The Marker of Tubular Injury, Kidney Injury Molecule-1 (KIM-1), in Acute Kidney Injury Complicating Acute Pancreatitis: A Preliminary Study

Acute pancreatitis (AP) may be associated with severe inflammation and hypovolemia leading to organ complications including acute kidney injury (AKI). According to current guidelines, AKI diagnosis is based on dynamic increase in serum creatinine, however, creatinine increase may be influenced by nonrenal factor and appears late following kidney injury. Kidney injury molecule-1 (KIM-1) is a promising marker of renal tubular injury and it has not been studied in AP. Our aim was to assess if urinary KIM-1 may be used to diagnose AKI complicating the early stage of AP. We recruited 69 patients with mild to severe AP admitted to a secondary care hospital during the first 24 h from initial symptoms of AP. KIM-1 was measured in urine samples collected on the day of admission and two subsequent days of hospital stay. AKI was diagnosed based on creatinine increase according to Kidney Disease: Improving Global Outcomes 2012 guidelines. Urinary KIM-1 on study days 1 to 3 was not significantly higher in 10 patients who developed AKI as compared to those without AKI and did not correlate with serum creatinine or urea. On days 2 and 3, urinary KIM-1 correlated positively with urinary liver-type fatty acid-binding protein, another marker of tubular injury. On days 2 and 3, urinary KIM-1 was higher among patients with systemic inflammatory response syndrome, and several correlations between KIM-1 and inflammatory markers (procalcitonin, urokinase-type plasminogen activator receptor, C-reactive protein) were observed on days 1 to 3. With a limited number of patients, our study cannot exclude the diagnostic utility of KIM-1 in AP, however, our results do not support it. We hypothesize that the increase of KIM-1 in AKI complicating AP lasts a short time, and it may only be observed with more frequent monitoring of the marker. Moreover, urinary KIM-1 concentrations in AP are associated with inflammation severity.

Download Full-text

Potential Prognostic Markers of Acute Kidney Injury in the Early Phase of Acute Pancreatitis

International Journal of Molecular Sciences ◽

10.3390/ijms20153714 ◽

2019 ◽

Vol 20 (15) ◽

pp. 3714 ◽

Cited By ~ 5

Author(s):

Justyna Wajda ◽

Paulina Dumnicka ◽

Małgorzata Maraj ◽

Piotr Ceranowicz ◽

Marek Kuźniewski ◽

...

Keyword(s):

Acute Kidney Injury ◽

Acute Pancreatitis ◽

Binding Protein ◽

Kidney Injury ◽

Current Evidence ◽

Serum Cystatin C ◽

Fatty Acid Binding ◽

Number Of Patients ◽

Kidney Injury Molecule 1 ◽

The Impact

Acute kidney injury (AKI) is a serious complication of acute pancreatitis (AP), which occurs in up to 70% of patients with severe AP and significantly increases the risk of mortality. At present, AKI is diagnosed based on dynamic increase in serum creatinine and decreased urine output; however, there is a need for earlier and more accurate biomarkers. The aim of the study was to review current evidence on the laboratory tests that were studied as the potential biomarkers of AKI in AP. We also briefly summarized the knowledge coming from the studies including sepsis or ICU patients since severe acute pancreatitis is associated with systemic inflammation and organ failure. Serum cystatin C and serum or urine NGAL have been shown to predict or diagnose AKI in AP; however, this evidence come from the single center studies of low number of patients. Other markers, such as urinary kidney injury molecule-1, cell cycle arrest biomarkers (tissue inhibitor metalloproteinase-2 and urine insulin-like growth factor-binding protein 7), interleukin-18, liver-type fatty acid-binding protein, or calprotectin have been studied in other populations suffering from systemic inflammatory states. In AP, the potential markers of AKI may be significantly influenced by either dehydration or inflammation, and the impact of these factors may be difficult to distinguish from kidney injury. The subject of AKI complicating AP is understudied. More studies are needed, for both exploratory (to choose the best markers) and clinical (to evaluate the diagnostic accuracy of the chosen markers in real clinical settings).

