bluuebunny/crossref_metadata_2025_split huggingface dataset:
#2740 Pregnancy outcomes in patients with IgA nephropathy and the impact of pregnancy on the renal disease
Authors: Tummala Snikitha , Menda Jaideep , Bagchi Soumita , Subbiah Arunkumar , Bhowmik Dipankar , Mahajan Sandeep 
Published: May 2024

Abstract

Background and Aims
IgA nephropathy (IgAN), the predominant primary glomerulonephritis in adults,, frequently affects women in childbearing age. There is a dearth of information about the impact of pregnancy on the outcome in IgAN especially in the Indian population where it is known to have an aggressive disease phenotype. This retrospective cohort study examines pregnancy outcomes in women with biopsy-proven IgAN and the impact on renal outcome.

Method
In a retrospective cohort study, we assessed the medical records of women in child bearing age (18-40 years) diagnosed with biopsy proven primary IgAN from 2012-2022. Patients with end stage kidney disease (ESKD) at the time of biopsy and/or at time of conception and those who had undergone kidney transplantation were excluded. Maternal (pre-eclampsia, relapse, renal disease progression, etc.) and fetal outcomes (neonatal death, preterm delivery, intra-uterine growth retardation-IUGR, etc.) were recorded. Relapse was defined as increase in proteinuria to ≥1 g/day during pregnancy and renal disease progression as &gt;40% sustained decline in eGFR and/or ESKD.

Results
Of 75 women assessed, 25 were lost to follow up. 34 did not conceive after biopsy. 20 pregnancies were documented in 14 patients. Three (15%) were medically terminated, 7 (35%) resulted in spontaneous abortions, and 10 (50%) culminated in live births. There was one neonatal death. 6/20(30%) pregnancies occurred while the patient was on ACEi/ARBs of which 5 pregnancies resulted in live births. 7/10 (70%) births were premature, 5 being moderate preterm (34-37 weeks) and 2 late preterm (32-34 weeks). IUGR below the 5th percentile affected 7/10(70%) of births. The mode of delivery was evenly split between vaginal (5, 50%) and Caesarian (5, 50%). From a maternal perspective, preeclampsia affected 3/10 (30%) patients. 5/10(50%) patients who delivered had a relapse during pregnancy with 2 developing nephrotic range proteinuria. 4 of them receiving steroids during pregnancy. All relapsed patients had persistent proteinuria &gt;1 g/day postpartum. In 2 (20%) pregnancies, relapse developed during immediate post-partum period. In 4 patients, eGFR decreased by &gt; 40 percent compared to their baseline (at biopsy) following the pregnancy.

Conclusion
Pregnancy is associated with adverse maternal and fetal outcomes in women with IgA nephropathy.
eGFR, estimated glomerular filtration rate. IUGR, Intra-uterine growth restriction (based on birth weight percentile, adjusted for gender and gestational age).
*Serum creatine of one patient during pregnancy is not available, analysis is done using values of other 9 patients. **Urine Protein of one patient is not available at the latest follow-up, analysis is done using values of 9 other patients.
#2538 Asymptomatic perirenal lymphoma: an unusual presentation of primary lymphoma
Authors: Bjedov Jelena , Djuric Petar , Stanucevic Milica , Markovic Katarina , Peslac Dragana , Naumovic Radomir 
Published: May 2024

Abstract

Background and Aims
Isolated perinephric lymphoma is uncommon clinicopathological entity, reported in less than 10% of cases. Although this is rare finding, every perirenal mass require prompt diagnosis and multidisciplinary approach if needed.

Method
We described a case of a asymptomatic young woman who presented with accidental ultrasound finding of a „kidney sweat sign“.

