bluuebunny/crossref_metadata_2025 huggingface dataset:
#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

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

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 >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 < 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

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 < 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 < 0.05 for fasting and p < 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 < 0.01). The increased relative density of urine in patients with diabetes of the CIN+ group compared to patients with CI- (p < 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

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

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

< Clinical research> 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.

< In vivo study> 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

< Clinical research> 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.

< In vivo study> 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

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

Background and Aims

Chronic kidney disease (CKD) is defined as an estimated glomerular filtration rate (eGFR)  < 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

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

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.
#2871 Effect of parathyroidectomy on kidney function in adults with primary hyperparathyroidism
Authors: Bandovas João Pedro , Candeias Henrique , Mourao Mariana , Dhanani Anjum , Monteiro Nuno , Crespo Ana , Tavares Paula , Marques Hugo Pinto
Published: May 2024

Background and Aims

Multidisciplinary guidelines recommend parathyroidectomy to slow the progression of chronic kidney disease in patients with primary hyperparathyroidism (PHPT) and an estimated glomerular filtration rate (eGFR) less than 60 mL/min/1.73 m2. However, this is a weak recommendation, based on low-quality evidence. The objective of this study was to evaluate the estimated glomerular filtration rate change 12 months after parathyroidectomy for primary hyperparathyroidism according to preoperative kidney function.

Method

Patients who underwent parathyroidectomy for PHPT between 2017 and 2020 were retrospectively enrolled (n = 90). Patients without 1-year follow-up or with missing data were excluded (n = 42). Patients were dichotomized according to their baseline eGFR:  < 60 mL/min (group 1; n = 13) and ≥60 mL/min (group 2; n = 35). Variables were measured before and then at 12 months after parathyroidectomy. Statistical analyses was made using SPSS 28.

Results

The cohort included 38 female patients (79.2%) with a mean age of 68.4 ± 11.27 years. Hypertension was present in 36 patients (75%) and 16 patients (33.3%) were diabetic. Thirty-two patients were being treated with ACEI/ARAII. The mean baseline eGFR was 44.6 ± 9.5 mL/min and 88.0 ± 12.7 mL/min in groups 1 and 2, respectively. Group 1 patients had a higher median baseline serum parathyroid hormone level (p = 0.002). At 12 months, all patients were normocalcemic. The eGFR decreased significantly after parathyroidectomy in group 2 (−5.8 mL/min, p = 0.012), while in group 1 the eGFR remain stable (−0.46 mL/min, p = 0.931). We didn't find any predictive factor of eGFR variation.

Conclusion

Further studies are needed to understand the progression of renal disease after parathyroidectomy. The etiology of the disease, the use of nephroprotective measures or in the other hand nephrotoxins may have an higher impact than restore normocalcemia alone.
#2411 Inflammation in hypervolemic hemodialysis patients is linked to increased caspase-4 activity
Authors: Ulrich Christof , Canim Zeynep , Herberger Eva , Girndt Matthias , Fiedler Roman
Published: May 2024

Background and Aims

Hypervolemia is associated with inflammation in hemodialysis patients (HD). How hypervolemia triggers inflammation is not entirely known. We hypothesized that hypervolemia affects signaling via the NF-kB transcription factor system and thus analyzed the phosphorylated forms of RelA and RelB in immune cells of hypervolemic (H) and normovolemic (N) patients. Further on, we speculated that the higher inflammatory load in H in comparison to N patients could affect the sensor of intracellular LPS activity, namely caspase-4.

Method

Forty HD patients were categorized by bioimpedance measurement in normovolemic (N; 23) and hypervolemic (H; 17) groups. A caspase activity assay in combination with a specific Caspase-4/-5 inhibitor was used to detect Caspase-4/-5 activity in isolated PBMCs by flow-cytometry. The transcription factors RelA (pS529) and RelB (pS552) were analyzed by phopho-flow cytometry. Endotoxin as well as IL-6 and TNF-α were detected by ELISA technique.

