Correlation of gestational age and age at death in sudden infant death syndrome: another pointer to the role of critical developmental period?

BACKGROUND: Filiano and Kinney proposed a triple-risk model for the sudden infant death syndrome (SIDS) that involves the intersection of three risks: (1) a vulnerable infant, (2) a critical developmental period in homeostatic control, and (3) an exogenous stressor(s). The primary evidence for the role of a critical developmental period in SIDS etiology is the peak of cases around the third month of life. Independently, several studies pointed to correlation between gestational age and age at death in SIDS, but used that to assess the SIDS risk for preterm infants, ignoring further ramifications. METHODS: We did a detailed analysis of CDC data spanning over two decades (1983-2011). We focused not only on the correlation between two age variables (gestational and age at death), but also on the possibility of misdiagnosis. Also, we attempted to account for potential biases in the data induced by the ICD-9/ICD-190 transition or the "Back to Sleep" campaign. RESULTS: The peak of deaths in the third month of life, that was the main argument for the role of the critical development period, wasn't unique to SIDS. However, we confirmed an almost linear and negative correlation between gestational age and the week of death due to SIDS. This pattern (slope of correlation < 0 and significance of correlation p < 0.05) is characteristic of SIDS among all diseases analyzed in the study. CONCLUSIONS: We interpret the results as the evidence of the role of the critical development period in SIDS etiology. Possibly more attention in the future research should be put to theories that are based on homeostatic control.

Concentrations of Transition Metal Ions in Rat Lungs after Tobacco Smoke Exposure and Treatment with His-Leu Dipeptide.

Tobacco smoking is deleterious to the lungs because it exposes them to many toxic substances. These include transition metal ions, such as cadmium. However, there is a lack of information about the influence of endogenous metal-binding peptides, such as His-Leu (HL), on the lung distribution of transition metals in smokers. To address this, we administered HL subcutaneously to rats exposed to tobacco smoke for six weeks, then we measured the concentrations of transition metal ions in the lungs. We found that exposure to tobacco smoke elevates the concentrations of Cd(II) and Cu(II). Administration of the HL peptide, whose elevation is a consequence of angiotensin receptor blocker anti-hypertension therapy, increases the concentration of Fe in the lungs of rats exposed to smoke. These findings suggest that smoking is a risk factor for patients receiving angiotensin receptor blockers to treat hypertension.

The molecular phenotypes of injury, steatohepatitis, and fibrosis in liver transplant biopsies in the INTERLIVER study.

To extend previous molecular analyses of rejection in liver transplant biopsies in the INTERLIVER study (ClinicalTrials.gov #NCT03193151), the present study aimed to define the gene expression selective for parenchymal injury, fibrosis, and steatohepatitis. We analyzed genome-wide microarray measurements from 337 liver transplant biopsies from 13 centers. We examined expression of genes previously annotated as increased in injury and fibrosis using principal component analysis (PCA). PC1 reflected parenchymal injury and related inflammation in the early posttransplant period, slowly regressing over many months. PC2 separated early injury from late fibrosis. Positive PC3 identified a distinct mildly inflamed state correlating with histologic steatohepatitis. Injury PCs correlated with liver function and histologic abnormalities. A classifier trained on histologic steatohepatitis predicted histologic steatohepatitis with cross-validated AUC = 0.83, and was associated with pathways reflecting metabolic abnormalities distinct from fibrosis. PC2 predicted histologic fibrosis (AUC = 0.80), as did a molecular fibrosis classifier (AUC = 0.74). The fibrosis classifier correlated with matrix remodeling pathways with minimal overlap with those selective for steatohepatitis, although some biopsies had both. Genome-wide assessment of liver transplant biopsies can not only detect molecular changes induced by rejection but also those correlating with parenchymal injury, steatohepatitis, and fibrosis, offering potential insights into disease mechanisms for primary diseases.

Label-Free Mass Spectrometry-Based Quantitative Proteomics to Evaluate the Effects of the Calcium-Sensing Receptor Agonist Cinacalcet on Protein Expression in Rat Brains and Livers.

