bluuebunny/crossref_metadata_2025_split huggingface dataset:
P0302NEUTROPHIL TO LYMPHOCYTE AND PLATELET TO LYMPHOCYTE RATIO IN PATIENTS UNDERGOING KIDNEY TRANSPLANT
Authors: Velasco Ramirez Sandra Fabiola , Flores Fonseca Milagros Melissa , Ramirez Anguiano Ana Cristina , Cueto Casilla Martha Rosa , Diaz Burke Yolanda , Baltazar Rodriguez Luz Margarita , Villalvazo Osoria Priscila Berenice , Ruiz Cruz Norma Cecilia , Medina Perez Miguel , Gomez Navarro Benjamin 
Published: June 2020

Abstract

Background and Aims
Inflammation plays a central role before and after a kidney transplant recipients (KTR). Despite survival improvement, several factors are associated with poor outcomes after transplantation. In search of a cost effective inflammatory marker neutrophil to lymphocyte ratio (NLR) and the platelet to lymphocyte ratio (PLR) have shown a prognostic value. Therefore, the objective of this study was to determine the association of NLR and PLR and acute kidney allograft dysfunction as markers of inflammatory state in KTR.

Method
A single center, retrospective study. Our study group included 41 KTR with acute kidney allograft dysfunction from our center at Centro Medico Nacional de Occidente, Jalisco, Mexico. NLR and PLR were collected and evaluated 1 month prior KT, at the time, 6 months and one year after transplantation. Statistical analysis: Data were expressed as the mean ± SD, median and range or frequency, as appropriate. Intergroup comparisons were performed with a chi-squared test for categorical variables and Student’s t test or the Mann-Whitney test for continuous variables. Putative associations between clinical factors, biological factors and mortality were assessed in univariate and multivariate Cox models. Statistical analyses were performed using SPSS v26.0 (IBM Corporation, NY, USA); p &lt; 0.05 was considered statistically significant.

Results
Mean age was 29.54 ± 7.32 years, and 56% were women. Of those patients, all received living donor kidney transplantation. All patients in the study groups received standardized immunosuppressive regimen consisting of calcineurin inhibitors, mycophenolate mofetil and steroids. Median serum creatinine levels after KT were between 1.11 ± 0.36 mg/dl. The median NLR and PLR levels were significantly higher in the study group, with a median of 3.34 (1.83 –5.14) and 8.65 (343.47 – 360.59), not statistically associated. The best set of predictors in multiple regression analysis of higher levels of NLR were serum albumin (r = -0.432; p = 0.007) and C reactive protein (r = 0.641; p = 0.002). The best set of predictors in multiple regression analysis of higher levels of PLR were hematocrit (r = -0.313; p = 0.055) and serum glucose (r = 0.360; p = 0.026).

Conclusion
Our data showed that higher values of NLR and PLR are associated with inflammatory markers, leading to the conclusion that this finding must be confirmed with larger, prospective and controlled follow up.
P0306ACUTE KIDNEY INJURY AFTER CHECKPOINT INHIBITOR TREATMENT: FACING THE FUTURE
Authors: Garcã­a Carro Clara , Bolufer Mónica , Oleas Diana , Azancot María A , Agraz Irene , Ramos Terrada Natalia , Espinel Eugenia , Seron Micas Daniel , Soler María José 
Published: June 2020

Abstract

Background and Aims
Checkpoint inhibitors (CPI) are used to treat solid organ metastatic malignancies. They act on by triggering a vigorous immune response against tumoral cells, preventing their proliferation. CPIs reinvigorate antitumor immune responses by interrupting co-inhibitory signaling pathways and promote immune-mediated elimination of tumor cells.This is not a selective response, deriving in immune related adverse events (irAEs). The kidney can potentially be damaged with an incidence of 13-29%. The most frequent type of toxicity is acute interstitial nephritis (AIN).

