Efficacy and Safety of Intravenous Ferric Carboxymaltose in Geriatric Inpatients at a German Tertiary University Teaching Hospital: A Retrospective Observational Cohort Study of Clinical Practice.

Current iron supplementation practice in geriatric patients is erratic and lacks evidence-based recommendations. Despite potential benefits in this population, intravenous iron supplementation is often withheld due to concerns regarding pharmacy expense, perceived safety issues, and doubts regarding efficacy in elderly patients. This retrospective, observational cohort study aimed to evaluate the safety and efficacy of intravenous ferric carboxymaltose (FCM, Ferinject) in patients aged >75 years with iron deficiency anaemia (IDA). Within a twelve-month data extraction period, the charts of 405 hospitalised patients aged 65-101 years were retrospectively analysed for IDA, defined according to WHO criteria for anaemia (haemoglobin: <13.0 g/dL (m)/<12.0 g/dL (f)) in conjunction with transferrin saturation <20%. Of 128 IDA patients screened, 51 (39.8%) received intravenous iron. 38 patient charts were analysed. Mean cumulative dose of intravenous FCM was 784.4 ± 271.7 mg iron (1-3 infusions). 18 patients (47%) fulfilled treatment response criteria (≥1.0 g/dL increase in haemoglobin between baseline and hospital discharge). AEs were mild/moderate, most commonly transient increases of liver enzymes (n = 5/13.2%). AE incidence was comparable with that observed in patients <75 years. No serious AEs were observed. Ferric carboxymaltose was well tolerated and effective for correction of Hb levels and iron stores in this cohort of IDA patients aged over 75 years.

[Efficacy and tolerability of ferric carboxymaltose in geriatric patients with anemia. Data from three non-interventional studies]. / Wirksamkeit und Verträglichkeit einer intravenösen Eisentherapie bei geriatrischen Patienten mit Anämie. Gepoolte Daten aus drei nicht-interventionellen Studien.

BACKGROUND: Anemia in the elderly is a common clinical finding. Prevalence in hospitalized geriatric patients approximates up to 40% presenting as iron deficiency anemia associated with absolute iron deficiency, anemia of chronic disease associated with functional iron deficiency or unexplained anemia. In patients with functional iron deficiency oral iron substitution is ineffective due to elevated hepcidin levels, such as in renal anemia. In these patients intravenous iron substitution represents a cornerstone. However, data among geriatric patients are limited. We conducted three non-interventional studies collecting data with respect to efficacy and tolerance of ferric carboxymaltose (ferinject) in three patient groups (cancer, chronic kidney disease [CKD], chronic inflammatory bowel disease [CIBD]) with anemia and functional iron deficiency. The present sub-analysis describes the results among the geriatric patients (age > 70 years) observed in all three observational studies. PATIENTS, METHODS: 264 patients were analyzed (mean age of 76.9 years [70-90 years; SD +/- 5.2 years]). Patients received an average amount of 1200 mg ferric carboxymaltose (746-1575 mg). RESULTS: Hemoglobin levels (p < 0.001), serum ferritin (p < 0.001) and transferrin saturation (p < 0.05) rose significantly in CKD patients; in CIBD patients hemoglobin and transferrin saturation rose significantly (p < 0.05) while the rise of ferritin failed to be significant. In oncologic patients the rise of hemoglobin and ferritin levels was of high statistic significance (p < 0.001) and transferrin saturation also rose significantly (p = 0.02) Fatigue, mental capacities as well as dyspnea improved among CKD-and CIBD-groups. No severe adverse reactions occurred. CONCLUSION: Administration of ferric carboxymaltose in geriatric patients is well tolerated and offers an effective treatment option for the treatment of functional iron deficiency.

An etiologic profile of anemia in 405 geriatric patients.

Background. Anemia is a common condition in the elderly and a significant risk factor for increased morbidity and mortality, reducing not only functional capacity and mobility but also quality of life. Currently, few data are available regarding anemia in hospitalized geriatric patients. Our retrospective study investigated epidemiology and causes of anemia in 405 hospitalized geriatric patients. Methods. Data analysis was performed using laboratory parameters determined during routine hospital admission procedures (hemoglobin, ferritin, transferrin saturation, C-reactive protein, vitamin B12, folic acid, and creatinine) in addition to medical history and demographics. Results. Anemia affected approximately two-thirds of subjects. Of 386 patients with recorded hemoglobin values, 66.3% were anemic according to WHO criteria, mostly (85.1%) in a mild form. Anemia was primarily due to iron deficiency (65%), frequently due to underlying chronic infection (62.1%), or of mixed etiology involving a combination of chronic disease and iron deficiency, with absolute iron deficiency playing a comparatively minor role. Conclusion. Greater awareness of anemia in the elderly is warranted due to its high prevalence and negative effect on outcomes, hospitalization duration, and mortality. Geriatric patients should be routinely screened for anemia and etiological causes of anemia individually assessed to allow timely initiation of appropriate therapy.