Results

Hypervolemic patients were older and had more frequent diabetes. Although the endotoxin levels (EU/ml) in the serum of both groups were not different (N: 3.3 ± 1.6 vs. H 2.9 ± 1.4), Caspase-4/-5 activity (frequency of CD14+Caspase-4+), linked to intracellular endotoxin detection, was significantly elevated in H patients (N: 52 + 17% vs. H: 65 + 17%, p < 0.01). While the frequency and expression density of Rel A expressing immune cells were not different, the monocytic frequency of cells staining positive for RelB (pS552) was significantly elevated in N patients (N: 37.7 ± 27.1 vs. H: 20.4 ± 17.1, p=0.038). Among inflammatory cytokines (pg/ml) measured in the serum of patients, only IL-6 (N: 5.8 ± 10.5 vs H: 7.2 ± 6.8, p = 0.01) but not TNF-α (N: 7.7 ± 1.1 vs. H: 7.5 ± 0.7, p = 0.580) was increased in H patients.

Conclusion

The lower frequency of pRelB-positive monocytes in hypervolemic patients may be linked to a functional impairment to resolve inflammatory circles. The elevated caspase-4/-5 activity in H patients, however, can be interpreted as a higher intracellular LPS-load in H patients. Therefore, both higher inflammatory load and lower inflammatory resolution capacities are characteristics of H patients.
#322 Are platelet-related parameters prognostic predictors of renal and cardiovascular outcomes in IgA nephropathy?
Authors: Kovács Tibor , Sági Balázs , Vas Tibor , Csiky Botond , Nagy Judit
Published: May 2024

Background and Aims

IgA nephropathy (IgAN) is associated with chronic inflammation. Platelet-related parameters, such as platelet (PLT) count, platelet-to-albumin ratio (PAR) and platelet-to-lymphocyte ratio (PLR), were examined as potential prognostic indicators for renal and cardiovascular (CV) outcomes in IgAN.

Method

150 IgAN patients were involved and divided into two groups based on the cut-off value of PAR. All-cause mortality, major CV events and end-stage renal disease were the primary combined endpoints. Secondary endpoints, such as CV or renal endpoints, were also analyzed separately.

Results

Seventy-four per cent of patients were male and had a mean age of 43.7 ± 13.5 years. Mean follow-up time: 124 ± 67 months. The K-M curve showed that PLT, PLR and PAR were strongly associated with primary combined and renal outcomes, but not with cardiovascular outcomes in IgAN. In the case of combining PAR with LVH, the K-M curves showed significant differences in both the primary (p  <  0.001) and secondary outcomes (p = 0.001 and p = 0.038). When we combined PAR with metabolic syndrome, the primary (p  <  0.001) and secondary (p = 0.001 and p = 0.015) outcomes were also significant in the low and high PAR groups. PAR was correlated with gender (r = -0.273, p = 0.001) and segmental glomerulosclerosis on histology (r = 0.161, p = 0.047). PLR correlated with microalbuminuria (r = -0.165, p = 0.033) and left ventricular hypertrophy (r = -0.178, p = 0.025). PLT was correlated with gender (r = -0.201, p = 0.013) and eGFR (r = 0.158, p = 0.040). PLR, gender, dyslipidemia and microalbuminuria were associated with the primary composite endpoints; left ventricular hypertrophy and microalbuminuria with the secondary renal endpoints; and gender, age and diabetes with the cardiovascular endpoints by multivariate Cox regression.

Conclusion

Elevated PAR and PLR may predict end-stage renal disease progression, but in combination with LVH and MetS, they showed CV events also in IgAN. The determination of PAR and PLR can be useful and cost-effective parameters for assessing both cardiovascular and renal risks in CKD.
#2191 Platelet function in chronic kidney disease; can flow cytometry guide in the difficult balance between risk for bleeding versus thrombotic events?
Authors: Lund Gustav , Christensson Anders , Malm Johan , Biglarnia Alireza , Norstrom Eva
Published: May 2024

Background and Aims

Increased risk of bleeding is a well-known complication of chronic kidney disease (CKD). However, these patients also have an increased risk of thrombotic events. Several studies have implicated both impaired and enhanced platelet function in patients with chronic kidney disease, but results vary between different studies and methods. Flow cytometry has emerged as a new method to study platelet function. Our aim was to investigate platelet function using flow cytometry in patients with chronic kidney disease.

