Serum PTH Associated with Malnutrition Determined by Bioelectrical Impedance Technology in Chronic Kidney Disease Patients.

Purpose: Chronic malnutrition and cachexia are common in chronic kidney disease (CKD), and importance should be given to these complications because they affect the patient's quality of life and prognosis. This study analyzed the correlation between the serum PTH level, nutritional status, and body composition of patients with CKD.

Methods: CKD patients were enrolled in Center for Kidney Disease, Second Affiliated Hospital of Nanjing Medical University, from December 1, 2016, to November 30, 2020.

A single-center experience of parathyroidectomy in 1500 cases for secondary hyperparathyroidism: a retrospective study.

Background: Chronic kidney disease (CKD) is a global public health problem. With the deterioration of renal function, a certain proportion of CKD patients enter the uremic stage, and secondary hyperparathyroidism (SHPT) becomes a challenge. For refractory hyperparathyroidism, parathyroidectomy (PTX) plays a key role in reducing mortality and improving prognosis.

Risk Factors for Severe Hypocalcemia in Patients with Secondary Hyperparathyroidism after Total Parathyroidectomy.

Background: Hypocalcemia is the most common complication of total parathyroidectomy in secondary hyperparathyroidism (SHPT) and is associated with adverse consequences such as spasms, epilepsy, and arrhythmia and even death if the serum calcium level decreases rapidly. Previous studies have identified several risk factors for postoperative severe hypocalcemia (SH) in patients with SHPT, but the sample sizes were small and thus the results may not be reliable.

Objectives: This study was performed to investigate the risk factors for SH after total parathyroidectomy without autotransplantation (tPTX) in a large sample of patients with uremic hyperparathyroidism.

Changes in bone mineral density after total parathyroidectomy without autotransplantation in the end-stage renal disease patients with secondary hyperparathyroidism.

Background: The patients with secondary hyperparathyroidism (SHPT) usually had reduced bone mineral density, which might lead to a substantial increase in osteoporosis, fracture and mortality. Although surgical intervention is effective in reducing parathyroid hormone (PTH) levels in suitable candidates refractory to medical therapy, the effect of surgery on bone mass changes still requires further evaluation. Thus, the aim of this study was to evaluate the characteristics of BMD changes after total parathyroidectomy (PTX) without autotransplantation and its associated factors.

Effect of parathyroid hormone on serum magnesium levels: the neglected relationship in hemodialysis patients with secondary hyperparathyroidism.

Chronic kidney disease-mineral and bone disorder (CKD-MBD) is an important complication in patients with end-stage renal disease. Since recent studies have shown that magnesium (Mg) disturbance plays an important role in CKD-MBD and cardiovascular mortality, the interest on magnesium has grown recently. Although much concern focused on the effect of Mg on parathyroid hormone (PTH) levels, however, the influence of PTH on serum Mg levels is nearly unexplored.

Relationship between parathyroid mass and parathyroid hormone level in hemodialysis patients with secondary hyperparathyroidism.

Background: To evaluate the influence of parathyroid mass on the regulation of parathyroid hormone (PTH) secretion, we investigated the relationship between the resected parathyroid gland in total parathyroidectomy and the parathyroid hormone level in hemodialysis patients with secondary hyperparathyroidism.

Methods: From January 2009 to July 2014, 223 patients undergoing total parathyroidectomy were included. The size and the weight of parathyroid gland were measured during the operation.

Secreted fibroblast-derived miR-34a induces tubular cell apoptosis in fibrotic kidney.

Tubular epithelial cell apoptosis contributes to tubulointerstitial fibrosis but its regulation remains unclear. Here, in fibrotic kidney induced by unilateral ureteral obstruction (UUO), we demonstrate that miR-34a is markedly upregulated in tubulointerstitial spaces and microvesicles isolated from obstructed kidney. However, miR-34a is not de novo synthesized by proximal tubular epithelial cells but by fibroblasts after incubation with TGF-β1.

miR-21-containing microvesicles from injured tubular epithelial cells promote tubular phenotype transition by targeting PTEN protein.

Renal fibrosis is inevitably progressive no matter what the initial insult is or whether the insult persists. In an experimental fibrosis model induced by unilateral ureteral obstruction, the accelerated pathological changes could hardly be explained by aggravated pressure caused by hydronephrosis after ligation. Moreover, at the initial stage, tubular phenotype transition and matrix deposition in obstructive kidneys are always local and scattered; however, these renal lesions expand and progress with time.

Sp1 mediates microRNA-29c-regulated type I collagen production in renal tubular epithelial cells.

Specificity protein 1 (Sp1), a ubiquitously expressed transcription factor, plays a potential pathogenic role for fibrotic disease in many organs by regulating the expression of several fibrosis-related genes, however, its role in kidney fibrosis and the mechanisms regulating its expression remain incompletely clarified. Here, we found that Sp1 was markedly induced and closely correlated with interstitial type I collagen accumulation in kidney tubular epithelia from obstructive nephropathy. In vitro, both Sp1 and type I collagen expression were up-regulated in TGF-β1-treated kidney tubular epithelial cells (NRK-52E), whereas knockdown of Sp1 largely abolished TGF-β1-induced type I collagen production, suggesting that Sp1 induction is partially responsible for type I collagen expression.

The miR-200 family regulates TGF-β1-induced renal tubular epithelial to mesenchymal transition through Smad pathway by targeting ZEB1 and ZEB2 expression.

Most chronic kidney injuries inevitably progress to irreversible renal fibrosis. Tubular epithelial-to-mesenchymal transition (EMT) is recognized to play pivotal roles in the process of renal fibrosis. However, a comprehensive understanding of the pathogenesis of renal scar formation and progression remains an urgent task for renal researchers.

Mice lacking the matrix metalloproteinase-9 gene reduce renal interstitial fibrosis in obstructive nephropathy.

Matrix metalloproteinase-9 (MMP-9) is one of the major components of the matrix proteolytic network, and its role in the pathogenesis of renal interstitial fibrosis remains largely unknown. Here, we demonstrate that ablation of MMP-9 attenuated renal interstitial fibrotic lesions in obstructive nephropathy. Mice lacking MMP-9 were less likely to develop morphological injury, which was characterized by a reduced disruption of tubular basement membrane (TBM) and expression of fibronectin as well as deposition of total tissue collagen in the kidneys after sustained ureteral obstruction compared with their wild-type counterparts.

Uric acid increases fibronectin synthesis through upregulation of lysyl oxidase expression in rat renal tubular epithelial cells.

Urate is produced as the major end product of purine metabolism. In the last decade, the incidence of hyperuricemia increased markedly, and similar trends in the epidemiology of metabolic syndrome have been observed. Hyperuricemia is associated with renal disease, and recent studies have reported that mild hyperuricemia results in hypertension, intrarenal vascular disease, and renal injury.

Role of TGF-beta1 in bone matrix production in vascular smooth muscle cells induced by a high-phosphate environment.

Aims: We demonstrated a relationship between transforming growth factor-beta(1) (TGF-beta(1)) and production of bone matrix in vascular smooth muscle cells (VSMCs) induced by a high-phosphate environment.

Methods: Rat VSMCs were incubated in a high-phosphate (2.5 or 3.