International Conference on Kidney September 29-30, 2016 Orlando, Florida, USA

Biography:

Michael F Michelis has been the Director of the Division of Nephrology at Lenox Hill Hospital for more than three decades. He is a Clinical Professor of Medicine at the New York University School of Medicine. He received a BA at Columbia College, Columbia University in New York City, and his MD degree at George Washington School of Medicine in Washington DC. He received his Nephrology Training at the University of Pittsburgh, School of Medicine. He has been selected for inclusion in the listing of top doctors in New York for the past several years. He is the Co-Editor of several medical textbooks, and he has published dozens of articles in the area of general nephrology, electrolyte disorders, hypertension and geriatric renal disease. He has lectured extensively throughout the United States, Hawaii, Japan and in various European cities. He has served on the Editorial Board of several medical journals, and he also reviews articles for established journals in nephrology. He has received many awards and lectureships for his work in Nephrology.

Abstract:

A variety of therapeutic interventions are available to alter the abnormalities seen in patients with chronic kidney disease (CKD). Programs can now be developed to slow the progression of CKD. This delay can be achieved by using accepted recommendations for optimal diabetes therapy (HbA1c target 7%), goals for blood pressure levels, reduction of proteinuria and the proper use of ACE/ARB therapies. For example, limits on dietary sodium and protein intake and reduction of body weight will decrease proteinuria. Proper treatment for elevated serum phosphorus and parathyroid hormone levels as well as therapy for dyslipidemias and anemia can mitigate renal loss. Other less widely appreciated measurable abnormalities such as elevated FGF-23 levels, hyperuricemia and metabolic acidosis have more recently been recognized to be associated with progressive renal insufficiency. Efforts aimed at correction of these disorders may have an important role in altering the course of renal dysfunction. Data will be presented to support this strategy. 

Biography:

Dr. Zinselmeyer’s scientific education is broad and interdisciplinary. Earning his PhD in pharmaceutical science (University of Strathclyde 2006) has inspired him to focus on translational science, with an emphasis on research that has relevance to clinical medicine. The main focus of his work over the past 10 years has been intravital-multi-photon-imaging of cells of the immune system and the CNS. He was part in the team using these technique for the first time observing leucocyte dynamics in transplanted lungs in living mice and the beating heart. Dr. Zinselmeyer authored over 40 peer-reviewed articles cited over 2000 times

Abstract:

The combination of murine transplantation models, fluorescent reporter mice and intravital 2-photon microscopy enables an unprecedented view on the initiation of transplant rejection. In murine allogeneic models of lung transplantation we could observe the innate arm of the immune-system of the host. Minutes after transplantation neutrophils of the host regularly aggregated in dynamic clusters that formed and dispersed in the allogeneic transplant. These clusters were associated with CD115+ F4/80+ Ly6C+ host cells that had immediately entered the lung. Observing the adaptive arm of the immune system we could explain why allogenic lungs can be rejected in the absence of secondary lymphoid organs. Two-photon microscopy revealed that recipient T-cells are activated predominantly around lung-resident, donor-derived CD11c+ cells. These findings might be singular for the lung; however they demonstrate the value of intravital multiphoton imaging in the study of transplant rejection. Very recently we started using two-photon microscopy to study the three-dimensional structure of mouse podocytes in high temporal resolution in the present absence of inflammation. We found that healthy podocytes remained non-motile and maintained a canopy-shaped structure over time. On expression of constitutively active Rac1 or after induction of nephrotoxic nephritis podocytes changed shape by retracting processes and clearly exhibited domains of increased membrane activity. Furthermore, drastic activation of Rac1 also led to podocyte detachment from the glomerular basement membrane, and we observed detached podocytes crawling on the surface of the tubular epithelium and occasionally, in contact with peritubular capillaries. These findings potentially explaining the extinction of foot-process in a wide range of severe kidney-disease

Biography:

