Urine Biomarkers of Kidney Tubule Health, Injury, and Inflammation are Associated with Progression of CKD in Children

2021 ◽  
pp. ASN.2021010094
Author(s):  
Jason H. Greenberg ◽  
Alison G. Abraham ◽  
Yunwen Xu ◽  
Jeffrey R. Schelling ◽  
Harold I. Feldman ◽  
...  
Keyword(s):  
Kidney Injury ◽  
Ckd Progression ◽  
Creatinine Concentration ◽  
Clinical Model ◽  
Content Type ◽  
Monocyte Chemoattractant Protein 1 ◽  
Urine Biomarkers ◽  
Urine Creatinine ◽  
Kidney Injury Molecule 1

BackgroundNovel urine biomarkers may improve identification of children at greater risk of rapid kidney function decline, and elucidate the pathophysiology of CKD progression.MethodsWe investigated the relationship between urine biomarkers of kidney tubular health (EGF and α-1 microglobulin), tubular injury (kidney injury molecule-1; KIM-1), and inflammation (monocyte chemoattractant protein-1 [MCP-1] and YKL-40) and CKD progression. The prospective CKD in Children Study enrolled children aged 6 months to 16 years with an eGFR of 30–90ml/min per 1.73m2. Urine biomarkers were assayed a median of 5 months [IQR: 4–7] after study enrollment. We indexed the biomarker to urine creatinine by dividing the urine biomarker concentration by the urine creatinine concentration to account for the concentration of the urine. The primary outcome was CKD progression (a composite of a 50% decline in eGFR or kidney failure) during the follow-up period.ResultsOverall, 252 of 665 children (38%) reached the composite outcome over a median follow-up of 6.5 years. After adjustment for covariates, children with urine EGF concentrations in the lowest quartile were at a seven-fold higher risk of CKD progression versus those with concentrations in the highest quartile (fully adjusted hazard ratio [aHR], 7.1; 95% confidence interval [95% CI], 3.9 to 20.0). Children with urine KIM-1, MCP-1, and α-1 microglobulin concentrations in the highest quartile were also at significantly higher risk of CKD progression versus those with biomarker concentrations in the lowest quartile. Addition of the five biomarkers to a clinical model increased the discrimination and reclassification for CKD progression.ConclusionsAfter multivariable adjustment, a lower urine EGF concentration and higher urine KIM-1, MCP-1, and α-1 microglobulin concentrations were each associated with CKD progression in children.

Kidney tubule health, mineral metabolism, and adverse events in persons with CKD in SPRINT

2021 ◽  
Author(s):  
Simon B Ascher ◽  
Rebecca Scherzer ◽  
Michelle M Estrella ◽  
Jarett D Berry ◽  
James A de Lemos ◽  
...  
Keyword(s):  
Adverse Events ◽  
Proportional Hazards ◽  
Mineral Metabolism ◽  
Fibroblast Growth Factor 23 ◽  
Kidney Injury ◽  
Cox Proportional Hazards ◽  
Hypertension Treatment ◽  
Kidney Tubule ◽  
Monocyte Chemoattractant Protein 1 ◽  
Kidney Injury Molecule 1

