Publications by authors named "D K Nagata"

A considerable amount of NaCl reabsorption in proximal tubules (PTs) occurs via the paracellular transport regulated by the tight junction proteins claudins (Cldns). However, the paracellular transport properties in mouse superficial PTs remain unclear. We characterized these properties in superficial PT S1-S3 segments from mice expressing [wild-type (WT, WTS1-WTS3)] or lacking [knockout (KO, KOS1-KOS3)] claudin-2.

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Chronic kidney disease (CKD) and hypertension share a complex relationship, each exacerbating the progression of the other. CKD contributes to hypertension by decreasing renal function, leading to fluid retention and increased plasma volume, whereas hypertension exacerbates CKD by increasing glomerular pressure and causing renal damage. This review examines the intertwined nature of CKD and hypertension, exploring the factors driving hypertension in CKD and how hypertension accelerates CKD progression.

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Article Synopsis
  • The main goal in treating chronic kidney disease (CKD) is to maintain kidney function and prevent it from worsening to end-stage renal disease.
  • Glomerular hypertension and low oxygen supply to kidney tubules are key factors that contribute to CKD progression, complicating treatment due to the kidney's unique blood flow dynamics.
  • Promising treatment options include sodium-glucose cotransporter 2 inhibitors and angiotensin receptor-neprilysin inhibitors, as they can help regulate the blood flow and pressure in the kidneys, potentially protecting renal function.
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Article Synopsis
  • Chronic kidney disease (CKD) and hypertension often occur together, complicating treatment, and while renin-angiotensin system (RAS) inhibitors are useful, their effectiveness for advanced CKD is still debated.
  • Angiotensin receptor-neprilysin inhibitors (ARNI) show promise in managing heart failure and may help protect kidney function, but direct evidence for their renal benefits is limited.
  • There are concerns about ARNI use in patients with severe renal failure due to the risk of low blood pressure, thus careful monitoring is crucial to balance its potential benefits and risks.
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Sodium-glucose cotransporter 2 (SGLT2) inhibitors increase urine volume with glucosuria and natriuresis. We recently reported that osmotic diuresis by the SGLT2 inhibitor ipragliflozin induces fluid homeostatic action via the stimulation of fluid intake and vasopressin-induced water reabsorption in euvolemic rats. However, the effects of SGLT2 inhibitors on these parameters in hypervolemic animals remain unclear.

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