bluuebunny/crossref_metadata_2025_split huggingface dataset:
MO411ACUTE KIDNEY INJURY AFTER PARATHYROIDECTOMY FOR PRIMARY HYPERPARATHYROIDISM: PREVALENCE, PREDICTORS AND RISK ASSESSEMENT
Authors: Parshina Ekaterina , Zulkarnaev Aleksei , Kislyy Pavel , Chernikov Roman , Mikhailova Svetlana 
Published: May 2021

Abstract

Background and Aims
Surgery is the most effective and the only definitive treatment of primary hyperparathyroidism (PHPT). We aimed to assess the prevalence of acute kidney injury (AKI) among patients underwent surgery for PHPT, to determine the possible risk factors.

Method
A retrospective cohort study included 290 patients who underwent successful selective parathyroidectomy (PTx) for PHPT. We did not include patients who underwent re-operative surgeries. AKI was defined according to KDIGO-2012 criteria.

Results
In our cohort, 106 patients (36,6%) met AKI criteria after PTx. Most of the patients developed AKI stage 1. In univariate analysis preoperative serum PTH level (р=0,0004) aa well as degree of its decrease before/after PTx (р&lt;0,0001), preoperative serum total calcium level (р=0,0158), size of the parathyroid adenoma (р=0,0184), presence of proteinuria (RR=1,9 [95%CI: 1,19; 3,54], р=0,0061), hypertension (р=0,019) and anemia (р=0,0313), older age (RR=1,32 [95%CI: 1,03; 1,72], р=0,0265) were significant risk factors of AKI development. In multivariate analysis age (OR 1,05 [95%CI: 1,02; 1,08] per a year, р=0,002), body-mass index (OR 1,07 [95%CI: 1,02; 1,13] per each kg/m2, р=0,005), anemia (yes/no OR 3,38 [95%CI: 1,38; 8,2], р=0,008), preoperative PTH (OR 1,03 [95%CI: 1,01; 1,05] per each pmol/l, р=0,002), proteinuria (yes/no OR 3,45 [95%CI: 1,34; 8,93], р=0,011), use of ACE inhibitors/ARBs (yes/no OR 2,84 [95%CI: 1,58; 5,12], р=0,001) were discovered as independent predictors of AKI.
Considering the most significant risk factors we developed two regression models for AKI risk assessment: the model 1 for patients with preserved kidney function (estimated glomerular filtration rate (eGFR ≥60 ml/min/1,73 m2) and the model 2 for those with decreased kidney function (eGFR less than 60 ml/min/1,73 m2) – tab. 1 and 2. Both models were statistically significant: χ2=25,39, df=5, р&lt;0,001, RN2=0,341 for the model 1, χ2=19,355, df=3, р&lt;0,001, RN2=0,428 for the model 2. The proposed models had good discrimination to predict AKI with area under the receiver operating characteristic curves (AUC-ROC) of 0,792 [95%CI: 0,691; 0,894], р&lt;0,001 for the model 1 (normal kidney function) and 0,84 [95%CI: 0,73; 0,951], р&lt;0,001 for the model 2 (decreased kidney function). Optimal cut-off values for predicted probability of AKI to define high-risk individuals were &gt; 0,57 (Youden’s index 0,525) for the model 1 and &gt; 0,439 (Youden’s index 0,589) for the model 2.

Conclusion
We observed high prevalence of AKI in patients after PTx for primary HPT. Developed risk models predict AKI with adequate accuracy. Risk factors of AKI should be considered when planning PTx, special attention should be paid to modifiable ones.
MO412THE RISK FACTORS OF ACUTE KIDNEY INJURY CAUSED BY HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS
Authors: Wang Siwen , Yang Jia , Xuelian Chen , Zhou Jiaojiao , Yang Lichuan 
Published: May 2021

Abstract

Background and Aims
Hemophagocytic lymphohistiocytosis (HLH) is a syndrome characterized by overproduction of proinflammatory cytokines and hemophagocytosis. Acute kidney injury (AKI) is the most common complication of HLH in the kidney, which is a strong predictor of poor prognosis. In this retrospective study, we aimed to find the risk factors of AKI in patients with HLH.

