Journal: American Journal of Physiology. Renal Physiology

Abbreviation

Am J Physiol Renal Physiol

Publisher

American Physiological Society

Journal Volumes

ISSN

0363-6127
1522-1466

Description

Filters

2010 - 201942020 - 20241
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Publications 1 - 5 of 5
  • A novel method for automated crystal visualization and quantification in murine folic acid-induced acute kidney injury
    Item type: Journal Article
    Hamid, Ahmad Kamal; Pastor Arroyo, Eva Maria; Lee, Sung Sik; et al. (2024)
    American Journal of Physiology. Renal Physiology
    Folic acid (FA)-induced acute kidney injury (FA-AKI) is an increasingly prevalent rodent disease model involving the injection of a high dose of FA that culminates in renal FA crystal deposition and injury. However, the literature characterizing the FA-AKI model is sparse and dated in part due to the absence of a well-described methodology for the visualization and quantification of renal FA crystals. Using widely available materials and tools, we developed a straightforward and crystal-preserving histological protocol that can be coupled with automated imaging for renal FA crystal visualization and generated an automated macro for downstream crystal content quantification. The applicability of the method was demonstrated by characterizing the model in male and female C57BL6/JRj mice after 3 and 30 h of FA treatment. Kidneys from both sexes and timepoints showed a bimodal distribution of FA crystal deposition in the cortical and medullary regions while, compared with males, females exhibited higher renal FA crystal content at the 30-h timepoint accompanied by greater kidney weight and higher plasma urea. Despite comparable plasma phosphate concentrations, FA-AKI resulted in a substantially more elevated plasma intact fibroblast growth factor 23 (FGF23) in females, reflected by a similar pattern in osseous Fgf23 mRNA expression. Therefore, the presented method constitutes a valuable tool for the quantification of renal FA crystals, which can aid the mechanistic characterization of the FA-AKI model and serves as a means to control for confounding changes in FA crystallization when using the model for investigating early and prophylactic AKI therapeutic interventions.
  • Regulation of the creatine transporter by AMP-activated protein kinase in kidney epithelial cells
    Item type: Journal Article
    Li, Hui; Thali, Ramon F.; Smolak, Christy; et al. (2010)
    American Journal of Physiology. Renal Physiology
  • Vacuolar H+-ATPase apical accumulation in kidney intercalated cells is regulated by PKA and AMP-activated protein kinase
    Item type: Journal Article
    Gong, Fan; Alzamora, Rodrigo; Smolak, Christy; et al. (2010)
    American Journal of Physiology. Renal Physiology
  • AMP-activated protein kinase regulates the vacuolar H+-ATPase via direct phosphorylation of the A subunit (ATP6V1A) in the kidney
    Item type: Journal Article
    Alzamora, R.; Al-Bataineh, M. M.; Liu, W.; et al. (2013)
    American Journal of Physiology. Renal Physiology
  • Anti-VEGF antibody treatment accelerates polycystic kidney disease
    Item type: Journal Article
    Raina, Shagun; Honer, Michael; Krämer, Stefanie-Dorothea; et al. (2011)
    American Journal of Physiology. Renal Physiology
    Polycystic kidney growth implies expansion of the vasculature, suggesting that vascular endothelial growth factor (VEGF)-dependent processes play a critical role and that VEGF is a putative therapeutic target. Whether an anti-VEGF antibody improves renal cystic disease has not been determined. We administrated 5 mg/kg B20.4.1, an anti-VEGF-A antibody, or vehicle intraperitoneally twice weekly to 4-wk-old male normal (+/+) and cystic (Cy/+) Han:SPRD rats for 6 wk. Renal function, urinary protein excretion, organ/body weight ratios, cyst volume, tubular epithelial cell (TEC) proliferation, renal VEGF, hypoxia-inducible factor (HIF)-1α and -2α expression, renal histology, and kidney hypoxia visualized by [18F]fluoromisonidazole positron emission tomography were assessed. The treated compared with untreated +/+ rats had lower TEC proliferation rates, whereas Cy/+ rats receiving B20.4.1 displayed an increased proximal TEC proliferation rate, causing enhanced cyst and kidney growth. The +/+ and Cy/+ rats receiving B20.4.1 had severe renal failure and extensive glomerular damage. Proteinuria, which was highest in anti-VEGF-treated Cy/+ and lowest in untreated normal littermates, was positively correlated with renal HIF-1α and negatively correlated with VEGF expression. The untreated Cy/+ vs. +/+ rats had higher overall [18F]fluoromisonidazole uptake. The +/+ rats receiving B20.4.1 vs. untreated had increased [18F]fluoromisonidazole uptake, whereas the uptake was unchanged among treated vs. untreated Cy/+ animals. In conclusion, B20.4.1 caused an exaggerated cystic response of the proximal tubules in cystic rats and severe kidney injury that was associated with low renal VEGF and high HIF-1α levels. Anti-VEGF drug therapy may therefore not be a treatment option for polycystic kidney disease.
Publications 1 - 5 of 5