Method

20 patients were included between February and May 2023. Pre-dialytic patients with an eGFR between 8-20 mL/min/1,73 m2 were included, mean eGFR 14.7 mL/min/1,73 m2. Patients with platelet levels >100 × 109/L were included. Medication in the form of anticoagulants, NSAIDs, platelet inhibitors or SSRIs were used as exclusion criteria. Platelet activation assay was performed with flow cytometry. The expression of activation markers PAC-1 (activated GPIIb/IIIa), CD62P (P-selectin) and CD63 (dense granules) were analysed before and after activation with ADP, CRP-XL (collagen stimulating peptide, activates GPVI) or TRAP-6 (stimulates platelet activating receptor 1, PAR1). Platelets from 20 healthy control subjects were analysed for comparison.

Results

The level and size of platelets (MPV) were comparable in both groups. There were significantly higher levels of D-dimer in the CKD group vs healthy controls (1,17 mg/L FEU vs 0,27 mg/L FEU). Except for the decreased expression of activated GPIIb-IIIa receptor after activation with ADP and CRP-XL in one patient, the platelet activation did not significantly differ between CKD patients and healthy controls.

Conclusion

No significant differences in the activation of platelets were observed between the CKD population and the healthy controls when analysed by flow cytometry. Elevated levels of D-dimer in CKD patients have previously been described and are believed to be due to increased fibrin formation, lysis and decreased renal clearance. Further studies in a larger patient population, including thrombocytopenic patients are planned, with greater focus to be placed on dense granula quantities which may correlate with decreased levels in the CKD population.
#619 Serum aldosterone to potassium ratio and hyperkalemia risk in patients with chronic kidney disease
Authors: Kim Hyunwoo , Ko Ara
Published: May 2024

Background and Aims

Angiotensin converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) have demonstrated efficacy in improving outcomes in patients with chronic kidney disease (CKD). However, these medications have also been associated with the development of hyperkalemia. The aim of this study was to evaluate the relation of serum aldosterone to potassium ratio to the risk of the development of hyperkalemia in CKD patients receiving ACEIs or ARBs.

Method

Between January 2017 and December 2021, 186 patients with CKD 3-4 (estimated glomerular filtration rate, eGFR, of 15-59 ml/min/1.73 m2) who were receiving an ACEI or an ARB for at least 3 months and had serum aldosterone and potassium measured simultaneously were analyzed. Serum aldosterone to potassium (Aldo/K) ratio was calculated (ng/ml per mmol/l) and patients were divided into two groups according to the median value of serum Aldo/K ratio above or below 2.42. Follow-up serum potassium concentrations were measured every 2 to 3 months. The primary outcome was the occurrence of hyperkalemia (defined as serum potassium level > 5.5 mEq/l). Incidence rates for hyperkalemic events were computed as the ratio of the total number of hyperkalemic events to the total patient-time at risk. In addition, the times from the index date to the first occurrence of hyperkalemia for were computed. Cox proportional hazards models were used to identify patients at the risk of the occurrence of hyperkalemia.

Results

During a median follow-up period of 3.1 years, 2505 times of serum potassium were measured (mean ± standard deviation number of annual potassium measurements per patient, 4.5 ± 1.7 measurements/year per patient). A total of 144 hyperkalemic events in 81 patients (43.5%) were identified, yielding an incidence rate of 24.6 per 100 person-years (95% confidence intervals [CIs] 20.4–28.8). The incidence of hyperkalemic events was significantly higher in patients with low serum Aldo/K ratio than in those with high serum Aldo/K ratio (35.8 events/100 patient-years, 95% CI 28.9‒42.7 events/100 patient-years vs. 12.9 events/100 patient-years, 95% CI 8.8‒17.0 events/100 patient-years, p < 0.001). In multivariate Cox proportional hazards analysis, diabetes mellitus (Hazard ratio [HR], 1.842; 95% CI, 1.046-3.243; P=0.034), prior history of hyperkalemia (HR, 2.288; 95% CI, 1.372-3.815; P=0.002), low baseline eGFR (HR, 0.973; 95% CI, 0.948-0.998; P=0.037) and a low serum Aldo/K ratio (HR, 3.654; 95% CI, 2.066-6.463; P < 0.001) were predictors of subsequent development of hyperkalemia.