Method
We evaluated all the patients with solid organ metastatic malignancies treated with immunotherapy that developed acute renal injury (AKI) and underwent to kidney biopsy from March 2018 to November 2019 at Vall d’Hebron University Hospital.

Results
11 patients with solid organ metastatic malignancies treated with immunotherapy developed AKI and underwent to kidney biopsy during the study period. The most frequent malignancy was lung cancer - in 6 patients-, followed by 3 patients with melanoma. 8 patients (72%) had already received previous oncological therapy, and for the remaining 3 patients (27%), CPI was the first line therapy. 8 patients (72%) were treated with anti-PD1 (programmed cell death protein 1), 4 patients (36 %) received anti PDL-1 (programmed death-ligand 1) 1 of these patients in combination with an anti CTLA-4 (cytotoxic T-lymphocyte antigen 4) and another patient received both anti PD1 and anti PDL-1. The time between the start of CPI and the onset of the AKI ranged between 2-11 months. The most frequent urine findings were subnephrotic range proteinuria with a mean protein/creatinine (mg/g creatinine) 503.6 ± 190.5 and leukocyturia in 9 of 11 patients. Mean creatinine (mg/dl) at diagnosis was 3.4 ± 1.3. 10 out of the 11 patients were diagnosed of AIN after performing a kidney biopsy. The remaining patient presented chronic changes (IFTA and glomerulosclerosis) in the biopsy, performed after receiving steroids for a month. 3 patients who presented AIN received pulses of methylprednisolone 250-500mg as induction treatment and 7 patients received prednisone 1mg/kg/day. Mean prednisone accumulated dose (mg) during the first month of treatment was 1387.5 ± 540. 9 patients experienced complete recovery of kidney function and two patients progressed to CKD.

Conclusion
We reported 11 patients who presented AKI associated to CPI treatment and underwent to kidney biopsy in the last 20 months at our center. 10 out of 11 presented biopsy confirmed CPI related AIN. In our experience, CPI related AIN is the most frequent renal lesion associated to the novel immunotherapy treatments. This entity seems to have good renal prognosis as long as steroid treatment is early started.
P0324SODIUM ZIRCONIUM CYCLOSILICATE TO PREVENT HYPERKALAEMIA IF HAEMODIALYSIS IS POSTPONED DUE TO VASCULAR ACCESS COMPLICATIONS: EXPERIENCE FROM CLINICAL PRACTICE
Authors: Brooks Owain , Mikhail Ashraf , Brown Chris , Gumbleton Mark , Jenkins Justine , Boyle Kaitlin 
Published: June 2020

Abstract

Background and Aims
Vascular access is a fundamental aspect of haemodialysis (HD) treatment. Vascular access may be compromised due to central venous catheter (CVC) thrombosis, arterio-venous fistula (AVF) or graft (AVG) stenosis, infections or perioperative complications that require urgent resolution or the formation of alternative emergency or definitive access. Sodium zirconium cyclosilicate (SZC) (Lokelma®) is a new oral potassium binder. We offer an insight into SZC treatment to prevent hyperkalaemia in patients where HD is postponed due to vascular access complications.

Method
Adult prevalent HD patients were included for analysis. Each patient was unable to receive their full scheduled HD treatment due to a vascular access complication. SZC was prescribed on the day HD was not possible (D1) until the vascular access issue was resolved and HD could recommence. The primary efficacy measures were the prevention of increases in serum potassium (sK+), the safe postponement of HD and the avoidance of emergency hospital admission.

