Increased susceptibility to structural acute kidney injury in a mouse model of presymptomatic cardiomyopathy

The early events that signal renal dysfunction in presymptomatic heart failure are unclear. We tested the hypothesis that functional and mechanistic changes occur in the kidney that precede the development of symptomatic heart failure. We employed a transgenic mouse model with cardiomyocyte-specific overexpression of mutant α-B-crystallin that develops slowly progressive cardiomyopathy. Presymptomatic transgenic mice displayed an increase in serum creatinine (1.17 ± 0.34 vs. wild type 0.65 ± 0.16 mg/dl, P < 0.05) and in urinary neutrophil gelatinase-associated lipocalin (NGAL; 278.92 ± 176.24 vs. wild type 49.11 ± 22.79 ng/ml, P < 0.05) but no renal fibrosis. Presymptomatic transgenic mouse kidneys exhibited a twofold upregulation of the Ren1 gene, marked overexpression of renin protein in the tubules, and a worsened response to ischemia-reperfusion injury based on serum creatinine (2.77 ± 0.66 in transgenic mice vs. 2.01 ± 0.58 mg/dl in wild type, P < 0.05), urine NGAL (9,198.79 ± 3,799.52 in transgenic mice vs. 3,252.94 ± 2,420.36 ng/ml in wild type, P < 0.05), tubule dilation score (3.4 ± 0.5 in transgenic mice vs. 2.6 ± 0.5 in wild type, P < 0.05), tubule cast score (3.2 ± 0.4 in transgenic mice vs. 2.5 ± 0.5 in wild type, P < 0.05), and TdT-mediated dUTP nick-end labeling (TUNEL)-positive nuclei (10.1 ± 2.1 in the transgenic group vs. 5.7 ± 1.6 per 100 cells counted in wild type, P < 0.01). Our findings indicate functional renal impairment, urinary biomarker elevations, and induction of renin gene and protein expression in the kidney that occur in early presymptomatic heart failure, which increase the susceptibility to subsequent acute kidney injury.

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MO066GASDERMIND MUTATION IS PROTECTIVE AGAINST RENAL ISCHEMIA REPERFUSION INJURY

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfaa140.mo066 ◽

2020 ◽

Vol 35 (Supplement_3) ◽

Author(s):

Natasha Rogers ◽

Jennifer Li ◽

Stephen Alexander

Keyword(s):

Bone Marrow ◽

Acute Kidney Injury ◽

Cell Death ◽

Serum Creatinine ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Kidney Injury ◽

Chimeric Mice ◽

Wild Type ◽

Donor Bone Marrow

Abstract Background and Aims Ischemia reperfusion injury (IRI) is an important contributor to acute kidney injury (AKI) and manifests as delayed graft function following kidney transplantation. Limiting the damage of IRI has implications on graft outcomes and has driven further exploration of the underlying pathophysiology. We hypothesize that pyroptosis, a pro-inflammatory form of cell death, has an important role in IRI and AKI. The pyroptosis pathway converges to the cleavage and release of N-terminal of the Gasdermin-D protein, leading to pore formation in the cell membrane and cell death. We examined the effects of Gasdermin-D mutation on inflammation in acute kidney injury. Method Male C57BL/6 mice were exposed to ethyl-N-nitrosourea mutagenesis, leading to a loss-of-function, single nucleotide polymorphism (isoleucine to asparagine mutation, I105N) in the Gasdermin-D gene. Age- and gender-matched littermate control wild-type, heterozygous and homozygous Gasdermin-DI105N mice were subjected to bilateral renal IRI (36°C, 22mins) and sacrificed 24-hours post-reperfusion for analysis of renal function, histology and biomolecular phenotyping. To delineate if the GasderminD mutation in renal parenchymal or hematopoietic cells were key drivers of IRI, we generated chimeric mice with whole body irradiation and infusion of syngeneic donor bone marrow. Following 8 weeks of engraftment, bilateral renal IRI was performed with analysis at 24 h reperfusion. Results Homozygote and heterozygote Gasdermin-DI105N mice were protected from renal IRI in a gene dose-dependent manner when compared to wild-type, with lower mean serum creatinine (15.7, 48.1 and 85.5µmol/L respectively, p<0.001), less histological tubular injury and cell death (1.8, 3.6 and 5.1 TUNEL+ cells/hpf, p<0.01) and significantly decreased expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, RANTES). Homozygote GasderminDI105N chimeric mice (reconstituted with wild-type donor bone marrow) were more susceptible to IRI, and serum creatinine was similar to that of wild-type chimeric control mice, indicating that hematopoietic cells rather than parenchymal cells, are likely predominant drivers of injury. Similarly, adoptive transfer of CpG-activated CD11c+ dendritic cells into homozygous Gasdermin-DI105N mice augmented renal injury compared to GpC-treated cells. Conclusion GasderminDI105N mice were protected from IRI and demonstrates the importance of the pyroptosis pathway on acute kidney injury. Manipulation of GasderminD is potentially an attractive target to mitigate inflammation and cellular death following injury.