Conclusion

This study revealed that low serum Aldo/K ratio ( <  2.42) was strongly associated with the occurrence of hyperkalemia in CKD patients receiving ACEIs or ARBs, suggesting that the identification of patients at a risk for subsequent hyperkalemia could be made by measuring serum aldosterone and potassium levels simultaneously on these drugs.
#1440 Analysis of risk factors for the development of coronary events in patients with chronic kidney disease stage 5
Authors: Daminova Lola , Rasulev Yorkin , Nigmanov Bahodir , Adylova Durdona , Abdullayev Akbar
Published: May 2024

Background and Aims

To analyze the number and presence of certain risk factors for the development of coronary events in patients with chronic kidney disease receiving program hemodialysis.

Method

To achieve this goal, we first conducted an information search in electronic databases of articles: in English - in PubMed, the search depth was from 2010 to 2020, after which we selected the most common risk factors for the development of coronary events in the conditions of Uzbekistan (Table 1). The study and recruitment of patients took place in the department of nephrology and hemodialysis of the Republican Specialized Scientific and Practical Medical Center for Nephrology and Kidney Transplantation in 2023. The study involved 73 (42.95%) men and 97 (57.05%) women; the average age of the patients was 54.00 ± 13.72 years.

The main causes of chronic renal failure in the structure of the overall morbidity of the prospective study were: diabetic nephropathy - 41% (69), chronic glomerulonephritis - 40% (68), chronic pyelonephritis - 12.9% (22).

Results

All 170 patients were assessed for risk factors for the development of coronary events according to Table 1. Based on the current literature, we selected 30 risk factors for the development of coronary events.

The most common risk factors for the development of coronary events were, that is, 2/3: albumin, body mass index, calcium, cardiovascular diseases, clinical and ambulatory blood pressure, chronic heart failure, diastolic blood pressure, hemoglobin, left ventricular hypertrophy, mean arterial pressure, systolic blood pressure, diuretic (urea), years with hypertension.

The least significant risk factors for the development of coronary events were, that is, 1/3: diabetes, diabetic nephropathy, dyslipidemia, coronary heart disease, left ventricular end-diastolic volume, metabolic syndrome, parathyroid hormone, peripheral vascular disease, phosphorus, potassium, pulse pressure, sodium (in plasma), sodium-potassium ratio, smoking, total cholesterol.

Conclusion

In 2/3 of the studied patients of the main group, the presence of 15 risk factors for the development of coronary events was noted, in 1/3 of the patients, 21 risk factors for the development of coronary events were identified. The above risk factors together increase the incidence of coronary events in patients with stage 5 CKD several times. Coronary events are the leading causes of death in all groups. The most common were: acute left ventricular failure and sudden cardiac death. And predictors of the risk factor for death for coronary events include: blood albumin levels, BMI, blood hemoglobin, LVH, SBP, DAS, CHF, blood calcium, years since hypertension.
#1534 Risk of CKD progression taken into account of metabolic changes
Authors: Egamberdieva Dano , Ruzmetova Iroda
Published: May 2024

Background and Aims

The purpose of this study was to study the relationship between metabolic syndrome and the risk of progression of CKD in a representative sample of patients who were hospitalized in the nephrology department of the 3rd clinic of the Tashkent Medical Academy and in the department of cardiology and interventional cardiology of the Russian National Medical Research and Medical Center.

Method

In the retrospective part of the study, 1000 case histories of patients with CKD who were inpatient treatment from 2013 to 2019 in the nephrology department of the 3rd clinic of the Tashkent Medical Academy and in the department of cardiology and interventional cardiology of the Russian National Medical Research Center for Medical Sciences were studied. In the prospective part of the study, information on demographic characteristics, including age, gender, education, and profession, was collected during medical visits using a standard questionnaire. Metabolic syndrome was defined according to international guidelines as the presence of three or more of the following risk factors: waist circumference >102 cm in men or >88 cm in women; serum triglyceride level ≥1.70 mmol/L; HDL cholesterol  < 1.04 mmol/L in men or  < 1.30 mmol/L in women; Blood pressure ≥ 130/85 mm Hg, including achieved; serum glucose level ≥6.11 mmol/L. Metabolic syndrome definition criteria used

Results

The demographic characteristics of the patients are presented in the table. Mean serum creatinine was similar, but GFR was estimated to be lower among those with metabolic syndrome compared with those without. The percentage of individuals with CKD and elevated serum creatinine was statistically significantly higher among individuals with metabolic syndrome. Low HDL cholesterol, elevated plasma glucose, and abdominal obesity were found to be statistically significantly associated with the risk of developing C5 CKD and elevated serum creatinine. In addition, a significant relationship was observed between the number of metabolic syndrome components and the percentage of CKD C5 or elevated serum creatinine (P  <  0.015 and P = 0.02, respectively). In the multivariate model, patients with 1, 2, 3 and 4 or 5 components of the metabolic syndrome had 1.51; 1.50; 2.13 and 2.72 times higher odds of CKD C5 CKD, respectively, compared with individuals without metabolic syndrome components. Overall, patients with metabolic syndrome had a 64% increased odds of CKD compared with a comparison group without metabolic syndrome.