Results
A 40 year old woman was reported to nephrologist after ultrasonography incidentally revealed a „kidney sweat sign“. The patient had normal kidney function and was symptom-free. Also, all laboratory findings were within the reference range. She was admitted to the nephrology department and CT urography, followed by the ultrasound guided coarse needle biopsy was performed. CT scan revealed right perirenal area completely filled with soft tissue mass that was making an external compression of the right kidney with no infiltration of renal tissue, while pathohistology examination of the biopsy core showed non Hodgkin B cell lymphoma of marginal zone. Immunohistochemistry study demonstrated CD20+, CD3-,CD5-, bcl 2+, bcl 6-, CD10-, CD21-, CD23-, CD38+, cyclin D1-, Ki67+ in 5–10 tumor cells.
The patient was reported to hematologist where she underwent bone marrow biopsy which did not show evidence of lymphoma involvement. She was initiated on chemotherapeutic treatment R- COP (Rituximab, cyclophosphamide, vincristine and prednisone). Until now she received three doses of immunochemotherapy and showed good response to the therapy with decrease in the mass dimensions at the repeated CT scan without signs of disease dissemination.

Conclusion
This case report highlights the importance of an urgent and expeditious work up, including both CT scan and biopsy. Multidisciplinary approach in order to get timely diagnosis and treatment are imperative to achieve improved outcomes.
#1679 Relationship between initial eGFR DIP with proteinuria after SGLT2i treatment, in patients with IgA nephropathy. A real-world clinical study
Authors: Xydakis Dimitris , Antonaki Ergini , Tzali Eleni , Papapanagiotou Michalis , Petra Christina , Kostakis Kostantinos , Vardaki Eleftheria 
Published: May 2024

Abstract

Background and Aims
Sodium-glucose cotransporter 2 inhibitors (SGLT2i) are associated with better cardiovascular outcomes and with nephroprotection independent of diabetes status. Recent data suggest that SGLT2i significantly reduce proteinuria in patients with IgA nephropathy (IgAN). However, they often cause an initial decline in estimated glomerular filtration rate (eGFR). The aim of our study was to assess the degree of proteinuria reduction after SGLT2i treatment in IgAN and its possible association with the initial functional dip in eGFR.

Method
63 adult patients with biopsy-proven IgA nephropathy, eGFR ≥ 30 mL/min/1.73 m2 (CKD-epi), and total urine protein of &gt;0.5 grams/day at screening were included. Patients with secondary IgAN were excluded. All receiving maximally tolerated RASi for at least 12 weeks. All patients started dapagliflozin 10 mg once per day after baseline data were registered. The total follow-up was 12 months. The main outcome was the decline in eGFR and the reduction in 24-hour proteinuria from SGLT2i initiation to 1,3, 6, 9, 12 months, end-stage renal disease, or kidney or cardiovascular death.

Results
55 patients (38/17 M/F), with mean age of 44,2±18,3 years, completed follow up. 8 patients discontinued treatment due to adverse events attributed to dapagliflozin. At baseline eGFR was 66.17±19,7 ml/min/1.73 m2 and Upr: 2356±1023 mg/24H. There was a transient decline in eGFR, 30 days after initiation of dapagliflozin (66.17±19,7 min/1.73 m2 at baseline to 57 ml/min/1.73 m2) but then, there was an improvement at month 3 from baseline. The Upr/24H difference for dapagliflozin was −25.1% (95% CI −27.5, −23.2; p &lt; 0.001) at the end of follow-up (month 12). Proteinuria reduction was similar across all eGFRs.
Notably, a significant correlation was found between the initial eGFR dip and percentage proteinuria reduction in the 12th month. (R = –0.23; p = 0.03).
Consistent results of dapagliflozin treatment on proteinuria were found in all analysis subgroups including sex, baseline proteinuria, systolic blood pressure, and body mass index. No hypoglycaemic events were reported and no deaths occurred.