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Comparison of In-Hospital Outcomes Between Patients With or Without Acute Kidney Injury Developed After Hospitalization Following Acute Coronary Syndrome

University Heart Journal ◽

10.3329/uhj.v16i1.44815 ◽

2020 ◽

Vol 16 (1) ◽

pp. 3-10

Author(s):

Md Sajjad Safi ◽

Msi Tipu Chowdhury ◽

Tanjima Parvin ◽

Khurshed Ahmed ◽

Md Ashraf Uddin Sultana ◽

...

Keyword(s):

Heart Failure ◽

Acute Kidney Injury ◽

Serum Creatinine ◽

Cardiogenic Shock ◽

Hospital Stay ◽

Kidney Injury ◽

Duration Of Hospital Stay ◽

Group A ◽

Hospital Stays ◽

Group B

Background: Acute Kidney Injury (AKI), a common complication of acute coronary syndromes (ACS), is associated with higher mortality and longer hospital stays. ACS patients with renal impairment during hospitalization are associated with adverse in-hospital outcomes in the form of heart failure, cardiogenic shock, arrhythmia, dialysis requirement and mortality. Objective: To compare the in-hospital adverse outcomesof patients with ACS with or without AKI. Materials and Methods: This prospective comparative study was conducted in the Department of Cardiology, BSMMU, Dhaka, during the period of August 2017 to July 2018. A total of 70 eligible patients were included in this study of which 35 patients were included in group A (ACS with AKI) and 35 patients were included in group B (ACS without AKI). AKI was diagnosed, on the basis of increased serum creatinine level 0.3mg/dL from baseline within 48 hours after hospitalization. They were subjected to electrocardiography, blood test for serum creatinine (on admission, 12 hours, 48 hours and at the time of discharge), lipid profile, 2-D echocardiography along with serum troponin, CK MB and electrolytes. Results: It was observed that mean age was 58.0±8.5 years in group A and 55.6±12.3 years in group B. Heart failure was more common in group A than in Group B (74.3% vs 34.2% p=0.001 respectively) and arrhythmia was more common in group A than in Group B (100% vs 74.2% respectively). 7(20%) patients of group A required dialysis. The mean duration of hospital stay was significantly higher in Group A than in the Group B (9.4±2.3 vs 7.2±0.6; p=0.001) days. Multiple logistic regression analysis revealed that heart failure, cardiogenic shock, duration of hospital stay were found to be the independently significant predictors of outcome of the patients with AKI with odds ratio being 5.53 (p=0.001), 4.353 (p=0.001) and 6.92 (p=0.001) Conclusion: This study shows that, heart failure, cardiogenic shock, arrhythmia, dialysis requirement, were more common in the patients with AKI (group A) than in the patients without AKI (group B). The duration of hospital stays were longer in patients with AKI (group A) than in the patients without AKI (group B). Therefore, an important research target is the identification of high-risk patients with ACS experiencing AKI, thereby appropriate medication and follow-up should be implemented. University Heart Journal Vol. 16, No. 1, Jan 2020; 3-10

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A mouse model of Townes-Brocks syndrome expressing a truncated mutant Sall1 protein is protected from acute kidney injury

AJP Renal Physiology ◽

10.1152/ajprenal.00222.2015 ◽

2015 ◽

Vol 309 (10) ◽

pp. F852-F863 ◽

Cited By ~ 4

Author(s):

Sara Hirsch ◽

Tarek El-Achkar ◽

Lynn Robbins ◽

Jeannine Basta ◽

Monique Heitmeier ◽

...