Effects of enzyme replacement therapy in adult patients with Fabry disease on cardiac structure and function: a retrospective cohort study of the Fabry Munster Study (FaMuS) data.

OBJECTIVE: Fabry disease (FD) is an X-linked inborn error of glycosphingolipid catabolism caused by deficient lysosomal α-galactosidase A activity. Progressive accumulation of globotriaosylceramide and related glycosphingolipids in vascular endothelial lysosomes of the heart, kidneys and brain is responsible for the main disease manifestations. The aim of our study was to assess short-term and long-term effects of enzyme replacement therapy (ERT) on cardiac mass and function. DESIGN: Retrospective cohort study. SETTING: Hospital outpatient clinic. PARTICIPANTS: 40 FD patients (21 men, 19 women) receiving agalsidase ß-ERT. OUTCOME MEASURES: The focus at baseline and follow-up examinations was on structural, functional (Doppler-echocardiography) as well as electrical changes (ECG) and blood pressure. RESULTS: In the Early Group, systolic and diastolic blood pressures significantly decreased. Left-ventricular (LV) also decreased; however, wall thickness and LV mass index showed no further increase. VE as an indicator for diastolic function significantly improved (64±21 vs 75±27 cm/s, p=0.038). There were no significant changes of ECG parameters. There were few relevant changes in the Late Group, albeit systolic blood pressure significantly decreased and QRS duration significantly increased. In conclusion, echocardiographic left-ventricular mass index, interventricular septum thickness, left-ventricular posterior wall, left-ventricular end-diastolic dimension) and diastolic function parameters are valuable for follow-up and guidance of therapy. CONCLUSIONS: The primary positive impact of ERT appears to be an early effect after the start of therapy, and early initiation of ERT should be recommended.

Signaling by the matrix proteoglycan decorin controls inflammation and cancer through PDCD4 and MicroRNA-21.

The mechanisms linking immune responses and inflammation with tumor development are not well understood. Here, we show that the soluble form of the extracellular matrix proteoglycan decorin controls inflammation and tumor growth through PDCD4 (programmed cell death 4) and miR-21 (microRNA-21) by two mechanisms. First, decorin acted as an endogenous ligand of Toll-like receptors 2 and 4 and stimulated production of proinflammatory molecules, including PDCD4, in macrophages. Second, decorin prevented translational repression of PDCD4 by decreasing the activity of transforming growth factor-ß1 and the abundance of oncogenic miR-21, a translational inhibitor of PDCD4. Moreover, increased PDCD4 abundance led to decreased release of the anti-inflammatory cytokine interleukin-10, thereby making the cytokine profile more proinflammatory. This pathway operates in both pathogen-mediated and sterile inflammation, as shown here for sepsis and growth retardation of established tumor xenografts, respectively. Decorin was an early response gene evoked by septic inflammation, and protein concentrations of decorin were increased in the plasma of septic patients and mice. In cancer, decorin reduced the abundance of anti-inflammatory molecules and increased that of proinflammatory molecules, thereby shifting the immune response to a proinflammatory state associated with reduced tumor growth. Thus, by stimulating proinflammatory PDCD4 and decreasing the abundance of miR-21, decorin signaling boosts inflammatory activity in sepsis and suppresses tumor growth.

Perforating vein fistula is superior to forearm fistula in elderly haemodialysis patients with diabetes and arterial hypertension.