Conclusion
In the present study, the use of SGLT2i was associated with a significant reduction of proteinuria in patients with IgA nephropathy in patients with maximally tolerated RASi. Higher initial eGFR dip after treatment initiation was a predictor of a significantly higher reduction in proteinuria at the end of follow-up. The correlation between eGFR dip and proteinuria reduction perhaps reflects the intraglomerular pressure reduction, mediated by tubuloglomerular feedback, one of the numerous.
#731 The role of diabetes mellitus in the development of contrast-induced nephropathy in patients during x-ray endovascular procedures
Authors: Daminova Lola , Muminov Shavkat , Muminova Sitora , Nigmonov Baxodir 
Published: May 2024

Abstract

Background and Aims
To identify the role of diabetes mellitus in the development of contrast-induced nephropathy (CIN) in patients during X-ray endovascular procedures (REP).

Method
The study included 150 patients with coronary artery disease who underwent X-ray endovascular procedures (REP) using the contrast agent unihexone. The mean age of the patients was 55.69±1.27 years, including 83 men and 67 women, which accounted for 55.3% and 44.7% of the total number of patients, respectively. Diabetes mellitus was detected in 73 patients (49%). To isolate patients whose REP in the postoperative period was complicated by CIN on days 1, 2, 3, 5, 7, and 10, dynamic determination of serum creatinine concentration was carried out with glomerular filtration rate calculation. According to the results, all patients were divided into 2 groups: patients with uncomplicated postoperative REP (CIN- group, 99 patients, 66%) and patients who developed contrast-induced nephropathy (CIN+ group, 51 patients, 34%). As a control group, 20 healthy volunteers were examined. The validity of intergroup comparisons was carried out using the Student's test for paired and unpaired differences.

Results
In the course of the study, it was revealed that in the group of patients who developed CIN, there were significantly more people who developed CIN against the background of type II diabetes mellitus (p &lt; 0.05), which is probably explained by their tendency to develop diabetic microangiopathy, one of the variants of which is nephropathy. The study of glycemic features in patients with CIN included in the study demonstrated that among patients with diabetes who developed CIN, the level of glycemia was significantly higher than in patients with uncomplicated course of REP (p &lt; 0.05 for fasting and p &lt; 0.001 for postprandial glycemia), that is, the higher level of glycemia in patients with CIN of the CINgroup is explained not only by the large number of patients with diabetes, but also by the large number of patients with diabetes. but also its less control. In parallel with higher glycemia, patients with diabetes of the CIN+ group were also distinguished by more pronounced uricemia (p &lt; 0.01). The increased relative density of urine in patients with diabetes of the CIN+ group compared to patients with CI- (p &lt; 0.05) is explained by the osmotic effect of glycosuria.

Conclusion
Thus, the presence of background DM, and especially its decompensation, is a risk factor for the development of CIN after REP.
#2366 Beneficial effects of TRIM33 on myokine-mediated renal function recovery in diabetic and obese mice
Authors: Chang Se-Ho , Kim Hyun-Jung , Kim Jin Hyun , Lee Seunghye , Jung Sehyun , Jeon Hyejin , Jang Hani 
Published: May 2024

Abstract

Background and Aims
Myokines secreted from myocytes are related to improving metabolic diseases such as diabetes, obesity, and chronic kidney disease (CKD). Patients with diabetic kidney disease (DKD) have lower irisin levels, suggesting that a low level of irisin is a risk factor for the progression of CKD. However, it is not well known how myokines can alleviate metabolic kidney injury. This study aimed to investigate the effect of TRIM33, a negative regulator of TGF-β1 signaling, as a novel strategy to treat multiple metabolic complications simultaneously in the kidneys and muscles of obese db/db mice.

Method
For the in vivo experiment, five-week-old male db/db mice were assigned to three groups: db/m+, db/db, and db/db with TRIM33 plasmid mice. TRIM33 plasmid (40 μg/mice) was administered intraperitoneally. Serum glucose and myokine levels, urinary albumin excretion, renal and muscle morphology, and myokine expression in muscles were assessed. In vitro, C2C12 cells were cultivated with 2% horse serum and lipid insult in the absence or presence of TRIM33 plasmid and were analyzed for myocyte differentiation and myokines expression or production.