Keyword(s):

Acute Kidney Injury ◽

Mouse Model ◽

Congenital Anomalies ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Kidney Injury ◽

Acute Injury ◽

Null Alleles ◽

Heme Oxygenase 1 ◽

Adult Kidney

It has been postulated that developmental pathways are reutilized during repair and regeneration after injury, but functional analysis of many genes required for kidney formation has not been performed in the adult organ. Mutations in SALL1 cause Townes-Brocks syndrome (TBS) and nonsyndromic congenital anomalies of the kidney and urinary tract, both of which lead to childhood kidney failure. Sall1 is a transcriptional regulator that is expressed in renal progenitor cells and developing nephrons in the embryo. However, its role in the adult kidney has not been investigated. Using a mouse model of TBS ( Sall1 TBS), we investigated the role of Sall1 in response to acute kidney injury. Our studies revealed that Sall1 is expressed in terminally differentiated renal epithelia, including the S3 segment of the proximal tubule, in the mature kidney. Sall1 TBS mice exhibited significant protection from ischemia-reperfusion injury and aristolochic acid-induced nephrotoxicity. This protection from acute injury is seen despite the presence of slowly progressive chronic kidney disease in Sall1 TBS mice. Mice containing null alleles of Sall1 are not protected from acute kidney injury, indicating that expression of a truncated mutant protein from the Sall1 TBS allele, while causative of congenital anomalies, protects the adult kidney from injury. Our studies further revealed that basal levels of the preconditioning factor heme oxygenase-1 are elevated in Sall1 TBS kidneys, suggesting a mechanism for the relative resistance to injury in this model. Together, these studies establish a functional role for Sall1 in the response of the adult kidney to acute injury.

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Human amniotic epithelial cells ameliorate kidney damage in ischemia-reperfusion mouse model of acute kidney injury

Stem Cell Research & Therapy ◽

10.1186/s13287-020-01917-y ◽

2020 ◽

Vol 11 (1) ◽

Cited By ~ 1

Author(s):

Yifei Ren ◽

Ying Chen ◽

Xizi Zheng ◽

Hui Wang ◽

Xin Kang ◽

...

Keyword(s):

Bone Marrow ◽

Acute Kidney Injury ◽

Renal Function ◽

Mouse Model ◽

Reperfusion Injury ◽

Ischemia Reperfusion ◽

Kidney Injury ◽

Mouse Bone Marrow ◽

Tissue Integration

Abstract Background Acute kidney injury (AKI) is a common clinical disease with complex pathophysiology and limited therapeutic choices. This prompts the need for novel therapy targeting multiple aspects of this disease. Human amnion epithelial cell (hAEC) is an ideal stem cell source. Increasing evidence suggests that exosomes may act as critical cell–cell communicators. Accordingly, we assessed the therapeutic potential of hAECs and their derived exosomes (hAECs-EXO) in ischemia reperfusion mouse model of AKI and explored the underlying mechanisms. Methods The hAECs were primary cultured, and hAECs-EXO were isolated and characterized. An ischemic-reperfusion injury-induced AKI (IRI-AKI) mouse model was established to mimic clinical ischemic kidney injury with different disease severity. Mouse blood creatinine level was used to assess renal function, and kidney specimens were processed to detect cell proliferation, apoptosis, and capillary density. Macrophage infiltration was analyzed by flow cytometry. hAEC-derived exosomes (hAECs-EXO) were used to treat hypoxia-reoxygenation (H/R) injured HK-2 cells and mouse bone marrow-derived macrophages to evaluate their protective effect in vitro. Furthermore, hAECs-EXO were subjected to liquid chromatography-tandem mass spectrometry for proteomic profiling. Results We found that systematically administered hAECs could improve mortality and renal function in IRI-AKI mice, decrease the number of apoptotic cells, prevent peritubular capillary loss, and modulate kidney local immune response. However, hAECs showed very low kidney tissue integration. Exosomes isolated from hAECs recapitulated the renal protective effects of their source cells. In vitro, hAECs-EXO protected HK-2 cells from H/R injury-induced apoptosis and promoted bone marrow-derived macrophage polarization toward M2 phenotype. Proteomic analysis on hAECs-EXO revealed proteins involved in extracellular matrix organization, growth factor signaling pathways, cytokine production, and immunomodulation. These findings demonstrated that paracrine of exosomes might be the key mechanism of hAECs in alleviating renal ischemia reperfusion injury. Conclusions We reported hAECs could improve survival and ameliorate renal injury in mice with IRI-AKI. The anti-apoptotic, pro-angiogenetic, and immunomodulatory capabilities of hAECs are at least partially, through paracrine pathways. hAECs-EXO might be a promising clinical therapeutic tool, overcoming the weaknesses and risks associated with the use of native stem cells, for patients with AKI.