Method
We screened all adult patients with HLH admitted to West China Hospital of Sichuan University from January 2009 to June 2019. Patients in this study were secondary HLH according to the HLH diagnostic criteria revised by the Histocyte Society in 2004. Patients with HLH were excluded from the study if they had a functioning kidney transplant, received renal replacement therapy (RRT) in the past month, suffered from end-stage renal disease (ESRD), or had the renal malignant tumor. We collected basic information, clinical manifestations, and laboratory data of patients from electronic medical records.

Results
A total of 600 patients with confirmed diagnosis of secondary HLH are included in our analysis. There are 199(33.2%)HLH-induced AKI patients, among whom 37.2%, 32.7%, and 30.2% are classified as AKI I, II, and III, respectively, according to the 2012 KDIGO (Kidney Disease: Improving Global Outcomes) guideline. Overall hospital mortality is 176(29.3%), and the number of deaths in patients with AKI was much higher than that in patients without AKI (53.3% versus 17.5%, P &lt; 0.001). The risk factors of AKI in patients with HLH were hyperphosphatemia (P&lt;0.001, OR 5.448, 95%CI 2.951-10.059) , vasopressor(P&lt;0.001, OR 3.485, 95%CI 2.114-5.746), heart failure (P=0.044, 0R 2.336, 95%CI 1.022-5.340), gastrointestinal symptoms (P=0.043, OR 1.877, 95%CI 1.021-3.453), increased heart rate (P=0.005, OR 1.017, 95%CI 1.005-1.029), elevated total bilirubin level(P&lt;0.001, OR 1.004, 95%CI 1.002-1.007), and hypoproteinemia (P=0.034, OR 0.939, 95%CI 0.886-0.995).

Conclusion
The incidence of AKI was higher in patients with HLH, and the risk of death was significantly higher in HLH patients with AKI. A variety of risk factors are related to the occurrence of HLH-induced AKI. Identifying and correcting them early in clinical diagnosis and treatment may reduce the incidence of AKI in patients with HLH and improve the prognosis of them.
MO413EFFECTS OF CHRONIC, LONG-TERM ACE-INHIBITOR TREATMENT ON CYTOKINE STORM AND RENAL FUNCTION AFTER CARDIO-PULMONARY BYPASS: A PROSPECTIVE OBSERVATIONAL STUDY
Authors: Presta Pierangela , Bolignano Davide , Coppolino Giuseppe , Zicarelli Mariateresa , Serraino Filiberto , Mastroroberto Pasquale , Fuiano Giorgio , Andreucci Michele 
Published: May 2021

Abstract

Background and Aims
Cardiopulmonary bypass (CPB) may trigger organs damage, including kidney injury, due to a massive cytokine release. In this observational, prospective study, we have analyzed the possible impact of chronic treatment with ACE-Inhibitors (ACE-I) on the inflammatory response and renal function after CPB.

Method
Sixty-nine patients undergoing major cardiac surgery with CPB were enrolled. Patients were stratified according to long-term (&gt;6 mo.) ACE-I use (n=38) or not (n=31). The primary endpoint was to analyze the changes in their IL-1 alpha, IL-1beta, IL-2, IL-4, IL-6, IL-8, IL-10, TNF alpha, EGF and VEGF plasma levels. Secondary (renal) endpoints were: postoperative acute kidney injury (AKI), recovery of baseline GFR values and the absolute changes in renal function indexes.

Results
After CPB, IL-1alpha, IL-1beta, IL-4 and TNF-alpha remained stable overtime, while a significant decrease in IL-2 plasma levels was noticed in the ACE-I group (p=0.01). IL-6 and IL-8 plasma levels increased after surgery and tended to decrease after 48h. IL-10 plasma levels showed a similar variation, but both their rise and decrease were more pronounced in patients under ACE-I treatment (p=0.007). Finally, VEGF and EGF showed a marked initial decrease with a tendency to normalization 10 days after surgery (p for trend ranging from 0.01 to 0.001) (Figure 1-2).
The occurrence of AKI within 2 days after surgery, the rate of GFR recovery and the absolute changes in renal function indexes were not statistically different between groups (Figure 3).

