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 ◽  
...  

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.

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Bancha Satirapoj

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.


2013 ◽  
Vol 40 (5) ◽  
pp. 674-683 ◽  
Author(s):  
Jason G. Lieberthal ◽  
David Cuthbertson ◽  
Simon Carette ◽  
Gary S. Hoffman ◽  
Nader A. Khalidi ◽  
...  

Objective.Glomerulonephritis (GN) is common in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), but tools for early detection of renal involvement are imperfect. We investigated 4 urinary proteins as markers of active renal AAV: alpha-1 acid glycoprotein (AGP), kidney injury molecule-1 (KIM-1), monocyte chemoattractant protein-1 (MCP-1), and neutrophil gelatinase-associated lipocalin (NGAL).Methods.Patients with active renal AAV (n = 20), active nonrenal AAV (n = 16), and AAV in longterm remission (n = 14) were identified within a longitudinal cohort. Urinary biomarker concentrations (by ELISA) were normalized for urine creatinine. Marker levels during active AAV were compared to baseline remission levels (from 1–4 visits) for each patient. Areas under receiver-operating characteristic curves (AUC), sensitivities, specificities, and likelihood ratios (LR) comparing disease states were calculated.Results.Baseline biomarker levels varied among patients. All 4 markers increased during renal flares (p < 0.05). MCP-1 discriminated best between active renal disease and remission: a 1.3-fold increase in MCP-1 had 94% sensitivity and 89% specificity for active renal disease (AUC = 0.93, positive LR 8.5, negative LR 0.07). Increased MCP-1 also characterized 50% of apparently nonrenal flares. Change in AGP, KIM-1, or NGAL showed more modest ability to distinguish active renal disease from remission (AUC 0.71–0.75). Hematuria was noted in 83% of active renal episodes, but also 43% of nonrenal flares and 25% of remission samples.Conclusion.Either urinary MCP-1 is not specific for GN in AAV, or it identifies early GN not detected by standard assessment and thus has potential to improve care. A followup study with kidney biopsy as the gold standard is needed.


2020 ◽  
Vol 26 (7) ◽  
pp. 1643-1649
Author(s):  
Elliyeh Ghadrdan ◽  
Sholeh Ebrahimpour ◽  
Sanambar Sadighi ◽  
Samira Chaibakhsh ◽  
Zahra Jahangard-Rafsanjani

Introduction Cisplatin-associated acute kidney injury (AKI) is the major limitation to the use of cisplatin-based chemotherapy regimens. Serum creatinine as a traditional marker did not increase in a timely enough fashion in AKI patients. Therefore, recently, the novel markers such as neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) were considered for early detection of AKI. The aim of this study was to compare the sensitivity and specificity of urinary NGAL and KIM-1 with serum creatinine in cisplatin related AKI. Methods Patients ≥18 years with solid tumors who received cisplatin-based chemotherapy were included. Urine samples were collected 0, 6 and 24 h after cisplatin infusion and the urinary NGAL, KIM-1, and creatinine concentrations were evaluated. NGAL and KIM-1 concentrations were adjusted based on urine creatinine to eliminate hydration effects. Serum creatinine levels were assessed at the base and 72 h after cisplatin administration. Results Seven out of the 35 recruited patients (20%) suffered from AKI defined by Acute Kidney Injury Network criteria. In AKI patients, the ratio of urinary KIM-1–creatinine at 24 h compared to baseline (24 h/baseline) and NGAL–creatinine 24 h/baseline were significantly higher than those of non-AKI group ( p = 0.037 and 0.047 respectively). The area under the receiver-operating characteristic curve for KIM-1–creatinine 24 h/baseline and NGAL–creatinine 24 h/baseline were 0.78 (0.59–0.96, p = 0.032) and 0.77 (0.57–0.97, p = 0.036) respectively. Conclusions Our findings showed that the changes in urinary NGAL–creatinine and KIM-1–creatinine ratios, 24 h after cisplatin administration can be utilized to predict AKI in cisplatin recipients.


2020 ◽  
Author(s):  
Hannah Harjen ◽  
Tove Nicolaysen ◽  
Tale Negard ◽  
Hege Lund ◽  
Bente Sævik ◽  
...  

Abstract Background Acute kidney injury (AKI) is associated with high morbidity and mortality in dogs, but diagnosis may be impaired due the insensitivity of routine renal function biomarkers to detect earlier or milder forms of injury. Snake envenomation is one of several causes of AKI in dogs and humans. Dogs are commonly envenomated by the European adder (Vipera berus) between April and October each year, but few studies exist examining serial serum creatinine (sCr) measurements and AKI biomarkers in these dogs. Novel urinary biomarkers could improve clinical outcome by allowing earlier diagnosis of and intervention in AKI. The aim of this study was to assess the presence of AKI in dogs envenomated by V. berus at 12, 24 and 36 hours after bite, as well as 14 days later, using sCr and a panel of urinary AKI biomarkers normalised to urine creatinine (uCr), compared to a group of healthy control dogs.Results Thirty-five envenomated dogs and 37 control dogs were included. Serum creatinine did not exceed the upper reference limit at any time point in any dog after envenomation. Compared to controls, urinary albumin /uCr, neutrophil gelatinase-associated lipocalin/uCr and monocyte chemotactic protein-1 /uCr were significantly elevated 12 hours (p < 0.001, p< 0.001, p = 0.01), 24 hours (p < 0.001, p < 0.001, p = 0.003) and 36 hours ( p < 0.001, p< 0.001, p = 0.001) after bite. Osteopontin /uCr was higher 24 and 36 hours after bite (p < 0.001), kidney injury molecule-1 /uCr, interleukin-8 /uCr and γ- glutamyl transferase /uCr were significantly higher 36 hours after bite (p = 0.0007, p = 0.0005, p= 0.001). Urinary cystatin C /uCr was not significantly different to controls at any timepoint. Biomarker/uCr ratios were not significantly different 14 days after envenomation compared to controls. Conclusion Urinary biomarker/Cr ratios are indicative of transient non-azotaemia AKI in dogs envenomated by V. berus.


