scholarly journals SAT-158 RENAL TUBULAR DYSFUNCTION, COAGULATION DISTURBANCES AND NOVEL BIOMARKES IN ACUTE KIDNEY INJURY DUE TO SNAKEBITES

2019 ◽  
Vol 4 (7) ◽  
pp. S71
Author(s):  
P.L.M.M. Albuquerque ◽  
G. Da Silva Jr. ◽  
G.C. Meneses ◽  
A.M.C. Martins ◽  
J. Raubenheimer ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Renal Tubular

Serial Quantification of Urinary Protein Biomarkers to Predict Drug-induced Acute Kidney Injury

2019 ◽  
Vol 20 (8) ◽  
pp. 656-664 ◽  
Author(s):  
Yi Da ◽  
K. Akalya ◽  
Tanusya Murali ◽  
Anantharaman Vathsala ◽  
Chuen-Seng Tan ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cystatin C ◽  
Calcineurin Inhibitors ◽  
Kidney Injury ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Protein Biomarkers ◽  
Drug Induced ◽  
Beta 2 ◽  
Beta 2 Microglobulin

Background: : Drug-induced Acute Kidney Injury (AKI) develops in 10-15% of patients who receive nephrotoxic medications. Urinary biomarkers of renal tubular dysfunction may detect nephrotoxicity early and predict AKI. Methods:: We prospectively studied patients who received aminoglycosides, vancomycin, amphotericin, or calcineurin inhibitors, and collected their serial urine while on therapy. Patients who developed drug-induced AKI (fulfilling KDIGO criteria) were matched with non-AKI controls in a 1:2 ratio. Their urine samples were batch-analyzed at time-intervals leading up to AKI onset; the latter benchmarked against the final day of nephrotoxic therapy in non- AKI controls. Biomarkers examined include clusterin, beta-2-microglobulin, KIM1, MCP1, cystatin-C, trefoil-factor- 3, NGAL, interleukin-18, GST-Pi, calbindin, and osteopontin; biomarkers were normalized with corresponding urine creatinine. Results:: Nine of 84 (11%) patients developed drug-induced AKI. Biomarkers from 7 AKI cases with pre-AKI samples were compared with those from 14 non-AKI controls. Corresponding mean ages were 55(±17) and 52(±16) years; baseline eGFR were 99(±21) and 101(±24) mL/min/1.73m2 (all p=NS). Most biomarker levels peaked before the onset of AKI. Median levels of 5 biomarkers were significantly higher in AKI cases than controls at 1-3 days before AKI onset (all µg/mmol): clusterin [58(8-411) versus 7(3-17)], beta-2-microglobulin [1632(913-3823) versus 253(61-791)], KIM1 [0.16(0.13-0.76) versus 0.07(0.05-0.15)], MCP1 [0.40(0.16-1.90) versus 0.07(0.04-0.17)], and cystatin-C [33(27-2990) versus 11(7-19)], all p<0.05; their AUROC for AKI prediction were >0.80 (confidence intervals >0.50), with average accuracy highest for clusterin (86%), followed by beta-2-microglobulin, cystatin-C, MCP1, and KIM1 (57%) after cross-validation. Conclusion: : Serial surveillance of these biomarkers could improve the lead time for nephrotoxicity detection by days.

scholarly journals Use of the kidney injury molecule-1 as a biomarker for early detection of renal tubular dysfunction in a population chronically exposed to cadmium in the environment

SpringerPlus ◽  
2013 ◽  
Vol 2 (1) ◽  
pp. 533 ◽  
Author(s):  
Werawan Ruangyuttikarn ◽  
Amnart Panyamoon ◽  
Kowit Nambunmee ◽  
Ryumon Honda ◽  
Witaya Swaddiwudhipong ◽  
...  
Keyword(s):  
Early Detection ◽  
Kidney Injury ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Renal Tubular ◽  
Kidney Injury Molecule 1

Renal tubular injury as an uncommon presentation of Wilson’s disease

2021 ◽  
Vol 2 (3) ◽  
Author(s):  
Hadar Mudrik-Zohar ◽  
◽  
Keren Cohen-Hagai ◽  
Danny Alon ◽  
◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Wilson’S Disease ◽  
Renal Involvement ◽  
Clinical Manifestations ◽  
Kidney Injury ◽  
Wilson's Disease ◽  
Tubular Dysfunction ◽  
Tubular Injury ◽  
Uncommon Presentation ◽  
Renal Tubular

Wilson's disease is an autosomal recessive disorder caused by a mutant ATP7B gene on chromosome 13. This mutation causes a reduction in hepatic copper excretion, which accumulates in hepatocytes and deposits in other tissues and organs (brain, cornea, kidney, etc.) as the disease progresses. Wilson's disease was described worldwide, with estimated prevalence of one case per 30,000 live births. Age of presentation is usually 4-60 years; however, the disease may present at any age. Clinical manifestations are predominantly hepatic, neurologic and psychiatric. Renal involvement is less common and characterized by proximal tubular dysfunction, Glomerular Filtration Rate (GFR) decline, renal tubular acidosis, aminoaciduria and nephrolithiasis. Herein, we aimed to report a case which describes an uncommon path to the diagnosis of this rare, yet well-known disease. The diagnosis resulted from an investigation of acute kidney injury in a 48-year-old man. Keywords: Wilson’s disease; Acute kidney injury; Renal tubular injury.

scholarly journals miRNA Profiles of Tubular Cells: Diagnosis of Kidney Injury

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Naoko Kito ◽  
Kosuke Endo ◽  
Masahiro Ikesue ◽  
Huachun Weng ◽  
Naoharu Iwai
Keyword(s):  
Small Intestine ◽  
Mirna Expression ◽  
Early Stage ◽  
Expression Profiles ◽  
Kidney Injury ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Small Noncoding Rnas ◽  
Mirna Expression Profiles ◽  
Renal Tubular

