Background: The renal cortex volume is associated with the kidney function and chronic kidney disease (CKD) risk factors, and it may also be a prognostic factor. We aimed to create an equation to estimate the renal cortex volume of CKD patients in day-to-day clinical practice.
Methods: The subjects included 116 ethnic Japanese CKD patients who were ≥ 18 years of age. The renal size (length, width and thickness) was measured by ultrasound. The body height, weight, year of age, sex, birth weight, gestational age, diabetes status, hypertension status, family history of CKD and dialysis and estimated glomerular filtration rate (eGFR) were collected as expected dependent variables. We made models for the equation regarding the renal cortex volume measured by non-contrast magnetic resonance imaging as a true renal cortex volume. Stepwise multiple linear regression analyses were performed with the log-transformation of dependent and independent variables. The accuracy of the models was compared using the leave one out cross-validation method.
Results: The estimated volume of the renal cortex (cm) = 0.012 × renal length (cm) × width (cm) × body weight (kg) × body height (cm) × eGFR (ml/min/1.73 m) × 1.12 if diabetes. The adjusted R value and the accuracy within 30 and 50% were 0.73, 0.94 and 0.99, respectively.
Conclusions: This study provided a new method for estimating the renal cortex volume in day-to-day clinical practice.
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http://dx.doi.org/10.1007/s10157-017-1492-8 | DOI Listing |
Front Biosci (Landmark Ed)
January 2025
Department of Zoology, College of Science, King Saud University, 11451 Riyadh, Saudi Arabia.
Background: We investigated chitosan's protective effects against tertiary butylhydroquinone (TBHQ)-induced toxicity in adult male rats, focusing on cognitive functions and oxidative stress in the brain, liver, and kidneys.
Methods: Rats were divided into four groups (n = 8/group): (1) Control, (2) Chitosan only, (3) TBHQ only, and (4) Chitosan + TBHQ.
Results: TBHQ exposure led to significant cognitive impairments and increased oxidative stress, marked by elevated malondialdehyde (MDA) and decreased superoxide dismutase (SOD) and glutathione (GSH) levels.
Int J Mol Sci
January 2025
Department of Nephrology, Carol Davila University of Medicine and Pharmacy, 020021 Bucharest, Romania.
Autophagy and mitophagy are critical cellular processes that maintain homeostasis by removing damaged organelles and promoting cellular survival under stress conditions. In the context of diabetic kidney disease, these mechanisms play essential roles in mitigating cellular damage. This review provides an in-depth analysis of the recent literature on the relationship between autophagy, mitophagy, and diabetic kidney disease, highlighting the current state of knowledge, existing research gaps, and potential areas for future investigations.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Laboratory of Molecular and Cellular Nephrology, Mossakowski Medical Research Institute, Polish Academy of Sciences, 80-308 Gdansk, Poland.
Microalbuminuria is the earliest clinical abnormality in diabetic kidney disease. High glucose (HG) concentrations are associated with the induction of oxidative stress in podocytes, leading to disruption of the glomerular filtration barrier. Our recent study revealed a significant decrease in the membrane-bound fraction of Klotho in podocytes that were cultured under HG conditions.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Department of Pathology, Albert Szent-Györgyi Medical Center, Faculty of Medicine, University of Szeged, 6720 Szeged, Hungary.
Fibronectin glomerulopathy (FG) is caused by fibronectin 1 () gene mutations. A renal biopsy was performed on a 4-year-old girl with incidentally discovered proteinuria (150 mg/dL); her family history of renal disease was negative. Markedly enlarged glomeruli (mean glomerular diameter: 196 μm; age-matched controls: 140 μm), α-SMA-positive and Ki-67-positive mesangial cell proliferation (glomerular proliferation index 1.
View Article and Find Full Text PDFBiomedicines
January 2025
Institute of Pathology "Dr. Ðorđe Joannović", Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia.
Background: Congenital mesoblastic nephroma represents 3-10% of all pediatric renal tumors. With the advancement of ultrasound diagnostics and magnetic resonance imaging, the diagnosis of this renal neoplasm is increasingly being established prenatally and at birth. It usually presents as a benign tumor, but it can severely affect pregnancy outcomes, contributing to perinatal morbidity and mortality.
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