Ayman Aly Seddik was born in 1972,Graduated from in Shams University school of medicine 1996 very good with honour ,interenship and residency programm in Internal medicine and Nephrology 1997-2001 Assistant lecturere and Nephrology specialist in ain Shams University hospital , Nasser institute for research 2001-2006 , after obtaining md degree in Internal Medicine & Nephrology 2006 ain Shams University , work as consultant Nephrologist and lecturer Nephrologist in Ain Shams University hospitals ,senior specialist Nephrologist king fahd armed force hospital jeddah saudia arabia 2006-2008,consultant Nephrologist Northeren area armed force hospital 2009-2011 , programme director of Internal medicine residency programme in northeren area armed force hospital ,degree of assistant profeessor of Internal Medicine and Nephrology Ain Shams University, cairo, egypt 2012.Currently working as Nephrologist , Dubai hospital -Dubai health authority 2011-present.

Abstract:

Introduction: Peritonitis in the peritoneal dialysis (PD) patient is defined by the International Society for Peritoneal Dialysis (ISPD) as the presence of two of the following three criteria: (1) signs and symptoms such as fever, abdominal pain/tenderness; (2) >100 white blood cells/mL dialysate fluid, of which >50% are neutrophils; and (3) identification of the organism in the PD fluid (1). Peritonitis still represents the main acute complication of peritoneal dialysis (PD) and is a leading cause of hospitalization catheter loss, and technique failure (2).

Patients and Methods: Quantitative approach, retrospective study. We analyzed a database of patients from the Nephrology Service at Dubai hospital, Dubai health authority from January 1999 till December 2012 The analysis included patients in PD for more than 3 months and with complete information. We collected data regarding the catheter and patient outcome following recorded peritonitis episodes. The rate of peritonitis was expressed as risk of a peritonitis episode per year (ep./year) and calculated in accordance with the  ISPD recommendations.

Biography:

Helene is Managing Vice-President and Global Head of Real-World Modeling at LASER Analytica, a cutting-edge population health consultancy with operations in 8 countries. She develops and coordinates LASER’s offer in analytics, and has 15 years of experience in quantitative methods applied to impact decisions in health care – as an academic, a drug developer, a start-up board member, and a consultant. In particular, she gained hands-on drug development experience in roles of increasing responsibility at Novartis from discovery to market launch. Hélène holds a physics degree from Ecole Polytechnique, France and a PhD in computer science and biology from MIT, USA.

Abstract:

The present study aims to compare overall survival (OS) in metastatic RCC (mRCC) between nivolumab and cabozantinib from two recent pivotal studies comparing, respectively, each one of the two emerging treatments against everolimus in patients who relapse following first-line treatment. Comparison is traditionally carried out using the Bucher method, which assumes proportional hazard. Since OS curves intersected in one of the pivotal studies, models not assuming proportional hazards were also considered to refine the comparison. Four Bayesian parametric survival network meta-analysis models were implemented on overall survival (OS) data digitized from the Kaplan-Meier curves reported in the studies. Three models allowing hazard ratios (HR) to vary over time were assessed against a fixed-HR model. The Bucher method favored cabozantinib, with a fixed HR for OS vs. nivolumab of 1.09 (95% confidence interval: [0.77, 1.54]). However, all models with time-varying HR showed better fits than the fixed-HR model. The log-logistic model fitted the data best, exhibiting a HR for OS initially favoring cabozantinib, the trend inverting to favor nivolumab after month 5. Numerical differences in study-adjusted OS estimates between the two treatments remained small. This study evidences that HR for OS of nivolumab vs. cabozantinib varies over time, favoring cabozantinib in the first months of treatment but nivolumab afterwards, a possible indication that patients with poor prognosis benefit more from cabozantinib in terms of survival, nivolumab benefiting patients with better prognosis. More evidence, including real-world observational data, is needed to compare effectiveness between cabozantinib and nivolumab

Biography:

Paulo Roberto Santos is Associate Professor at Federal University of Ceará, Brazil, and coordinates the Graduate Program in Health Sciences of the Sobral Faculty of Medicine. His main research interests are self-perceived outcomes (quality of life, depression, coping strategies and sexuality) among end-stage renal disease patients.