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Concordant Changes of Plasma and Kidney MicroRNA in the Early Stages of Acute Kidney Injury: Time Course in a Mouse Model of Bilateral Renal Ischemia-Reperfusion

PLoS ONE ◽

10.1371/journal.pone.0093297 ◽

2014 ◽

Vol 9 (4) ◽

pp. e93297 ◽

Cited By ~ 29

Author(s):

Melissa A. Bellinger ◽

James S. Bean ◽

Melissa A. Rader ◽

Kathleen M. Heinz-Taheny ◽

Jairo S. Nunes ◽

...

Keyword(s):

Acute Kidney Injury ◽

Mouse Model ◽

Time Course ◽

Ischemia Reperfusion ◽

Kidney Injury ◽

Renal Ischemia ◽

Early Stages

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The Efficacy of Cinnamon Extract ( Cinnamomum burmannii ) on Reducing Staging Acute Kidney Injury in Ischemia Reperfusion (IR) Model

BioScientia Medicina ◽

10.32539/bsm.v5i1.203 ◽

2020 ◽

Vol 5 (1) ◽

pp. 178-181

Author(s):

Evi Lusiana ◽

Nia Savitri Tamzil ◽

Desi Oktarina

Keyword(s):

Acute Kidney Injury ◽

Serum Creatinine ◽

Filtration Rate ◽

Ischemia Reperfusion ◽

Kidney Injury ◽

Sham Operation ◽

Cinnamon Extract ◽

Model Method ◽

Before And After ◽

Cinnamomum Burmannii

A B S T R A C TIntroduction. Acute kidney injury (AKI) is defined as sudden decline in theglomerular filtration rate, resulting in the retention of nitrogenous wastes, such asurea and creatinine in plasma. Cinnamomum burmannii is known as a anti-inflammatory renoprotective agent, although the precise mechanism is not wellunderstood. This study aimed to elucidate the effectiveness of Cinnamomumburmannii extract in decreasing creatinine level of acute kidney injury Ischemiareperfusion (IR) model. Method. We performed Ischemia reperfusion (IR) in maleWistar rat to induce acute kidney injury. The rat (n=30) were divided into six groups:IR, 1 group treated with methylprednisolone as a control (IR+M), 3 groups treatedwith different oral Cinnamomum burmannii extract doses (50mg/kg (IR+EKM1),100mg/kg (IR+EKM2), and 200 mg/kg (IR+EKM3), and a Sham operation (SO)group. AKI stage reduction based on serum creatinine levels, before and aftermodeling, before and after the cinnamon extract intervention. Creatinine levels werequntified by spectrophotometry and analyzed by SPSS. Result. Cinnamomumburmannii extract lowers creatinine levels; significant (P <0.05). 200 mg / kgbb isthe effective dose of lowering creatinine levels in the IR model. Conclusion.Cinnamomum burmannii extract reduced serum creatinine levels associated withdecreased acute renal staging in the IR model.

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Human amniotic epithelial cells improve kidney repair in ischemia-reperfusion mouse model of acute kidney injury

10.21203/rs.3.rs-28766/v1 ◽

2020 ◽

Author(s):

Yifei Ren ◽

Ying Chen ◽

Xizi Zheng ◽

Hui Wang ◽

Xin Kang ◽

...