BACKGROUND Cinacalcet is a calcium-sensing receptor agonist that is clinically approved for the treatment of secondary hyperparathyroidism in chronic kidney disease and hypercalcemia in patients with parathyroid carcinoma. This study aimed to use quantitative mass spectrometry-based label-free proteomics to evaluate the effects of cinacalcet on protein expression in rat brains and livers. MATERIAL AND METHODS We randomly assigned 18 Wistar rats to 2 groups: an untreated control group (n=6) and a group treated with cinacalcet at a dose corresponding to the maximum dose used in humans (2 mg/kg/body weight, 5 days/week) divided into 7-day (n=6) and 21-day (n=6) treatment subgroups. A mass-spectrometry-based label-free quantitative proteomics approach using peptides peak area calculation was used to evaluate the changes in protein expression in examined tissues. Bioinformatics analysis of quantitative proteomics data was done using MaxQuant and Perseus environment. RESULTS No changes in protein expression were revealed in the 7-day treatment subgroup. We detected 10 upregulated and 3 downregulated proteins in the liver and 1 upregulated protein in the brain in the 21-day treatment subgroup compared to the control group. Based on Gene Ontology classification, all identified differentially expressed proteins were indicated as molecular functions involved in the enzyme regulator activity (36%), binding (31%), and catalytic activity (19%). CONCLUSIONS These findings indicate that long-term cinacalcet therapy can impair phase II of enzymatic detoxication and can cause disturbances in blood hemostasis, lipid metabolism, and inflammatory mediators or contribute to the acceleration of cognitive dysfunction; therefore, appropriate patient monitoring should be considered.

Crosstalk between microRNA and Oxidative Stress in Heart Failure: A Systematic Review.

Heart failure is defined as a clinical syndrome consisting of key symptoms and is due to a structural and/or functional alteration of the heart that results in increased intracardiac pressures and/or inadequate cardiac output at rest and/or during exercise. One of the key mechanisms determining myocardial dysfunction in heart failure is oxidative stress. MicroRNAs (miRNAs, miRs) are short, endogenous, conserved, single-stranded non-coding RNAs of around 21-25 nucleotides in length that act as regulators of multiple processes. A systematic review following the PRISMA guidelines was performed on the evidence on the interplay between microRNA and oxidative stress in heart failure. A search of Pubmed, Embase, Scopus, and Scopus direct databases using the following search terms: 'heart failure' AND 'oxidative stress' AND 'microRNA' or 'heart failure' AND 'oxidative stress' AND 'miRNA' was conducted and resulted in 464 articles. Out of them, 15 full text articles were eligible for inclusion in the qualitative analysis. Multiple microRNAs are involved in the processes associated with oxidative stress leading to heart failure development including mitochondrial integrity and function, antioxidant defense, iron overload, ferroptosis, and survival pathways.

Fluorine-Containing Drug Administration in Rats Results in Fluorination of Selected Proteins in Liver and Brain Tissue.

In many pharmaceuticals, a hydrogen atom or hydroxyl group is replaced by a fluorine to increase bioavailability and biostability. The fate of fluorine released from fluorine-containing drugs is not well investigated. The aim of this study was to examine possible fluorination of proteins in rat liver and brain after administration of the fluorinated drug cinacalcet. We assigned 18 Wistar rats to a control group (n = 6) and a group treated with cinacalcet (2 mg kg-1/body weight, 5 days/week), divided into 7 day (n = 6) and 21 day (n = 6) treatment subgroups. Fluorinated proteins were identified using a free proteomics approach; chromatographic separation and analysis by high-resolution mass spectrometry; peptide/protein identification using the Mascot search algorithm; manual verification of an experimentally generated MS/MS spectrum with the theoretical MS/MS spectrum of identified fluorinated peptides. Three fluorinated proteins (spectrin beta chain; carbamoyl-phosphate synthase [ammonia], mitochondrial; 6-phosphofructo-2-kinase/fructose-2, 6-bisphosphatase 1) were identified in the liver and four (spectrin beta chain, dihydropyrimidinase-related protein 4, prominin-2, dihydropyrimidinase-related protein 4) in the brain tissue after 21 days of cinacalcet treatment, but not in the control group. Introduction of fluorine into an organism by administration of fluorinated drugs results in tissue-specific fluorination of proteins.

EBV load is associated with cfDNA fragmentation and renal damage in SLE patients.

