- Email: [email protected]
Differences in Patient and Allograft Survival Following Kidney Transplantation Among Glomerulonephritis Subtypes in the United States
NKF 2016 Spring Clinical Meetings Abstracts
Case Report 253 DIALYSIS REQUIREMENT AND LONG-TERM MAJOR ADVERSE CARDIOVASCULAR EVENTS (MACE) IN CKD PATIENTS WITH SUPERIMPOSED AKI – A PROPENSITYMATCHED COHORT STUDY Bolanle A. Omotoso1,2, Emaad M. Abdel-Rahman1, Wenjun Xin1, Jennie Z. Ma1, Kenneth Scully1, Fatiu A Arogundade2, Rasheed A. Balogun1, University of Virginia, Charlottesville, VA, USA1, Obafemi Awolowo University Teaching Hospital, Ile Ife, Nigeria2 CKD is a widely known risk factor for AKI. CKD patients who experience superimposed AKI has been shown to be at higher risk of long term sequelae of AKI when compared with those who do not experience AKI. It remains unclear whether the need for temporary dialysis intervention following superimposed AKI in patients with CKD has effect on the long-term major adverse cardiovascular event (MACE). The study population consists of adults who developed AKI while on admission at the University of Virginia Medical Center between January 1, 2002, and December 31, 2012, and who had preadmission eGFR between 20-60 ml/min per 1.73 m2 and survived beyond 30 days of AKI (n=6634). Of these, 380 received temporary hemodialysis. AKI was defined as an absolute increase in serum creatinine by ≥0.3mg/dl from the baseline occurring within 48hrs and or requirement for acute dialysis during the index hospitalization. MACE was defined as subsequent admission for Myocardial Infarction (MI), cerebrovascular disease (CVD) and heart failure using ICD 9 codes. Demographic and premorbid clinical variables were used to generate propensity score. Survivors who had temporary dialysis were matched to those managed conservatively according to propensity score in a ratio of 1:3 After the propensity score matching, covariates were well balanced between groups. The overall hazard ratio for MACE in dialyzed versus non dialyzed patients was 1.147(95% CI: 0.964 to 1.364). Treatment of AKI with temporary dialysis in hospitalized patients with baseline eGFR between 20- 60ml/min per1.73m2 was NOT associated with an increased risk for subsequent admission for MACE. Clinicians may not need to worry that the need for temporary dialysis procedure itself may confer additional risk for long-term MACE in CKD patients with superimposed AKI
254 MAJOR DEPRESSION: A RISK FACTOR FOR LONG-TERM MAJOR CARDIOVASCULAR EVENTS (MACE) AND MORTALITY IN ACUTE KIDNEY INJURY. Bolanle A.Omotoso1,2, Emaad M. Abdel-Rahman1, Kenneth Scully1, Fatiu A Arogundade2, Rasheed A. Balogun1, University of Virginia, Charlottesville, VA, USA1, Obafemi Awolowo University Teaching Hospital, Ile Ife, Nigeria2 The point prevalence of depression and its relationship to poor outcomes in chronic kidney disease (including ESRD) has been established. Such prognostic impact in acute kidney injury (AKI) population is not known. This study aims to determine the prognostic implication of a clinical diagnosis of depression on renal recovery and long-term outcomes following AKI. A retrospective cohort study comprising of adults admitted to the University of Virginia Medical Center between January 1, 2002 and December 31, 2012 who sustained AKI, as defined by the KDIGO guidelines, during the admission. Complete recovery was defined as a return of SCr to less than 1.25 times the baseline value and not dialysis dependent. The cohort with existing ICD 9 codes for major depression was identified and formed the comparison group. Long-term outcomes, specifically renal recovery, major adverse cardiovascular events (MACE) and all-cause mortality were compared in both groups. A total of 11,425 patients survived beyond 90 days of AKI and had a complete data available for analysis. Diagnosis of Major depression was present in 2519 (22%) of the entire population. The cohort with major depression had a higher risk for MACE and all-cause mortality: fully adjusted hazard ratio (HR) were 1.186; CI, 1.092-1.289; p <0.001 and 1.226; 95% CI, 1.123 -1.339; p<0.001respectively. The presence of major depression was not a predictor of renal recovery. Patients who sustain AKI in hospital and who have been diagnosed with major depression are at higher long-term risk of MACE and allcause mortality. To improve long–term outcomes, interventions that identify and target these patients for additional treatment(s) may be necessary.