Keyword(s):

Bone Marrow ◽

Acute Kidney Injury ◽

Renal Function ◽

Epithelial Cells ◽

Mouse Model ◽

Ischemia Reperfusion ◽

Kidney Injury ◽

Mouse Bone Marrow ◽

Tissue Integration

Abstract Background: Acute kidney injury (AKI) is a common clinical disease with complex pathophysiology and very limited therapeutic choices. This prompts the need for novel therapy targeting multiple aspects of this disease. Human amnion epithelial cells (hAECs) are ideal alternative stem cell source for regenerative medicine. Increasing evidence suggests that hAEC-derived exosomes (hAECs-EXO) may act as novel cell–cell communicators. Accordingly, we assessed the therapeutic potential of hAECs in ischemia reperfusion mouse model of AKI and explored the underlying mechanisms.Methods: The hAECs were primary cultured and hAECs-EXO were isolated and characterized. An ischemic renal injury mouse model was established to mimic different severity of the kidney injury. Mouse blood creatinine level was used to assess renal function and kidney specimens were processed to detect cell proliferation, apoptosis and angiogenesis. Immune cells infiltration was analyzed by flow cytometry. hAECs-EXO was used to treat hypoxia-reoxygenation (H/R) injured HK2 cells and mouse bone marrow-derived macrophages to evaluate their protective effect in vitro. Furthermore, hAEC exosomes were subjected to liquid chromatography-tandem mass spectrometry for proteomic profiling. Results: We found that systematically administered hAECs could improve mortality and renal function in IRI mice; decrease the number of apoptotic cells; promote peritubular capillary regeneration and modulate kidney local immune response. However, hAECs showed very low kidney tissue integration. Exosomes isolated from hAECs recapitulated the renal protective effects of their parent cells. In vitro, hAECs-EXO protected HK-2 cells from H/R injury-induced apoptosis and promoted bone marrow-derived macrophage polarization toward M2 phenotype. Proteomic analysis on hAECs-EXO revealed proteins involved in extracellular matrix organization, growth factor signaling pathways, cytokine production and immunomodulation. These findings demonstrated that paracrine of exosomes might be a key mechanism by hAECs mediating kidney functional recovery in AKI.Conclusions: We first reported hAECs could improve mortality and renal repair in mice with ischemia-reperfusion injury. The anti-apoptotic, pro-angiogenetic, and immunomodulatory capabilities of hAECs at least partially, through paracrine pathways. The renoprotective effects of hAECs-EXO might be a promising clinical therapeutic tool, overcoming the weaknesses and risks associated with the use of native stem cells for patients with AKI.

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MO331LINEAGE TRACING OF REGENERATING PROXIMAL TUBULE CELLS (STC) BY SINGLE CELL PROFILING IN ACUTE KIDNEY INJURY

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfab084.004 ◽

2021 ◽

Vol 36 (Supplement_1) ◽

Author(s):

Eleni Stamellou ◽

Mingbo Cheng ◽

Viktor Sterzer ◽

Katja Leuchtle ◽

Thiago Strieder ◽

...

Keyword(s):

Acute Kidney Injury ◽

Proximal Tubule ◽

Single Cell ◽

Transgenic Mouse ◽

Ischemia Reperfusion ◽

Expression Patterns ◽

Kidney Injury ◽

Multiple Time ◽

Proximal Tubule Cells ◽

Tubule Cells

Abstract Background and Aims Acute tubular injury accounts for the most common intrinsic cause for acute kidney injury (AKI). The scattered tubular cell (STC) phenotype was discovered as a uniform reaction of tubule cells triggered by injury. Our group was the first to identify an inducible transgenic mouse (PEC-rtTA-mouse) specifically labeling STCs with eGFP. Analysis of the transcriptional factors and associated signaling pathways might reveal the function and role of STCs in AKI. Method Here, we performed single-cell RNA sequencing of unilateral ischemia-reperfusion murine model of AKI 8, 24, 48 hours and 6 and 12 days after AKI induction. Results Genes expressing proximal tubular proteins and transporters were markedly downregulated during transition into the STC phenotype upon injury; but expression recovered over time and upon resolution and tubular cells re-differentiated into proximal tubule cells. This provides evidence for the first time that the STC phenotype is a transient and reversible phenotype triggered by injury. Among cells in the STC phenotype, we could identify 2 sub-clusters; a highly proliferating sub-cluster that in the cell cycle analysis showed the highest proportion of cycling cells. The second eGFP-positive cluster appeared very early after AKI and expressed a distinct set of genes (defined by 7 anchor genes). Some of the highly up-regulated genes are known markers of STCs hence confirming the specificity of our transgenic mouse line. Conclusion Our study provides gene expression patterns specifically in STCs upon injury and repair at multiple time points and suggests that the STC phenotype is a transient and reversible phenotype triggered by injury.

