The latest medical research on Chronic Kidney Disease

The research magnet gathers the latest research from around the web, based on your specialty area. Below you will find a sample of some of the most recent articles from reputable medical journals about chronic kidney disease gathered by our medical AI research bot.

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Influence of carnosine and carnosinase-1 on diabetes-induced afferent arteriole vasodilation: implications for glomerular hemodynamics.

Renal Physiology

Dysregulation in glomerular hemodynamics favors hyperfiltration in diabetic kidney disease (DKD). Although carnosine supplementation ameliorates features of DKD, its effect on glomerular vasoregulation is not known. We assessed the influence of carnosine and carnosinase-1 (CN1) on afferent glomerular arteriole vasodilation and its association with glomerular size, hypertrophy and nephrin expression in diabetic BTBRob/ob mice.

Two cohorts of mice including appropriate controls were studied i.e., diabetic mice receiving oral carnosine supplementation (cohort 1) and human CN1 (hCN1) transgenic (TG) diabetic mice (cohort 2). Lumen area ratio (LAR) of the afferent arterioles and glomerular parameters were measured by conventional histology. Three-dimensional analysis using a tissue clearing strategy was also employed.

In both cohorts, LAR was significantly larger in diabetic BTBRob/ob vs non-diabetic BTBRwt/ob mice (0.41±0.05 vs 0.26±0.07; p<0.0001) and (0.42±0.06 vs 0.29±0.04; p<0.0001), and associated with glomerular size (cohort 1: r =0.55, p=0.001; cohort 2: r=0.89, p<0.0001). LAR was partially normalized by oral carnosine supplementation (0.34±0.05 vs 0.41±0.05; p=0.004), but did not differ between hCN1 TG and wild type (WT) BTBRob/ob mice. In hCN1 TG mice, serum CN1 concentrations correlated with LAR (r=0.90; p=0.006). Diabetic mice displayed decreased nephrin expression and increased glomerular hypertrophy. This was not significantly different in hCN! TG BTBRob/ob mice (p=0,06 and p=0,08, respectively).

Carnosine and CN1 may affect intra-glomerular pressure in an opposing manner through regulation of afferent arteriolar tone. This study corroborates previous findings on the role of carnosine in the progression of DKD.

Single-Cell versus Single-Nucleus: Transcriptome differences in murine kidney after ischemia-reperfusion injury.

Renal Physiology

The kidney is a complex organ, which consists of multiple components with highly diverse cell types. A detailed understanding of these cell types i...

Inhaled Silica Nanoparticles Causes Chronic Kidney Disease in Rats.

Renal Physiology

Silica nanoparticles (SiNPs) released during the burning of sugarcane have been postulated to have a role in chronic kidney disease of unknown etiology. We tested the hypothesis that pristine SiNPs of the size present in sugarcane might cause chronic kidney injury when administered through the lung in rats.

We administered 200 nm or 300 nm amorphous SiNPs twice weekly (4 mg/dose) or vehicle by oropharyngeal aspiration for 13 weeks to rats followed by sacrifice after an additional 13 weeks (26 weeks total). Tissues were evaluated for presence of SiNPs and evidence of histologic injury.

Both sizes of SiNPs caused kidney damage, with early tubular injury and inflammation (at week 13) that continued to inflammation and chronic fibrosis at week 26 despite discontinuing the SiNP administration. Both sizes of SiNPs caused local inflammation in the lung and kidney and were detected in the serum and urine at week 13, and the 200 nm particles also localized to the kidney with no evidence of retention of the 300 nm particles. At week 26 there was some clearance of the 200 nm silica from the kidneys, and urinary levels of SiNPs were reduced but still significant in both the 200 and 300 nm exposed rats.

Inhaled SiNPs causes chronic kidney injury that progresses despite stopping the SiNP administration. These findings are consistent with the hypothesis that human exposure to amorphous silica nanoparticles found in burned sugarcane fields could have a participatory role in chronic kidney disease of unknown etiology.

Contribution of Afferent Renal Nerves to Cystogenesis and Arterial Pressure Regulation in a Preclinical Model of Autosomal Recessive Polycystic Kidney Disease.