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EFFECTS OF ICODEXTRIN AND GLUCOSE BICARBONATE/LACTATE-BUFFERED PERITONEAL DIALYSIS FLUIDS ON EFFLUENT CELL POPULATION AND BIOCOMPATIBILITY MARKERS IL-6 AND CA125 IN INCIDENT PERITONEAL DIALYSIS PATIENTS Fuchsova, Sylvie Opatrna, Anna Popperlova, Daniel Lysak, Radka Laith Al-Rabadi, MBBS,1,* Rivka Ladislav Trefil, Jaroslav Racek, Ondrej Topolcan, Charles Jennifer E. Ballard, MD,2,y Alan University Medical School and Teaching Hospital Plzen, Czech Republic David J. Salant, MD,1 Icodextrin peritoneal dialysis (PD) solution has been shown to increase interleukin-6(IL-6) levels in PD effluent as well as leukocyte and mesothelial cell count. Mesothelial cells release cancer antigen 125(CA125) which is used as a There marker is of little information about pregnancy o especially those with circulating autoantibod mesothelial cell mass. This 1 year prospective study was designedautoantigen to compare peritoneal in primary MN. We present what effluent cell population, its inflammatory phenotype and a 39-year-old woman with PLA2R-associate biocompatibility biomarkers IL-6 and CA125 between icodextrin (E) and glucose bicarbonate/lactate (P) basedanasarca, PD solutions.hypoalbuminemia (albumin, 1.3-2. opsy 19 revealed Using baseline peritoneal ultrafiltration capacity, stable MN with staining for PLA2R, a incident PD patients were allocated either to P onlydid (n=8) to P She notorrespond to conservative therapy a plus E for the overnight dwell (n=11). Flow cytometry used after to Several was weeks presentation, she was fou measure white blood cell count and differential and the expression treatment. Protei of inflammatory molecules on peritoneal cellsfurther isolatedimmunosuppressive from timed Circulating anti-PLA2R levels declined but w overnight peritoneal effluents. Compared to P, E effluent showed higher leukocyte vs 7.9), at birth or at her subseque without (10.9 proteinuria macrophages (6.1 vs 2.5) and mesothelial cells (0.3detectable vs 0.1)*106/Lcirculating anti-PLA R of imm had 2 count, as well as expression of HLA DR on mesothelial cells and low titers. Onlyvstrace amounts of IgG4 ant IL-6 (320.5 vs 141.2 pg/min) and CA125 appearance rate (159.6 discrepancy between anti-PLA2R levels in th 84.3 IU/min), all p<0.05. In E group, correlation between IL-6 and CA125 effluent levels (r=0.503,p<0.05) as well rates 67(5):775-778. ª 2016 by AmasJappearance Kidney Dis. (r=0.774,p<0.001) was demonstrated. No effect on systemic inflammatory markers or peritoneal permeability was found. INDEX without WORDS: Membranous nephropathy ( Icodextrin PD solution activates local inflammation receptor (PLA2R); autoantibody; placenta; ritu systemic consequences so the clinical relevance of this observation remains obscure. Correlation between effluent IL-6 and CA125 suggests that CA125 might be upregulated due to inflammation and thus not a reliable marker of mesothelial cell mass and/or biocompatibility.
Pregnancy in a Patient Wit and Circulating Anti-P
P
regnant patients with autoimmune disease deliver newborns with a spectrum of cl manifestations due to the transplacental passa 256 circulating autoantibodies. Pregnant patients DIFFERENCES IN PATIENT AND ALLOGRAFT SURVIVAL lupus or myasthenia FOLLOWING KIDNEY TRANSPLANTATION AMONG gravis can deliver babies GLOMERULONEPHRITIS corresponding SUBTYPES IN THE UNITED diseaseSTATES. in the neonate.1,2 Neo Michelle O’Shaughnessy1, Maria Montez-Rath1, Sai Liu1, Richard 2 1 membranous nephropathy (MN) not associated Lafayette1, Wolfgang Winkelmayer . Division of Nephrology, 2 Stanford University School of Medicine, Paloinfection Alto, CA, USA. congenital wasSection first described in 199 of Nephrology, Baylor College of Medicine, Houston, TX, USA. to thehave passive Patient outcomes followingattributed kidney transplantation not been transfer of maternal compared among glomerulonephritis subtypes at renal the population bodies(GN) to putative antigens.3 More than a d level in the United States, and little is known about specific barriers to 4 Debiec et al identified the first antigen inv kidney transplantation withinlater, individual GN subtypes. We identified from the U.S.inRenal Data System adultneutral (≥18 years)endopeptidase (NE such casesallas patients who received a first kidney transplant between 1996 and 2011 metalloprotease present on the surface of the pod and with a diagnosis of ESRD attributed to any of four primary (focal segmental glomerulosclerosis, IgA involved nephropathy [IgAN, and in thereference proteolytic regulation of va group], membranous nephropathy, membranoproliferative GN) or two tive peptides. Debiec et al described a