Background: This study aimed to determine the association between the urinary protein-to-creatinine ratio (UPCR) and chronic kidney disease (CKD) progression in a cohort study, and to determine whether body mass index (BMI) modifies this association.
Methods: The study population consisted of 856 hypertensive patients with CKD stages 2-5, enrolled between 2010 and 2011 in Japan. Generalized linear models with a logit link were used to evaluate the independent and combined effects of the UPCR and BMI on CKD progression RESULTS: During a median follow-up of 25 months, 242 patients developed CKD progression during follow-up. A notably higher risk of CKD progression was found in participants in tertiles 2 [odds ratio (OR): 5.46, 95% confidence interval (95% CI): 2.49-11.99] and 3 (OR 27.74, 95% CI 12.34-62.38) comparing with tertiles 1 for UPCR levels. Moreover, an interaction was found between UPCR and BMI on CKD progression (P for interaction = 0.006). Participants in both the highest tertile of UPCR and overweight (UPCR ≥ 248.9 mg/mmol and BMI ≥ 25 kg/m) had a 45.59-times higher risk of CKD progression compared with those in the lowest tertile of UPCR and nonoverweight (UPCR < 36.2 mg/mmol and BMI < 25 kg/m) CONCLUSIONS: The present study demonstrates that the combination of elevated UPCR and BMI may contribute to an increased risk of CKD progression.
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http://dx.doi.org/10.1007/s11255-024-03984-z | DOI Listing |
Can J Kidney Health Dis
January 2025
Can Tho University of Medicine and Pharmacy, Can Tho, Vietnam.
Objectives: Chronic kidney disease (CKD) is associated with disability, low quality of life, and mortality. However, most cases are asymptomatic, often detected incidentally, or only recognized when they have progressed to the later stages with complications. The present study aimed to determine the prevalence of CKD and develop a predictive nomogram for CKD in Vietnamese adults.
View Article and Find Full Text PDFBackground: Patients with chronic kidney disease (CKD) have serum, bone, and vascular abnormalities presenting as chronic kidney disease-mineral bone disorder (CKD-MBD) syndrome. This study sought to identify the parameters with the greatest relative impact on progression of CKD-MBD abnormalities.
Materials And Methods: This prospective study measured 237 parameters including serum markers, clinical variables, dual-energy X-ray absorptiometry (DXA) measurements, vascular calcifications, and histomorphometric results from bone samples obtained at baseline and after 2 - 3 years.
Nephrology (Carlton)
January 2025
Faculty of Medicine, Dentistry & Health Sciences Melbourne, The University of Melbourne, Melbourne, Victoria, Australia.
Chronic kidney disease is characterised by the progressive loss of kidney function. However, predicting who will progress to kidney failure is difficult. Artificial Intelligence, including Machine Learning, shows promise in this area.
View Article and Find Full Text PDFAm J Physiol Cell Physiol
January 2025
Department of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China.
Arterial stiffening is a hallmark of chronic kidney disease (CKD) related cardiovascular events and is primarily attributed to the elevated matrix stiffness. Stiffened arteries are accompanied by low-grade inflammation, but the causal effects of matrix stiffness on inflammation remain unknown. For analysis of the relationship between arterial stiffness and vascular inflammation, pulse wave velocity (PWV) and aortic inflammatory markers were analyzed in an adenine-induced mouse model of CKD in chronological order.
View Article and Find Full Text PDFPLoS One
January 2025
Nephrological Department, Herlev Hospital, University of Copenhagen, Copenhagen, Denmark.
Secondary hyperparathyroidism (sHPT) is a significant clinical complication of CKD leading to bone abnormalities and cardiovascular disease. Current treatment based on activating the parathyroid calcium-sensing receptor (CaSR) using calcimimetics such as Cinacalcet, aims to decrease plasma PTH levels and inhibit the progression of parathyroid hyperplasia. In the present study, we found significant diurnal rhythmicity of Casr, encoding the Cinacalcet drug target in hyperplastic parathyroid glands (p = 0.
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