Results
Four patients receiving thrice-weekly HD (mean age 69 years, all male) received SZC for a mean duration of 3.5 days (min 2 days, max 6 days). No patients were admitted during these acute episodes. The mean pre-dialysis sK+ on D1 was 6.0mmol/L (K1). No post-dialysis sK+ values were obtained on D1 because HD was not possible or cut-short (Table 1).
For patients 2 and 3, one and 10 HD treatments preceded the next sK+ (K2) respectively. sK+ reduced from 5.8mmol/L (K1) to 4.8mmol/L (K2) for patients 1 and 4 (Table 1). No statistical analyses were undertaken due to the low patient numbers.
HD was delayed beyond the scheduled treatment date for 3 of the 4 patients, with a mean delay of 1.75 days (min 0 days, max 3 days) (Table 2). There was no delay between HD treatments for patient 2, who only received 1 hour HD treatment on D1. The last full HD treatment for patient 2 was 3 days prior to D1. A gap between SZC initiation (D1) and the next HD treatment was seen for all four patients, with a mean gap of 2 days (min 1 day, max 3 days) (Table 2).

Conclusion
Sodium zirconium cyclosilicate can be used to successfully reduce, or avoid an increase in sK+ in mild to moderate hyperkalaemia, avoid emergency hospital admission and allow HD to be postponed for a valuable short period until HD vascular access can be re-established.
P0326EFFECT OF PRAVASTATIN ON ERYTHROCYTE MEMBRANE FATTY ACID CONTENTS IN PATIENTS WITH CHRONIC KIDNEY DISEASE
Authors: Lee Sumi , Choi DongHo , Jeong Yu In , Son Young Ki , Kim Seong Eun , An Won Suk 
Published: June 2020

Abstract

Background and Aims
Treatment with statin has been decreased the risk of cardiovascular events in patients with chronic kidney disease (CKD). Erythrocyte membrane oleic acid contents are significantly higher in patients with acute coronary syndrome than control subjects. Still, there is no report about the effect of statin on erythrocyte membrane fatty acid (FA) including oleic acid. The aim of this study was to evaluate the effect of pravastatin on the erythrocyte membrane FA in patients with CKD.

Method
Sixty two CKD patients were enrolled in this single arm randomized clinical trial and this trial was conducted at two centers from Jan 2017 to March 2019 (NCT02992548). Pravastatin with dose of 20mg was initially treated for 24 weeks. Pravastatin dose was increased to 40mg after 12 weeks, if it is necessary to control dyslipidemia. The primary outcome of this study was the change of erythrocyte membrane FA including oleic acid after pravastatin treatment for 24 weeks. We checked total cholesterol, triglyceride, LDL-cholesterol, HDL-cholesterol and adiponectin for secondary outcome at baseline and after 24 weeks. Erythrocyte membrane FA contents were measured by gas chromatography at baseline and after 24 weeks.

Results
Forty-five patients finished this study (age: 59.2±12.4 years, male: 42.2%, diabetes: 48.9%). There was no adverse effect related with pravastatin. Baseline serum creatinine was 1.5±0.7 mg/dL and estimated glomerular filtration rate was 54.2±27.3 ml/min/1.73 m2. Compared to baseline, total cholesterol (223.1±50.8 mg/dL vs. 168.4±32.5 mg/dL), LDL-cholesterol (149.1±35.3mg/dL vs. 100.1±25.4 mg/dL) and C-reactive protein were significantly decreased after pravastatin treatment. There were no significant changes in triglyceride, HDL-cholesterol, serum creatinine, amounts of proteinuria and adiponectin levels. Saturated FA, oleic acid and arachidonic acid contents of erythrocyte membrane were significantly increased after pravastatin treatment compared to baseline levels. Polyunsaturated FA (PUFA) and linoleic acid were significantly decreased after pravastatin treatment compared to baseline. Decreased tendency of eicosapentaenoic acid and omega-3 index were found after pravastatin treatment.

