cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.19422302.v1
title: Anti-phospholipase A2 receptor antibodies directly induced podocyte damage <i>in vitro</i>

description: The pathogenesis of primary membranous nephropathy (MN) involves the antibodies against antigens on the cell surface of podocytes, with the majority of M-type phospholipase A2 receptor (PLA2R), and a profound podocyte dysfunction. The effects of anti-PLA2R antibodies directly to the podocytes remain unclear. Anti-PLA2R antibodies from patients with PLA2R-associated MN were affinity-purified using a column coupled with recombinant human PLA2R protein. Their effects on conditionally immortalized human podocytes were assessed by apoptosis assays, cellular calcium detection, wound healing assay, and immunofluorescent staining. Proteomics analysis was performed by LC-MS/MS and on PANTHER database. The stimulation by anti-PLA2R antibodies could induce early-stage apoptosis of podocytes (MFI of Annexin <i>V</i> = 104.3 ± 19.2 vs. 36.7 ± 7.6, <i>p</i> = 0.004). The increase of calcium concentration in podocytes (MFI = 3309.3 ± 363.6 vs. 1776.3 ± 212.7, <i>p</i> = 0.015) might attribute to the endoplasmic reticulum calcium efflux. The expression of calcium/calmodulin-dependent protein kinase IV (CaMK4) was also increased (MFI = 134.4 ± 9.8 vs. 105.3 ± 10.1, <i>p</i> = 0.011). Proteomics results suggested that anti-PLA2R antibody treatment led to damage on cellular structure, and produced functional disorders on protein binding, actin filament binding, and microtubule motor activity. The staining of F-actin on foot process was reduced (MFI = 27.3 ± 2.8 vs. 47.5 ± 1.0, <i>p</i> = 0.001) and the motility and adherence capacity of podocytes were reduced (number of migrated cells = 44.7 ± 3.1 vs. 53.3 ± 4.9, <i>p</i> = 0.001) after incubation with anti-PLA2R antibodies. These data indicate that anti-PLA2R antibodies may directly induce podocyte damage independent of the complement system, which expands the mechanism of anti-PLA2R antibodies on MN.
DOI: 10.18738/t8/uoes4s/57zpn8
title: timestamps.txt
DOI: 10.6084/m9.figshare.19354008
title: Risk factors for hypocalcemia in dialysis patients with refractory secondary hyperparathyroidism after parathyroidectomy: a meta-analysis

description: Hypocalcemia after parathyroidectomy (PTX) results in tetany, diarrhea, cardiac arrhythmia, and even sudden death. However, a meta-analysis or systematic evaluation of risk factors with the occurrence and development of hypocalcemia in patients with secondary hyperparathyroidism (SHPT) after PTX has never been performed. A thorough search of electronic databases, including PubMed, Web of Science, the Cochrane Library, and EMBASE, was performed to retrieve relevant studies from database inception to June 2021. Quality of the included studies was assessed by two independent reviewers using the Newcastle–Ottawa Scale. Review Manager 5.3 and Stata 16.0 were used for meta-analysis. The random-effects model was adopted to calculate the 95% CIs (<i>I</i><sup>2</sup>&gt; 50% or <i>p</i> &lt; 0.05) of the combined effect size and the corresponding homogeneous data. Otherwise, a fixed-effects model was used. Thirteen studies including 2990 participants who met the inclusion criteria were enrolled in the present meta-analysis. The overall quality of the enrolled studies had a score of &gt;7 points. Risk factors significantly related to hypocalcemia in patients with SHPT after PTX were preoperative serum calcium (OR 0.19, 95%CI 0.11–0.31), preoperative alkaline phosphatase (ALP) (OR 1.01, 95% CI 1.01–1.02), and preoperative intact parathyroid hormone (iPTH) (OR 1.38, 95%CI 1.20–1.58). Meanwhile, age (OR 0.97, 95%CI 0.87–1.10) was not significantly correlated with hypocalcemia after PTX. Based on the current evidence, preoperative serum calcium, preoperative ALP, and preoperative iPTH were significant predictors of hypocalcemia in patients with SHPT after PTX. More attention should be given to patients with these risk factors for the prevention of postoperative hypocalcemia.
DOI: 10.6084/m9.figshare.19354008.v1
title: Risk factors for hypocalcemia in dialysis patients with refractory secondary hyperparathyroidism after parathyroidectomy: a meta-analysis