Abstract Background Measures of kidney tubule health are risk markers for acute kidney injury (AKI) in persons with chronic kidney disease (CKD) during hypertension treatment, but their associations with other adverse events (AEs) are unknown. Methods Among 2,377 Systolic Blood Pressure Intervention Trial (SPRINT) participants with CKD, we measured at baseline eight urine biomarkers of kidney tubule health and two serum biomarkers of mineral metabolism pathways that act on the kidney tubules. Cox proportional hazards models were used to evaluate biomarker associations with risk of a composite of pre-specified serious AEs (hypotension, syncope, electrolyte abnormalities, AKI, bradycardia, and injurious falls) and outpatient AEs (hyperkalemia and hypokalemia). Results At baseline, the mean age was 73 ±9 years and mean eGFR was 46 ±11 ml/min/1.73m2. During a median follow-up of 3.8 years, 716 (30%) participants experienced the composite AE. Higher urine interleukin-18, kidney injury molecule-1, neutrophil gelatinase-associated lipocalin (NGAL), and monocyte chemoattractant protein-1 (MCP-1), lower urine uromodulin (UMOD), and higher serum fibroblast growth factor-23 were individually associated with higher risk of the composite AE outcome in multivariable-adjusted models including eGFR and albuminuria. When modeling biomarkers in combination, higher NGAL (HR: 1.08 per 2-fold higher biomarker level, 95% CI: 1.03, 1.13), higher MCP-1 (HR: 1.11, 95% CI: 1.03, 1.19), and lower UMOD (HR: 0.91, 95% CI: 0.85, 0.97) were each associated with higher composite AE risk. Biomarker associations did not vary by intervention arm (P >0.10 for all interactions). Conclusions Among persons with CKD, several kidney tubule biomarkers are associated with higher risk of AEs during hypertension treatment, independent of eGFR and albuminuria.

scholarly journals HMOX1 and Acute Kidney Injury in Sickle Cell Anemia

Blood ◽  
2017 ◽  
Vol 130 (Suppl_1) ◽  
pp. 686-686
Author(s):  
Santosh L. Saraf ◽  
Maya Viner ◽  
Ariel Rischall ◽  
Binal Shah ◽  
Xu Zhang ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Risk Factor ◽  
Kidney Disease ◽  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Kidney Injury ◽  
Ckd Progression ◽  
Kdigo Guidelines

Abstract Acute kidney injury (AKI) is associated with tubulointerstitial fibrosis and nephron loss and may lead to an increased risk for subsequently developing chronic kidney disease (CKD). In adults with sickle cell anemia (SCA), high rates of CKD have been consistently observed, although the incidence and risk factors for AKI are less clear. We evaluated the incidence of AKI, defined according to Kidney Disease Improving Global Outcomes (KDIGO) guidelines as a rise in serum creatinine by ≥0.3mg/dL within 48 hours or ≥1.5 times baseline within seven days, in 158 of 299 adult SCA patients enrolled in a longitudinal cohort from the University of Illinois at Chicago. These patients were selected based on the availability of genotyping for α-thalassemia, BCL11A rs1427407, APOL1 G1/G2, and the HMOX1 rs743811 and GT-repeat variants. Median values and interquartile range (IQR) are provided. With a median follow up time of 66 months (IQR, 51-74 months), 137 AKI events were observed in 63 (40%) SCA patients. AKI was most commonly observed in the following settings: acute chest syndrome (25%), an uncomplicated vaso-occlusive crisis (VOC)(24%), a VOC with pre-renal azotemia determined by a fractional excretion of sodium <1% or BUN-to-creatinine ratio >20:1 (14%), or a VOC with increased hemolysis, defined as an increase in serum LDH or indirect bilirubin level >1.5 times over the baseline value at the time of enrollment (12%). Compared to individuals who did not develop AKI, SCA adults who developed an AKI event were older (AKI: median and IQR age of 35 (26-46) years, no AKI: 28 (23 - 26) years; P=0.01) and had a lower estimated glomerular filtration rate (eGFR) (AKI: median and IQR eGFR of 123 (88-150) mL/min/1.73m2, no AKI: 141 (118-154) mL/min/1.73m2; P=0.02) by the Kruskal-Wallis test at the time of enrollment. We evaluated the association of a panel of candidate gene variants with the risk of developing an AKI event. These included loci related to the degree of hemolysis (α-thalassemia, BCL11A rs1427407), to chronic kidney disease (APOL1 G1/G2 risk variants), and to heme metabolism (HMOX1) . Using a logistic regression model that adjusted for age and eGFR at the time of enrollment, the risk of an AKI event was associated with older age (10-year OR 2.6, 95%CI 1.4-4.8, P=0.002), HMOX1 rs743811 (OR 3.1, 95%CI 1.1-8.7, P=0.03), and long HMOX1 GT-repeats, defined as >25 repeats (OR 2.5, 95%CI 1.01-6.1, P=0.04). Next, we assessed whether AKI is associated with a more rapid decline in eGFR and with CKD progression, defined as a 50% reduction in eGFR, on longitudinal follow up. Using a mixed effects model that adjusted for age and eGFR at the time of enrollment, the rate of eGFR decline was significantly greater in those with an AKI event (β = -0.51) vs. no AKI event (β = -0.16) (P=0.03). With a median follow up time of 66 months (IQR, 51-74 months), CKD progression was observed in 21% (13/61) of SCA patients with an AKI event versus 9% (8/88) without an AKI event. After adjusting for age and eGFR at the time of enrollment, the severity of an AKI event according to KDIGO guidelines (stage 1 if serum creatinine rises 1.5-1.9 times baseline, stage 2 if the rise is 2.0-2.9 times baseline, and stage 3 if the rise is ≥3 times baseline or ≥4.0 mg/dL or requires renal replacement therapy) was a risk factor for CKD progression (unadjusted HR 1.6, 95%CI 1.1-2.3, P=0.02; age- and eGFR-adjusted HR 1.6, 95%CI 1.1-2.5, P=0.03). In conclusion, AKI is commonly observed in adults with sickle cell anemia and is associated with increasing age and the HMOX1 GT-repeat and rs743811 polymorphisms. Furthermore, AKI may be associated with a steeper decline in kidney function and more severe AKI events may be a risk factor for subsequent CKD progression in SCA. Future studies understanding the mechanisms, consequences of AKI on long-term kidney function, and therapies to prevent AKI in SCA are warranted. Disclosures Gordeuk: Emmaus Life Sciences: Consultancy.

