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Thallium reabsorption via NKCC2 causes severe acute kidney injury with outer medulla-specific calcium crystal casts in rats.
Arch Toxicol
December 2024
Department of Nephrology and Hypertension, Dokkyo Medical University, Tochigi, Japan.
Article Synopsis
- Thallium (Tl) is a highly toxic heavy metal linked to accidental poisoning and can cause severe health issues including kidney failure.
- In a study on rats, intraperitoneal administration of Tl led to significant kidney dysfunction, characterized by high calcium deposits and mitochondrial issues in a specific kidney region called the medullary thick ascending limb (mTAL).
- The research found that inhibiting a specific kidney transporter helped reduce Tl accumulation and its damaging effects, which could lead to new treatment strategies for Tl poisoning and improve diagnostic methods for related kidney damage.
Experimental TET2 Clonal Hematopoiesis Predisposes to Renal Hypertension Through an Inflammasome-Mediated Mechanism.
Circ Res
October 2024
Cardiovascular Medicine and the Robert M. Berne Cardiovascular Research Center (A.H.P., L.M., K.-D.M., Y.Y., J.D.C., M.A.E., E.P., H.D., E.M.-Y., B.E.I., K.W.), University of Virginia School of Medicine, Charlottesville.
Background: Hypertension incidence increases with age and represents one of the most prevalent risk factors for cardiovascular disease. Clonal events in the hematopoietic system resulting from somatic mutations in driver genes are prevalent in elderly individuals who lack overt hematologic disorders. This condition is referred to as age-related clonal hematopoiesis (CH), and it is a newly recognized risk factor for cardiovascular disease.
View Article and Find Full Text PDFDistal convoluted tubule-specific disruption of the COP9 signalosome but not its regulatory target cullin 3 causes tubular injury.
Am J Physiol Renal Physiol
October 2024
Division of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, Portland, Oregon, United States.
Article Synopsis
- Familial hyperkalemic hypertension (FHHt), also known as Gordon syndrome, results from abnormal WNK4 accumulation that activates the NaCl cotransporter (NCC) in the kidneys, primarily affecting the distal convoluted tubule (DCT).
- Mutations in the cullin 3 (CUL3) gene disrupt its interaction with the COP9 signalosome, leading to WNK4 accumulation and potential kidney injury, but short-term experiments show no significant plasma electrolyte changes in DCT-specific knockout mice.
- Long-term DCT-specific deletion of CUL3 causes kidney injury and atrophy, indicating that CUL3's role in degrading WNK4 is crucial for preventing FHHt, highlighting how the
Kidney collecting duct-derived vasopressin is not essential for appropriate concentration or dilution of urine.
Am J Physiol Renal Physiol
June 2024
Division of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, United States.
We have previously shown that kidney collecting ducts make vasopressin. However, the physiological role of collecting duct-derived vasopressin is uncertain. We hypothesized that collecting duct-derived vasopressin is required for the appropriate concentration of urine.
View Article and Find Full Text PDFCharacterization of Diclofenac-induced Renal Damage in Normotensive and Hypertensive Rats: A Comparative Analysis.
Drug Res (Stuttg)
April 2024
Postgraduate Program in Pharmaceutical Sciences, Nucleus of Chemical-Pharmaceutical Investigations, University of Vale do Itajaí, Itajaí, Brazil.
Background: Diclofenac is the non-steroidal anti-inflammatory drug (NSAID) mostly prescribed worldwide, but it is highly associated with hypertension and acute kidney injury. Despite that, little information is available about the renal effects of diclofenac in hypertensive individuals, which led us to carry out this comparative study between the renal effects of this NSAID in normotensive (NTR) and spontaneously hypertensive rats (SHR).
Methods: Male Wistar NTR and SHR were orally treated with vehicle (V: 10 mL/kg) or diclofenac sodium (D: 100 mg/kg) once a day for 3 days.
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