Conclusion

The present study revealed a positive and significant association between metabolic syndrome and the risk of CKD C5 in those examined. The risk of CKD increased progressively with increasing number of metabolic syndrome components.
#2550 Micro(nano)plastics in human urine: a surprising contrast between Chongqing's urban and rural regions
Authors: Song Xuan , Feng Xiaoqian , Chen Tian , Tan Zhongyou , Du Lixia , Chen Zongwen , Qiu Xihong , Mo Yunbo , Li Yan , Zhang Yuxin , Zhu Yu
Published: May 2024

Background and Aims

Microplastics (100 nm-5 mm) and nanoplastics (<100 nm) collectively referred to as micro(nano)plastics (MNPs), which are emerging pollutants all over the world. Environmental differences affect its distribution. The content of MNPs differs between urban and rural environments, according to previous studies.

Method

To understand the actual situation of human exposure to MNPs in various environments, this study collected 12 urine samples from volunteers in urban and rural regions of Chongqing and used pyrolysis-gas chromatography/mass spectrometry (Py-GC/MS) and laser direct infrared spectroscopy (LDIR) to detect and analyze MNPs in urine.

Results

With an average abundance of 1.50 (2.31) mg/kg, MNPs were found in 9 samples by Py-GC/MS. Polyethylene (PE), polyvinyl chloride (PVC) and polyamide 66 (PA66), three different types of MNPs were found, with PE content being the highest among them. By using LDIR, MNPs were found in 7 samples, with an average abundance of 15.17 (23.13) particles/kg. Five different types of MNPs were found, with acrylates (ACR) being the main type, followed by polymethylmethacrylate (PMMA), polyurethane (PU), polypropylene (PP), polyethylene terephthalate (PET).

Conclusion

The findings demonstrated that urban region had much greater levels and more types of MNPs in human urine than rural. Additionally, regular contact with plastic toys and the use of personal care products are linked to the presence of MNPs. The influence of environmental factors on the actual exposure of the human body to MNPs was preliminary explored in this study, and two different methods were used for the first time to simultaneously detect and analyze MNPs in human urine. This allowed for the feasibility of comprehensively and effectively quantitatively analyzing the actual exposure of the human body to MNPs, and also provided the theoretical foundation for further research on the harm of MNPs to human health in different environments.
#1081 Associations of MRI-derived kidney volume, kidney function, body composition, and physical performance in >38 000 UK Biobank participants
Authors: Kim Jung-Hyun , Park Sehoon , Joo Kwon Wook
Published: May 2024

Background and Aims

Kidney volume is used as predictive and therapeutic marker for several clinical conditions. However, there is a lack of large-scale studies examining the relationship between kidney volume and various clinicodemographic factors, including kidney function, body composition, and physical performance.

Method

In this observational study, MRI-derived kidney volume measurements from 38,526 UK Biobank participants were analyzed. Major kidney volume-related measures included body surface area (BSA)-adjusted total kidney volume (TKV) and the difference of bilateral kidneys. Multivariable-adjusted linear regression and cubic spline analyses were used to explore the association between kidney volume-related measures and clinicodemographic factors. Cox regression was used to identify the risks of death, non-kidney cancer, myocardial infarction (MI), and ischemic stroke.

Results

The median of BSA-adjusted TKV and difference in kidney volume were 141.9 (128.1–156.9) mL/m2 and 1.08 (1.04–1.15) fold, respectively. Higher BSA-adjusted TKV was significantly associated with higher eGFR (beta [95% CIs], 0.43 [0.42–0.44]; P < 0.001), higher composition of muscle volume (beta [95% CIs], 0.50 [0.48–0.51]; P < 0.001), and higher mean handgrip strength (beta [95% CIs], 0.15 [0.13–0.16]; P < 0.001), while associated with lower visceral adipose tissue volume (VAT, beta [95% CIs], −0.09 [−0.11 – −0.07]; P < 0.001) in adjusted models. Higher difference in bilateral kidney volumes was associated with lower eGFR, muscle volume, and physical performance, while associated with higher proteinuria and VAT.