Renal Physiology

Polycystic kidney disease (PKD) is the most common inheritable cause of kidney failure, and the underlying mechanisms remain incompletely uncovered...

Transient Receptor Potential Cation Channel 6 (TRPC6) Contributes to Kidney Injury Induced by Diabetes and Hypertension.

Renal Physiology

Diabetes (DM) and hypertension (HTN) are major risk factors for chronic kidney injury, together accounting for >70% of end-stage renal disease. In ...

15-Lipoxygenase Worsens Renal Fibrosis, Inflammation, and Metabolism in a Murine Model of Ureteral Obstruction.

Renal Physiology

15-Lipoxygenase (15-LO) is a non-heme iron-containing dioxygenase that has both pro- and anti-inflammatory roles in many tissues and disease states. 15-LO is thought to influence macrophage phenotype; and silencing 15-LO reduces fibrosis after acute inflammatory triggers. The goal of this study was to determine if altering 15-LO expression influences inflammation and fibrogenesis in a murine model of unilateral ureteral obstruction (UUO).

C57BL/6J mice, 15-lipoxygenase knockout (Alox15-/-) mice, and 15-lipoxygenase transgenic overexpressing mice (15LOTG) were subjected UUO and kidneys were analyzed at 3, 10, and 14-days post injury. Histology for fibrosis, cytokine quantification, flow cytometry, and metabolomics were performed on injured tissues and controls. PD146176, a specific 15-LO inhibitor, was used to complement studies involving knockout animals.

Compared to WT animals undergoing UUO, Alox15-/- mouse kidneys had less pro-inflammatory, pro-fibrotic message along with less fibrosis. PD146176 inhibited 15-LO, and resulted in reduced fibrosis similar to Alox15-/- mice. Flow cytometry revealed that Alox15-/- UUO-injured kidneys had a dynamic change in macrophage phenotype, with an early blunting of CD11bHiLy6CHi "M1" macrophages and increase in anti-inflammatory CD11bHiLy6CInt "M2c" macrophages and reduced expression of the fractalkine receptor, CX3CR1. Many of these findings were reversed when UUO was performed on 15LOTG mice. Metabolomics analysis revealed that WT kidneys developed a glycolytic shift post-injury, while Alox15-/- kidneys exhibited increased oxidative phosphorylation.

15-LO manipulation by genetic or pharmacologic means induces dynamic changes in the inflammatory microenvironment in the UUO-model and appears to be critical in the progression of UUO-induced fibrosis.

Semaporin3A-inhibitor ameliorates renal fibrosis through the regulation of JNK signaling.

Renal Physiology

Renal fibrosis is the common pathological pathway in progressive renal diseases. In the study, we analyzed the roles of Semaphorin 3A (SEMA3A) on r...

Cubilin-, Megalin- and Dab2-dependent transcription revealed by CRISPR/Cas9 knockout in kidney proximal tubule cells.

Renal Physiology

The multiligand receptors megalin and cubilin and their endocytic adaptor protein Dab2 play essential roles in maintaining the integrity of the api...

Autophagy gene ATG7 regulates albumin transcytosis in renal tubule epithelial cells.

Renal Physiology

Receptor-mediated albumin transport in proximal tubule epithelial cells (PTECs) is important to control proteinuria. Autophagy is an evolutionarily...

Pathomorphological Sequence of Nephron Loss in Diabetic Nephropathy.

Renal Physiology

Following our reports on mesangial sclerosis and vascular proliferation in diabetic nephropathy (DN)(25,34) we now describe the advanced stages of ...

Critical role of the mineralocorticoid receptor in aldosterone-dependent and aldosterone-independent regulation of ENaC in the distal nephron.

Renal Physiology

The epithelial sodium channel (ENaC) constitutes the rate-limiting step for sodium absorption in the aldosterone-sensitive distal nephron (ASDN) co...

IFT88 deficiency in proximal tubular cells exaggerates cisplatin-induced injury by suppressing autophagy.

Renal Physiology

Primary cilia are widely regarded as specialized sensors in differentiated cells that have been implicated in the regulation of cell proliferation,...