Abstract 15934: Higher Midlife Serum Levels of Kidney-injury Molecule-1 (KIM-1) are Associated With Incident Fatal CHD Over Very Long-term Follow-up Among Men

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Rachel H Mackey ◽  
Greg G Grandits ◽  
Lewis H Kuller ◽  
Joel Estis ◽  
John A Todd ◽  
...  
Keyword(s):  
Risk Factor ◽  
Limit Of Detection ◽  
Kidney Injury ◽  
Multiple Risk Factor ◽  
Serum Samples ◽  
Increased Risk ◽  
Long Term Follow Up ◽  
Kidney Injury Molecule 1

Introduction: Higher levels of kidney-injury molecule-1 (KIM-1) measured in urine are associated with presence and progression of acute renal disease. A recent study reported similar results for KIM-1 measured in blood. Hypothesis: We hypothesized that KIM-1 measured in stored serum from middle-aged men who participated in the Multiple Risk Factor Intervention Trial (MRFIT) would differentiate very long-term risk of fatal CHD vs. survival to a mean age of 80 over approximately 30 year follow-up. Methods: We conducted a nested case-control study within MRFIT, which in 1973-76 randomized 12,866 high risk but CVD free men ages 35-57 to risk factor intervention vs. usual care. Serum samples were collected at baseline and stored for future use. The trial concluded in 1982 but long-term mortality follow-up was ascertained through 2005 using the National Death Index. From MRFIT participants with stored serum from baseline, we sampled 100 men who died of CHD (mean age 47.3 at baseline and 73.9 at death), and 100 men who survived to 2005 (mean age =48.4 at baseline and 80.1 in 2005.) KIM-1 was assayed from stored serum samples using high sensitivity single-molecule counting technology (Erenna ® Immunoassay System, Singulex), with limit of detection (LoD)=0.5 pg/ml, and lower limit of quantification (LLoQ)=2.0 pg/ml. Results were compared between cases and controls using Wilcoxon rank tests and logistic regression. Results: Inter-assay %CVs were 8%. Median KIM-1 was higher for smokers vs. non-smokers and for men with vs. without hypertension, but was not associated with high cholesterol. KIM-1 was significantly higher in cases (183 pg/ml (IQR: 137-239) versus controls, (161 pg/ml (IQR:109-212), p=0.03; OR (95%CI)for Q4 versus Q1 was 2.26 (1.02 - 5.02) Adjusted for age and smoking the OR(95%CI) of fatal CHD for Q4 vs. Q1 was 2.34 (1.02- 5.37), and further adjusted for diastolic BP and serum cholesterol at baseline, was 2.0 (95% CI: 0.8-4.7). Conclusions: Higher serum KIM-1 levels at midlife were associated with a ∼2-fold increased risk of fatal CHD vs. survival over ∼30 years of follow-up. This is the first report of a longitudinal association of circulating KIM-1 levels with fatal CHD in long-term follow-up.