BACKGROUND: For long Epstein-Barr virus (EBV) has been suspected to be involved in the pathogenesis of systemic lupus erythematosus (SLE). The aim of this study was to verify the association between EBV, cell-free DNA (cfDNA) and kidney disease in SLE. METHODS: Blood samples were obtained from 43 SLE patients and 50 healthy individuals. EBV load was measured via real-time PCR assay. Sizing and quantification of plasma cfDNA was performed on Bioanalyzer. We proposed that the uniformity of cfDNA fragmentation can be described using cfDNA fragmentation index. RESULTS: SLE patients with chronic kidney disease (CKD +) had higher EBV load compared to CKD(-) patients (P = 0.042). Patients with high cfDNA level had higher EBV load (P = 0.041) and higher cfDNA fragmentation index (P < 0.001) compared to patients with low cfDNA level. Among patients with high cfDNA level, EBV load was higher in CKD(+) group compared to CKD(-) group (P = 0.035). EBV load was positively correlated with the fragmentation index in all SLE patients (P = 0.028, R2 = 0.13), and the correlation was even more pronounced in CKD (+) patients (P < 0.001, R2 = 0.20). CONCLUSIONS: We showed that EBV load was associated with non-uniform cfDNA fragmentation, higher cfDNA levels, and kidney disease in SLE patients. Although the causality of this relationship could not be determined with the current study, it brings rationale for further investigations on the role of EBV and cfDNA interplay in SLE pathogenesis.

Gene Expression Profile of Human Mesenchymal Stromal Cells Exposed to Hypoxic and Pseudohypoxic Preconditioning-An Analysis by RNA Sequencing.

Mesenchymal stromal cell (MSC) therapy is making its way into clinical practice, accompanied by research into strategies improving their therapeutic potential. Preconditioning MSCs with hypoxia-inducible factors-α (HIFα) stabilizers is an alternative to hypoxic priming, but there remains insufficient data evaluating its transcriptomic effect. Herein, we determined the gene expression profile of 6 human bone marrow-derived MSCs preconditioned for 6 h in 2% O2 (hypoxia) or with 40 µM Vadadustat, compared to control cells and each other. RNA-Sequencing was performed using the Illumina platform, quality control with FastQC and adapter-trimming with BBDUK2. Transcripts were mapped to the Homo_sapiens. GRCh37 genome and converted to relative expression using Salmon. Differentially expressed genes (DEGs) were generated using DESeq2 while functional enrichment was performed in GSEA and g:Profiler. Comparison of hypoxia versus control resulted in 250 DEGs, Vadadustat versus control 1071, and Vadadustat versus hypoxia 1770. The terms enriched in both phenotypes referred mainly to metabolism, in Vadadustat additionally to vesicular transport, chromatin modifications and interaction with extracellular matrix. Compared with hypoxia, Vadadustat upregulated autophagic, phospholipid metabolism, and TLR cascade genes, downregulated those of cytoskeleton and GG-NER pathway and regulated 74 secretory factor genes. Our results provide valuable insight into the transcriptomic effects of these two methods of MSCs preconditioning.

Cirrhotic Liver of Liver Transplant Recipients Accumulate Silver and Co-Accumulate Copper.

Silver-based materials are widely used in clinical medicine. Furthermore, the usage of silver containing materials and devices is widely recommended and clinically approved. The impact on human health of the increasing use of silver nanoparticles in medical devices remains understudied, even though Ag-containing dressings are known to release silver into the bloodstream. In this study, we detected a widespread and sometimes significant silver accumulation both in healthy and sick liver biopsies, levels being statistically higher in patients with various hepatic pathologies. 28 healthy and 44 cirrhotic liver samples were investigated. The median amount of 0.049 ppm Ag in livers was measured in cirrhotic livers while the median was 0.0016 ppm for healthy livers (a more than 30-fold difference). The mean tissue concentrations of essential metals, Fe and Zn in cirrhotic livers did not differ substantially from healthy livers, while Cu was positively correlated with Ag. The serum levels of gamma-glutamyl transpeptidase (GGTP) was also positively correlated with Ag in cirrhotic livers. The increased Ag accumulation in cirrhotic livers could be a side effect of wide application of silver in clinical settings. As recent studies indicated a significant toxicity of silver nanoparticles for human cells, the above observation could be of high importance for the public health.

miRNA-16 as a predictive factor for intracranial aneurysms in autosomal dominant polycystic kidney disease.

