Historically, it takes an average of 17 years to move new treatments from clinical evidence to daily practice. Given the highly effective treatments now available to prevent or delay kidney disease onset and progression, this is far too long. The time is now to narrow the gap between what we know and what we do. Clear guidelines exist for the prevention and management of common risk factors for kidney disease, such as hypertension and diabetes, but only a fraction of people with these conditions worldwide are diagnosed, and even fewer are treated to target. Similarly, the vast majority of people living with kidney disease are unaware of their condition, because in the early stages it is often silent. Even among patients who have been diagnosed, many do not receive appropriate treatment for kidney disease. Considering the serious consequences of kidney disease progression, kidney failure, or death, it is imperative that treatments are initiated early and appropriately. Opportunities to diagnose and treat kidney disease early must be maximized beginning at the primary care level. Many systematic barriers exist, ranging from patient to clinician to health systems to societal factors. To preserve and improve kidney health for everyone everywhere, each of these barriers must be acknowledged so that sustainable solutions are developed and implemented without further delay.
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http://dx.doi.org/10.1111/jorc.12495 | DOI Listing |
Environ Int
December 2024
Department of Toxicology, School of Public Health, Sun Yat-sen University, Guangzhou, 510080, China. Electronic address:
Aristolochic Acid I (AAI) is widely present in traditional Chinese medicines derived from the Aristolochia genus and is known to cause significant damage to renal tubular epithelial cells. Genome-wide screening has proven to be a powerful tool in identifying critical genes associated with the toxicity of exogenous substances. To identify undiscovered key genes involved in AAI-induced renal toxicity, a genome-wide CRISPR library screen was conducted in the human kidney-2 (HK-2) cell line.
View Article and Find Full Text PDFClin Exp Nephrol
December 2024
Division of Diabetology and Metabolism, Department of Internal Medicine, Tokyo Women's Medical University School of Medicine, 8-1 Kawada-Cho, Shinjuku-Ku, Tokyo, 162-8666, Japan.
Background: Whether diabetic retinopathy (DR) can predict kidney disease progression in individuals with diabetes remains unclear. Furthermore, there are only a limited number of studies investigating the association between DR and kidney outcomes classified according to baseline kidney function and albuminuria status. Here, we examined the association of DR with kidney disease progression in individuals with type 2 diabetes.
View Article and Find Full Text PDFInt Urol Nephrol
December 2024
Department of Pediatrics, The First Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, 450000, China.
Purpose: Henoch-Schönlein purpura nephritis (HSPN) has a poor prognosis and variable pathophysiology. The present study aimed to analyze the kidney injury, clinicopathology, and prognosis of HSPN children.
Methods: This retrospective study examined 249 children with HSPN.
J Nephrol
December 2024
Vanderbilt Institute for Global Health (VIGH), Nashville, TN, USA.
Background: Pregnancy-Related Acute Kidney Injury (PRAKI) is an important contributor to maternal-fetal morbidity and mortality. The burden of PRAKI in sub-Saharan Africa is not well documented. We conducted a systematic literature review and meta-analysis to estimate the prevalence of PRAKI in sub-Saharan Africa.
View Article and Find Full Text PDFUrolithiasis
December 2024
Department of Nephro-urology, Nagoya City University Graduate School of Medical Sciences, 1, Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Japan.
The early stages of kidney crystal formation involve inflammation and hypoxia-induced cell injury; however, the role of the hypoxic response in kidney crystal formation remains unclear. This study investigated the effects of a prolyl hydroxylase domain inhibitor (roxadustat) on renal calcium oxalate (CaOx) crystal formation through in vitro and in vivo approaches. In the in vitro experiment, murine renal tubular cells (RTCs) were exposed to varying roxadustat concentrations and CaOx crystals.
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