Abstract:

End-stage renal disease (ESRD) is associated with several stressors that affect family dynamics and social relationships of hemodialysis (HD) patients. Social support is well known to influence quality of life and mortality among ESRD patients. Thus, it is crucial to understand the association between social support given to ESRD patients and demographic and clinical variables commonly used in clinical practice. We aimed to verify the association of social support perceived by ESRD patients undergoing HD with demographic and clinical variables. We studied 161 patients submitted to HD in the only two dialysis centers in northern Ceará state, northeast Brazil. We excluded patients under 18 years of age and on HD for less than three months. Social support was measured by The Medical Outcomes Study Social Support Survey (MOS-SS). MOS-SS comprises 19 items and generates scores from 0 (worst) to 100 (best) related to five dimensions of social support: Instrumental Support, Affection, Positive Social Interaction, Emotional Support and Informational Support. The following demographic variables were collected: gender, age, religion, marital status and economic class: E (lowest economic class) to A (highest). The clinical variables were etiology of renal disease, time on HD and an index based on comorbidity, as described by Khan: low-, medium- or high risk. We compared scores generated by the MOS-SS related to the five dimensions of social support between men and women; patients younger 60 years vs. 60 years or older; married vs. unmarried; Catholics vs. non-Catholics; economic classes B and C vs. D and E; time on HD up to 36 months vs. more than 36 months; diabetics vs. non-diabetics; low-risk vs. medium- and high-risk. Comparisons were performed by Student’s t test. Statistical significance was considered to be P < 0.05. The sample was formed mostly by men (65.3%), had mean of age of 50.3 years, and mostly came from economic classes C and D (91.3%). The main etiology of ESRD was hypertension (34.2%) followed by glomerulonephritis (25.2%) and diabetes (21.7%). Patients were undergoing HD for a mean of 46.2 months. More than half of them (50.9%) presented low risk based on comorbidity. Among five dimensions of social support, Affection was the best scored (mean score=87.7) and Positive Social Interaction the worst (mean sore=73.5). The demographic variables associated with social support were: age, marital status and economic class, in the following way: older patients perceived higher Instrumental Support; married patients perceived higher and Emotional Support compared to unmarried; patients from high economic classes perceived better Affection. Among clinical variables, only longer time on maintenance HD was associated with lower Instrumental Support. We concluded that  younger patients, single patients and patients from low economic class should be seen as having higher risk of receiving poor social support. For them, educational intervention, search for community resources and strengthening of patients’ interaction with family and friends should be promoted by social workers.

Biography:

Dr Praveen Kumar Kolla has completed his graduation in Medicine from Kurnool Medical college , Kurnool and post graduation in Internal Medicine from Manipal Academy of Higher Education . He was trained in Nephrology from Sri Ramachandra University, Chennai, India. He is the Professor and Head , Department of Nephrology, Narayana Medical College, Nellore. He has published more than 20 papers in reputed journals

Abstract:

Introduction: Invasive fungal infections cause significant morbidity and mortality in renal transplant recipients. The opportunistic pathogens such as Candida, Aspergillus, Mucormycosis, Cryptococcus, Histoplasma,Coccidioides are known to infect the kidneys in predisposed individuals with serious complications. Recipients of solid organ transplants have 24-40% incidence of opportunistic fungal infections with a very high mortality of 70-100%. Objective: To report the spectrum of fungal infections in renal allograft recipients at Narayana medical college -Nellore , Andhra Pradesh, INDIA. Materials and Methods: 70 patients who underwent kidney transplantation between march 2010-feb 2016 were reviewed. Among these, 65 were live related and 5 were deceased donor transplants. Only 16 patients received induction therapy with either ATG or Basiliximab and all were on triple immunosuppression with Tacrolimus, MMF and Steroids. Patients who were diagnosed having fungal infections were included in our study. Diagnosis was based on clinical, radiological, culture and histopathological examination. Results: Out of 11 patients with various fungal infections 4 were found to have aspergillus, 2 were infected with Candida , 3 with Pneumocystis, 1 with mucor mycosis,1 with chromoblastomycosis. Of these 3 were in the form of cutaneous nodules, 7 were invasive fungal infections, One had aneurysm of graft renal artery. Inspite of appropriate antifungal therapy 4 of these patients with invasive fungal infection expired . Conclusion: The mortality of invasive fungal infections is still high in renal allograft recipients despite newer antifungal agents. Early detection of invasive fungal infections and prompt initiation of therapy are important in reducing mortality.

Biography:

Tomasz KamiÅ„ski graduated Medical University of BiaÅ‚ystok (Poland) with a master degree in pharmacy and currently is a PhD student at international Interdisciplinary Doctoral Studies in English at Medical University of Bialystok and Hasselt University. Presently he is the principal investigator of two projects supported by Leading National Research Centre (The Centre for Innovative Research at Medical University of Bialystok) and the project supported by the Polish National Science Centre. All above-mentioned projects focus on searching connections between kidney diseases and hemostatic disorders. Furthermore, he has been granted with the award of Rector of Medical University of BiaÅ‚ystok for outstanding scientific achievements.

Abstract:

Objectives: Patients with chronic kidney disease (CKD) are at higher risk of incidence of thromboembolic events. The effect of continuous loss of function of nephrons is a progressive accumulation of uremic toxins. Indoxyl sulfate (IS) is an aggressive uremic toxin exerting proinflammatory and prooxidative properties, which affects multiple signaling pathways.

Aim: We examined the association between indoxyl sulfate and activation of the coagulation system in predialysis patients with CKD.

Methods: Studies have been conducted on a group of 53 patients with CKD on conservative treatment and 18 healthy volunteers. For the determination of parameters of coagulation ELISA-immuno-enzymatic kits were used,  whereas the IS levels were determined by HPLC. The hematological and biochemical parameters were assessed using standard laboratory methods.

Biography:

MaÅ‚gorzata Karbowska graduated Jagiellonian University Medical College with a master degree in pharmacy and currently is a PhD student at Medical University of Bialystok. As a young scientist she received Scholarship from the Minister of Science and Higher Education for outstanding achievement. Presently she is managing project supported by Leading National Research Centre (The Centre for Innovative Research at Medical University of Bialystok) and is co-investigator of Preludium project supported by the Polish National Science Centre – both projects focus on nephrology.

Abstract:

Objective: Chronic kidney disease (CKD) is associated with higher risk for thromboembolic events compared with general population. Indoxyl sulfate (IS) is a potent uremic toxin associated with the appearance of cardiovascular disease prevalence. However, mechanism underlying IS association with thromboembolic events is not fully understood.

Material and methods: We evaluated the effect of IS on thrombotic process after acute treatment in electrical current-induced arterial thrombosis in Wistar male rats. IS doses: 3, 10, and 30 mg/kg of body weight were administered intravenously. We assessed IS influence on parameters of coagulation, fibrinolysis, collagen-induced platelet aggregation and blood morphology.

Biography:

Beata Znorko completed her Master degree in Laboratory Medicine in 2013 at Medical University of BiaÅ‚ystok. Currently I am PhD student at Faculty of Pharmacy with the Division of Laboratory Medicine at Medical University of Bialystok. I am head of the project funded by National Science Centre Poland entitled: ‘Osteoprotegerin - ally or enemy of blood vessels calcification in the experimental model of chronic kidney disease in rat? ‘ and ‘Molecular mechanisms of vascular calcification in chronic kidney disease as a link between bone and vasculature’ funded by KNOW The Leading National Research Centre and The Centre for Innovative Research (CIR).