Conclusion
Linoleic acid or omega-3 FA supplementations may be necessary to recover erythrocyte membrane FA changes, when pravastatin is used for dyslipidemia treatment in CKD patients. Further study for reducing cardiovascular events are necessary by using combined PUFA and pravastatin treatment.
P0335PULMONARY HEMORRAHGE IN IG A NEPHROPATHY: A RARE MANIFESTATION
Authors: Hanen Abid , Amel Harzallah , Chifaa Trigui , Soumaya Chargui , Rim Goucha , Fathi Ben Hamida , Mondher Ounissi , Taieb Ben Abdallah 
Published: June 2020

Abstract

Background and Aims
Ig A nephropathy is the most frequent cause of glomerulonephritis worldwide. Renal-limited disease is the habitual clinical form of the disease. Pulmonary involvement may also be seen in rare cases. Capillaritis with pulmonary hemorrhage is the most frequent pulmonary involvement and is lifethreatening. We reported the case of patient presenting a rapidly progressive glomerulonephritis with pulmonary hemorrhage revealing Ig A nephropathy.

Method
A case report

Results
A 23 year-old man admitted for a rapidly progressesive glomerulonephritis with sever hypertension. He presented a respiratory distress with hemoptysis. At biology serum creatinine was at 2200µmol/l (eGFR = 2.4 ml/min) and Hemoglobin was at 5g/dl. Immunoassays of anti-glomerular basement antibodies and antineutrophil cytoplasmic autoantibodies were negatives.
Computed tomography scan showed diffuse intra alveolar hemorrhage associated with pleural effusion. Bronchoalveolar lavage confirms this diagnosis. Renal histology showed Ig A nephropathy.
Treatment consisted of daily depleted haemodialysis with blood transfusion and corticosteroids associated with monthly pulses of cyclophosphamide. His hemoptysis gradually resolved with a stable hemoglobin at 11 g/dL. However, renal failure persisted requiring maintenance hemodialysis regularly.

Conclusion
Pulmonary hemorrhage is a rare but serious complication of Ig A Nephropathy which is associated with significant morbidity and mortality. The exact cause for this “extra renal bleed” in Ig A Nephropathy is not known but it possibly represents IgA capillaritis. Though no evidence-based treatment protocol exists, therapeutic options includes steroids, plasmapheresis, cyclophosphamide and rituximab.
P0348THE DUAL ENDOTHELIN ETA AND ANGIOTENSIN AT1 RECEPTOR BLOCKER SPARSENTAN PROTECTS AGAINST THE DEVELOPMENT OF ALBUMINURIA AND GLOMERULOSCLEROSIS IN THE GDDY MOUSE MODEL OF IGA
Authors: Nagasawa Hajime , Suzuki Hitoshi , Jenkinson Celia , Ueda Seiji , Fukao Yusuke , Nakayama Maiko , Otsuka Tomoyuki , Liu Kai , Komers Radko , Suzuki Yusuke 
Published: June 2020

Abstract

Background and Aims
gddY mice are an IgA nephropathy (IgAN)-prone mouse model that develops albuminuria by 8 weeks (wks) of age with glomerular IgA, IgG, and C3 deposits and progressive mesangioproliferative glomerulonephritis. A previous study in the ddY mouse model, the more genetically heterogeneous predecessor of gddY mice, using the endothelin type A receptor (ETAR) antagonist FR139317 resulted in amelioration of proteinuria and preservation of kidney function. Treatment of ddY mice with the angiotensin II type 1 receptor (AT1R) blocker valsartan resulted in significant protection from glomerulosclerosis (GS) without a significant prevention in proteinuria. Here we examined the effect of sparsentan (SP), a dual ETAR and AT1R blocker, currently in phase 3 trials for focal segmental glomerulosclerosis and IgAN, on the development of albuminuria and GS in gddY mice.

Method
gddY mice at 4 wks of age were fed with control (C) chow (n=5) or chow containing 900 ppm (n=10) or 1800 ppm (n=10) SP (approximately 180 and 360 mg/kg/day) for 8 wks. Albuminuria (U-Alb) was assessed at 4, 6, 8, and 12 wks of age and plasma levels of SP were determined at 8 am and 4 pm at wks 6, 8, and 12. Kidney biopsies were taken at the end of the study at 12 wks of age for processing and 30 glomeruli per animal were scored for the percentage of GS.