mother w secondary (lupus nephritis [LN], vasculitis) GN subtypes. Hazard ratios mutation NEP expression who had fo (HRs) with 95% confidence intervals (CIs)preventing for death, all-cause allograft failure, and allograft failure excluding deathantibodies as a cause were due computed anti-NEP to fetomaternal alloi using proportional hazards regression, adjusting for demographic, nization from a previous miscarriage; these antib socioeconomic, and clinical characteristics at time of transplantation. Among the 32,152 patientswere studied,to baseline patient cross thecharacteristics placenta and cause subepit (e.g. age, race, dialysis vintage, donor type) differed considerably by deposits inpatients the fetal GN subtype. Prior to adjusting for case mix, with anykidney of the 5 of a subsequent comparator GN subtypes were significantly more likely than patients nancy. M-type phospholipase A2 receptor (PL with IgAN to experience each outcome. After adjustment, relative risks was later identified as the major autoantigen fo remained significantly elevated for all subtypes except vasculitis: for 5 death, HRFSGS 1.28 (95% CI mary 1.10-1.50), HRMNin 1.33adults. (95% CI 1.08-1.64), MN Little literature exists HRMPGN 1.59 (95% CI 1.27-1.99), HRLN 1.56 (95% CI 1.28-1.89), pregnancy outcomes in patients with nephrotic HRvasculitis 1.24 (95% CI 0.97-1.59); for death-censored allograft failure, drome to primary HRFSGS 1.37 (95% CI 1.19-1.58), HRMNdue 1.54 (95% CI 1.25-1.89),MN, with no data ava HRMPGN 1.82 (95% CI 1.48-2.24), HRLN 1.21 (95% CI 1.01-1.44), about pregnancy in PLA2R-associated disease HRvasculitis 0.91 (95% CI 0.68-1.21). present believe to be the first known ca Independent associations between GNwhat subtypewe and post-transplant patient and allograft survivalpregnancy exist, thus challenging current with PLA R-associated in a the patient 2 research paradigm to group all GN subtypes together when examining who for was seropositive forstudy. anti-PLA2R autoantib disparities require further post-transplant outcomes. Reasons throughout the course of her pregnancy. Am J Kidney Dis. 2016;67(5):A1-A118
Case Report 253 DIALYSIS REQUIREMENT AND LONG-TERM MAJOR ADVERSE CARDIOVASCULAR EVENTS (MACE) IN CKD PATIENTS WITH SUPERIMPOSED AKI – A PROPENSITYMATCHED COHORT STUDY Bolanle A. Omotoso1,2, Emaad M. Abdel-Rahman1, Wenjun Xin1, Jennie Z. Ma1, Kenneth Scully1, Fatiu A Arogundade2, Rasheed A. Balogun1, University of Virginia, Charlottesville, VA, USA1, Obafemi Awolowo University Teaching Hospital, Ile Ife, Nigeria2 CKD is a widely known risk factor for AKI. CKD patients who experience superimposed AKI has been shown to be at higher risk of long term sequelae of AKI when compared with those who do not experience AKI. It remains unclear whether the need for temporary dialysis intervention following superimposed AKI in patients with CKD has effect on the long-term major adverse cardiovascular event (MACE). The study population consists of adults who developed AKI while on admission at the University of Virginia Medical Center between January 1, 2002, and December 31, 2012, and who had preadmission eGFR between 20-60 ml/min per 1.73 m2 and survived beyond 30 days of AKI (n=6634). Of these, 380 received temporary hemodialysis. AKI was defined as an absolute increase in serum creatinine by ≥0.3mg/dl from the baseline occurring within 48hrs and or requirement for acute dialysis during the index hospitalization. MACE was defined as subsequent admission for Myocardial Infarction (MI), cerebrovascular disease (CVD) and heart failure using ICD 9 codes. Demographic and premorbid clinical variables were used to generate propensity score. Survivors who had temporary dialysis were matched to those managed conservatively according to propensity score in a ratio of 1:3 After the propensity score matching, covariates were well balanced between groups. The overall hazard ratio for MACE in dialyzed versus non dialyzed patients was 1.147(95% CI: 0.964 to 1.364). Treatment of AKI with temporary dialysis in hospitalized patients with baseline eGFR between 20- 60ml/min per1.73m2 was NOT associated with an increased risk for subsequent admission for MACE. Clinicians may not need to worry that the need for temporary dialysis procedure itself may confer additional risk for long-term MACE in CKD patients with superimposed AKI