description: Hypocalcemia after parathyroidectomy (PTX) results in tetany, diarrhea, cardiac arrhythmia, and even sudden death. However, a meta-analysis or systematic evaluation of risk factors with the occurrence and development of hypocalcemia in patients with secondary hyperparathyroidism (SHPT) after PTX has never been performed. A thorough search of electronic databases, including PubMed, Web of Science, the Cochrane Library, and EMBASE, was performed to retrieve relevant studies from database inception to June 2021. Quality of the included studies was assessed by two independent reviewers using the Newcastle–Ottawa Scale. Review Manager 5.3 and Stata 16.0 were used for meta-analysis. The random-effects model was adopted to calculate the 95% CIs (<i>I</i><sup>2</sup>&gt; 50% or <i>p</i> &lt; 0.05) of the combined effect size and the corresponding homogeneous data. Otherwise, a fixed-effects model was used. Thirteen studies including 2990 participants who met the inclusion criteria were enrolled in the present meta-analysis. The overall quality of the enrolled studies had a score of &gt;7 points. Risk factors significantly related to hypocalcemia in patients with SHPT after PTX were preoperative serum calcium (OR 0.19, 95%CI 0.11–0.31), preoperative alkaline phosphatase (ALP) (OR 1.01, 95% CI 1.01–1.02), and preoperative intact parathyroid hormone (iPTH) (OR 1.38, 95%CI 1.20–1.58). Meanwhile, age (OR 0.97, 95%CI 0.87–1.10) was not significantly correlated with hypocalcemia after PTX. Based on the current evidence, preoperative serum calcium, preoperative ALP, and preoperative iPTH were significant predictors of hypocalcemia in patients with SHPT after PTX. More attention should be given to patients with these risk factors for the prevention of postoperative hypocalcemia.
DOI: 10.6084/m9.figshare.20268989
title: Coronary artery lesion distribution in patients with chronic kidney disease undergoing percutaneous coronary intervention

description: To determine the location of coronary atherosclerosis distribution observed in patients with chronic kidney disease (CKD). A cross-sectional study was conducted using the database of cardiovascular medicine data from Saitama Sekishinkai Hospital to clarify the association between renal function and angiographic characteristics of coronary atherosclerosis. In total, 3268 patients who underwent percutaneous coronary intervention were included. Propensity score matching revised the total to 1772. The association of renal function with the location and/or distribution of coronary atherosclerosis lesions was then examined. Overall, coronary lesion was observed in the left anterior descending coronary artery (LAD) in 56% patients, whereas 28% and 22% were in the right coronary artery (RCA) and left circumflex coronary artery (LCX), respectively. LAD was most affected and observed in 57% patients with stage 1 CKD. RCA was second-most affected, at 26% CKD stage 1, but it increased to 31%, 38%, and 59% in CKD 3, 4, and 5, respectively. In CKD 5 patients, the RCA was the most affected artery (59%), with 41% LAD lesions. Logistic regression analysis after propensity score matching showed that the odds ratios for an RCA lesion was 3.658 in CKD 5 (<i>p</i> = .025) compared with CKD 1 after adjusting for traditional risk factors. The prevalence of RCA lesions, but not LAD or LCX lesions, increased with increasing CKD stage. The pathophysiology of coronary atherosclerosis may differ by lesion location. Deterioration of renal function may affect progression of atherosclerosis more in the RCA than in the LAD or LCX.
DOI: 10.6084/m9.figshare.20268989.v2
title: Coronary artery lesion distribution in patients with chronic kidney disease undergoing percutaneous coronary intervention