INTRODUCTION: Autosomal dominant polycystic kidney disease (ADPKD) is the most common genetic renal disorder. It leads to multiple extra-renal complications, with intracranial aneurysms (IA) among the most serious. Biological markers could become tools in identifying patients at risk of an IA. MicroRNAs 16 (miR-16) and 25 (miR-25) have been proposed as being markers of IAs in the general population. In the current study, we attempted to discover if they may also be considered markers of IAs in ADPKD. MATERIAL AND METHODS: 64 renal transplant recipients with ADPKD were included. After magnetic resonance angiography of the brain, they were divided into a case group (IA+, n = 13) and a control group (IA-, n = 51). Expression of miRNAs in plasma was analysed by qRT-PCR. RESULTS: The expression of miR-16 was higher in the control (IA-) group. There was no statistically significant difference between the groups in terms of miR-25 expression. CONCLUSIONS AND CLINICAL IMPLICATIONS: MicroRNA-16 is a potential marker of IAs in renal transplant recipients with ADPKD. It may become a tool to identify patients who should undergo screening for an IA.

The molecular diagnosis of rejection in liver transplant biopsies: First results of the INTERLIVER study.

Molecular diagnosis of rejection is emerging in kidney, heart, and lung transplant biopsies and could offer insights for liver transplant biopsies. We measured gene expression by microarrays in 235 liver transplant biopsies from 10 centers. Unsupervised archetypal analysis based on expression of previously annotated rejection-related transcripts identified 4 groups: normal "R1normal " (N = 129), T cell-mediated rejection (TCMR) "R2TCMR " (N = 37), early injury "R3injury " (N = 61), and fibrosis "R4late " (N = 8). Groups differed in median time posttransplant, for example, R3injury 99 days vs R4late 3117 days. R2TCMR biopsies expressed typical TCMR-related transcripts, for example, intense IFNG-induced effects. R3injury displayed increased expression of parenchymal injury transcripts (eg, hypoxia-inducible factor EGLN1). R4late biopsies showed immunoglobulin transcripts and injury-related transcripts. R2TCMR correlated with histologic rejection although with many discrepancies, and R4late with fibrosis. R2TCMR , R3injury , and R4late correlated with liver function abnormalities. Supervised classifiers trained on histologic rejection showed less agreement with histology than unsupervised R2TCMR scores. No confirmed cases of clinical antibody-mediated rejection (ABMR) were present in the population, and strategies that previously revealed ABMR in kidney and heart transplants failed to reveal a liver ABMR phenotype. In conclusion, molecular analysis of liver transplant biopsies detects rejection, has the potential to resolve ambiguities, and could assist with immunosuppressive management.

Cell-free DNA profiling in patients with lupus nephritis.

BACKGROUND: Increased level of cell-free DNA (cf-DNA) is associated with systemic lupus erythematosus (SLE) and might be related to disease activity. The aim of this study was to evaluate whether cfDNA integrity, size distribution and concentration of different cfDNA fractions is associated with lupus activity and kidney involvement. METHODS: Blood samples were collected from 43 SLE patients and 50 healthy controls. Nuclear and mitochondrial fractions of cfDNA and intracellular DNA were quantified by real-time qPCR. Sizing and quantification of total cfDNA level was performed on Bioanalyzer. RESULTS: We determined four parameters that characterized cfDNA profile: fragmentation index, ratio of intra- to extracellular mtDNA copy number, cfDNA concentration, and presence of 54-149 bp and 209-297 bp fragments. Patients with healthy-like cfDNA profile had higher eGFR (P = 0.009) and more often no indications for kidney biopsy or less advanced lupus nephritis (LN) (P = 0.037). In contrary, SLE patients with distinct cfDNA profile (characterized by increased cfDNA concentration and fragmentation, higher discrepancy between intra- to extracellular mtDNA copy number, and the presence of 54-149 bp and 209-297 bp fragments) had lower eGFR (P = 0.005) and more often advanced LN or history of renal transplantation (P = 0.001). CONCLUSIONS: We showed that cfDNA profiling may help to distinguish SLE patients with renal involvement and severe disease course from patients with more favorable outcomes. We suggest cfDNA profile a promising SLE biomarker.

Age-Related Decline in Renal Blood Flow Could Be a Beneficial and Compensatory Mechanism.

Aging is a time-dependent process affecting all organs and tissues in the human body. The process of aging in the kidney is characterized by structural and functional changes, of which the main feature is a reduction in size, a decreased number of functioning glomeruli, and vascular changes. These changes result in functional deterioration, mainly involving a decrease in renal blood flow and the glomerular filtration rate. Additionally, impaired regulation of electrolyte and water homeostasis due to structural changes in the tubulo-interstitial system can occur. A reduced glomerular filtration rate does not necessarily result in serious clinical complications, and other selected parameters of kidney function may remain within reference value ranges in the elderly. Aging is also accompanied by decreased perfusion of other organs, including the heart and brain, which can induce more serious conditions in the elderly, including cardiac insufficiency or impairment of mental function. Thus, the decrease in renal blood flow in the aging kidney could be regarded as a compensatory mechanism to maintain perfusion of other organs and therefore, it could be also treated as being a beneficial reordering of blood-flow allocation.