Download Full-text

Acute kidney injury in children

Srpski arhiv za celokupno lekarstvo ◽

10.2298/sarh1406371p ◽

2014 ◽

Vol 142 (5-6) ◽

pp. 371-377 ◽

Cited By ~ 1

Author(s):

Amira Peco-Antic ◽

Dusan Paripovic

Keyword(s):

Acute Kidney Injury ◽

Serum Creatinine ◽

Kidney Injury ◽

Developed Countries ◽

Multiple Organ ◽

Critically Ill Children ◽

Creatinine Concentration ◽

Fatty Acid Binding ◽

Kidney Injury Molecule 1 ◽

Sudden Decrease

Acute kidney injury (AKI) is a clinical condition considered to be the consequence of a sudden decrease (>25%) or discontinuation of renal function. The term AKI is used instead of the previous term acute renal failure, because it has been demonstrated that even minor renal lesions may cause far-reaching consequences on human health. Contemporary classifications of AKI (RIFLE and AKIN) are based on the change of serum creatinine and urinary output. In the developed countries, AKI is most often caused by renal ischemia, nephrotoxins and sepsis, rather than a (primary) diffuse renal disease, such as glomerulonephritis, interstitial nephritis, renovascular disorder and thrombotic microangiopathy. The main risk factors for hospital AKI are mechanical ventilation, use of vasoactive drugs, stem cell transplantation and diuretic-resistant hypervolemia. Prerenal and parenchymal AKI (previously known as acute tubular necrosis) jointly account for 2/3 of all AKI causes. Diuresis and serum creatinine concentration are not early diagnostic markers of AKI. Potential early biomarkers of AKI are neutrophil gelatinase-associated lipocalin (NGAL), cystatin C, kidney injury molecule-1 (KIM-1), interleukins 6, 8 and 18, and liver-type fatty acid-binding protein (L-FABP). Early detection of kidney impairment, before the increase of serum creatinine, is important for timely initiated therapy and recovery. The goal of AKI treatment is to normalize the fluid and electrolyte status, as well as the correction of acidosis and blood pressure. Since a severe fluid overload resistant to diuretics and inotropic agents is associated with a poor outcome, the initiation of dialysis should not be delayed. The mortality rate of AKI is highest in critically ill children with multiple organ failure and hemodynamically unstable patients.

Download Full-text

Diagnostic Utility of Serial Microscopic Examination of the Urinary Sediment in Acute Kidney Injury

Kidney360 ◽

10.34067/kid.0004022020 ◽

2020 ◽

pp. 10.34067/KID.0004022020

Author(s):

Vipin Varghese ◽

Maria Soledad Rivera ◽

Ali A. Alalwan ◽

Ayman M. Alghamdi ◽

Manuel E. Gonzalez ◽

...

Keyword(s):

Acute Kidney Injury ◽

Serum Creatinine ◽

Microscopic Examination ◽

Odds Ratio ◽

Positive Likelihood Ratio ◽

Kidney Injury ◽

Diagnostic Utility ◽

Tubular Injury ◽

Urinary Sediment ◽

Unclear Etiology

Background. Microscopic examination of the urinary sediment (MicrExUrSed) is an established diagnostic tool for acute kidney injury (AKI). Single inspection of urine during the course of AKI is a mere snapshot affected by timing. We hypothesized that longitudinal MicrExUrSed provides information not identified in a single inspection. Methods. MicrExUrSed was undertaken in patients with AKI stage >= 2 and suspected intrinsic cause of AKI seen for nephrology consultation over a 2-year period. MicrExUrSed was performed on the day of consultation and repeated at a second (2 - 3 days later) and/or third (4 - 10 days later) interval. Cast scores were assigned to each specimen. Chawla scores (CS) 3 to 4 and Perazella scores (PS) 2 to 4 were categorized as consistent with acute tubular injury (ATI), whereas CS 1 to 2 and PS 0 to 1 were categorized as non-diagnostic for ATI (non-ATI). Non-recovering AKI was defined as a rise in serum creatinine (sCr) ≥ 0.1 mg/dL between microscopy intervals. Results. At least 2 consecutive MicrExUrSed were performed in 121 patients [46% women, mean age 61 ± 14, mean sCr at consult of 3.3 +/- 1.9 mg/dL]. On day 1, a CS and PS consistent with non-ATI was assigned to 64 (53%) and 70 (58%) patients, respectively. After a subsequent MicrExUrSed, CS and PS changed to ATI in 14 (22%) and 16 (23%) patients. Thus, 20 - 24% of patients only revealed evidence of ATI after serial MicrExUrSed was performed. Patients with non-recovering AKI were more likely to change their PS to ATI category [odds ratio: 5.8 (CI:1.7-19.3; p=0.005) and positive likelihood ratio: 2.0 (CI: 1.3-2.9)]. Conclusion. Serial MicrExUrSed revealed diagnostic findings of ATI not identified in a single examination. A repeat MicrExUrSed may be warranted in cases of AKI of unclear etiology or not recovering.