BACKGROUND: Access-related problems are one of the major causes of morbidity in elderly patients with chronic kidney disease. The aim of this study was to assess potential risks and benefits in elderly patients comparing forearm arteriovenous fistula (AVF) and perforating vein AVF below the elbow for primary vascular access. METHODS: A retrospective comparison of elderly patients (65.7 ± 9.3 years, 70.4% male patients, 36.2% late referral) undergoing primary vascular access surgery using forearm AVF (n = 50) and perforating vein AVF (n = 55) was performed over a 2-year period, including a multivariate analysis of potential risk factors and benefits of primary patency (PP = intervention-free access survival) and secondary patency (SP = access survival until abandonment). RESULTS: Patency rates after 24 months were significantly higher in patients with perforating vein AVF (PP + SP: 78.2%) compared to forearm AVF (PP: 62%, SP: 56%, P = 0.04). Presence of diabetes mellitus in patients with forearm AVF was associated with a decreased PP [odds ratio (OR): 3.6, 95% confidence interval (CI): 0.9-13.8] and SP (OR: 4.8, 95% CI: 1.3-17.9), and arterial hypertension was associated with a lower PP (OR: 6.7, 95% CI: 0.8-53.9), whereas the presence of hyperparathyroidism was associated with higher PP and SP (OR: 0.2, 95% CI: 0.1-0.7). In contrast, PP and SP in patients with perforating vein AVF were not influenced by comorbidities. CONCLUSIONS: Perforating vein AVF is superior to forearm AVF in elderly patients with diabetes and arterial hypertension due to the proximal fistula location, probably caused by an improved artery distensibility during fistula maturation.

The proteoglycan biglycan regulates expression of the B cell chemoattractant CXCL13 and aggravates murine lupus nephritis.

CXCL13 is a key B cell chemoattractant and marker of disease activity in patients with SLE; however, the mechanism of its induction has not been identified yet. Here, we have shown that the proteoglycan biglycan triggers CXCL13 expression via TLR2/4 in macrophages and dendritic cells. In vivo, levels of biglycan were markedly elevated in the plasma and kidneys of human SLE patients and lupus-prone (MRL/lpr) mice. Overexpression of soluble biglycan in MRL/lpr mice raised plasma and renal levels of CXCL13 and caused accumulation of B cells with an enhanced B1/B cell ratio in the kidney, worsening of organ damage, and albuminuria. Importantly, biglycan also triggered CXCL13 expression and B cell infiltration in the healthy kidney. Conversely, biglycan deficiency improved systemic and renal outcome in lupus-prone mice, with lower levels of autoantibodies, less enlargement of the spleen and lymph nodes, and reduction in renal damage and albuminuria. This correlated with a marked decline in circulating and renal CXCL13 and a reduction in the number of B cells in the kidney. Collectively, our results describe what we believe to be a novel mechanism for the regulation of CXCL13 by biglycan, a host-derived ligand for TLR2/4. Blocking biglycan-TLR2/4 interactions might be a promising strategy for the management of SLE and other B cell-mediated inflammatory disease entities.

Department-related tasks and organ-targeted therapy in Fabry disease: an interdisciplinary challenge.

Fabry disease is a rare X-linked storage disorder leading to an accumulation of globotriaosylceramides in all cells carrying lysosomes. As the accumulation occurs in most organs, different medical specialties are involved in the diagnostics and therapy of Fabry disease. With this review of the 3 main specialties (cardiology, nephrology, and neurology) and, in addition, the adjacent specialties (ophthalmology and dermatology), we aim to discuss the division-related responsibilities and want to suggest an organ-related additional therapy besides enzyme replacement therapy.

Dialysis and transplantation in Fabry disease: indications for enzyme replacement therapy.

ESRD is a major cause of morbidity and premature mortality in Fabry disease, particularly in classically affected males. The decline of renal function in Fabry nephropathy is adversely affected by male gender, advanced chronic kidney disease (CKD), and severe proteinuria. The diagnosis of Fabry nephropathy may be missed if not specifically addressed in progressive CKD and patients have been first identified in screening programs of dialysis patients. Fabry patients have worse 3-year survival rates on dialysis as compared with nondiabetic controls. The 5-year survival rate of transplanted Fabry patients is also lower than that of controls. However, because Fabry nephropathy does not recur in the allograft and transplanted Fabry patients appear to have better overall outcomes than those maintained on dialysis, kidney transplantation should be recommended as a first choice in renal replacement therapy (RRT) for Fabry disease. Appropriately designed and powered studies are not available to answer the question whether enzyme replacement therapy (ERT) influences outcomes, the course of cardiomyopathy, events, or survival in Fabry patients on RRT. The authors are not aware of compelling indications for ERT in RRT patients because progression of cardiomyopathy was documented during ERT. Whether the excess mortality risk of Fabry patients on RRT can be prevented by ERT is unknown. Despite observational reports of symptomatic improvement, the available evidence supporting ERT for such patients is not compelling enough. To clarify this issue, studies are needed to test the effectiveness of agalsidases in preventing cardiac and cerebrovascular complications in Fabry patients with ESRD.