scholarly journals P0599THE LYSOSOMAL URINE ENZYMES ACTIVITY IN CHILDREN AFTER ACUTE KIDNEY INJURI

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Olga Lavrenchuk ◽  
Lesya Korol ◽  
Ludmila Migal ◽  
Ingretta Bagdasarova
Keyword(s):  
Enzyme Activity ◽  
Kidney Disease ◽  
Lysosomal Enzymes ◽  
Reference Group ◽  
Kidney Injury ◽  
Activity Levels ◽  
Healthy Children ◽  
Ckd Progression ◽  
One Year

Abstract Background and Aims The urgency of the problem of acute kidney injury (AKI) in children is due to the high risk of chronic kidney disease (CKD) as an outcome. Lysosomal enzymes in urine are considered to be informative markers of renal parenchyma damage. The aim of study was to determine the activity of lysosomal enzymes β-galactosidase (GAL) and N-acetyl-β-D-glucosamynidase (NAG) in urine as markers of CKD progression in children after AKI. Method 41 children were examined after AKI with achieving self-diuresis and clinical improvement. The functional state of the kidneys was evaluated by the glomerular filtration rate (Schwartz GFR), the level of albuminuria. Urine enzyme activity was determined and cross-linked to mmol urinary creatinine. The control (reference) group consisted of 28 children who were conditionally healthy, without kidney disease. Results The NAG activity was 8 times higher level than in the reference group of healthy children (87/46;193 vs. 15/11;18, p<0.001), and GAL was elevated in 3 times either (34/22;45 vs. 10/6;13, p<0.001) in patients with a disease period of up to 2 years after AKI. In patients with follow-up period 2 or more years enzyme activity levels decreased, but remained 4 times higher (NAG: 49/31;109, p <0.001 compared to control; GAL: 35/25;44, p <0.001 compared to control). The high levels of enzyme activity was documented in 73.2% of patients after one year of follow up, but the GFR decrease was found in 22.0%, and albuminuria - only in 34.1%. Conclusion The urine activity of NAG and GAL in children is an informative marker for diagnosing recovery after AKI or CKD progression with renal function decline. This method is non-invasive, inexpensive, and simple to conduct.

scholarly journals Postangiography Increases in Serum Creatinine and Biomarkers of Injury and Repair

2020 ◽  
Vol 15 (9) ◽  
pp. 1240-1250 ◽  
Author(s):  
Caroline Liu ◽  
Maria K. Mor ◽  
Paul M. Palevsky ◽  
James S. Kaufman ◽  
Heather Thiessen Philbrook ◽  
...  
Keyword(s):  
Serum Creatinine ◽  
Kidney Injury ◽  
Tubular Damage ◽  
Serious Adverse Events ◽  
Monocyte Chemoattractant Protein 1 ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Iodinated Contrast ◽  
Injury And Repair ◽  
Kidney Injury Molecule 1 ◽  
Major Adverse Kidney Events