Download Full-text

Screening of early diagnostic markers of gentamicin-induced acute kidney injury in canines

Journal of Veterinary Research ◽

10.2478/jvetres-2019-0048 ◽

2019 ◽

Vol 63 (3) ◽

pp. 405-411

Author(s):

Jia-San Zheng ◽

Jing-Nie ◽

Ting-Ting Zhu ◽

Hong-Ri Ruan ◽

Xue-Wei ◽

...

Keyword(s):

Acute Kidney Injury ◽

Characteristic Curve ◽

Kidney Tissue ◽

Kidney Injury ◽

Fatty Acid Binding ◽

Neutrophil Gelatinase Associated Lipocalin ◽

Transmission Electron ◽

Renal Tubular ◽

Kidney Injury Molecule 1 ◽

Neutrophil Gelatinase

Abstract Introduction The value of neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (Kim-1), and liver-type fatty acid binding protein (L-FABP) was assessed in early diagnosis of gentamicin-induced acute kidney injury (AKI) in dogs. Material and Methods Subcutaneous gentamicin injection in 16 healthy adult beagles made the AKI model. Blood was sampled every 6 h to detect NGAL, Kim-1, L-FABP, and serum creatinine (SCr) concentrations. Kidney tissue of two dogs was taken before the injection, as soon as SCr was elevated (78 μmol/L), and when it had risen to 1.5 times the baseline, and haematoxylin-eosin staining and transmission electron microscopy (TEM) were used to observe changes. Results NGAL, Kim-1, and SCr levels were significantly increased (P < 0.05) at 18, 30, and 78 h post injection, but L-FABP concentration was not associated with renal injury. At the earliest SCr elevation stage, findings were mild oedema, degeneration, and vacuolisation in renal tubular epithelial cells in pathology, and mild cytoplasmic and mitochondrial oedema in TEM. At this time point, NGAL and Kim-1 concentrations were significantly increased (P < 0.05), indicating that these two molecules biomark early kidney injury in dogs. Using receiver operating characteristic curve analysis, their warning levels were > 25.31 ng/mL and > 48.52 pg/mL. Conclusion Plasma NGAL and Kim-1 above warning levels are early indicators of gentamicin-induced AKI in dogs.

Download Full-text

Serum Cystatin C, Kidney Injury Molecule-1, Neutrophil Gelatinase-Associated Lipocalin, Klotho and Fibroblast Growth Factor-23 in The Early Prediction of Acute Kidney Injury Associated With Sepsis in a Chinese Emergency Cohort Study

10.21203/rs.3.rs-1059386/v1 ◽

2021 ◽

Author(s):

Yuanyuan Pei ◽

Guangping Zhou ◽

Pengfei Wang ◽

Fang'e Shi ◽

Xiaolu Ma ◽

...