Results
gddY mice fed SP in the diet for 8 wks from 4 wks of age demonstrated significantly (*P&lt;0.05) decreased U-Alb compared to mice fed the C diet in a dose-dependent manner (Figure 1). The development of GS in mice fed the diet containing 1800 ppm SP was significantly (*P&lt;0.05) attenuated compared to C diet (Figure 2). Plasma levels of SP taken at 8 am and 4 pm after 8 wks of treatment were (mean±SD) 281±107 and 105±62 ng/ml for 900 ppm SP respectively, and 774±674 and 304±176 ng/ml for 1800 ppm SP, respectively. Weight gain in mice fed SP was not different from mice that received C diet.

Conclusion
Eight weeks of treatment with SP attenuated increases in albuminuria and GS associated with the development of IgAN in gddY mice. If translated to the clinic, these data support SP as a new approach to the treatment of IgAN.
P0349A MISSPROCESSED FORM OF APOLIPOPROTEIN A-I IS SPECIFICALLY ASSOCIATED TO RECURRENT FOCAL SEGMENTAL GLOMERULOSCLEROSIS
Authors: Jacobs Cachá Conxita , Puig Gay Natàlia , Helm Dominic , Rettel Mandy , Sellares Joana , Meseguer Anna , Savitski Mikhail M , Moreso Francesc , Soler María José , Seron Micas Daniel , López Hellín Joan 
Published: June 2020

Abstract

Background and Aims
Recurrence of idiopathic FSGS, a glomerular disease of unknown aetiology, is a serious complication after kidney transplantation. There are no accurate means to diagnose the relapses or to detect the patients at risk. In an exploratory study we detected Apolipoprotein A-Ib (ApoA-Ib), a high molecular weight form of ApoA-I, specifically in urine of kidney transplanted patients that relapsed of FSGS. The diagnostic performance of ApoA-Ib has been assessed in two independent cohorts obtaining high specificity (94,1 %) and sensitivity (87,5 %) to detect FSGS relapses. It has also a potential to detect patients at risk of relapse as ApoA-Ib predates the recurrence episodes in most of the cases. As urinary ApoA-Ib is strongly associated to primary FSGS we aimed to unravel the nature of the modification present in ApoA-Ib.

Method
The whole APOA1 gene was sequenced in ApoA-Ib positive and negative patients and the protein structure was studied using 2D electrophoresis followed by mass spectrometry.

Results
No genetic variations in the APOA1 gene were found in the ApoA-Ib positive patients that could explain the increase in the molecular mass. The mass spectrometry analysis revealed three extra amino acids at the N-Terminal end of ApoA-Ib that were not present in the standard plasmatic form of ApoA-I. These amino acids corresponded to half of the propeptide sequence of the immature form of ApoA-I (proApoA-I). These results suggest that proApoA-I is miss-cleaved producing ApoA-Ib probably due to an altered protease activity in recurrent FSGS patients

Conclusion
ApoA-Ib, found specifically in urine of recurrent FSGS patients, is a misprocessed form of ApoA-I that retains three aminoacids of the six-aminoacid N-terminal propeptide of proApoA-I. The description of ApoA-Ib could be relevant not only to allow the automated analysis of this biomarker in the clinical laboratory but also to shed light into the molecular mechanism of idiopathic FSGS.
P0353EFFECT OF RITUXIMAB IN PATIENTS WITH RELAPSED OR REFRACTORY PRIMARY MEMBRANOUS NEPHROPATHY
Authors: Akyildiz Arif , Uludag Omer , Mirioglu Safak , Ucar Ali Riza , Demir Erol , Caliskan Yasar Kerem , Ozluk Yasemin , Turkmen Aydin , Sever Mehmet Sukru , Yazici Halil 
Published: June 2020

Abstract

Background and Aims
Membranous nephropathy (MN) is the most common cause of glomerulonephritis in non-diabetic adults. B-cell dysfunction is an important pathway involved in pathogenesis. We, therefore, investigated effects of rituximab (RTX) on the outcome of patients with relapsed or refractory primary MN.