Results
TRIM33 treatment showed beneficial effects on tubular injury, tubulointerstitial fibrosis, mesangial expansion, renal dysfunction, variations in skeletal muscle fiber size and arrangement, skeletal muscle activity, and serum myokines levels in db/db mice. During the differentiation of C2C12 cells, myokine mRNA and protein expression and secretion were increased in TRIM33-transfected cells. Reduced levels of myokines expression and secretion in C2C12 cells with palmitate were improved by TRIM33 transfection. In coculture with HK-2 and C2C12 cells, increased EMT transition in TGF-b-treated HK-2 cells by coculture with palmitate-treated C2C12 cells was decreased in coculture with palmitate-treated C2C12 cells with TRIM33 transfection.

Conclusion
This study showed that TRIM33 is involved in the recovery of renal dysfunction via myokine in mice with diabetes and obesity.
#648 Relationship between renal tubular damage, interstitial fibrosis and semaphorin class 3C
Authors: Suzuki Natsuko , Tomohiro Takehara , Otaki Yoichiro , Ichikawa Kazunobu , Watanabe Masafumi , Miyata Masahiro , Kamei Keita , Watanabe Sayumi , Matsuki Eri , Kon Soichiro , Konta Tsuneo 
Published: May 2024

Abstract

Background and Aims
The detailed mechanism of interstitial fibrosis in CKD has not been clarified. In this study, we focused on semaphorin class 3C (SEMA3C), a secreted protein expressed in the renal tubules, that is involved in embryonic kidney development [1], and investigated the relationship between SEMA3C and renal tubular damage and interstitial fibrosis.

Methods
&lt; Clinical research&gt; We investigated the correlation between serum SEMA3C concentration and the renal tubular damage marker urinary β2 microglobulin (β2MG) concentration in the 191 patients who underwent kidney biopsy from 2017 to 2021 at Yamagata University.
&lt; In vivo study&gt; We generated proximal tubule-specific SEMA3C knockout mice (PT-SEMA3C KO) from male mice (C57BL/6) using the Cre/loxP system. The PT-SEMA3C KO group and control group were fed a 0.2% adenine diet for 5 weeks to induce CKD. The area of interstitial fibrosis/tubular atrophy (IFTA) region was assessed by Masson-Trichrome staining.

Results
&lt; Clinical research&gt; The median age of the patients was 54 (IQR 38-68) years, 94 men and 97 women. Median serum SEMA3C concentration was 0.14 (IQR 0.07-0.35) ng/ml. Median urinary β2MG levels was 0.22 (IQR 0-1.79) mg/gCr. Spearman's correlation analysis showed a significant negative correlation between serum SEMA3C and urinary β2MG levels (r=-0.208, P=0.005), but no correlation between eGFR and Urinary protein/ creatinine.
&lt; In vivo study&gt; IFTA region was 5.6% in the control group, compared to 11.2% in the PT-SEMA3C KO group (p=0.031). Interstitial fibrosis was significantly suppressed in the PT-SEMA3C KO mice (Fig. 1).

Conclusion
Our clinical and in vivo results indicate that serum SEMA3C is associated with renal tubular damage and interstitial fibrosis.
#794 LncRNA NEAT1 protects uremic toxin-induced intestinal epithelial barrier injury by regulating miR-122-5p/Occludin axis
Authors: Han Meng , Tian Na , Pathuama Pathuama 
Published: May 2024

Abstract

Background and Aims
Long non-coding RNA(LncRNA) has been reported to be associated with intestinal barrier damage. The aim of this study was to explore the mechanism of lncRNA Nuclear enriched abundant transcript 1 (NEAT1) in uremic toxin-induced intestinal epithelial barrier injury.

Method
Human colon cancer cells (Caco-2) were used to establish intestinal epithelial injury models with the urea treatment in different conditions. Cell Counting Kit-8 (CCK-8) and Western blot screening the best concentration and time. The expressions of lncRNA NEAT1 and miR-122-5p were measured by quantitative real-time polymerase chain reaction (qRT-PCR). Western blot and immunofluorescence were used to detect the expression of tight junction proteins Occludin, ZO-1 and Claudin-1. Sodium fluorescein was used to detect the paracellular permeability of intestinal epithelial injury models. The binding of miR-122-5p to lncRNA NEAT1 and Occludin was determined by bioinformatics analysis and dual luciferase reporter assay.