Keyword(s):

Acute Kidney Injury ◽

Serum Creatinine ◽

Cystatin C ◽

Fibroblast Growth Factor 23 ◽

Kidney Injury ◽

Serum Levels ◽

Serum Cystatin C ◽

Serum Cystatin ◽

Kidney Injury Molecule 1 ◽

Fgf 23

Abstract Background: Acute kidney injury (AKI) was a common and critical complication of sepsis, and is associated with unacceptable morbidity and mortality. Current diagnostic criteria for AKI was insensitive for early detection. Novel biomarkers included cystatin C, KIM-1, NGAL, klotho and FGF-23 which can predict AKI earlier may allow immediate interventions. We aimed to determine the diagnostic performance of these biomarkers for detecting AKI in sepsis patients.Methods: This prospective observational study was conducted from May 2018 and November 2020, enrolling sequential 162 sepsis patients. AKI’s definition was according to 2012 KDIGO criteria and we divided patients into non-AKI (n=102) and AKI (n=60) groups. Serum levels of several AKI biomarkers were detected by ELISA. The relationship between biomarker levels on admission of AKI were analyzed and discrimination performances comparison were performed.Results: AKI incidence was up to 37.0% (60/162) during hospitalization. Compared with non-AKI group, both serum cystatin C, KIM-1, NGAL and FGF-23 were significantly elevated at admission in septic AKI patients. The areas under the receiver operating curves demonstrated that serum cystatin C had modest discriminative powers for predicting AKI after sepsis, and cystatin C combined with serum creatinine in the prediction of septic AKI increased the diagnostic sensitivity prominently.Conclusion: Serum cystatin C, KIM-1, NGAL and FGF-23 levels are both increased in septic AKI patients. Our study provides reliable evidence that cystatin C solely and combined with serum creatinine may accurately and sensitively predict septic AKI when patients on admission.

Download Full-text

Gene deletion of the Na+-glucose cotransporter SGLT1 ameliorates kidney recovery in a murine model of acute kidney injury induced by ischemia-reperfusion

AJP Renal Physiology ◽

10.1152/ajprenal.00111.2019 ◽

2019 ◽

Vol 316 (6) ◽

pp. F1201-F1210 ◽

Cited By ~ 10

Author(s):

Josselin Nespoux ◽

Rohit Patel ◽

Kelly L. Hudkins ◽

Winnie Huang ◽

Brent Freeman ◽

...

Keyword(s):

Acute Kidney Injury ◽

Proximal Tubule ◽

Gene Deletion ◽

Ischemia Reperfusion ◽

Plasma Osmolality ◽

Kidney Injury ◽

Tubular Injury ◽

Outer Medulla ◽

Glucose Reabsorption ◽

Kidney Injury Molecule 1

Renal Na+-glucose cotransporter SGLT1 mediates glucose reabsorption in the late proximal tubule, a hypoxia-sensitive tubular segment that enters the outer medulla. Gene deletion in mice ( Sglt1−/−) was used to determine the role of the cotransporter in acute kidney injury induced by ischemia-reperfusion (IR), including the initial injury and subsequent recovery phase. On days 1 and 16 after IR, absolute and fractional urinary glucose excretion remained greater in Sglt1−/− mice versus wild-type (WT) littermates, consistent with a sustained contribution of SGLT1 to tubular glucose reabsorption in WT mice. Absence of SGLT1 did not affect the initial kidney impairment versus WT mice, as indicated by similar increases on day 1 in plasma concentrations of creatinine and urinary excretion of the tubular injury marker kidney injury molecule-1 as well as a similar rise in plasma osmolality and fall in urine osmolality as indicators of impaired urine concentration. Recovery of kidney function on days 14/16, however, was improved in Sglt1−/− versus WT mice, as indicated by lower plasma creatinine, higher glomerula filtration rate (by FITC-sinistrin in awake mice), and more completely restored urine and plasma osmolality. This was associated with a reduced tubular injury score in the cortex and outer medulla, better preserved renal mRNA expression of tubular transporters ( Sglt2 and Na+-K+-2Cl– cotransporter Nkcc2), and a lesser rise in renal mRNA expression of markers of injury, inflammation, and fibrosis [kidney injury molecule-1, chemokine (C-C motif) ligand 2, fibronectin 1, and collagen type I-α1] in Sglt1−/− versus WT mice. These results suggest that SGLT1 activity in the late proximal tubule may have deleterious effects during recovery of IR-induced acute kidney injury and identify SGLT1 as a potential therapeutic target.