description: To determine the location of coronary atherosclerosis distribution observed in patients with chronic kidney disease (CKD). A cross-sectional study was conducted using the database of cardiovascular medicine data from Saitama Sekishinkai Hospital to clarify the association between renal function and angiographic characteristics of coronary atherosclerosis. In total, 3268 patients who underwent percutaneous coronary intervention were included. Propensity score matching revised the total to 1772. The association of renal function with the location and/or distribution of coronary atherosclerosis lesions was then examined. Overall, coronary lesion was observed in the left anterior descending coronary artery (LAD) in 56% patients, whereas 28% and 22% were in the right coronary artery (RCA) and left circumflex coronary artery (LCX), respectively. LAD was most affected and observed in 57% patients with stage 1 CKD. RCA was second-most affected, at 26% CKD stage 1, but it increased to 31%, 38%, and 59% in CKD 3, 4, and 5, respectively. In CKD 5 patients, the RCA was the most affected artery (59%), with 41% LAD lesions. Logistic regression analysis after propensity score matching showed that the odds ratios for an RCA lesion was 3.658 in CKD 5 (<i>p</i> = .025) compared with CKD 1 after adjusting for traditional risk factors. The prevalence of RCA lesions, but not LAD or LCX lesions, increased with increasing CKD stage. The pathophysiology of coronary atherosclerosis may differ by lesion location. Deterioration of renal function may affect progression of atherosclerosis more in the RCA than in the LAD or LCX.
DOI: 10.18738/t8/uoes4s/vjm8ka
title: description.txt
DOI: 10.6084/m9.figshare.19169669
title: Is hyperuricemia an independent prognostic factor for IgA nephropathy: a systematic review and meta-analysis of observational cohort studies

description: Hyperuricemia has been reported to be correlated with IgA nephropathy (IgAN). However, whether hyperuricemia or elevated serum uric acid (SUA) is an independent prognostic factor of IgAN remains unknown. Therefore, this systematic review and meta-analysis evaluated the prognostic value of hyperuricemia and elevated SUA in IgAN. Databases including PubMed, EMBASE, the Cochrane Central Register of Controlled Trials (CENTRAL), and Open Gray were reviewed systematically. The kidney failure events of IgAN were defined as a doubling of serum creatinine, halving of eGFR, end-stage renal disease (ESRD), or death. The risk ratio (RR) between hyperuricemia and IgAN-caused kidney failure was evaluated before and after adjustment for relevant covariates. The RR between elevated SUA and IgAN-caused kidney failure was evaluated after adjustment for relevant covariates. A total of 11 548 patients from 14 studies were included in this meta-analysis. Hyperuricemia was found to be an independent prognostic factor of IgAN (unadjusted RR = 2.79, 95% CI = 1.93–4.03, <i>p</i> for heterogeneity &lt;0.00001, <i>I</i><sup>2</sup> = 91%; adjusted RR = 2.12, 95% CI = 1.64–2.73, <i>p</i> for heterogeneity = 0.86, <i>I</i><sup>2</sup> = 0%). Subgroup and sensitivity analyses confirmed the stability of these results. Similarly, elevated SUA was positively correlated with kidney failure events of IgAN (adjusted RR = 1.25, 95% CI = 1.19–1.31, <i>p</i> for heterogeneity = 0.6, <i>I</i><sup>2</sup> = 0%). Our meta-analysis showed that hyperuricemia and elevated SUA were both independently associated with an increased incidence of kidney failure events in IgAN patients.
DOI: 10.6084/m9.figshare.19169669.v1
title: Is hyperuricemia an independent prognostic factor for IgA nephropathy: a systematic review and meta-analysis of observational cohort studies