MicroRNAs (miRNAs) are small noncoding RNAs of 18–23 nucleotides that regulate gene expression. Recently, plasma miRNAs have been investigated as biomarkers for various physiological and pathological conditions. The present study details the conserved miRNA expression profiles of tubular tissues, and discusses whether they could be used to distinguish between proximal tubule injury, diagnose acute kidney injury (AKI), and the early-stage renal tubular dysfunction. miRNA expression was assessed with miRNA array and real-time reverse transcription polymerase chain reaction using the TaqMan system. The expression profiles of miR-200a/b/c, miR-145, miR-192, miR-194, miR-216a/b, miR-217, and miR-449a in human and rat tubular tissues such as the kidneys, lung, small intestine, and various exocrine glands were adequate for discriminating tubular tissues. In the kidney, miR-192 and miR-194 were highly expressed, whereas miR-145 and miR-449a were absent. miR-145 and miR-449a were relatively specifically expressed in small intestine and lung, respectively. Therefore, the combined levels of miR-200a/b/c, miR-192, and miR-194 in plasma were very useful in diagnosing AKI induced by contact freezing in mice. Moreover, urinary miR-200a levels were useful for the diagnosis of renal tubular dysfunction in Dahl salt-sensitive rat with high salt administration. Our results indicate that miRNA expression profiles are useful as biomarkers for identification of various kidney injuries.

1,2,3,4,6-Penta-O-Galloyl-β-D-Glucose from Galla rhois Ameliorates Renal Tubular Injury and Microvascular Inflammation in Acute Kidney Injury Rats

2018 ◽  
Vol 46 (04) ◽  
pp. 785-800 ◽  
Author(s):  
Ji Hun Park ◽  
Min Chol Kho ◽  
Hyun Cheol Oh ◽  
Youn Chul Kim ◽  
Jung Joo Yoon ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Urine Volume ◽  
Kidney Injury ◽  
Tubular Damage ◽  
Tubular Dysfunction ◽  
Tubular Injury ◽  
Microvascular Inflammation ◽  
Renal Tubular

Renal ischemia-reperfusion injury (IRI), an important cause of acute kidney injury (AKI), causes increased renal tubular injury and microvascular inflammation. 1,[Formula: see text]2,[Formula: see text]3,[Formula: see text]4,[Formula: see text]6-penta-O-galloyl-[Formula: see text]-D-glucose (PGG) from Galla rhois has anticancer, anti-oxidation and angiogenesis effects. We examined protective effects of PGG on IRI-induced acute AKI. Clamping both renal arteries for 45[Formula: see text]min induced isechemia and then reperfusion. Treatment with PGG (10[Formula: see text]mg/kg/day and 50[Formula: see text]mg/kg/day for four days) significantly ameliorated urine volume, urine osmolality, creatinine clearance (Ccr) and blood urea nitrogen (BUN). In addition, PGG increased aquaporine 1/2/3, Na[Formula: see text]-K[Formula: see text]-ATPase and urea transporter (UT-B) and decreased ICAM-1, MCP-1, and HMGB-1 expression. In this histopathologic study, PGG improved glomerular and tubular damage. Immunohistochemistry results showed that PGG increased aquaporine 1/2, and Na[Formula: see text]-K[Formula: see text] ATPase and decreased ICAM-1 expression. These findings suggest that PGG ameliorates tubular injury including tubular dysfunction and microvascular inflammation in IRI-induced AKI rats.

Renal Sodium Handling in Relation to Environmental and Genetic Factors in Untreated Chinese

2020 ◽  
Author(s):  
Yuan-Yuan Kang ◽  
Yi-Bang Cheng ◽  
Qian-Hui Guo ◽  
Chang-Sheng Sheng ◽  
Qi-Fang Huang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Multiple Testing ◽  
Genetic Factors ◽  
Blood Pressure Monitoring ◽  
Lithium Concentration ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Renal Sodium Handling ◽  
Renal Tubular ◽  
Sodium Handling

Abstract Background We investigated proximal and distal renal tubular sodium handling, as assessed by fractional excretion of lithium (FELi) and fractional distal reabsorption rate of sodium (FDRNa), in relation to environmental and genetic factors in untreated patients. Methods Our study participants were suspected hypertensive patients being off antihypertensive medication for ≥2 weeks and referred for 24-hour ambulatory blood pressure monitoring. We collected serum and 24-hour urine for measurement of sodium, creatinine and lithium concentration, and calculated FELi and FDRNa. We genotyped 19 SNPs associated with renal sodium handling or blood pressure using the ABI SNapShot method. Results The 1409 participants (664 men, 47.1%) had a mean (±SD) age of 51.0±10.5 years. After adjustment for host factors, both FELi and FDRNa were significantly (P≤0.01) associated with season and humidity, explaining ~1.3% and ~3.5% of the variance, respectively. FELi was highest in autumn and lowest in summer and intermediate in spring and winter (P=0.007). FDRNa was also highest in autumn but lowest in winter and intermediate in spring and summer (P&lt;0.001). Neither FELi nor FDRNa was associated with outdoor temperature or atmospheric pressure (P≥0.13). After adjustment for host and environmental factors and Bonferroni multiple testing, among the 19 studied genetic variants, only rs12513375 was significantly associated with FELi and FDRNa (P≤0.004) and explained about 1.7% of the variance. Conclusions Renal sodium handling as measured by endogenous lithium clearance was sensitive to major environmental and genetic factors. Our finding is towards the use of these indexes for the definition of renal tubular dysfunction.

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