Conclusion
Chronic, long-term ACE-I treatment may influence the inflammatory response following CPB. On the other hand, this drug class apparently has neutral impact on perioperative renal outcomes.
MO414ACUTE KIDNEY INJURY AFTER ELECTIVE ENDOCRINE SURGERY: ARE PATIENTS WITH PRIMARY HYPERPARATHYROIDISM AT RISK?
Authors: Parshina Ekaterina , Zulkarnaev Aleksei , Chernikov Roman , Kislyy Pavel 
Published: May 2021

Abstract

Background and Aims
Development of acute kidney injury (AKI) after elective endocrine surgery is underreported. We aimed to assess the prevalence of AKI among patients underwent surgery for primary hyperparathyroidism (PHPT) and thyroid surgery and compare risk of AKI between these cohorts.

Method
A retrospective cohort study included 299 patients who underwent successful selective parathyroidectomy (PTx) for PHPT, and 40 patients after thyroid surgery with comparable scope of the intervention (thyroid follicular cells tumor, non-invasive papillary thyroid carcinoma). AKI was defined according to KDIGO-2012 criteria.

Results
Change of serum creatinine before/after surgery differed significantly between PHPT and thyroid surgery group: type of surgery*time interaction p&lt;0,0001 (repeated measures ANOVA after Box-Cox transformation) – fig.1. 109 patients (36,5%) in the PHPT group and 2 patients (5%) in the thyroid group met AKI criteria after PTx. Most of the patients developed AKI stage 1. Risk of AKI was significantly higher in the PHPT patients: RR=7,3 [2,19; 26,6], OR=10,9 [2,82; 46,6], р&lt;0,0001. Patients in the thyroid surgery group were significantly younger than those in the PHPT group (41,5 [Q1-Q3: 30; 51] years vs 59 [Q1-Q3: 50,8; 67] years, respectively, p&lt;0,0001), had higher mean baseline estimated glomerular filtration rate (eGFR) (91,1 ± 18 vs 78,8 ± 18,6 ml/min/1,73 m2 respectively, p=0,0001) and had less comorbidity index (p&lt;0,0001). Hypertension encountered much more often in PHPT group vs thyroid group (69% and 22,5%, respectively, χ2 p&lt;0,0001). Duration of surgery also differed between groups: 25 min [Q1-Q3: 20; 40] min in PHPT group vs 50 [Q1-Q3: 31; 62,5] min in thyroid group, p&lt;0,0001.
We hypothesized that acute decline of parathyroid hormone after PTx increases risk of AKI in the PHPT group. To evaluate whether type of surgery (PTx/thyroid surgery) is independently associated with risk of AKI, we used 1:1 pseudorandomization (Propensity Score Matching, “matchit” package, “nearest” method in R) to balance the baseline characteristics (age, BMI, comorbidity, baseline eGFR, duration of surgery, presence of hypertension). The 40 patients in the thyroid surgery group were matched to 40 patients in the PHPT group according to these confounders. After PSM the prevalence of AKI remained significantly higher in the PHPT group than in the thyroid surgery group (30% vs. 5%, respectively, RR=6 [95%CI: 1,7; 23,1], p=0,006), confirming that PTx is the independent risk factor of AKI.

Conclusion
We observed higher prevalence of AKI after PTx for PHPT comparing with patients after thyroid surgery. Our data suggests that PTx itself is the main risk factor of AKI development after elective endocrine surgery.
MO415DOES LOW CONTRAST VOLUMES REDUCE RATES OF CONTRAST-INDUCED NEPHROPATHY IN PATIENTS UNDERGOING CORONARY ANGIOGRAPHY?
Authors: Chaabouni Emna , Jbali Hela , Mariem Najjar , Khadija Mzoughi , Mohamed karim Zouaghi 
Published: May 2021

Abstract

Background and Aims
Coronary angiography (CAG) necessitates administration of iodinated contrast, which may precipitate an acute deterioration in renal function (contrast-induced nephropathy).
Previous work on contrast-induced nephropathy (CIN) has identified contrast volume as a risk factor and suggested that there is a toxic contrast dose above which the risk of CIN is markedly increased.
The focus of this study is to provide a critical appraisal of this modifiable risk factor.