Results
The best condition for the injury model was urea treatment in 144 mg/dl for 48 hours. With the increase of urea intervention time and concentration, the damage degree of intestinal epithelial cells is aggravated. Based on the qRT-PCR results, lncRNA NEAT1 was significantly down-regulated in the model group. Meanwhile, the tight junction proteins Occludin, ZO-1 and Claudin-1 were significantly reduced. The permeability of sodium fluorescein was significantly increased in the model group. Overexpression of lncRNA NEAT1 can alleviate the above performances. As the target gene of lncRNA NEAT1, miR-122-5p is significantly up-regulated in the model group. The dual luciferase reporter assay proved that miR-122-5p was targets to Occludin. The protective effect of overexpression lncRNA NEAT1 on intestinal epithelial barrier function is reversed by miR-122-5p mimics.

Conclusion
LncRNA NEAT1 protects uremic toxin-induced intestinal epithelial barrier injury by regulating miR-122-5p/Occludin axis.
#2671 Renal tubular epithelial FFAR4 improves cellular senescence to alleviate interstitial fibrosis in CKD
Authors: Yang Letian , Liu Dekai , Fu Ping , MA Liang 
Published: May 2024

Abstract

Background and Aims
Chronic kidney disease (CKD) is defined as an estimated glomerular filtration rate (eGFR) &lt; 60 ml/min/1.73 m2 or pathological albuminuria, which is known as one of the major contributors to worldwide mortality. Although there have been substantial advances in understanding CKD mechanisms, at present, there are no effective therapies to treat it. We had formerly found that TUG891, a free fatty acid receptor 4 (FFAR4) (a member of the G protein-coupled receptor (GPCR) family) agonist, alleviated tubular damage as well as interstitial fibrosis in mice with CKD. Nevertheless, the multifunctional effects of FFAR4 in the kidney have not been well described.

Method
In the current research, the FFAR4 expression was abnormally reduced in tubular epithelial cells (TECs) of unilateral ureteral obstruction (UUO) and adenine-induced CKD mice. Systemic and conditional TEC-specific knockout of FFAR4 aggravated renal function, pathological damage and interstitial fibrosis, whereas FFAR4 activation by TUG-891 alleviated the severity of disease in UUO and adenine-induced CKD mice.

Results
Notably, FFAR4, as a key determinant, was firstly explored to regulate the cellular senescence in TECs and CKD mice injured kidneys, as represented through the activity of senescence associated β-galactosidase (SA-β-gal), marker protein p21, p53, Lamin B1, phospho-histone H2A.X, phospho-Rb expression, and secretory phenotype IL-6 level. Mechanistically, pharmacological activation and overexpression of FFAR4 reversed the decrease of aging-related SirT3 protein, where FFAR4 regulated SirT3 expression to exhibit anti-senescent effect via Gq subunit-mediated CaMKKβ/AMPK signaling in UUO and adenine-induced CKD mice.

Conclusion
These results underline the primordial role of renal tubular FFAR4 in the cellular senescence through AMPK/SirT3 signaling and define FFAR4 as a target for underlying drugs against CKD.
#1172 Identification of phenyl sulfate producer phenotypes by an oral tyrosine challenge test: a microbiota-based personalized nutritional approach
Authors: Hung Szu-Chun , Lin Ting-Yun 
Published: May 2024

Abstract

Background and Aims
Phenyl sulfate (PS) has been implicated in the pathogenesis of diabetic kidney disease (DKD). PS is converted from phenol, a gut microbial metabolite of dietary tyrosine, and sulfated into PS by aryl sulfotransferases in the host liver. We hypothesized that the effects of a particular diet on metabolic responses might differ from person to person. In the present study, we aimed to characterize various PS producer phenotypes using an oral tyrosine challenge test (TCT).