2020 ◽  
Vol 32 (5) ◽  
pp. 656-663
Author(s):  
Jennifer Davis ◽  
Anthea L. Raisis ◽  
David W. Miller ◽  
Gabriele Rossi

Interest is growing in measurement of novel biomarkers for the diagnosis of acute kidney injury. Multiplex assays may provide a rapid and cost-effective way of measurement; however, sparse information is published regarding their use in dogs. We aimed to validate a commercial magnetic bead–based assay for 5 biomarkers: clusterin (Clus), cystatin C (CysC), kidney injury molecule 1 (KIM-1), monocyte chemoattractant protein 1 (MCP-1), and neutrophil gelatinase–associated lipocalin (NGAL). Intra- and inter-assay imprecision, linearity under dilution (LUD), spike recovery (S-R), and hemoglobin interference were evaluated using serum from healthy and diseased dogs. Additionally, the effect of sample type (serum vs. plasma) was investigated. All values for Clus and MCP-1 were outside the assay’s measurable range. Intra- and inter-assay precision were acceptable for NGAL (CVs 8.8% and 13.2%, respectively). Regression analysis of LUD and S-R indicated good linearity for CysC and NGAL. Hemolysis did not affect measurement of any biomarker. Measured concentrations of CysC ( p = 0.018) and NGAL ( p = 0.015) were significantly lower in sodium citrate plasma compared to serum. We conclude that this magnetic bead–based assay is precise and accurate for NGAL measurement in canine serum. Inappropriate standards for MCP-1 and Clus, and poor accuracy for KIM-1 measurement, suggest that this assay cannot reliably quantify those biomarkers in canine blood. Measurements of CysC in canine blood using this assay must be interpreted with caution given inter-assay imprecision.


2016 ◽  
Author(s):  
Lee Grodin ◽  
Joshua McHugh ◽  
Richard Sinert

Acute kidney injury (AKI) is defined as a syndrome in which there is an abrupt (hours to days) absolute increase in serum creatinine (SCr) of 0.5 mg/dL or a 25% increase from baseline. Even a modest rise in SCr of 0.3 mg/dL during hospitalization is associated with increased mortality and morbidity. Because of difficulties using SCr as a determinant of AKI, a variety of serum (neutrophil gelatinase–associated lipocalin, interleukin-18) and urine (kidney injury molecule–1) biomarkers of AKI are currently undergoing intense investigation. AKI may be defined pathophysiologically, as a decrease in renal blood flow (prerenal), or an intrinsic renal parenchymal disease (renal), or obstruction of urine flow (postrenal). Indications for emergent dialysis include hyperkalemia, fluid overload, acidosis, and signs and symptoms of uremia. If AKI is diagnosed in the emergency department, the patient should be admitted for further workup. In the majority of patients who survive AKI, renal function essentially returns to normal.  Key words: acute kidney injury, dialysis, hyperkalemia, serum creatinine This review contains 3 highly rendered figures, 11 tables, and 49 references.


2021 ◽  
pp. oemed-2021-107989
Author(s):  
Erik Hansson ◽  
David H Wegman ◽  
Catharina Wesseling ◽  
Jason Glaser ◽  
Zachary J Schlader ◽  
...  

ObjectivesSerum creatinine (SCr) is a routine marker of kidney injury but also increases with dehydration and muscular work. This study was to elucidate whether increase in SCr is associated with more specific markers of kidney tubular and interstitial injury and function, during prolonged heat stress among workers at high risk of chronic kidney disease of non-traditional origin (CKDnt).MethodsUrine monocyte chemoattractant protein-1 (MCP-1), kidney injury molecule-1 (KIM-1), calbindin, glutathione S-transferase-π (GST-π), clusterin, interleukin 18 and albumin, fractional excretion of potassium (FEK), blood haemoglobin, serum potassium, ferritin and erythropoietin were measured before and after harvest in a sample of 30 workers with a ≥0.3 mg/dL SCr increase across harvest (cases), and 53 workers with stable SCr (controls).ResultsUrine MCP-1 (p for differential cross-harvest trend <0.001), KIM-1 (p=0.002), calbindin (p=0.02), GST-π (p=0.04), albumin (p=0.001) and FEK (p<0.001) increased in cases, whereas blood haemoglobin (p<0.001) and serum erythropoietin (p<0.001) decreased.ConclusionSeveral markers of tubular and interstitial injury and function changed as SCr increased across a harvest season, supporting the use of SCr as an indicator of kidney injury in physically active workers regularly exposed to heat stress. Repeated injury similar to that described here, and continued work under strenuous and hot conditions with similarly elevated injury markers is likely to worsen and possibly initiate CKDnt.


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