Abstract:

Chronic kidney disease-mineral and bone disorders (CKD-MBD) are common during the course of CKD and related to disturbances in bone strength and metabolism. Recent research shows that the osteoprotegerin (OPG) and receptor activator of NF-κB ligand (RANKL) play a significant role in the development of CKD-MBD. The aim of the study was to investigate if the OPG/RANKL system affects biomechanical properties in young, growing rats with experimental model of chronic renal failure (CRF). The animals were divided into two groups: sham-operated and subtotal nephrectomized rats. Left femurs were excised one and three months after nephrectomy for determination of biomechanical properties: three-point-bending test in femoral diaphysis and bending test in femoral neck. Soluble RANKL(sRANKL) and OPG were measured in homogenates from trabecular and cortical bone tissue. Trabecular and cortical OPG was increased in CRF in comparison to control three months after surgery, whereas trabecular sRANKL was increased one month after nephrectomy. At the level of femoral neck, OPG in trabecular bone tissue
correlated positively with stiffness (r=0.539,p=0.017) and ultimate load (Fu) (r=0.611,p=0.05), and inversely with work to fracture (W) (r=-0.465,p=0.044). sRANKL in both and cortical bone tissue was positively correlated with W (r=0.648,p=0.01; r=0.420;p=0.05, respectively) and inversely with stiffness (r=0,474,p=0.026). At the level offemoral diaphysis, sRANKL was inversely associated with Fu  (r=-0.503,p=0.017) and there were no associations between cortical OPG levels and these parameters in both femoral neck and diaphysis. In young, rapidly growing rats OPG and sRANKL exerts opposite effect on biomechanical bone strength in experimental CRF.

Biography:

Rajendra Bhimma, MB, ChB, MD, DCH (SA), FCP (Paeds)(SA), MMed (Natal), is Associate Professor of Pediatrics, Principal Specialist, Department of Pediatrics and Child Health, Nelson R Mandela School of Medicine,  University of KwaZulu-Natal, South Africa. He has published over 50 articles in peer-reviewed journals. He is a member of the following Societies: American Association for the Advancement of Science, International Pediatric Transplant Association, International Society of Nephrology, South African Medical Association, South African Paediatric Association, South African Transplant Society. Research interest in glomerular diseases, especially HIV associated kidney diseases. He is also a long-standing member of the Biomedical Research Ethics Committee of the University of KwaZulu-Natal and an editorial board member of two international journals.

Abstract:

To review the changing paradigms in the diagnosis, investigation and management of urinary tract infections (UTIs) in children beyond the neonatal period.

UTIs are the second most common cause of serious bacterial infections in early childhood, thus placing a huge financial burden on the health budget.  Despite increasing resistance to several first-line antibiotics, appropriate antibiotic treatment has almost eliminated mortality. 

Early guidelines advocated aggressive treatment and extensive imaging studies, particularly for the detection of serious ureteric reflex and kidney scarring. Treatment in the acute episode is aimed at eradication of bacteriuria and alleviation of symptoms.  Long-term goals include prevention of recurrent attacks of UTIs, kidney scarring and correction of urological lesions that may predispose to recurrent infections.   Although there is increasing evidence to show that long-term antimicrobial prophylaxis may be associated with a reduced risk of recurrent infection in selected groups of patients, but not renal scarring, more studies are needed to confirm this.

Surgical intervention is now restricted to cases with severe vesicoureteric reflux and failed medical management with endoscopic surgery being increasingly used in most centres compared to open surgery.

Biography:

Sudip Kumar Datta has completed his MD in Clinical Biochemistry and currently working as an Assistant Professor in the Department of Laboratory Medicine, AIIMS, India since 2014. He has published more than 10 papers in national and international journals of repute and is also serving as Assistant Editor for the Journal of Laboratory Physicians. His area of interest is gene-environment interaction in CKD patients so as to identify potential biomarkers for the disease progression.