description: Hyperuricemia has been reported to be correlated with IgA nephropathy (IgAN). However, whether hyperuricemia or elevated serum uric acid (SUA) is an independent prognostic factor of IgAN remains unknown. Therefore, this systematic review and meta-analysis evaluated the prognostic value of hyperuricemia and elevated SUA in IgAN. Databases including PubMed, EMBASE, the Cochrane Central Register of Controlled Trials (CENTRAL), and Open Gray were reviewed systematically. The kidney failure events of IgAN were defined as a doubling of serum creatinine, halving of eGFR, end-stage renal disease (ESRD), or death. The risk ratio (RR) between hyperuricemia and IgAN-caused kidney failure was evaluated before and after adjustment for relevant covariates. The RR between elevated SUA and IgAN-caused kidney failure was evaluated after adjustment for relevant covariates. A total of 11 548 patients from 14 studies were included in this meta-analysis. Hyperuricemia was found to be an independent prognostic factor of IgAN (unadjusted RR = 2.79, 95% CI = 1.93–4.03, <i>p</i> for heterogeneity &lt;0.00001, <i>I</i><sup>2</sup> = 91%; adjusted RR = 2.12, 95% CI = 1.64–2.73, <i>p</i> for heterogeneity = 0.86, <i>I</i><sup>2</sup> = 0%). Subgroup and sensitivity analyses confirmed the stability of these results. Similarly, elevated SUA was positively correlated with kidney failure events of IgAN (adjusted RR = 1.25, 95% CI = 1.19–1.31, <i>p</i> for heterogeneity = 0.6, <i>I</i><sup>2</sup> = 0%). Our meta-analysis showed that hyperuricemia and elevated SUA were both independently associated with an increased incidence of kidney failure events in IgAN patients.
DOI: 10.6084/m9.figshare.19187301
title: Endoplasmic reticulum stress mediates parathyroid hormone-induced apoptosis in vascular smooth muscle cells

description: Vascular calcification is one of the most common complications of chronic kidney disease (CKD), which is closely associated with increased mortality and morbidity rates of CKD patients. It has been reported that increased parathyroid hormone (PTH) aggravates vascular calcification in CKD patients. However, the direct role of PTH in vascular smooth muscle cells (VSMCs) is less elucidated. Here, we present evidence that PTH promotes apoptosis of VSMCs and endoplasmic reticulum (ER) stress participates in this process. Human aorta vascular smooth muscle cells (HASMCs) were treated with different concentrations of PTH for various time. HASMC apoptosis was detected by flow cytometry. Expression of phosphorylated (p)-PERK, CHOP, IRE1, p-JNK, and cleaved caspase 3 was determined by Western blotting. We found that PTH induced HASMC apoptosis and increased the expression of cleaved caspase 3. Furthermore, PTH activated PERK-CHOP and IRE1-JNK ER stress pathways. Either inhibition of JNK by SP600125 or CHOP by siRNA ameliorated PTH-induced apoptosis in HASMCs. We therefore suggest that ER stress participates in PTH-induced apoptosis of VSMCs, which may be a possible mechanism of PTH-promoted vascular calcification in CKD patients.
DOI: 10.6084/m9.figshare.20268989.v1
title: Coronary artery lesion distribution in patients with chronic kidney disease undergoing percutaneous coronary intervention

