Dynamic changes in serum albumin and ferritin indicate higher risk of early-onset peritonitis in peritoneal dialysis patients.

Introduction: The objective of this study is to investigate the dynamic changes in serum albumin and ferritin as potential predictors for early-onset peritoneal dialysis-related peritonitis (PDRP) in patients undergoing peritoneal dialysis (PD).

Methods: This retrospective study included 215 patients with end-stage renal disease who initiated PD at Huadong Hospital. Patients were followed up to 24 months, during which episodes of PDRP were recorded.

Clinical classification of hyperuricemia in patients with chronic kidney disease.

Purpose: Clinical classification of hyperuricemia (HUA) could help to guide therapy of HUA. Studies on the classification of HUA with chronic kidney disease (CKD) are rare. Therefore, we aimed to investigate the classification of HUA with CKD.

The Association between Urinary Glucose and Renal Uric Acid Excretion in Non-diabetic Patients with Stage 1-2 Chronic Kidney Disease.

: To test the hypothesis that in non-diabetic patients with early-stage chronic kidney disease (CKD), the renal excretion of urate and glucose transportation are coupled and interconnected. : A cross-sectional study of 255 non-diabetic participants with stage 1-2 CKD recruited from our department was conducted. Spearman's correlation and multiple linear regression analyses were used to study the correlation between urinary glucose and renal uric acid excretion.

Atorvastatin promotes bone formation in aged apoE mice through the Sirt1-Runx2 axis.

Background: Statins are the most widely used drugs in elderly patients; the most common clinical application of statins is in aged hyperlipemia patients. There are few studies on the effects and mechanisms of statins on bone in elderly mice with hyperlipemia. The study is to examine the effects of atorvastatin on bone phenotypes and metabolism in aged apolipoprotein E-deficient (apoE) mice, and the possible mechanisms involved in these changes.

Efficacy of different urinary uric acid indicators in patients with chronic kidney disease.

Background: Mounting studies have shown that hyperuricemia is related to kidney diseases through multiple ways. However, the application of urinary uric acid indicators in patients with reduced renal function is not clear. In this study, we aim to determine the effects of renal function on various indicators reflecting uric acid levels in patients with chronic kidney disease (CKD).

The urinary β microglobulin-creatinine ratio is inversely associated with lumbar spine bone mineral density in the elderly Chinese males.

Unlabelled: Renal tubule cells play a pivotal role in maintaining bone homeostasis. Hence, renal tubular function may be associated with bone mineral density. Our study found that urinary β microglobulin-creatinine ratio (UBCR) levels correlated negatively with lumbar spine bone mineral density (BMD) and T and Z values, and may be a marker for osteoporosis in Chinese elderly male adults.

The association of renal tubular inflammatory and injury markers with uric acid excretion in chronic kidney disease patients.

Aim: To investigate the correlation of renal tubular inflammatory and injury markers with renal uric acid excretion in chronic kidney disease (CKD) patients.

Methods: Seventy-three patients with CKD were enrolled. Fasting blood and morning urine sample were collected for routine laboratory measurements.

The association of urinary uric acid excretion with ambulatory blood pressure values in patients with chronic kidney disease.

Background: To analyze the association between hypertension and urinary uric acid excretion in patients with chronic kidney disease (CKD).

Methods: We screened 87 patients who had been admitted at the Dept of Nephrology, Huadong hospital between April 2017 to April 2019 who had completed 24-h ambulatory blood pressure monitoring and retained 24-h urine biochemical test specimens, thirty adult patients (age ≤ 65 years) with CKD 1-2 stages were recruited in the study. Pearson's correlation analysis and multiple linear regression analysis were used to study the correlation of urinary uric acid excretion with ambulatory blood pressure values and the association of morning mean diastolic pressure (mMDP), night mean diastolic pressure (nMDP) and CV of dMSP (coefficient of variation of day mean systolic pressure) with fractional excretion of uric acid (FEua) and uric acid clearance rate (Cur).

SGK1 Attenuates Oxidative Stress-Induced Renal Tubular Epithelial Cell Injury by Regulating Mitochondrial Function.

Mitochondrial dysfunction has been implicated in the early stages or progression of many renal diseases. Improving mitochondrial function and homeostasis has the potential to protect renal function. Serum- and glucocorticoid-induced kinase 1 (SGK1) is known to regulate various cellular processes, including cell survival.

Adiponectin protects against uric acid‑induced renal tubular epithelial inflammatory responses via the AdipoR1/AMPK signaling pathway.

Adiponectin (APN) exerts anti‑inflammatory effects in various cells. Uric acid (UA) induces inflammation in proximal renal tubular epithelial cells (PTECs). It remains unknown whether APN protects against UA‑induced inflammation.

The Association of Urinary Sodium and Potassium with Renal Uric Acid Excretion in Patients with Chronic Kidney Disease.

Background/aims: Hypertension and hyperuricemia are closely associated with an intermingled cause and effect relationship. Additionally, urinary sodium and potassium excretion is related to blood pressure. Whether or not it is associated with urinary uric acid excretion is not clear.

Urinary excretion of uric acid is negatively associated with albuminuria in patients with chronic kidney disease: a cross-sectional study.

Background: Increasing evidence has shown that albuminuria is related to serum uric acid. Little is known about whether this association may be interrelated via renal handling of uric acid. Therefore, we aim to study urinary uric acid excretion and its association with albuminuria in patients with chronic kidney disease (CKD).

Ischemic Preconditioning Promotes Autophagy and Alleviates Renal Ischemia/Reperfusion Injury.

