was used to assess mortality risk. Results: The hazard ratio of death was significantly high in both the eGFR <60 mL/min/1.73 m2 and in the eGFR ≥120 mL/ min/1.73 m2 groups in univariable and multivariable regression analyses when compared to those within the reference range (eGFR of 90–120 mL/min/1.73 m2). The results were similar for death by cardiovascular, cancer, infection, endocrine, respiratory, and digestive causes. We also found that albuminuria was associated with higher risk of death regardless of eGFR range, and those in the higher categories of dipstick albuminuria showed higher risk. Conclusion: We reconfirmed the significant association between eGFR, albuminuria, and mortality. Healthcare providers should keep in mind that albuminuria and decreased eGFR as well as kidney hyperfiltration are independent predictors of mortality.

Background: Obstructive sleep apnea (OSA) is a sleep disorder associated with an increased risk of cardiovascular and metabolic complications. Albuminuria, an early marker of kidney damage, is a proposed risk factor for OSA and its adverse outcomes. The study explored the association between OSA and albuminuria in Korean adults. Methods: We screened participants from the cross-sectional Korean National Health and Nutrition Examination Survey (2019– 2021). The study included participants aged 40 years and older who completed the STOP-BANG questionnaire, a tool used to assess the OSA risk. Albuminuria was defined as a urine albumin-to-creatinine ratio ≥30 mg/g Cr. The participants were categorized based on albuminuria presence and severity. A multivariate logistic regression analysis examined the association between albuminuria and OSA. Results: This study included 10,923 participants. Participants with albuminuria had significantly higher STOP-BANG scores than those without. Moreover, albuminuria remained strongly associated with an increased risk of OSA (odds ratio, 2.01; 95% confidence interval, 1.66–2.43), after multivariate adjustment. This association was more pronounced as albuminuria severity increased. Participants with high STOP-BANG scores were more likely to have albuminuria (odds ratio, 2.51; 95% confidence interval, 1.89–3.31), highlighting the bidirectional relationship between albuminuria and OSA. Conclusion: The present study demonstrated a significant association between albuminuria and an elevated risk of OSA. These findings underscore the importance of early screening for OSA in patients with albuminuria, particularly in those with additional metabolic risk factors, to improve their long-term outcomes.

Key Points: Lower bone mineral density was associated with a higher risk of fracture, irrespective of eGFR. At a similar bone mineral density, the fracture risk was higher with lower eGFR, more prominently for hip fractures than for vertebral fractures. The higher risk of fracture associated with lower eGFR was more pronounced in individuals with poor static balance. Background: Although both lower bone mineral density (BMD) and impaired kidney function are well-established risk factors for fracture, large-scale studies evaluating their effects and interaction on fracture, particularly site-specific fractures including vertebra and hip, are still limited. Methods: The main study population included female participants aged 66 years who underwent BMD assessment through dual-energy x-ray absorptiometry through the Korean National Screening Program between 2010 and 2016. BMD was categorized as normal, osteopenia, and osteoporosis on the basis of T -score. Kidney function was classified as eGFR ≥60, 45–59, and <45 ml/min per 1.73 m ² . Primary outcome was any fracture, including vertebral, hip, and other fractures, defined using International Classification of Diseases, Tenth Revision codes. Subgroup analysis was performed by physical performance, including the single-leg stance test. Results: Among 551,548 participants included in the main study population, 80,514 developed any fracture over a median follow-up of 8.2 (interquartile range, 6.7–10.0) years. The prevalence of osteoporosis was 36%, and those with lower BMD showed higher eGFR and lower body mass index. Lower BMD was associated with a higher risk of any fracture, irrespective of eGFR, with nonsignificant interaction ( P for interaction = 0.54). Among participants with normal BMD, those with eGFR <45 ml/min per 1.73 m ² showed a greater risk of hip fracture than those with normal eGFR (adjusted hazard ratio, 2.44 [1.88–3.18]), whereas vertebral fracture risks were similar across different eGFR categories at a given BMD status. Furthermore, a higher fracture risk with lower eGFR was more pronounced in women with poor static balance assessed by the single-leg stance test than in those with normal static balance. Conclusions: In postmenopausal women, lower BMD was associated with a higher fracture risk, irrespective of eGFR. However, at any given BMD, lower eGFR was associated with a greater risk for hip fracture, but not for vertebral fracture.

Rationale: Non-autoimmune hypothyroidism is a rare but significant cause of rhabdomyolysis and myocarditis, which can mimic acute coronary syndrome. Early recognition and treatment of hypothyroidism are crucial, especially in patients with chronic kidney disease (CKD), where delayed diagnosis may lead to life-threatening complications such as acute kidney injury. Patient concerns: A 71-year-old male with diabetes, CKD stage G3aA3, and a history of chronic myelogenous leukemia presented with myalgia, anorexia, and anuria. He also reported intermittent chest pain for 1 month, progressing to severe symptoms including decreased urine output and anuria. Diagnoses: Laboratory findings revealed acute kidney injury (serum creatinine: 12.14 mg/dL), extreme elevations in muscle enzymes (creatine kinase: 250,000 IU/L), and cardiac biomarkers (troponin-T: 543 ng/L). Initial management did not improve his condition. On day 15, thyroid function tests confirmed non-autoimmune hypothyroidism (TSH: 55.58 μIU/mL, free T4: 0.06 ng/dL). Interventions: The patient underwent hemodialysis and conservative treatment initially, followed by levothyroxine replacement therapy on day 16. Outcomes: Renal function, urine output, and muscle enzyme levels gradually improved after thyroid hormone supplementation. By discharge on day 40, the patient’s serum creatinine decreased to 3.08 mg/dL, and hemodialysis was discontinued. At 7 months posttreatment, his renal function stabilized at CKD stage G3bA2 with normal thyroid function. Lessons: This case highlights the importance of considering hypothyroidism in patients with unexplained rhabdomyolysis and persistent cardiac symptoms, particularly in those with CKD. Early thyroid function testing can lead to timely treatment and improved outcomes in such complex cases.