Method
We prospectively enrolled 158 patients who CAG with or without percutaneous coronary intervention from December 2017 to February 2018 at a cardiology department .
CIN was defined as an increase in serum creatinine level &gt;25% or 0.5 mg/dL after 48 hours postcardiac catheterization.
Toxic contrast dose was defined as a ratio volume of contrast media to estimated glomerular filtration rate (V/eGFR) &gt; 2 . Multivariable regression was conducted to evaluate the effect of exceeding the toxic contrast dose on CIN.

Results
Of 158 patients (females = 36.1%, mean age 60.0 ± 11 years) who underwent CAG , 15 (9,5%) developed CIN .
The volume administered of contrast was not related to the existence of postprocedure CIN (96,6±35,9 ml vs 102,5±33,7ml , p=0,16). However , it was associated with a higher incidence of CIN in patients with chronic renal failure (90±19,1 ml vs 116,6±73,7ml , p=0,008) .
The mean V/eGFR value was 1,2±0,7.Nine percent of patients exceeded the toxic contrast dose.
After adjusting for other known predictors of CIN, a V/eGFR ratio &gt; 2 remained significantly associated with CIN (odds ratio 4.7, 95% confidence interval 1.28-17.7, P=0,02).

Conclusion
Low incidences of CIN suggest that a reduced dose of contrast agent is safe in high-risk patients with impaired renal function. A ratio volume of contrast media to estimated glomerular filtration rate &gt; 2 is a significant and independent predictor of CIN after CAG.
MO341VALUE OF THE CELL CYCLE ARREST BIOMARKERS IN THE DIAGNOSIS OF PREGNANCY RELATED ACUTE KIDNEY INURY
Authors: Keryakos Hesham Kamal Habeeb , El-Minshawy Osama , Khedr Mahmoud , Yousuf Ayman , Abo Elela Moustafa , Kamel Fatma 
Published: May 2021

Abstract

Background and Aims
Pregnancy related acute kidney injury (PRAKI) is still a common serious problem in developing countries. Insulin-like growth factor-binding protein 7 (IGFBP7) and tissue inhibitor metalloproteinases-2 (TIMP-2) can identify critically ill patients at risk for the development of severe AKI. Aims: To identify main causes and timing of PRAKI and to study the G1 cell cycle arrest biomarkers in cases diagnosed with (PRAKI) as a diagnostic tool.

Method
80 pregnant women diagnosed with PRAKI were recruited from a single hospital as well as 30 age-matched pregnant women with normal pregnancy participated in this study. A urine specimen was collected from all study participants with established AKI within 24 hours of ICU admission to measure [TIMP-2]*[IGFBP7].

Results
The incidence of PRAKI was 1.1%. The most common cause of PRAKI is preeclampsia/eclampsia spectrum (61%). Most of the cases occur in the third trimester (60%) and postpartum period (23%). At a cutoff 0.33 ng/mL, the estimated sensitivity and specificity of urinary [TIMP-2]*[IGFBP7] in predicting PRAKI is 100% (95% CI) with NPV and PPV are 100%.

Conclusion
Urinary [TIMP-2]*[IGFBP7] serves as a sensitive and specific biomarker in the diagnosis of PRAKI.
MO343SERUM RESPONSE FACTOR, A NOVEL EARLY DIAGNOSTIC BIOMARKER OF ACUTE KIDNEY INJURY
Authors: Zhao Long , Xu Yan 
Published: May 2021

Abstract

Background and Aims
Studies have shown that serum response factor (SRF) is increased in chronic kidney injury, such as diabetic nephropathy, hyperuricemic nephropathy and renal cell carcinoma. The objective is to explore the early diagnostic value of SRF in acute kidney injury (AKI).

Method
AKI-related microarray data were analyzed, and the expression and location of SRF were investigated in the early phase of AKI.