Platelets level variability during the first year after liver transplantation in the risk prediction model for recipients mortality.

INTRODUCTION AND OBJECTIVES: Many scoring systems in liver diseases use static values of liver function parameters. These parameters may change significantly in liver transplant (LTx) recipients over time due to various processes. The study was aimed at building a new model for survival prediction after LTx based on variability of selected parameters. MATERIALS AND METHODS: The study included 450 LTx recipients who survived a minimum one year after transplantation. We analyzed liver enzymes and hematology parameters static values and their variability during the first year after transplantation. Modeling patients' survival was performed using Cox regression. Various sets of parameters (both static and variability and trends values) were tested to predict survival in our study group. Models' performance was measured using the concordance index. RESULTS: The single predictors of the patients survival were the static values of AST with C-index 0.706 (0.5883-0.7494), ALT 0.6102 (0.4843-0.6857) and bilirubin 0.6224 (0.5537-0.6695). High prediction scores were observed for variability in creatinine 0.6023 (0.5409-0.6451), PLT 0.6350 (0.5491-0.7043), RBC 0.5689 (0.5065-0.6213) and WBC 0.6506 (0.5095-0.7124). Our best-fitted and proposed model for patients survival after LTx has C-index 0.8273 (IQR 0.7767-0.8649). The model uses the following indicators for mortality prediction: the static value of AST, variability measure of PLT and trend measures of WBC and PLT. CONCLUSIONS: Adding variability and trend measures increases predictive accuracy in modeling patients survival after LTx. We propose a high-accuracy survival model in which variability and trend of PLT measures in the first year after transplantation are strong predictors of long-term mortality.

Biocompatibility of Hemodialysis.

This study was designed to investigate the biocompatibility of hemodialysis procedures, largely depending on the contact of patient's blood with the dialysis membranes. We addressed the issue by comparing the content of the proteolytic enzymes collagenase and cathepsin B and that of neutrophil myeloperoxidase (MPO) and C-reactive protein (CRP) in the blood before and after a single session treatment and a full course of successive 8-week-long therapies with three types of hemodialysis: low-flux (lfHD), high-flux (hfHD), and post-dilution hemodiafiltration (HDF). The study included 19 patients with chronic nephropathy. We found that collagenase significantly increased after a single session of each type of hemodialysis. Cathepsin B tended to decrease after single sessions; the decrease reached significance only after hfHD. CRP increased significantly after single hfHD and HDF treatments. These changes were meager, with no differences depending on the dialysis type, and their significance was lost after 8-week-long therapy, except the persisting increase in CRP after HDF. Neutrophil MPO apparently was not activated during any type of dialysis, as its content was below the detection threshold. We conclude that all three types of hemodialysis are compatible with the biological system, so that they would rather unlikely lead to clinically harmful effects in chronically hemodialyzed patients. Nonetheless, proteolytic enzymes and myeloperoxidase seem hardly appropriable estimators of hemodialysis biocompatibility due to meager and variable changes. Upregulation of C-reactive protein, on the other hand, expresses a general pro-inflammatory propensity of hemodialysis and is not a suitable estimator of biocompatibility either.

IL 6 but not TNF is linked to coronary artery calcification in patients with chronic kidney disease.

INTRODUCTION: Patients with chronic kidney disease (CKD) have a high risk of death mainly due to cardiovascular diseases (CVD). Early risk identification may allow interventions and prevention of fatal events. OBJECTIVES: The study aim was to assess the usefulness of selected CVD biomarkers as predictors of 5-year mortality in patients with different CKD stages. PATIENTS AND METHODS: Study included 57 CKD patients: 38 in stage 5 (ESRD), 19 in stage 3 and 4 (CKD3-4), and 19 healthy controls. Blood samples were obtained once to measure fetuin A, adiponectin, leptin, tumor necrosis factor (TNF), interleukin-6 (IL-6), metalloproteinase-9 (MMP9), intracellular-1 (ICAM1) and vascular-1 (VCAM1) adhesion molecules (ELISA or Luminex platform). Computed tomography was performed to assess the calcium score (CS). Patients were prospectively followed for 5 years to evaluate their all-cause mortality. RESULTS: Serum VCAM1, TNF and IL-6 were significantly higher in more advanced CKD stages. VCAM1 correlated significantly with ICAM1, TNF and IL-6. TNF and IL-6 were also significantly correlated with each other. No significant changes were detected for other markers. IL-6 correlated significantly with CS, age, renal function and CRP. Elevated CS and IL-6 increased over 3 times the 5-year all-cause and cardiovascular mortality risks in patients with CKD or ESRD at baseline. CONCLUSIONS: IL-6 and CS were significantly associated with 5-year risk of all-cause mortality in CKD patients. Our study suggests an involvement of chronic inflammation linked to coronary artery calcification that is likely to contribute to the cardiovascular mortality in patients with impaired renal function.