Abstract:

Till date there is no clear answer regarding whether high levels of organochlorine pesticides (OCP) found associated with chronic kidney disease (CKD) cause kidney damage or they get accumulated due to falling glomerular function rate (GFR). We have observed that blood OCP levels as analyzed by gas chromatography, show significantly higher levels in CKD patients. Spearman’s correlation analysis of OCP levels with eGFR exhibited significant negative correlation for most individual OCPs which persisted even after statistical adjustments for age, sex, BMI, total cholesterol and triglycerides. Another of our studies pointed out association of higher OCP loads in patients with genetic polymorphisms involving CYP1A1. Subjects carrying at least one mutant allele of CYP1A1*2A (TC, CC) and *2C (AG, GG) were found to have a modest rise of odds (1.4-2) of association with CKD. However, genotypic combinations of heterozygous/homozygous mutants were found to be significantly associated with CKD with odds ratios ranging from 1.8-3. Another of our studies, where we also analyzed genetic polymorphisms of GSTM1 and GSTT1, showed similar results. We observed that, presence of GSTM1(-)/GSTT1(-) genotype was associated with 1.8-fold higher odds of association with CKD compared to wild genotypes i.e., GSTM1(+)/GSTT1(+). Logistic regression analysis by taking wild genotypes GSTM1(+)/GSTT1(+) as reference revealed that, in CKD patients several pesticides showed significant association with either null or both null genotypes. The above results suggest that decreasing GFR and genetic polymorphisms involving xenobiotic metabolising genes both play a role in accumulation of OCPs in CKD patients.

Biography:

Coming soon

Abstract:

In this study, seven human urinary stones were collected from Istanbul, Turkey. They labeled S1 to S7, their XRD, FT-IR, FT-Raman and EDX spectra as well as SEM images have been recorded to determine their chemical compositions, morphologies, crystal structures, and crystallite sizes. XRD and vibrational (FT-IR and FT-Raman) analyses indicate that S1 is apatite and S2 contains both calcium oxalate monohydrate and apatite, S3–S7 are composed of calcium oxalate monohydrate. The ratios of organic and inorganic contents of the stones have been determined by their thermogravimetric analyses and these analyses also demonstrate characteristic peaks for the dehydration and the decomposition of calcium oxalate and apatite. The present characterization study is especially useful for the future classification studies of renal studies needed for treating urinal diseases

Biography:

Varun Kumar Bandi has completed his PhD from Ramachandra University, India in the Department of Nephrology and he has published more than 25 papers in reputed journals.

Abstract:

Patients receiving a solid organ transplant have an increased risk of developing post-transplant lymphoproliferative disorder (PTLD). Incidence of PTLD is 1% in renal allograft recipients. Most of the PTLDs are of B cell origin, and are found to have evidence of Epstein–Barr virus (EBV) infection. The immunosuppressant mediated decrease in activity of the natural cytotoxic T-cells is probably one of the contributing factors. We report a case of PTLD occurring in the transplanted kidney of a 45 year old male, 7 years after transplant who presented with graft dysfunction. The graft biopsy revealed presence of lymphoid proliferation, confirmed by histochemistry and a diagnosis of monomorphic B-cell lymphoma was made. He was treated by reducing the immunosuppression and is doing well on follow up with stable graft function at 8 months follow up. We suggest that allograft dysfunction in renal transplant recipients should have a detailed evaluation, including for PTLD involving the allograft. PTLD limited to the renal allograft in renal transplant patients has a benign behavior; therefore it is important to screen renal recipients with allograft dysfunction for early diagnosis of PTLDs.