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Netrin-1 and kidney injury. II. Netrin-1 is an early biomarker of acute kidney injury

AJP Renal Physiology ◽

10.1152/ajprenal.00507.2007 ◽

2008 ◽

Vol 294 (4) ◽

pp. F731-F738 ◽

Cited By ~ 78

Author(s):

W. Brian Reeves ◽

Osun Kwon ◽

Ganesan Ramesh

Keyword(s):

Acute Kidney Injury ◽

Folic Acid ◽

Serum Creatinine ◽

Renal Injury ◽

Ischemia Reperfusion ◽

Kidney Injury ◽

Peak Level ◽

Urine Samples ◽

Mortality And Morbidity ◽

Early Biomarker

Acute kidney injury is an important complication in hospitalized patients often diagnosed late and associated with high mortality and morbidity. Although biomarkers for nephrotoxicity are available, they often lack sensitivity and specificity for detecting tubular injury. Netrin-1 is a laminin-like molecule highly expressed in many organs including kidney. To determine the value of netrin-1 as a biomarker of renal injury, we analyzed its urinary excretion following ischemia-reperfusion-, cisplatin-, folic acid-, and endotoxin-induced renal injury in mice. Urinary netrin-1 levels increased markedly within 3 h of ischemia-reperfusion (40 ± 14-fold, P < 0.01 vs. baseline), reached a peak level at 6 h, and decreased thereafter, returning to near baseline by 72 h. Serum creatinine significantly increased only after 24 h of reperfusion. Similarly, in cisplatin-, folic acid-, and lipopolysaccharide-treated mice, urine netrin-1 excretion increased as early as 1 h and reached a peak level at 6 h after injection. However, serum creatinine was raised significantly after 6, 24, and 72 h after folic acid, lipopolysaccharide, and cisplatin administration, respectively. NGAL excretion in folic acid- and lipopolysaccharide-treated mice urine samples could only be detected by 24 h after drug administration. Furthermore, urinary netrin-1 excretion increased dramatically in 13 acute renal failure patients, whereas none was detected in 6 healthy volunteer urine samples. Immunohistochemical localization showed that netrin-1 is highly expressed in tubular epithelial cells in transplanted human kidney. We conclude that urinary netrin-1 is a promising early biomarker of renal injury.

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Heart failure and contrast-induced acute kidney injury in patients with coronary artery disease

Consilium Medicum ◽

10.26442/20751753.2020.10.200352 ◽

2020 ◽

Vol 22 (10) ◽

pp. 61-63

Author(s):

Olga Iu. Mironova ◽

◽

Olga A. Sivakova ◽

Aleksandr D. Deev ◽

Viktor V. Fomin ◽

...

Keyword(s):

Heart Failure ◽

Coronary Artery Disease ◽

Acute Kidney Injury ◽

Coronary Artery ◽

Serum Creatinine ◽

Contrast Media ◽

Kidney Injury ◽

Baseline Serum ◽

Artery Disease ◽

Contrast Media Administration

Aim. To assess the influence of heart failure on the risk of contrast-induced acute kidney injury (CI-AKI) in patients with stable coronary artery disease (CAD) with indications to diagnostic procedures requiring intra-arterial administration of contrast media. Materials and methods. 1023 patients, who were receiving optimal medical therapy and had indications to coronary angiography and possible coronary angio-plasty, with stable CAD were included in the study. We conducted an observational open prospective cohort study, which was registered in clinicaltrials.gov with ID NCT04014153. CI-AKI was defined as 25% or more increase of baseline serum creatinine, or more than 0.5 mg/dl and was assessed 48 hours after contrast media administration. The primary endpoint was the CI-AKI development according to KDIGO criteria. Most of the patients, included in the study, were males aged 66.3±10 years with arterial hypertension and overweight (BMI 29.14±5 kg/m2). Results. The study included 1023 patients, 76 suffered from heart failure. The rate of CI-AKI in this group was 13.2% (10 patients). The rate of CI-AKI using the absolute creatinine rise definition was 4% cases (3 cases). Conclusion. Female patients suffering from heart failure with higher levels of serum creatinine and low glomerular filtration rate need more attention, less amount of contrast and adequate preventive measures before contrast media administration in order to lower the risk of CI-AKI development.

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