Download Full-text

Different Biomarkers of Acute kidney Injury in Cancer Patients

Iranian Journal of Pediatric Hematology & Oncology ◽

10.18502/ijpho.v11i2.5845 ◽

2021 ◽

Author(s):

Reza Kazemi ◽

Shirin Saberianpour ◽

Hanieh Salehi ◽

Mohammad Hatampour ◽

Elnaz Sheikhpour

Keyword(s):

Acute Kidney Injury ◽

Cancer Patients ◽

Early Stage ◽

Kidney Injury ◽

The Body ◽

Main Task ◽

Waste Products ◽

Fatty Acid Binding ◽

Neutrophil Gelatinase Associated Lipocalin ◽

Kidney Injury Molecule 1

Acute Kidney Injury (AKI) occurs if the kidneys suddenly lose their ability to remove waste products. When the kidneys lose their ability to filter, dangerous levels of waste products can accumulate, which can upset the chemical composition of the blood and urine. Chemotherapy is one of the methods used to treat or temporarily reduce cancer by using certain medications. The main task of this treatment is to kill cancer cells without seriously damaging the surrounding tissues. However, this type of treatment also has destructive effects on healthy cells and tissues in the body. Researchers studying cancer patients undergoing chemotherapy found that people undergoing this type of treatment may develop serious kidney problems and be forced to use treatments such as dialysis and kidney transplants. Research showed that people with more severe cancers and advanced tumors are more likely to have acute kidney injury than those with early-stage cancer. AKI biomarkers can be selected from the patient's serum, urine, or body imaging components. Various studies showed that urine is a source of the best markers in AKI. Biomarkers in plasma and urine, such as N-acetyl-β-glucosaminidase, Cystatin-C, β2-microglobulin , Cysteine-Rich Protein, Osteopontin, Fetuin-A, Kidney Injury Molecule-1, Liver-type fatty acid-binding protein, Netrin-1, Neutrophil gelatinase-associated lipocalin, and interleukin-18 are effective tools for early detection of AKI. In this review study, an attempt was made to collect biomarkers related to AKI disease.

Download Full-text

Kidney injury molecule-1 identifies antemortem injury in postmortem adult and fetal kidney

AJP Renal Physiology ◽

10.1152/ajprenal.00060.2018 ◽

2018 ◽

Vol 315 (6) ◽

pp. F1637-F1643 ◽

Cited By ~ 2

Author(s):

Wenqing Yin ◽

Ping L. Zhang ◽

Jacqueline K. Macknis ◽

Fan Lin ◽

Joseph V. Bonventre

Keyword(s):

Serum Creatinine ◽

Tissue Damage ◽

Kidney Injury ◽

Postmortem Examination ◽

Tubular Injury ◽

Fetal Kidney ◽

Pulmonary Alveoli ◽

Kidney Injury Molecule 1 ◽

Postmortem Autolysis

There is currently no technique to unambiguously diagnose antemortem kidney injury on postmortem examination since postmortem tissue damage and autolysis are common. We assessed the ability to detect kidney injury molecule-1 (KIM-1) expression in adult and fetal kidneys examined at autopsy. In adult kidneys ( n = 52 subjects), we found that the intensity of KIM-1 staining significantly correlated with the antemortem level of serum creatinine, and this was independent of the extent of tissue autolysis. In addition, kidneys from a total of 52 fetal/neonatal subjects, 30 stillborns and 22 liveborns, were assessed for KIM-1 staining. Given that serum creatinine is unreliable and often unavailable in fetuses and newborns, we assessed preterminal hypoxia in fetuses by the presence of squames in pulmonary alveoli and by required intubation. KIM-1 expression correlated with these clinical indexes of hypoxia. The expression of KIM-1 was seen in a majority of the fetal and neonatal autopsy kidneys (77%, 40/52) as early as 16 wk of gestation, even in the presence of autolysis. Thus KIM-1 is a specific and stable marker of antemortem tubular injury in kidneys of adults and fetuses despite postmortem autolysis.