Results
Bioinformatics results demonstrated that SRF was dramatically elevated 2-4 h after ischemia/reperfusion (I/R) in mouse renal tissue. In I/R rats, SRF was mostly expressed and located in renal tubular epithelial cells (TECs). SRF started to increase at 1 h, peaked at 3-9 h and started to decrease at 12 h after I/R. The areas under the ROC curve of renal SRF mRNA, renal SRF protein, urinary SRF, serum SRF and serum creatinine (Scr) were 87.9%, 83.0%, 81.3%, 78.8%, 68.8%, respectively.

Conclusion
SRF is remarkably upregulated in early (before 24 h) AKI and can replace Scr as a potential new early diagnostic biomarker of AKI.
MO344INCIDENCE AND RISK FACTORS FOR ACUTE POSTOPERATIVE RENAL FAILURE
Authors: Failal Imane , Ezzaki Sanae , Elafifi Rania , Zamd Mohamed , Mtioui Naoufal , Elkhayat Salma , Medkouri Ghizlaine , Benghanem Mohamed , Ramdani Benyounes 
Published: May 2021

Abstract

Background and Aims
Postoperative acute renal failure (AKI) is a particular form of acute failure with several triggers. Decreased renal blood flow and the resulting ischemia seem to be the most common cause of kidney damage. The objective was to study the incidence and risk factors associated with post-operative AKI.

Method
It was a retrospective, descriptive study spanning a 3-year period from January 1, 2017 to December 31, 2019. The patients in this series were admitted to the various surgical departments.

Results
Our study included 618 cases of AKI. The incidence of postoperative AKI was 8.73%. The average age of our patients was 40.4 +/- 12.3 years, a male predominance with a sex ratio of 1.2. The main history was diabetes found in 39%, hypertension in 27.5% and an injection of contrast product a few days before the intervention in 14.5%. General surgery topped the list in 49.5% of our patients, followed by trauma in 25%, gyneco-obstetrics in 14.5%, and 11% for the rest of the surgeries. The associated risk factors were: hypovolemic shock, diabetes, severe sepsis.

Conclusion
The occurrence of acute renal failure in the postoperative period results from factors related to the field and surgery. Hence the need for early identification of risk situations, in order to reduce the incidence of renal damage during the perioperative period.
MO331LINEAGE TRACING OF REGENERATING PROXIMAL TUBULE CELLS (STC) BY SINGLE CELL PROFILING IN ACUTE KIDNEY INJURY
Authors: Stamellou Eleni , Cheng Mingbo , Sterzer Viktor , Leuchtle Katja , Strieder Thiago , Boor Peter , Floege Jürgen , Costa Ivan G , Möller Marcus Johannes 
Published: May 2021

Abstract

Background and Aims
Acute tubular injury accounts for the most common intrinsic cause for acute kidney injury (AKI). The scattered tubular cell (STC) phenotype was discovered as a uniform reaction of tubule cells triggered by injury. Our group was the first to identify an inducible transgenic mouse (PEC-rtTA-mouse) specifically labeling STCs with eGFP. Analysis of the transcriptional factors and associated signaling pathways might reveal the function and role of STCs in AKI.

Method
Here, we performed single-cell RNA sequencing of unilateral ischemia-reperfusion murine model of AKI 8, 24, 48 hours and 6 and 12 days after AKI induction.

Results
Genes expressing proximal tubular proteins and transporters were markedly downregulated during transition into the STC phenotype upon injury; but expression recovered over time and upon resolution and tubular cells re-differentiated into proximal tubule cells. This provides evidence for the first time that the STC phenotype is a transient and reversible phenotype triggered by injury. Among cells in the STC phenotype, we could identify 2 sub-clusters; a highly proliferating sub-cluster that in the cell cycle analysis showed the highest proportion of cycling cells. The second eGFP-positive cluster appeared very early after AKI and expressed a distinct set of genes (defined by 7 anchor genes). Some of the highly up-regulated genes are known markers of STCs hence confirming the specificity of our transgenic mouse line.

