Hemodilution Impacts Assessment of Thyroid Status before and after Hemodialysis in Patients with End-Stage Renal Disease.

Background: To elucidate the role of hemodilution in the alteration of thyroid hormone levels in end-stage renal disease (ESRD), we compared thyroid function before and after hemodialysis (HD).

Methods: Twenty-three male ESRD patients (age <65 years) with either chronic glomerulonephritis (CGN) or diabetic nephropathy (DN), who were enrolled between June 2019 and August 2019, were included in the study. The free thyroxine (fT4), free tri-iodothyronine (fT3), and thyroid-stimulating hormone (TSH), thyroxine-binding globulin (TBG), and thyroglobulin (Tg), measured before and after HD in 12 patients with CGN (48.

A serine protease inhibitor attenuates aldosterone-induced kidney injuries via the suppression of plasmin activity.

Emerging evidence has suggested that aldosterone has direct deleterious effects on the kidney independently of its hemodynamic effects. However, the detailed mechanisms of these direct effects remain to be elucidated. We have previously reported that camostat mesilate (CM), a synthetic serine protease inhibitor, attenuated kidney injuries in Dahl salt-sensitive rats, remnant kidney rats, and unilateral ureteral obstruction rats, suggesting that some serine proteases would be involved in the pathogenesis of kidney injuries.

Renal tubular acidosis complicated with hyponatremia due to cortisol insufficiency.

Adrenocortical insufficiency such as occurs in Addison's disease causes hyponatremia and renal tubular acidosis (RTA). Hyponatremia results from both aldosterone and cortisol insufficiency. RTA is due to aldosterone insufficiency.

The serine protease prostasin regulates hepatic insulin sensitivity by modulating TLR4 signalling.

The effects of high-fat diet (HFD) and postprandial endotoxemia on the development of type 2 diabetes are not fully understood. Here we show that the serine protease prostasin (PRSS8) regulates hepatic insulin sensitivity by modulating Toll-like receptor 4 (TLR4)-mediated signalling. HFD triggers the suppression of PRSS8 expression by inducing endoplasmic reticulum (ER) stress and increases the TLR4 level in the liver.

The antifibrotic effect of a serine protease inhibitor in the kidney.

Interstitial fibrosis is a final common pathway for the progression of chronic kidney diseases. Activated fibroblasts have an extremely important role in the progression of renal fibrosis, and transforming growth factor (TGF)-β₁ is a major activator of fibroblasts. Since previous reports have indicated that serine protease inhibitors have a potential to inhibit TGF-β₁ signaling in vitro, we hypothesized that a synthetic serine protease inhibitor, camostat mesilate (CM), could slow the progression of renal fibrosis.

Effect of a serine protease inhibitor on the progression of chronic renal failure.

The number of the chronic renal failure (CRF) patients is increasing explosively. Hypertension, proteinuria, inflammation, fibrosis, and oxidative stress are intertwined in a complicated manner that leads to the progression of CRF. However, the therapeutic strategies to delay its progression are limited.

In vivo contribution of serine proteases to the proteolytic activation of γENaC in aldosterone-infused rats.

Aldosterone plays an important role in the regulation of blood pressure by modulating the activity of the epithelial sodium channel (ENaC) that consists of α-, β-, and γ-subunits. Aldosterone induces a molecular weight shift of γENaC from 85 to 70 kDa that is necessary for the channel activation. In vitro experiments demonstrated that a dual cleavage mechanism is responsible for this shift.

Palladium(II)-Catalyzed Oxidation of Alcohols to Aldehydes and Ketones by Molecular Oxygen.

A novel combination of Pd(OAc)(2)/pyridine/MS3A catalyzes the aerobic oxidation in toluene of a variety of primary and secondary alcohols into the corresponding aldehydes and ketones in high yields. Various substituents and protecting groups are compatible with this oxidation. The ca.