description: To determine the location of coronary atherosclerosis distribution observed in patients with chronic kidney disease (CKD). A cross-sectional study was conducted using the database of cardiovascular medicine data from Saitama Sekishinkai Hospital to clarify the association between renal function and angiographic characteristics of coronary atherosclerosis. In total, 3268 patients who underwent percutaneous coronary intervention were included. Propensity score matching revised the total to 1772. The association of renal function with the location and/or distribution of coronary atherosclerosis lesions was then examined. Overall, coronary lesion was observed in the left anterior descending coronary artery (LAD) in 56% patients, whereas 28% and 22% were in the right coronary artery (RCA) and left circumflex coronary artery (LCX), respectively. LAD was most affected and observed in 57% patients with stage 1 CKD. RCA was second-most affected, at 26% CKD stage 1, but it increased to 31%, 38%, and 59% in CKD 3, 4, and 5, respectively. In CKD 5 patients, the RCA was the most affected artery (59%), with 41% LAD lesions. Logistic regression analysis after propensity score matching showed that the odds ratios for an RCA lesion was 3.658 in CKD 5 (<i>p</i> = .025) compared with CKD 1 after adjusting for traditional risk factors. The prevalence of RCA lesions, but not LAD or LCX lesions, increased with increasing CKD stage. The pathophysiology of coronary atherosclerosis may differ by lesion location. Deterioration of renal function may affect progression of atherosclerosis more in the RCA than in the LAD or LCX.
DOI: 10.6084/m9.figshare.19187301.v1
title: Endoplasmic reticulum stress mediates parathyroid hormone-induced apoptosis in vascular smooth muscle cells

description: Vascular calcification is one of the most common complications of chronic kidney disease (CKD), which is closely associated with increased mortality and morbidity rates of CKD patients. It has been reported that increased parathyroid hormone (PTH) aggravates vascular calcification in CKD patients. However, the direct role of PTH in vascular smooth muscle cells (VSMCs) is less elucidated. Here, we present evidence that PTH promotes apoptosis of VSMCs and endoplasmic reticulum (ER) stress participates in this process. Human aorta vascular smooth muscle cells (HASMCs) were treated with different concentrations of PTH for various time. HASMC apoptosis was detected by flow cytometry. Expression of phosphorylated (p)-PERK, CHOP, IRE1, p-JNK, and cleaved caspase 3 was determined by Western blotting. We found that PTH induced HASMC apoptosis and increased the expression of cleaved caspase 3. Furthermore, PTH activated PERK-CHOP and IRE1-JNK ER stress pathways. Either inhibition of JNK by SP600125 or CHOP by siRNA ameliorated PTH-induced apoptosis in HASMCs. We therefore suggest that ER stress participates in PTH-induced apoptosis of VSMCs, which may be a possible mechanism of PTH-promoted vascular calcification in CKD patients.
DOI: 10.6084/m9.figshare.19738347
title: Effect of goal-directed fluid therapy on renal function in critically ill patients: a systematic review and meta-analysis

description: To evaluate whether goal-directed fluid therapy (GDFT) reduces the risk of renal injury in critical illness. MEDLINE <i>via</i> PubMed, EMBASE, CENTRAL and CBM was searched from inception to 13 March 2022, for studies comparing the effect of GDFT with usual care on renal function in critically ill patients. GDFT was defined as a protocolized intervention based on hemodynamic and/or oxygen delivery parameters. A fixed or random effects model was applied to calculate the pooled odds ratio (OR) based on heterogeneity through the included studies. A total of 28 studies with 9,019 patients were included. The pooled data showed that compared with usual care, GDFT reduced the incidence of acute kidney injury (AKI) in critical illness (OR 0.62, 95% confidence interval (CI) 0.47 to 0.80, <i>p</i>&lt; 0.001). Sensitivity analysis with only low risk of bias studies showed the same result. Subgroup analyses found that GDFT was associated with a lower AKI incidence in both postoperative and medical patients. The reduction was significant in GDFT aimed at dynamic indicators. However, no significant difference was found between groups in RRT support (OR 0.88, 95% CI 0.74 to 1.05, <i>p</i>= 0.17). GDFT tended to increase fluid administration within the first 6 h, decrease fluid administration after 24 h, and was associated with more vasopressor requirements. This meta-analysis suggests that GDFT aimed at dynamic indicators may be an effective way to prevent AKI in critical illness. This may indicate a benefit from early adequate fluid resuscitation and the combined effect of vasopressors.
DOI: 10.6084/m9.figshare.19738347.v1
title: Effect of goal-directed fluid therapy on renal function in critically ill patients: a systematic review and meta-analysis