254 MAJOR DEPRESSION: A RISK FACTOR FOR LONG-TERM MAJOR CARDIOVASCULAR EVENTS (MACE) AND MORTALITY IN ACUTE KIDNEY INJURY. Bolanle A.Omotoso1,2, Emaad M. Abdel-Rahman1, Kenneth Scully1, Fatiu A Arogundade2, Rasheed A. Balogun1, University of Virginia, Charlottesville, VA, USA1, Obafemi Awolowo University Teaching Hospital, Ile Ife, Nigeria2 The point prevalence of depression and its relationship to poor outcomes in chronic kidney disease (including ESRD) has been established. Such prognostic impact in acute kidney injury (AKI) population is not known. This study aims to determine the prognostic implication of a clinical diagnosis of depression on renal recovery and long-term outcomes following AKI. A retrospective cohort study comprising of adults admitted to the University of Virginia Medical Center between January 1, 2002 and December 31, 2012 who sustained AKI, as defined by the KDIGO guidelines, during the admission. Complete recovery was defined as a return of SCr to less than 1.25 times the baseline value and not dialysis dependent. The cohort with existing ICD 9 codes for major depression was identified and formed the comparison group. Long-term outcomes, specifically renal recovery, major adverse cardiovascular events (MACE) and all-cause mortality were compared in both groups. A total of 11,425 patients survived beyond 90 days of AKI and had a complete data available for analysis. Diagnosis of Major depression was present in 2519 (22%) of the entire population. The cohort with major depression had a higher risk for MACE and all-cause mortality: fully adjusted hazard ratio (HR) were 1.186; CI, 1.092-1.289; p <0.001 and 1.226; 95% CI, 1.123 -1.339; p<0.001respectively. The presence of major depression was not a predictor of renal recovery. Patients who sustain AKI in hospital and who have been diagnosed with major depression are at higher long-term risk of MACE and allcause mortality. To improve long–term outcomes, interventions that identify and target these patients for additional treatment(s) may be necessary.
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EFFECTS OF ICODEXTRIN AND GLUCOSE BICARBONATE/LACTATE-BUFFERED PERITONEAL DIALYSIS FLUIDS ON EFFLUENT CELL POPULATION AND BIOCOMPATIBILITY MARKERS IL-6 AND CA125 IN INCIDENT PERITONEAL DIALYSIS PATIENTS Fuchsova, Sylvie Opatrna, Anna Popperlova, Daniel Lysak, Radka Laith Al-Rabadi, MBBS,1,* Rivka Ladislav Trefil, Jaroslav Racek, Ondrej Topolcan, Charles Jennifer E. Ballard, MD,2,y Alan University Medical School and Teaching Hospital Plzen, Czech Republic David J. Salant, MD,1 Icodextrin peritoneal dialysis (PD) solution has been shown to increase interleukin-6(IL-6) levels in PD effluent as well as leukocyte and mesothelial cell count. Mesothelial cells release cancer antigen 125(CA125) which is used as a There marker is of little information about pregnancy o especially those with circulating autoantibod mesothelial cell mass. This 1 year prospective study was designedautoantigen to compare peritoneal in primary MN. We present what effluent cell population, its inflammatory phenotype and a 39-year-old woman with PLA2R-associate biocompatibility biomarkers IL-6 and CA125 between icodextrin (E) and glucose bicarbonate/lactate (P) basedanasarca, PD solutions.hypoalbuminemia (albumin, 1.3-2. opsy 19 revealed Using baseline peritoneal ultrafiltration capacity, stable MN with staining for PLA2R, a incident PD patients were allocated either to P onlydid (n=8) to P She notorrespond to conservative therapy a plus E for the overnight dwell (n=11). Flow cytometry used after to Several was weeks presentation, she was fou measure white blood cell count and differential and the expression treatment. Protei of inflammatory molecules on peritoneal cellsfurther isolatedimmunosuppressive from timed Circulating anti-PLA2R levels declined but w overnight peritoneal effluents. Compared to P, E effluent showed higher leukocyte vs 7.9), at birth or at her subseque without (10.9 proteinuria macrophages (6.1 vs 2.5) and mesothelial cells (0.3detectable vs 0.1)*106/Lcirculating anti-PLA R of imm had 2 count, as well as expression of HLA DR on mesothelial cells and low titers. Onlyvstrace amounts of IgG4 ant IL-6 (320.5 vs 141.2 pg/min) and CA125 appearance rate (159.6 discrepancy between anti-PLA2R levels in th 84.3 IU/min), all p<0.05. In E group, correlation between IL-6 and CA125 effluent levels (r=0.503,p<0.05) as well rates 67(5):775-778. ª 2016 by AmasJappearance Kidney Dis. (r=0.774,p<0.001) was demonstrated. No effect on systemic inflammatory markers or peritoneal permeability was found. INDEX without WORDS: Membranous nephropathy ( Icodextrin PD solution activates local inflammation receptor (PLA2R); autoantibody; placenta; ritu systemic consequences so the clinical relevance of this observation remains obscure. Correlation between effluent IL-6 and CA125 suggests that CA125 might be upregulated due to inflammation and thus not a reliable marker of mesothelial cell mass and/or biocompatibility.