Biography:

Otgonchimeg Rentsendorj has more than 15 years of research-based experience in “Endothelial molecular biology, biomarkers, blood products, renal and lung injuries, toxicology, and virology”. She completed her PhD (Molecular biology) at the Hungarian Academy of Sciences in Szeged in 2006. She was a Visiting Scholar, Post-doctoral and a Research Associate at the Johns Hopkins University. In January 2015, she joined the Laboratory of Biochemistry and Vascular Biology, Division of Hematology Research and Review at CBER, FDA. Her current research focuses on “Animal models and tissue injuries induced by hemoglobin-mediated oxidative stress”. She has authored 50+ abstracts and papers.

Abstract:

Polymerized cell-free hemoglobins are being developed as oxygen and plasma volume-expanding therapeutics though their potential to promote oxidative tissue injury has raised safety concerns. Using a guinea pig exchange transfusion model, we explored oxidant mechanisms of polymerized bovine hemoglobin (HbG) in renal injury. Several renal injury markers including oxidative stress and inflammation markers were targeted. HbG infusion increased tubular injury markers including neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury marker-1 and reduced the transcription of glomerular filtration barrier components including podocin, and nephrin. Increased renal heme oxygensase-1 (HO-1) and decreased enzymatic antioxidants including SOD isoforms 1-3, GPx1, GPx3, GPx4, and CAT were also detected at the mRNA, protein, and activity levels. Furthermore, DNA methylation analyses identified CpG hypermethylation in the gene promoters for all enzymatic antioxidants that we studied suggested an epigenetic-based mechanism underlying the observed gene repression. HbG also induced oxidative stress as evidenced by increased renal lipid peroxidation end-products and 4-HNE immunostaining, which could be the result of the depleted antioxidant defenses and/or serve as a trigger for increased DNA methylation. Together, these findings provide evidence that the renal exposure to HbG suppresses the function of major antioxidant defense systems which may have relevant implications for understanding the safety of hemoglobin-based products and may serve as sensitive and specific biomarkers in kidney injury.

Biography:

Mohamed Siyab Eldin Elsadig Ahmed has completed his Doctorate from the University of Tuebingen. He is the Head of the Department of Molecular Biology. He has published about 10 papers in reputed journals. He is also an Editorial and Advisory Board Member of JBRC.

Abstract:

Anemia is a major complication of end stage renal disease. It is mainly the result of impaired formation of erythrocytes due to lack of erythropoietin and iron deficiency. However, compelling evidence points to the contribution of accelerated erythrocyte death, which decreases the life span of circulating erythrocytes. Erythrocytes may enter suicidal death or eryptosis, which is characterized by cell shrinkage and by cell membrane scrambling with phosphatidylserine exposure at the erythrocyte surface. Triggers of eryptosis include increase of cytosolic Ca²⁺-activity ([Ca²⁺]i). Erythrocytes could be sensitized to cytosolic Ca²⁺ by ceramide. In end stage renal disease, eryptosis may possibly be stimulated by uremic toxins. The present study explored, whether the uremic toxin acrolein could trigger eryptosis or not. Cell volume was estimated from forward scatter, phosphatidylserine exposure from annexin-V-binding, hemolysis from hemoglobin release, [Ca²⁺]i from Fluo3-fluorescence, and ceramide from fluorescent antibodies. In results a 48 h exposure to acrolein (30-50 μM) did not significantly modify [Ca²⁺]i but significantly decreased forward scatter and increased annexin-V-binding. Acrolein further triggered slight, but significant hemolysis and increased ceramide formation in erythrocytes. Acrolein (50 μM) induced annexin-V-binding was significantly blunted in the nominal absence of extracellular Ca²⁺. Acrolein augmented the annexin-V-binding following treatment with Ca²⁺ ionophore ionomycin (1 μM). Finally we concluded that acrolein stimulates suicidal erythrocyte death or eryptosis, an effect at least in part due to stimulation of ceramide formation with subsequent sensitization of the erythrocytes to cytosolic Ca²⁺.