Background and objectivesIt is unknown whether iodinated contrast causes kidney parenchymal damage. Biomarkers that are more specific to nephron injury than serum creatinine may provide insight into whether contrast-associated AKI reflects tubular damage. We assessed the association between biomarker changes after contrast angiography with contrast-associated AKI and 90-day major adverse kidney events and death.Design, setting, participants, & measurementsWe conducted a longitudinal analysis of participants from the biomarker substudy of the Prevention of Serious Adverse Events following Angiography trial. We measured injury (kidney injury molecule-1, neutrophil gelatinase-associated lipocalin, IL-18) and repair (monocyte chemoattractant protein-1, uromodulin, YKL-40) proteins from plasma and urine samples at baseline and 2–4 hours postangiography. We assessed the associations between absolute changes and relative ratios of biomarkers with contrast-associated AKI and 90-day major adverse kidney events and death.ResultsParticipants (n=922) were predominately men (97%) with diabetes (82%). Mean age was 70±8 years, and eGFR was 48±13 ml/min per 1.73 m2; 73 (8%) and 60 (7%) participants experienced contrast-associated AKI and 90-day major adverse kidney events and death, respectively. No postangiography urine biomarkers were associated with contrast-associated AKI. Postangiography plasma kidney injury molecule-1 and IL-18 were significantly higher in participants with contrast-associated AKI compared with those who did not develop contrast-associated AKI: 428 (248, 745) versus 306 (179, 567) mg/dl; P=0.04 and 325 (247, 422) versus 280 (212, 366) mg/dl; P=0.009, respectively. The majority of patients did not experience an increase in urine or plasma biomarkers. Absolute changes in plasma IL-18 were comparable in participants with contrast-associated AKI (−30 [−71, −9] mg/dl) and those without contrast-associated AKI (−27 [−53, −10] mg/dl; P=0.62). Relative ratios of plasma IL-18 were also comparable in participants with contrast-associated AKI (0.91; 0.86, 0.97) and those without contrast-associated AKI (0.91; 0.85, 0.96; P=0.54).ConclusionsThe lack of significant differences in the absolute changes and relative ratios of injury and repair biomarkers by contrast-associated AKI status suggests that the majority of mild contrast-associated AKI cases may be driven by hemodynamic changes at the kidney.

scholarly journals Tubulointerstitial Biomarkers for Diabetic Nephropathy

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Bancha Satirapoj
Keyword(s):  
Diabetic Nephropathy ◽  
Tissue Injury ◽  
Kidney Injury ◽  
Cardiovascular Complications ◽  
Renal Tissue ◽  
Monocyte Chemoattractant Protein 1 ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Potential Applications ◽  
Novel Biomarkers ◽  
Kidney Injury Molecule 1

Patients with diabetic nephropathy have a higher risk of mortality, mostly from cardiovascular complications. Standard biomarkers including serum creatinine, estimated glomerular filtration rate, and albuminuria are imprecise, do not directly measure renal tissue injury, and are relatively insensitive to small changes in renal function. Thus, availability of novel biomarkers that are sensitive, specific, and precise as well as able to detect kidney injury and predict clinically significant outcomes would be widely useful in diabetic nephropathy. Novel biomarkers of the processes that induce tubulointerstitial changes may ultimately prove to better predict renal progression and prognosis in type 2 diabetes. Recently, certain biomarkers, which were initially identified in acute kidney injury, also have been reported to confer value in evaluating patients with chronic kidney disease. Biomarkers such as cystatin C, kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), angiotensinogen, periostin, and monocyte chemoattractant protein-1 (MCP-1) reflect tubular injury. In this article, we focused on the potential applications of these biomarkers in diabetic nephropathy.

scholarly journals Importance of KIM-1 and MCP-1 in Determining the Leptospirosis-Associated AKI: A Sri Lankan Study

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Thilini Nisansala ◽  
Manjula Weerasekera ◽  
Nilantha Ranasinghe ◽  
Chamil Marasinghe ◽  
Chandika Gamage ◽  
...  
Keyword(s):  
Early Stage ◽  
Kidney Injury ◽  
Diagnostic Tools ◽  
Sri Lankan ◽  
Monocyte Chemoattractant Protein 1 ◽  
Median Serum ◽  
The Status ◽  
Medical Wards ◽  
Kidney Injury Molecule 1 ◽  
Prompt Diagnosis