Pregnancy in a Patient Wit and Circulating Anti-P
P
regnant patients with autoimmune disease deliver newborns with a spectrum of cl manifestations due to the transplacental passa 256 circulating autoantibodies. Pregnant patients DIFFERENCES IN PATIENT AND ALLOGRAFT SURVIVAL lupus or myasthenia FOLLOWING KIDNEY TRANSPLANTATION AMONG gravis can deliver babies GLOMERULONEPHRITIS corresponding SUBTYPES IN THE UNITED diseaseSTATES. in the neonate.1,2 Neo Michelle O’Shaughnessy1, Maria Montez-Rath1, Sai Liu1, Richard 2 1 membranous nephropathy (MN) not associated Lafayette1, Wolfgang Winkelmayer . Division of Nephrology, 2 Stanford University School of Medicine, Paloinfection Alto, CA, USA. congenital wasSection first described in 199 of Nephrology, Baylor College of Medicine, Houston, TX, USA. to thehave passive Patient outcomes followingattributed kidney transplantation not been transfer of maternal compared among glomerulonephritis subtypes at renal the population bodies(GN) to putative antigens.3 More than a d level in the United States, and little is known about specific barriers to 4 Debiec et al identified the first antigen inv kidney transplantation withinlater, individual GN subtypes. We identified from the U.S.inRenal Data System adultneutral (≥18 years)endopeptidase (NE such casesallas patients who received a first kidney transplant between 1996 and 2011 metalloprotease present on the surface of the pod and with a diagnosis of ESRD attributed to any of four primary (focal segmental glomerulosclerosis, IgA involved nephropathy [IgAN, and in thereference proteolytic regulation of va group], membranous nephropathy, membranoproliferative GN) or two tive peptides. Debiec et al described a mother w secondary (lupus nephritis [LN], vasculitis) GN subtypes. Hazard ratios mutation NEP expression who had fo (HRs) with 95% confidence intervals (CIs)preventing for death, all-cause allograft failure, and allograft failure excluding deathantibodies as a cause were due computed anti-NEP to fetomaternal alloi using proportional hazards regression, adjusting for demographic, nization from a previous miscarriage; these antib socioeconomic, and clinical characteristics at time of transplantation. Among the 32,152 patientswere studied,to baseline patient cross thecharacteristics placenta and cause subepit (e.g. age, race, dialysis vintage, donor type) differed considerably by deposits inpatients the fetal GN subtype. Prior to adjusting for case mix, with anykidney of the 5 of a subsequent comparator GN subtypes were significantly more likely than patients nancy. M-type phospholipase A2 receptor (PL with IgAN to experience each outcome. After adjustment, relative risks was later identified as the major autoantigen fo remained significantly elevated for all subtypes except vasculitis: for 5 death, HRFSGS 1.28 (95% CI mary 1.10-1.50), HRMNin 1.33adults. (95% CI 1.08-1.64), MN Little literature exists HRMPGN 1.59 (95% CI 1.27-1.99), HRLN 1.56 (95% CI 1.28-1.89), pregnancy outcomes in patients with nephrotic HRvasculitis 1.24 (95% CI 0.97-1.59); for death-censored allograft failure, drome to primary HRFSGS 1.37 (95% CI 1.19-1.58), HRMNdue 1.54 (95% CI 1.25-1.89),MN, with no data ava HRMPGN 1.82 (95% CI 1.48-2.24), HRLN 1.21 (95% CI 1.01-1.44), about pregnancy in PLA2R-associated disease HRvasculitis 0.91 (95% CI 0.68-1.21). present believe to be the first known ca Independent associations between GNwhat subtypewe and post-transplant patient and allograft survivalpregnancy exist, thus challenging current with PLA R-associated in a the patient 2 research paradigm to group all GN subtypes together when examining who for was seropositive forstudy. anti-PLA2R autoantib disparities require further post-transplant outcomes. Reasons throughout the course of her pregnancy. Am J Kidney Dis. 2016;67(5):A1-A118