Method
In this retrospective analysis, 48 patients with primary MN were evaluated. Patients, who had relapsed or refractory biopsy-proven disease, with a nephrotic-range proteinuria despite at least six months of prior immunosuppressive therapy using corticosteroids, calcineurin inhibitors or mycophenolic acid derivatives, which were used according to KDIGO guidelines. All patients received at least 2 doses of 375 mg/m2 of RTX. Proteinuria and serum albumin levels of the patients were recorded at baseline, and 3,6,12,18 and 24 months.

Results
Of 48 patients who participated in this study, 27(56.3%) were male. Mean age was 45.3±17.2 years. Results of serum anti-phospholipase-A2-receptor (PLA2R) were available in 31 patients, 23 of whom (74%) were positive. Proteinuria levels at 3, 6, 12, 18, and 24 months after treatment with RTX showed a significant decrease when compared to baseline (p&lt;0.05) (Figure 1): From 7±3.5 g/24h at baseline to 2.6±2.4 g/24h at 12 months. Serum albumin levels at 3, 6, 12, 18, and 24 months after RTX significantly increased compared to baseline values (p&lt;0.05) (Figure 2): From 2.97±0.76 g/dl at baseline to 3.88±0.67 g/dl at 12 months.

Conclusion
Treatment with RTXiseffective in patients suffering from relapsed or refractory primary MN.
P0365INCREASED LIFETIME RISK OF END-STAGE RENAL DISEASE IN FAMILIAL IGA NEPHROLOGY
Authors: Xie Jingyuan 
Published: June 2020

Abstract

Background and Aims
Familial IgA nephropathy (IgAN) has been widely reported around the world. However, it's clinico-histological characteristics and long-term prognosis are not clear.

Method
In this study, 348 familial IgAN cases from167 independent IgAN families were recruited and their clinico-histological characteristics were compared to 1,116 sporadic IgAN patients from the same geographic region. Inheritance patterns, clinical features, and treatment regimens of all recruited patients were recorded and lifetime risk of end-stage renal disease (ESRD) was compared between familial and sporadic cases.

Results
Of all familial IgAN patients, 60 (17%) came from 32 single-generation (SG, defined as all affected individuals are siblings) families, while 286 (82%) came from 134 multiple-generation (MG, affected individuals were present in at least two consecutive generations) families. There’re totally 178 transmissions, 79 of which (44%) were paternal transmission and 99 (56%) were maternal transmissions. We observed evidence for incomplete penetrance in 30 (22%) MG families. The lifetime risk of progression to ESRD was significantly higher in familial IgAN patients than sporadic patients after adjusted by gender [HR=1.40, 95%CI: 1.12-1.74, P=0.004], with 5-year younger in median ESRD onset age [median ESRD-free survival of 60 years vs. 65 years in familial and sporadic cases separately]. As expected, compared to the ones without progressive renal failure at disease onset (eGFR≥60ml/min), familial cases with progressive renal failure (eGFR&lt;60ml/min) had higher risk of lifetime ESRD [HR=6.32, 95%CI: 3.73-10.72, P&lt;0.001]. Interestingly, among familial cases, we found cases from SG families [vs MG families: HR=2.62, 95%CI: 1.59-4.31, P&lt;0.001] or with early onset (onset age &lt;30yrs) [vs late onset: HR=4.79, 95%CI: 3.16-7.26, P&lt;0.001] had higher lifetime risk of ESRD. Furthermore, among sporadic patients, compared to females, males had lower eGFR, higher urine protein, higher Oxford T score and resulted in a higher risk for lifespan ESRD (male vs female, 25% vs 17%, P=0.003) while these gender difference was not seen in familial patients.

Conclusion
In conclusion, familial IgAN cases had poorer renal outcomes and less gender differences compared to sporadic cases. These findings provide evidence that familial disease represent a distinct subtype of more progressive IgAN.