Proteoglycans: from structural compounds to signaling molecules.

Our knowledge of proteoglycan biology has significantly expanded over the past decade with the discovery of a host of new members of this multifunctional family leading to their present classification into three major categories: (1) small leucine-rich proteoglycans, 2) modular proteoglycans, and 3) cell-surface proteoglycans. In addition to being structural proteins, proteoglycans play a major role in signal transduction with regulatory functions in various cellular processes. Being mostly extracellular, they are upstream of many signaling cascades and are capable of affecting intracellular phosphorylation events and modulating distinct pathways, including those driven by bone morphogenetic protein/transforming growth factor superfamily members, receptor tyrosine kinases, the insulin-like growth factor-I receptor, and Toll-like receptors. Mechanistic insights into the molecular and cellular functions of proteoglycans have revealed both the sophistication of these regulatory proteins and the challenges that remain in uncovering the entirety of their biological functions. This review aims to summarize the multiple functions of proteoglycans with special emphasis on their intricate composition and the newly described signaling events in which these molecules play a key role.

The matricellular functions of small leucine-rich proteoglycans (SLRPs).

The small leucine-rich proteoglycans (SLRPs) are biologically active components of the extracellular matrix (ECM), consisting of a protein core with leucine rich-repeat (LRR) motifs covalently linked to glycosaminoglycan (GAG) side chains. The diversity in composition resulting from the various combinations of protein cores substituted with one or more GAG chains along with their pericellular localization enables SLRPs to interact with a host of different cell surface receptors, cytokines, growth factors, and other ECM components, leading to modulation of cellular functions. SLRPs are capable of binding to: (i) different types of collagens, thereby regulating fibril assembly, organization, and degradation; (ii) Toll-like receptors (TLRs), complement C1q, and tumor necrosis factor-alpha (TNFalpha), regulating innate immunity and inflammation; (iii) epidermal growth factor receptor (EGF-R), insulin-like growth factor receptor (IGF-IR), and c-Met, influencing cellular proliferation, survival, adhesion, migration, tumor growth and metastasis as well as synthesis of other ECM components; (iv) low-density lipoprotein receptor-related protein (LRP-1) and TGF-beta, modulating cytokine activity and fibrogenesis; and (v) growth factors such as bone morphogenic protein (BMP-4) and Wnt-I-induced secreted protein-1 (WISP-1), controlling cell proliferation and differentiation. Thus, the ability of SLRPs, as ECM components, to directly or indirectly regulate cell-matrix crosstalk, resulting in the modulation of various biological processes, aptly qualifies these compounds as matricellular proteins.

Enzyme replacement therapy for Fabry disease: a systematic review of available evidence.

Fabry disease is a progressive and life-threatening glycolipid storage disorder affecting both males and females. The primary driver of the disease is the accumulation of glycolipids (globotriaosylceramide [GL-3]) in a variety of cell types, including vascular endothelial cells, a range of renal cell types, cardiomyocytes and neurons, which is caused by deficient activity of the lysosomal enzyme, alpha-galactosidase. The disease typically presents during childhood or adolescence. First manifestations reflect involvement of small nerve fibres of the peripheral and autonomic nervous systems. With age, severe complications involving the kidneys, heart and brain cause considerable morbidity and premature death. Outside the US, enzyme replacement therapy (ERT) with agalsidase alfa 0.2 mg/kg every other week (EOW) and agalsidase beta 1.0 mg/kg EOW is available for the treatment of patients with Fabry disease, while agalsidase beta 1.0 mg/kg EOW is the only approved drug in the US. To analyse the evidence for ERT, a systematic review of the literature was performed to identify prospectively designed randomized, controlled trials (RCTs) and open-label studies on the efficacy of agalsidase alfa and agalsidase beta. MEDLINE and EMBASE databases were searched; inclusion criteria for the systematic review were prospectively designed clinical studies evaluating ERT with quantifiable endpoints: double-blind and open-label studies were eligible. Exclusion criteria were review articles, case reports, case studies, letters to the editor and articles based on registry data (Fabry Outcome Survey or Fabry Registry). In addition, any studies with a retrospective design or data based on post hoc analyses were excluded. The evidence was reviewed with respect to the clinical benefits of ERT at the level of the end organ. A total of 9 RCTs and 23 open-label studies were identified for inclusion. The efficacy of ERT in Fabry disease has been measured against a variety of endpoints, the majority of which were subclinical parameters rather than clinical outcomes. Plasma levels of GL-3 together with accumulation in the kidney, heart and skin were the most commonly studied endpoints, followed by renal endpoints of proteinuria and glomerular filtration rate, whereas cardiac and neurological endpoints were not commonly studied. To date, only one RCT with ERT defined hard clinical outcomes in the form of cardiac, renal or cerebrovascular events, or death as its primary endpoint. The currently available data from prospective RCTs and open-label studies in patients with Fabry disease are more robust for ERT at a dose of 1 mg/kg EOW than a dose of 0.2 mg/kg EOW, although the beneficial effects of ERT with either dose or preparation are variable.