description: To evaluate whether goal-directed fluid therapy (GDFT) reduces the risk of renal injury in critical illness. MEDLINE <i>via</i> PubMed, EMBASE, CENTRAL and CBM was searched from inception to 13 March 2022, for studies comparing the effect of GDFT with usual care on renal function in critically ill patients. GDFT was defined as a protocolized intervention based on hemodynamic and/or oxygen delivery parameters. A fixed or random effects model was applied to calculate the pooled odds ratio (OR) based on heterogeneity through the included studies. A total of 28 studies with 9,019 patients were included. The pooled data showed that compared with usual care, GDFT reduced the incidence of acute kidney injury (AKI) in critical illness (OR 0.62, 95% confidence interval (CI) 0.47 to 0.80, <i>p</i>&lt; 0.001). Sensitivity analysis with only low risk of bias studies showed the same result. Subgroup analyses found that GDFT was associated with a lower AKI incidence in both postoperative and medical patients. The reduction was significant in GDFT aimed at dynamic indicators. However, no significant difference was found between groups in RRT support (OR 0.88, 95% CI 0.74 to 1.05, <i>p</i>= 0.17). GDFT tended to increase fluid administration within the first 6 h, decrease fluid administration after 24 h, and was associated with more vasopressor requirements. This meta-analysis suggests that GDFT aimed at dynamic indicators may be an effective way to prevent AKI in critical illness. This may indicate a benefit from early adequate fluid resuscitation and the combined effect of vasopressors.
DOI: 10.18738/t8/uoes4s/2zjjaf
title: Vid2RealPhase2_P20_vectornavIMU.txt
DOI: 10.6084/m9.figshare.19752374
title: Role of tRNA derived fragments in renal ischemia–reperfusion injury

description: Ischemia–reperfusion injury (IRI) is one of the major causes of acute kidney injury (AKI). tRNA derived fragments (tRFs/tiRNAs) are groups of small noncoding RNAs derived from tRNAs. To date, the role of tRFs/tiRNAs in renal IRI has not been reported. Herein, we aimed to investigate the involvement of tRFs/tiRNAs in the occurrence and development of ischemia–reperfusion-induced AKI. Moderate/severe renal IRI mouse models were established by bilateral renal pedicle clamping. The tRF/tiRNA profiles of healthy controls and moderate/severe IRI-stressed kidney tissues were sequenced by Illumina NextSeq 500. Candidate differentially expressed tiRNAs were further verified by RT-qPCR. Biological analysis was also performed. Overall, 152 tRFs/tiRNAs were differentially expressed in the moderate ischemic injury group compared with the normal control group (FC &gt; 2, <i>p</i> &lt; 0.05), of which 47 were upregulated and 105 were downregulated; in the severe ischemic injury group, 285 tRFs/tiRNAs were differentially expressed (FC &gt; 2, <i>p</i> &lt; 0.05), of which 157 were upregulated, and 128 were downregulated. RT-qPCR determination of eight abundantly expressed tiRNAs was consistent with the sequencing results. Gene Ontology analysis for target genes of the tRFs/tiRNAs showed that the most enriched cell components, molecular functions and biological processes were Golgi apparatus, cytoplasmic vesicles, protein binding, cellular protein localization and multicellular organism development. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that these target genes were mainly involved in the natural killer cell mediated cytotoxicity pathway, citrate cycle, and regulation of actin cytoskeleton signaling pathway. Our results indicated that tRFs/tiRNAs were involved in renal IRI. These tRFs/tiRNAs may be effective partly <i>via</i> regulation of renal immunity, inflammation and metabolism processes. Candidate genes, including tiRNA-Gly-GCC-003, tiRNA-Lys-CTT-003, and tiRNA-His-GTG-002, might be potential biomarkers and therapeutic targets of ischemia–reperfusion injury-induced acute kidney injury.