Conclusion
Our study provides gene expression patterns specifically in STCs upon injury and repair at multiple time points and suggests that the STC phenotype is a transient and reversible phenotype triggered by injury.
MO333TARGETING HIGH MOBILITY GROUP BOX 1 WITH INHIBITORS ATTENUATE ACUTE KIDNEY INJURY IN POSTISCHEMIC KIDNEYS
Authors: Zhao Zhibo , Marschner Julian Aurelio , Li Chenyu , Hans-Joachim Anders 
Published: May 2021

Abstract

Background and Aims
HMGB1 (high mobility group box 1) is released from dying cells and hence works as a danger signal, which amplifies necroinflammation in postischemic acute kidney injury. If and to what extend small molecule HMGB1 inhibitors are capable to ameliorate the acute kidney injury is still unknown.

Method
Mice underwent 17 min unilateral renal ischemia followed by reperfusion (IR) for 4 or 7 days and were administered either 50 mg/kg glycyrrhizic acid, 80 mg/kg ethyl pyruvate, or PBS i.p. 1h before surgery and once daily until day 7.

Results
Administration of HMGB1 inhibitors consistently increased the glomerular infiltration rate at day 4 and day 7, in parallel with a reduction of plasma creatinine and circulating HMGB1 at day 7 of reperfusion. Histopathological analysis confirmed that HMGB1 inhibitors consistently attenuated tubule injury. In vitro, HMGB1 inhibitors protected primary murine tubular epithelial cells against H2O2-induced cell death.

Conclusion
Our data indicate that the treatment with glycyrrhizic acid or ethyl pyruvate ameliorates post-ischemic renal injury. This serves as a rationale to further study the role of extracellular HMGB1 and its inhibition in different models of acute kidney injury.
MO335URINARY CYTOKINES REFLECT THE ONGOING RENAL INFLAMMATION IN THE DIAGNOSTIC OF ACUTE TUBULOINTERSTITIAL NEPHRITIS: RESULTS OF A MULTIPLEX BEAD-BASED ASSAY ASSESSMENT
Authors: Martinez Valenzuela Laura , Draibe Juliana , Fulladosa Xavier , Gomez Preciado Francisco , Nadal Ernest , Jove Maria , Bestard Oriol , Cruzado Josep , Torras Joan 
Published: May 2021

Abstract

Background and Aims
Acute tubulointerstitial nephritis (ATIN) diagnostic lays on the kidney biopsy given the absence of non-invasive biomarkers for disease demonstration and follow-up. The aim of this study was to evaluate the accuracy of ten urinary inflammatory-related cytokines in the diagnostic of ATIN and its clinical distinction from acute tubular necrosis (ATN).

Method
Observational prospective study including 21 ATIN and 12 ATN patients, and 6 healthy controls. We determined the urinary levels of 10 inflammation-related cytokines using a multiplex bead-based Luminex assay. We registered clinical, analytical and histological data from the medical records.

Results
Urinary levels of I-TAC/CXCL11, CXCL10, IL-6, TNFα and MCP-1 were higher in ATIN compared to healthy controls. In contrast, healthy controls exhibited higher EGF urinary levels compared to ATIN patients. Follow-up samples available from 11/21 ATIN patients showed a significant decrease in I-TAC/CXCL11, MIG/CXCL9 and CXCL10 levels. Urinary levels of I-TAC/CXCL11, IL-6 and MCP-1 were significantly higher in ATIN compared to ATN patients, with I-TAC/CXCL11 as the best discriminatory biomarker based on its higher AUC in the ROC curve and likelihood ratio. The combinatory model of the three cytokines increased the sensitivity of the individual biomarkers in the distinction of ATIN/ATN but the best results were obtained when blood eosinophil count and leukocyturia were added to the model. We found a positive correlation of the extent of the tubulointerstitial infiltrate in kidney biopsies with the urinary concentration of I-TAC/CXCL11, MIG/CXCL9, CXCL10, IL17, IFNα, MCP1 and EGF, indicating the potential renal source of the cytokines

Conclusion
the higher cytokine levels in ATIN compared to ATN patients and healthy controls, the significant decline after treatment and the positive correlation of the cytokines with the grade of the inflammatory infiltrate allows us to propose I-TAC/CXCL11, CXCL10, IL6 and MCP-1 as candidate biomarkers in this disease.