Biglycan, a danger signal that activates the NLRP3 inflammasome via toll-like and P2X receptors.

The role of endogenous inducers of inflammation is poorly understood. To produce the proinflammatory master cytokine interleukin (IL)-1beta, macrophages need double stimulation with ligands to both Toll-like receptors (TLRs) for IL-1beta gene transcription and nucleotide-binding oligomerization domain-like receptors for activation of the inflammasome. It is particularly intriguing to define how this complex regulation is mediated in the absence of an infectious trigger. Biglycan, a ubiquitous leucine-rich repeat proteoglycan of the extracellular matrix, interacts with TLR2/4 on macrophages. The objective of this study was to define the role of biglycan in the synthesis and activation of IL-1beta. Here we show that in macrophages, soluble biglycan induces the NLRP3/ASC inflammasome, activating caspase-1 and releasing mature IL-1beta without the need for additional costimulatory factors. This is brought about by the interaction of biglycan with TLR2/4 and purinergic P2X(4)/P2X(7) receptors, which induces receptor cooperativity. Furthermore, reactive oxygen species formation is involved in biglycan-mediated activation of the inflammasome. By signaling through TLR2/4, biglycan stimulates the expression of NLRP3 and pro-IL-1beta mRNA. Both in a model of non-infectious inflammatory renal injury (unilateral ureteral obstruction) and in lipopolysaccharide-induced sepsis, biglycan-deficient mice displayed lower levels of active caspase-1 and mature IL-1beta in the kidney, lung, and circulation. Our results provide evidence for direct activation of the NLRP3 inflammasome by biglycan and describe a fundamental paradigm of how tissue stress or injury is monitored by innate immune receptors detecting the release of the extracellular matrix components and turning such a signal into a robust inflammatory response.

[Division-related function and organ-related therapy in Fabry's disease. An interdisciplinary challenge]. / Fachspezifische Aufgabe und organspezifische Therapie beim Morbus Fabry. Eine interdisziplinäre Herausforderung.

Fabry's disease is a rare X-linked lysosomal storage disorder leading to an accumulation of globotriaosylceramides in the lysosomes of all tissues. As the accumulation occurs in all organs, different medical faculties are involved in the diagnostics and therapy of Fabry's disease. With this review the three main faculties (cardiology, nephrology and neurology) as well as the adjacent faculties (ophthalmology and dermatology) want to discuss the division-related function and also to suggest an organ-related additional therapy besides enzyme replacement therapy.

Excessive Daytime Sleepiness Is a Common Symptom in Fabry Disease.

Fabry disease (FD) is an X-linked lysosomal storage disorder characterized by a deficient activity of the enzyme α-galactosidase A, resulting in a vasculopathic involvement of various organ systems, e.g. cerebral structures. Marked cerebral vasculopathy with subsequent white matter lesions (WML) are a frequent finding in FD patients. Recent studies discussed an association between cerebral white matter changes and sleep-related disturbances of breathing, which may lead to excessive daytime sleepiness (EDS). A 56-year-old Caucasian female FD patient with EDS was admitted to our sleep laboratory. Overnight polysomnography showed a Cheyne-Stokes respiration pattern with significant O(2) desaturation. MR imaging revealed confluent WML including the brain stem, but no renal or cardiac involvement. We then evaluated the clinical data of 49 genetically proven FD patients (27 males; mean age 43 years) from our FD centre. With a frequency of 68%, EDS exceeds the prevalence of other common symptoms of FD (angiokeratomas 61%; acroparaesthesia 51%; renal involvement 29%; cardiac involvement 27%), and the prevalence of chronic fatigue (48%). EDS was independently associated with the physical component summary of the SF-36 data (corrected R(2) = -0.323, p < 0.001). EDS and age explained a quarter of variance in mental component summary (corrected R(2) = -0.253, p < 0.001). We conclude that EDS is a common and underdiagnosed symptom in FD patients, accompanied by a significant impact on quality of life. EDS might be caused by central breathing disorders due to an affection of brain regions associated with respiratory control in FD.