Autophagy is important for cellular survival during renal ischemia/reperfusion (I/R) injury. Ischemic preconditioning (IPC) has a strong renoprotective effect during renal I/R. Our study here aimed to explore the effect of IPC on autophagy during renal I/R injury.

Impaired Na-K-ATPase signaling in renal proximal tubule contributes to hyperuricemia-induced renal tubular injury.

Hyperuricemia contributes to renal inflammation. We aimed to investigate the role of Na-K-ATPase (NKA) in hyperuricemia-induced renal tubular injury. Human primary proximal tubular epithelial cells (PTECs) were incubated with uric acid (UA) at increasing doses or for increasing lengths of time.

Ischemic preconditioning attenuates ischemia/reperfusion-induced kidney injury by activating autophagy via the SGK1 signaling pathway.

Ischemic preconditioning (IPC) has a strong renoprotective effect during renal ischemia/reperfusion (I/R) injury that is thought to relate to autophagy. However, the role of autophagy during IPC-afforded renoprotection and the precise mechanisms involved are unknown. In this study, an in vitro hypoxia/reoxygenation (H/R) model was established in which oxygen and glucose deprivation (OGD) was applied to renal cells for 15 h followed by reoxygenation under normal conditions for 30 min, 2 h or 6 h; transient OGD and subsequent reoxygenation were implemented before prolonged H/R injury to achieve hypoxic preconditioning (HPC).

Uric acid upregulates the adiponectin‑adiponectin receptor 1 pathway in renal proximal tubule epithelial cells.

Adiponectin (APN) is a protein hormone that is primarily derived from adipocytes. It can also be secreted by renal cells. Hypoadiponectinemia has been documented in patients with hyperuricemia, however, whether soluble uric acid (SUA) regulates the expression of APN and APN receptor 1 (AdipoR1) in renal proximal tubule epithelial cells (PTECs) remains to be elucidated.

Toll-like Receptor 4 Signaling Pathway in the Protective Effect of Pioglitazone on Experimental Immunoglobulin A Nephropathy.

Background: In vitro experiments have revealed that toll-like receptor 4 (TLR4) pathway is involved in the progression of immunoglobulin A nephropathy (IgAN) by induction of proinflammatory cytokines. Evidence showed that, in other disease models, peroxisome proliferator-activated receptor-γ (PPAR-γ) agonists have been shown to exert anti-inflammatory effects through suppression of the expression and activity of TLR4. However, the interaction between PPAR-γ and TLR4 in IgAN has not been fully studied both in vitro and in vivo.

Peroxisome proliferator-activated receptor γ prevents the production of NOD-like receptor family, pyrin domain containing 3 inflammasome and interleukin 1β in HK-2 renal tubular epithelial cells stimulated by monosodium urate crystals.

Recent evidence showed that peroxisome proliferator‑activated receptor γ (PPARγ) ameliorates a variety of inflammatory conditions. The present study aimed to investigate the role of PPARγ in regulating NOD-like receptor family, pyrin domain containing 3 (NALP3) inflammasome and interleukin (IL)‑1β levels during monosodium urate (MSU) crystal‑induced inflammation. HK‑2 cells were incubated with or without 200 µg/ml MSU crystals, and mRNA and protein levels of PPARγ were determined using reverse transcription quantitative polymerase chain reaction and western blot analysis, respectively.

Crosstalk between peroxisome proliferator-activated receptor-γ and mineralcorticoid receptor in TNF-α activated renal tubular cell.

Introduction: In our previous study, we observed the crosstalk between peroxisome proliferator-activated receptor-γ (PPAR-γ) and angiotensin II in activated renal tubular cells. The present study is aimed to further explore the crosstalk between PPAR-γ and mineralocorticoid receptor (MR) in tumor necrosis factor (TNF)-α activated renal tubular cells.

Methods: Human proximal renal tubular epithelial cells HK-2 were cultured with the pre-treatment of PPAR-γ agonist, pioglitazone (5 μM), MR antagonist, eplerenone (5 μM), or their combined treatment, followed by activation with TNF-α (20 ng/ml).

Soluble monosodium urate, but not its crystal, induces toll like receptor 4-dependent immune activation in renal mesangial cells.

Background: Uric acid has emerged as a novel and potential modifiable risk factor for the incidence and progression of kidney diseases, however, the deteriorate effect of uric acid on renal mesangial cells remains unclear. The present study is to examine the immune activation of soluble and crystal forms of uric acid in human mesangial cells.

Methods: We stimulated primary human mesangial cells (HMCs) with increasing concentrations (from 50 to 200 μg/ml) of soluble monosodium urate (MSU) or MSU crystals.

Soluble uric acid increases NALP3 inflammasome and interleukin-1β expression in human primary renal proximal tubule epithelial cells through the Toll-like receptor 4-mediated pathway.

Urate crystals activate innate immunity through Toll like receptor 4 (TLR4) activation, leading to the formation of the NACHT, LRR and PYD domains-containing protein 3 [NALP3; also known as NOD-like receptor family, pyrin domain containing 3 (NALP3) and cryopyrin] inflammasome, caspase-1 activation and interleukin (IL)-1β expression in gout. However, whether elevated serum uric acid (UA) levels are associated with the development and progression of renal diseases without renal urate crystal deposition remains unknown. In the present study, human primary renal proximal tubule epithelial cells were incubated with soluble UA (100 µg/ml) with or without the TLR4 inhibitor, TAK242 (1 µM).