Download Full-text

Etiology and Outcomes of Acute Kidney Injury in Patients Admitted to a Single Tertiary Care Hospital: Balochistan Institute of Nephrology-Urology Quetta

Pakistan Journal of Kidney Diseases ◽

10.53778/pjkd4429 ◽

2021 ◽

Vol 4 (4) ◽

pp. 319-323

Author(s):

Abdul Kareem Zarkoon Zarkoon ◽

Habib Ullah Rind ◽

Moin Khan ◽

Aijaz Ahmed ◽

Nasir Jakrani ◽

...

Keyword(s):

Acute Kidney Injury ◽

Tertiary Care Hospital ◽

Tertiary Care ◽

Age Groups ◽

Kidney Injury ◽

Complete Recovery ◽

Clinical Syndrome ◽

Obstructive Nephropathy ◽

Care Hospital ◽

Number Of Patients

Acute kidney injury (AKI) is a common clinical syndrome with broad spectrum of etiologies and an important cause of morbidity and mortality requiring hospitalization. Depending on the cause and nature of AKI it may complicate to be life threatening or even proceed to Chronic Kidney disease (CKD) compromising the quality of life. Methods: The current retrospective study determines the causes and outcomes of AKI in patients of different age groups, who required hospitalization at our tertiary care hospital from March 2018 to March 2020. Possible etiologic conditions for AKI were recorded during the study period and AKI was classified according to the causes, age and outcome. Results: records of total of 267 patients with diagnosis of AKI were obtained who were admitted during the study period. Obstetric related diagnosis was the commonest reason for AKI (n= 50 18.7%), another 42 (15.7%) had obstructive nephropathy, prerenal AKI in 35 patients (13.1%) and other causes such as glomerulonephritis, sepsis, pigment nephropathy and drug related interstitial nephritis among others. Majority of the patients needed dialytic support, n=190 (71.2%) and majority of patients n=181 patients (67.7%) recovered completely, and only 11 patients (4.2%) expired. Conclusion: Our study reveals that majority of patients with AKI presenting to BINUQ had reversible causes of AKI with complete recovery in significant number of patients. Community wise programs to early detect AKI with prompt treatment will decrease the likelihood of such patients adding to the CKD population.

Download Full-text

INCIDENCE AND CAUSES OF ACUTE KIDNEY INJURY IN SICK NEONATE : A STUDY FROM A TERTIARY CARE NEONATAL UNIT

10.36106/ijsr/4105010 ◽

2020 ◽

pp. 1-2

Author(s):

Krishnendu Karmakar ◽

Sumanta Laha ◽

Bhaswati Ghoshal ◽

Pradip Kumar Das

Keyword(s):

Acute Kidney Injury ◽

Birth Weight ◽

Kidney Disease ◽

Serum Creatinine ◽

Perinatal Asphyxia ◽

Tertiary Care ◽

Kidney Injury ◽

Care Hospital ◽

Cross Sectional ◽

Normal Birth

Objective To find out the incidence of Acute Kidney Injury(AKI) and various causes responsible for the AKI in sick neonates in a tertiary care hospital. Material and Method In this observational cross sectional study we included all neonates with features suggestive of AKI with exclusion criteria of extreme prematurity, chronic kidney disease and major congenital anomaly. We diagnose AKI according to the KIDIGO(Kidney Disease: Improving Global Outcome)guideline where we take serum creatinine value and urinary output as determinant. Serum creatinine value measured at 48 and 72 hrs of admission and repeated at 96 hrs if there is rising trend of creatinine..Now we find out the incidence of AKI in relation to gender, birth weight, mode of delivary . Among the AKI case we sort out the causative factors like perinatal asphyxia,sepsis, shock, prematurity etc and analysed all the results statistically. Results Out of total 1872 neonates admitted during the 18 months study period we found AKI in 111 neonates(5.93%).There is male preponderance and most neonates are of normal birth wt.Among the various causes of AKI perinatal asphyxia is the leading cause followed by sepsis and prematurity.Other imp causes are congenital heart disease,shock, PPHN , nephrotoxic drug use and RDS of newborn. We found asphyxia as the leading cause of AKI in normal vaginal delivary group whereas sepsis is the main cause of AKI in cesarean section group. Conclusion AKI is fairly common in sick neonates , even in normal birth weight babies and perinatal asphyxia and sepsis are the two most prevalent cause for AKI in this study.

Download Full-text