Background. Acute kidney injury (AKI) is one of most prevalent and serious complications of leptospirosis, a prevalent zoonotic disease in tropical countries. Prompt diagnosis of the leptospirosis-associated AKI is a challenge as there are no proper diagnostic tools that can identify patients in the early stage. Kidney injury molecule-1 (KIM-1) and monocyte chemoattractant protein-1 (MCP-1) are widely used novel AKI biomarkers that are studied in various disease conditions with AKI, but not in leptospirosis. Thus, this study is aimed at seeking the importance of KIM-1 and MCP-1 in determining the leptospirosis-associated AKI. Methods. Leptospirosis-suspected patients who were admitted to medical wards of two selected hospitals in the Western province of Sri Lanka were recruited. Leptospirosis was confirmed by three diagnostic tests: PCR, MAT, and culture, and the status of AKI was determined by Kidney Disease Improving Global Outcomes (KDIGO) criteria. Results. Of 170 leptospirosis-suspected patients, 79 were leptospirosis confirmed, and among them, 24.05% of patients were diagnosed to have AKI according to KDIGO criteria. Median serum KIM-1 ( p < 0.0001 ), urine KIM-1 (0.0053), serum MCP-1 (0.0080), and urine MCP-1 (0.0019) levels in those developing AKI were significantly higher than in patients not developing AKI. The biomarker levels associated with leptospirosis AKI had AUC-ROC of 0.8565, 0.7292, 0.7024, and 0.7282 for serum KIM-1, urine KIM-1, serum MCP-1, and urine MCP-1, respectively. Conclusion. This study revealed serum KIM-1 as a promising marker for leptospirosis-associated AKI among the tested biomarkers. Thus, further validation is recommended with a larger study group.

scholarly journals Evaluation of Urinary Big Endothelin-1 in Feline Spontaneous CKD

Animals ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 2144
Author(s):  
Marco Giraldi ◽  
Saverio Paltrinieri ◽  
Camilla Piazza ◽  
Paola Scarpa
Keyword(s):  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Serum Creatinine ◽  
Urine Samples ◽  
Ckd Progression ◽  
Creatinine Concentration ◽  
Endothelin 1 ◽  
Urine Creatinine ◽  
Advanced Stages

The endothelin-1 (ET-1) system has been implicated in the development and progression of chronic kidney disease (CKD). No information on big ET-1 in feline urine is available. The purpose of this study was to evaluate if urinary big endothelin-1 (bigET-1) is associated with feline CKD. Sixty urine samples were prospectively collected from 13 healthy cats at risk of developing CKD and 22 cats with CKD of different International Renal Interest Society (IRIS) stages (1–4). Urinary bigET-1 was measured using a commercially available ELISA. BigET-1 normalized to urine creatinine (bigET-1:UC) was compared amongst stages and substages, as proposed by IRIS, and correlated with serum creatinine concentration, proteinuria and blood pressure. BigET-1:UC at the time of inclusion was compared between cats that remained stable and cats that progressed after 12 months. BigET-1:UC was significantly higher (p = 0.002) in cats at IRIS stages 3–4 (median: 21.9; range: 1.88–55.6), compared to all other stages, and in proteinuric (n = 8, median: 11.0; range: 0.00–46.4) compared with nonproteinuric cats (n = 38 median: 0.33; range: 0.00–55.6) (p = 0.029). BigET-1:UC was not associated with CKD progression. Urinary bigET-1 increased in advanced stages of CKD and in proteinuric patients, suggesting that ET-1 may be indicative of the severity of feline CKD.

Incidence of contrast-induced acute kidney injury in patients with acute mesenteric ischemia and identification of potential predictive factors

Vascular ◽  
2021 ◽  
pp. 170853812110507
Author(s):  
Emmanuel Augène ◽  
Fabien Lareyre ◽  
Julien Chikande ◽  
Lucas Guidi ◽  
Grégoire Mutambayi ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Contrast Medium ◽  
Predictive Factors ◽  
Mesenteric Ischemia ◽  
Kidney Injury ◽  
Acute Mesenteric Ischemia ◽  
Creatinine Concentration ◽  
Increased Risk ◽  
Significant Difference