Glucose and Lipid Metabolism Abnormalities among Patients with Autosomal Dominant Polycystic Kidney Disease.

INTRODUCTION: Autosomal dominant polycystic kidney disease (ADPKD) is the most prevalent monogenic renal disease with a prevalence of 1:1,000 births and it is the 4th most common cause of dialysis-dependent end-stage renal disease (ESDR). Recent reports suggest an association between APDKD and metabolic derangements, particularly impaired glucose metabolism. METHODS: In this cross-sectional study we analyzed data obtained from case records of 189 patients with ADPKD, including kidney transplant recipients, managed in an outpatient department. RESULTS: The mean BMI was 25.4 ± 3.9; 25.25 before and 27.7 after transplan-tation. A fasting glucose level above 100 mg/dL (5.6 mmol/L) was observed in 60 patients (29%) - 27% without transplantation and 41% kidney transplant recipients. Diabetes mellitus was diagnosed in 17 patients (8.9%), including 3 (2.3%) without a history of transplantation and 14 (24.1%) after kidney transplantation (p < 0.01). We observed dyslipidemia in 30% and hyperuricemia in 53% of patients. CONCLUSION: Demonstrated metabolic abnormalities should be considered in maintenance of ADPKD patients, including kidney transplant recipients.

Protein-Bound Solute Clearance During Hemodialysis.

Indoxyl sulfate (IS) and p-cresol sulfate (p-CS) are protein-bound solutes that accumulate in the blood serum in chronic kidney disease and have a detrimental effect on the kidney and other organs' function. This study seeks to define the effectiveness of IS and p-CS clearance after single dialysis sessions and after 8-week-long cycles of hemodialysis using the following different dialysis modalities in succession: low-flux hemodialysis (lfHD), high-flux hemodialysis (hfHD), and post-dilution hemodiafiltration (HDF). We also investigated to what extent IS and p-CS serum content would associate with some other biochemical indices in patients with chronic kidney diseases. The study included 21 uremic patients. We found that a single session of each modality effectively decreased the content of both IS and p-CS, with the predominance of p-CS decrease. There were no appreciable differences depending on the modality of hemodialysis chosen. However, the leaching effect tended to wear off with the weeks' long dialysis cycles. We further found that a greater inflammation-prone level of hsCRP evoked by dialysis led to a greater removal of solutes, and thus their decrease in the serum, during a single dialysis session. Reversely, a greater protein level might result in a greater solute binding and a decrease in removal. We conclude that there are no major differences in the serum clearance of IS and p-CS depending on the dialysis modality. These protein-bound toxins are significantly cleared from the serum already during the first dialysis session, but their level tends to revert during weeks' long dialysis sessions.

Successful transplantation of kidneys from deceased donors with terminal acute kidney injury.

BACKGROUND: There are many doubts with regards to accepting deceased kidneys with acute kidney injury (AKI) for transplantation. PURPOSE: The aim of this study was to present the 5-years outcome of kidney transplantation cases where deceased donors developed AKI before organ procurement. METHODS: Two hundred twenty-six deceased renal transplants were analyzed. Data regarding donors and recipients were collected. Terminal AKI was defined as terminal serum creatinine concentration higher than 1.99 mg/dL and 66 such cases were diagnosed. All kidney transplant recipients were followed for 60 months. RESULTS: AKI group presented more episodes of delayed graft function (DGF) compared to the non-AKI group (56% vs 35%, p < .05). No differences were observed between the groups in the rate of acute rejection episodes, kidney function as well as patient and graft survival. CONCLUSIONS: Transplants with AKI present more often DGF and comparable graft survival to transplants without AKI. Kidneys with AKI can be a valuable source of organs provided attentive selection and appropriate care of deceased donors.