Method
We developed the TCT to determine the individual PS producing capacity. Plasma samples were collected at baseline after overnight fasting, and were then collected at 4, 8, 12, 24, 36 and 48 hours after oral administration of L-tyrosine at a dose of 100 mg/kg. PS concentrations were measured by high performance liquid chromatography. The gut microbiome was assessed by metagenomic shotgun sequencing.

Results
A total of 48 healthy volunteers were enrolled to undergo the TCT. The mean age of the participants was 32 ± 8 years; 50% were men, and 50% were vegetarians. The time-concentration curves of PS were similar among the participants, with the maximal increase of PS at the 24th hour (Fig. A). Participants were stratified into tertiles according to the PS levels at the 24th hour after the TCT. The 16 participants in the highest tertile were defined as high-PS producers, whereas those in the lowest tertile were defined as low-PS producers (Fig. B). We found that there was no difference in age, gender, dietary habit, BMI, eGFR, and baseline plasma PS levels between the 2 groups. However, the high-PS producers had higher levels of cholesterol, triglycerides, and low-density lipoprotein cholesterol. In addition, distinct differences in gut microbial composition were identified. At the species level, the relative abundance of Alistipes dispar, Clostridium sp. C5-48, and Butyricimonas faecihominis was markedly increased in the high-PS producers (Fig. C).

Conclusion
We found high PS variability in the response to a TCT, suggesting that universal dietary recommendations may have limited utility in reducing PS levels. Further studies are warranted to investigate the potential clinical applications of the TCT in patients with DKD.
#2302 Bleeding risk stratification following kidney biopsy using “MAJOR BLEEDING RISK SCORE”
Authors: Espada Paula Jara Caro , Nuñez Belén Alvarez , Lozano Claudia Yuste , Rodríguez-Gayo Lucía , Mérida Evangelina , Hernández-Velasco Paúl , Colina Julio , Gutiérrez Elena , Ruiz Enrique Morales 
Published: May 2024

Abstract

Background and Aims
Kidney biopsy (KB) is the gold standard in diagnosing the majority of kidney diseases. While generally KB is a safe procedure, a complication rate of 6-8% has been reported, mainly bleeding. Halimi et al. proposed “The Major Bleeding Risk Score” (MBRS) identifying 11 risk factors (out of a maximum of 41 points) associated with the likelihood of major complications (such bleeding requiring transfusion, arteriography, nephrectomy or death).

Method
In this retrospective study, we analyzed 358 native KB conducted between 2017 and 2022 by the interventional nephrology team in a tertiary hospital. Following the application of the MBRS, 273 KB were finally included to validate the score within our cohort.

Results
We analyzed 273 KB, 46.5% were male, with a mean age of 53.6 ± 18.5 years. The majority of KB were performed on the left kidney (82.4%), with an average of 2.1 ± 0.7 cylinders and 12.33 ± 6.27 glomeruli. The MBRS stratified patients into three risk groups: G1 for scores from 0 to 9 points (36.6% KB), G2 for scores between 10 to 19 points (38.8% KB) and G3 for scores from 20 to 29 points (24.5% KB).
Eleven patients (4%) had major complications (0.3% in G1, 1.5% in G2 and 2.2% in G3). The risk of bleeding increased proportionally with risk stage (G1 1% vs G2 3.8% vs G3 9%, p=0.037). Patients who experienced a complication after KB had a significantly higher MBRS than patients who did not develop complications (19 ± 5.23 points vs 13 ± 7.19 points, p=0,01). Patients who developed complications associated anaemia, thrombopenia and lower BMI more frequently than patients who did not develop complications (23.6 ± 5.9 vs. 27.3 ± 5.4, p=0.03). The pathology with the highest bleeding was thrombotic microangiopathy [OR 10,54 (2,39-46,51)].

Conclusion
The MBRS adequately stratifies patients according to bleeding risk and could be a valuable tool in the clinical practice guiding the decision to proceed with the kidney biopsy.