Conclusion

Higher BSA-adjusted TKV and lower discrepancies in bilateral kidney volumes are associated with higher renal function, muscle volume, and physical performance.
#1737 Kidney function, kidney function decline, and the risk of abdominal aortic aneurysm: the Stockholm CREAtinine Measurements (SCREAM) project
Authors: Tanaka Shigeru , Bosi Alessandro , Fu Edouard L , Faucon Anne-Laure , Carrero Juan-Jesus
Published: May 2024

Background and Aims

Small, cross-sectional, cohort studies suggest a relationship between low estimated glomerular filtration rate (eGFR) and risk of developing abdominal aortic aneurysm (AAA). We here explored the possible association between eGFR and annual eGFR decline with future risk of AAA in a large community-based sample.

Method

Observational study from the SCREAM project, including participants free from AAA history. We used Cox regression to explore associations between eGFR and the rate of incident AAA and fatal-AAA (followed by death within 30 days). Among those with repeated eGFR tests within a year, we used linear mixed models to explore associations between the annual slope in eGFR and AAA rates.

Results

We included 1 586,543 eligible participants (mean age 47 years, 53% female, median eGFR 97 ml/min/1.73 m2). During median 7.6 years, 5,248 (0.34%) participants experienced AAA, of which 317 were fatal. In multivariable analyses, compared with individuals with eGFR 90 mL/min/1.73 m2, the rates of AAA and fatal-AAA were higher across lower eGFR: for eGFR 30 mL/min/1.73 m2, the HR of AAA was 1.23 (95% CI 1.09-1.39), and for fatal-AAA was 2.59 (1.71-3.90); for eGFR 15 mL/min/1.73 m2, the HR of AAA was 1.58 (1.31-1.90) and for fatal-AAA was 3.92 (2.28-6.70). Total 639 607 participants had repeated eGFR measures within a year, and experienced 3,416 AAA events during median 8.8 years of follow-up. Compared with participants showing a stable eGFR slope (−1 to 1 mL/min/y), the rate of AAA was 10% higher (HR 1.10 [1.00-1.21]) in those with an eGFR decline of 1-3 mL/min/y, and 30% higher (HR 1.30 [1.03-1.65]) in those with an eGFR decline >3 mL/min/y.

Conclusion

Both a single point eGFR and the annual slope of eGFR decline were associated with future risks of AAA. The incidence rate of AAA, and particularly fatal AAA, was higher with greater severity of chronic kidney disease or speed of eGFR decline.
#208 Obesity is associated with incident chronic kidney disease in individuals with normal renal function
Authors: Bae Eun Hui , Kim Minah , Kim Jin , Song Su Hyun , Oh Tae Ryom , Suh Sang Heon , Choi Hong Sang , Kim Chang Seong , MA Seong Kwon , Kim Soo Wan
Published: May 2024

Background and Aims

Obesity is a representative modifiable risk factor for chronic kidney disease (CKD). This study aimed to investigate whether both body mass index (BMI), waist-to-hip ratio (WHR) and changes of WHR during follow-up are risk factors for development of incident CKD.

Method

A total of 2 711 participants from a community-based cohort with normal renal function were prospectively analyzed. Among participants with obesity, we analyzed the change in WHR to evaluate the association of obesity reduction with CKD development.

Results

During a mean follow-up of 11.03 ± 4.22 years, incident CKD occurred in 190 (7.0%) participants. In the fully adjusted multivariable Cox proportional hazard models, the risk of incident CKD increased with higher BMI (hazard ratio, 1.06; 95% confidence interval, 1.00–1.11; p = 0.033) and higher WHR (hazard ratio, 1.33; 95% confidence interval, 1.07–1.66; p = 0.009). In the Kaplan–Meier analysis, cumulative adverse renal events were significantly more common in the maintained obesity group than in the reduced obesity group (p = 0.001).

Conclusion

Both higher BMI and WHR were associated with development of CKD, but the magnitude of the effect of WHR was higher than that of BMI. Moreover, reducing obesity would be beneficial for renal prognosis.