Objective Contrast-enhanced computed tomography angiography (CTA) is commonly used to investigate acute abdominal conditions, but the risk of contrast-induced acute kidney injury (CI-AKI) has been poorly investigated in patients with acute mesenteric ischemia. The aim of the present study was to evaluate the incidence of CI-AKI in these patients and identify potential predictive factors. Methods Patients admitted for acute mesenteric ischemia who had a diagnostic CTA with contrast medium and a follow-up of creatinine concentration were retrospectively included. Results Among 53 patients included, 9 (16.9%) developed CI-AKI. The prevalence of chronic kidney disease did not differ significantly between those who developed CI-AKI and those who did not (33.3 vs 18.2%, p=.372). Plasma total bilirubin and conjugated bilirubin levels were significantly higher in patients who developed CI-AKI (17.5 vs 8.0 μmol/L, p=.013 and 8.0 vs 3.0 μmol/L, p=.031, respectively). The proportion of patients who had revascularization was similar between patients who developed CI-AKI and those who did not (11.1 vs 20.5%, p>.999). No significant difference was observed for 30-day mortality and all-cause mortality for a median follow-up of 168 days (22.2 vs 13.6%, p=.611; and 33.3 vs 61.4%, p=.153, respectively). Conclusion This study reports the incidence of CI-AKI in patients with acute mesenteric ischemia after diagnostic CTA with contrast medium. Plasma bilirubin levels were a predictive factor of CI-AKI in these patients. The administration of contrast media during revascularization was not associated with an increased risk of CI-AKI.

Searching for Perfect Marker - Differences and Dependencies in Serum Levels of Renalase, KIM-1, MCP-1, Calbindin and GST-Pi in Patients with Diabetes, Glomerulonephritis and Congenital Defects of the Kidney

2018 ◽  
Author(s):  
Natalia Maria Serwin ◽  
Magda Wiśniewska ◽  
Edyta Skwirczyńska ◽  
Karol Serwin ◽  
Oskar Wróblewski ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Kidney Function ◽  
Kidney Injury ◽  
Congenital Defects ◽  
Glutathione S Transferase ◽  
Kidney Toxicity ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Kidney Injury Molecule 1

Diagnosis of kidney diseases has recently become more comprehensive and accurate by using new renal markers. Despite the fact that creatinine and cystatin c have been sufficient in determining kidney function, they did not indicate the exact site of the damage and they were often insufficient in predicting the course of the disease. Aim of the study was to evaluate the potential correlations and differences in levels of six&nbsp; factors related to kidney function and injury: kidney injury molecule-1 (KIM-1), ncalbindin (CALB), glutathione S-transferase Pi (GST-Pi), calbindin and monocyte chemoattractant protein-1 (MCP-1), between renal patients with diabetic nephropathy (DM), congenital defects (CD) of the kidney and glomerulonephritis (GN). Study involved 75 patients: 49 with diabetic nephropathy, 12 with congenital defects and 14 with glomerulonephritis. Levels of renalase was measured using immunoenzymatic tests. Levels of other markers: calbindin, glutathione-S-transferase (GST-pi), interleukin-18 (IL-18), kidney injury molecule-1 (KIM-1) and monocyte chemoattractant protein-1 (MCP-1), were analyzed using Kidney Toxicity-1 Panel and BioPlex system, designed for analyses in urine and optimized by us for serum.From all analyzed markers, only levels of KIM-1 differed significantly between any subgroups, and that was for CD and DM. Renalase correlated significantly negatively with creatinine and positively with all other markers, apart from MCP-1. Obtained results indicate, that serum renalase, KIM-1, calbindin and GST-pi are related to kidney function, with KIM-1 being the most exact, while MCP-1 levels are unrelated to creatinine and glucose levels, does not differ between patients with diabetic nephropathy and other subgroups, and therefore seem to be independent of diabetes. Also, serum-optimized Kidney Toxicity Panel 1 kit for determination of selected markers gave results similar to previous ones and therefore the method can be valuable in determination of analyzed factors.

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