Characteristics of pole impacts to side of passenger cars in European traffic accidents and assessment of injury mechanisms--analysis of German and UK in-depth data.

The national accident statistics demonstrate that the situation of passenger car side impacts is dominated by car-to-car accidents. Car side-to-pole impacts are relatively infrequent events but result in disproportionate rates of serious and fatal injuries when compared to those in car-to-car side impact. Hence their importance has been highlighted in recent studies. For the present study two approaches were undertaken to better understand the scenario of car-to-pole impacts in Germany. The German in-depth database GIDAS (German In-Depth-Accident Study) and the UK-based database CCIS (Co-operative Crash Injury Study) were used. The first part or the study is a statistical analysis of passenger car side-to-pole impacts to describe the characteristics and their importance relevant to other types of impact and to gain further knowledge about the main factors influencing the accident outcome. The second part contains a case-by-case review of passenger cars first registered 1998 and onwards to further investigate this type of impact, including regression analysis to assess the relationship between injury severity and pole impact relevant factors. The study uses a methodology that merges in-depth-accident data from different nations and shows how in-depth cases can be used for finding injury-related technical parameters like deformation pattern, load circumstances for impact locations, and directions on the vehicle for the assessment of current and prospective test regulations. Delta-v can be identified as the most significant influencing factor for MAIS, especially for injury severity for thr thorax and abdomen. The vast majority of severe and fatal injuries are in accidents involving damage to the passenger compartment. The depth of deformation has significant influence on the injury severity level of the extremities. The most frequent direction of impact in car side-to-pole impacts is perpendicular (90 degrees +/-15 degrees ).

Predictors for contrast media-induced nephropathy and long-term survival: prospectively assessed data from the randomized controlled Dialysis-Versus-Diuresis (DVD) trial.

BACKGROUND: Among the numerous studies concerning contrast media-induced nephropathy (CIN), there was no prospective trial that provided data on the long-term outcomes. OBJECTIVES: To prospectively assess predictors of CIN and long-term outcomes of affected patients. METHODS: Four hundred twelve consecutive patients with serum creatinine levels of 115 micromol/L to 309 micromol/L (1.3 mg/dL to 3.5 mg/dL) undergoing elective coronary angiography were included. Patients were randomly assigned to periprocedural hydration alone, hydration plus one-time hemodialysis or hydration plus N-acetylcysteine. RESULTS: Multivariate logistic regression identified the following as predictors of CIN within 72 h (equivalent to an increase in creatinine 44.2 micromol/L [0.5 mg/dL] or more) : prophylactic postprocedural hemodialysis (OR 2.86, 95% CI 1.07 to 7.69), use of angiotensin-converting enzyme inhibitors (OR 6.16, 95% CI 2.01 to 18.93), baseline glomerular filtration rate (OR 0.94, 95% CI 0.90 to 0.98) and the amount of contrast media given (OR 1.01, 95% CI 1.00 to 1.01). With regard to long-term outcome (mean follow-up 649 days), multivariate Cox regression models found elevated creatinine levels at 30 days (hazard rate ratio [HRR] 5.48, 95% CI 2.85 to 10.53), but not CIN within 72 h (HRR 1.12, 95% CI 0.63 to 2.02), to be associated with increased mortality. In addition, independent predictors for death during follow-up included left ventricular ejection fraction lower than 35% (HRR 4.01, 95% CI 2.22 to 7.26), serum phosphate (HRR 1.64, 95% CI 1.10 to 2.43) and hemoglobin (HRR 0.80, 95% CI 0.67 to 0.96). CONCLUSION: From the present prospective trial, performance of postprocedural hemodialysis, use of angiotensin-converting enzyme inhibitors, reduced baseline glomerular filtration rate and amount of contrast media were independent predictors of CIN within 72 h after catheterization. Assessing renal function after 30 days, rather than within 72 h, seemed to be more predictive for patients' long-term survival.