scholarly journals Kidney Injury Molecule-1 and the Loss of Kidney Function in Diabetic Nephropathy: A Likely Causal Link in Patients With Type 1 Diabetes

Diabetes Care ◽  
2015 ◽  
Vol 38 (6) ◽  
pp. 1130-1137 ◽  
Author(s):  
Nicolae M. Panduru ◽  
Niina Sandholm ◽  
Carol Forsblom ◽  
Markku Saraheimo ◽  
Emma H. Dahlström ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Diabetic Nephropathy ◽  
Kidney Function ◽  
Kidney Injury ◽  
Causal Link ◽  
Kidney Injury Molecule 1

scholarly journals Serum Cystatin C as a Biomarker for Early Diabetic Nephropathy and Dyslipidemia in Young Type 1 Diabetes Patients

2020 ◽  
Author(s):  
Lina Radzeviciene ◽  
Ingrida Stankute ◽  
Ausra Monstaviciene ◽  
Rimantė Dobrovolskiene ◽  
Evalda Danyte ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Kidney Function ◽  
Cystatin C ◽  
Young Patients ◽  
Kidney Injury ◽  
Albumin Excretion Rate ◽  
Serum Cystatin C ◽  
Serum Cystatin ◽  
Long Term Follow Up

Abstract Background. Early capture of initial stages of complications is the destination of long term follow up of type 1 diabetes (T1D) patients. The aim of this study was to assess the clinical significance of serum cystatin C in the early diagnosis of renal injury and its association with dyslipidemia in young T1D patients.Methods. 779 subjects were evaluated for kidney function by estimating glomerular filtration rate (eGFR) based on serum creatinine (eGFRcreat) and cystatin C (eGFRcys). Results. Median age of study subjects was 16.2 years (2.1;26.4), diabetes duration – 5.3 years (0.51;24.0). The median of HbA1c was 8% (5.2;19.9) (64 mmol/mol (33.3;194)); 24.2% of participants had HbA1c <7% (53 mmol/mol). Elevated albumin excretion rate was found in 13.5% of subjects. The median of cystatin C was 0.8 mg/L (0.33;1.71), the median of creatinine – 63 µmol/L (6;126). Median of eGFRcys was lower than eGFRcreat (92 ml/min/1.73m2 vs. 101 ml/min/1.73m2, p<0.001). 30.2% of all patients were classified as having worse kidney function when using cystatin C vs. creatinine for eGFR calculation. Linear correlations were found between cystatin C and HbA1c, r=-0.088, p<0.05, as well as cystatin C and HDL, r=-0.097, p<0.01.Conclusion. This study showed that cystatin C might be used as an additional biomarker of early kidney injury for young patients with T1D.

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.

scholarly journals Increased plasma kidney injury molecule-1 suggests early progressive renal decline in non-proteinuric patients with type 1 diabetes

2016 ◽  
Vol 89 (2) ◽  
pp. 459-467 ◽  
Author(s):  
Natalia Nowak ◽  
Jan Skupien ◽  
Monika A. Niewczas ◽  
Masayuki Yamanouchi ◽  
Melissa Major ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Kidney Injury ◽  
Kidney Injury Molecule 1

scholarly journals T Cell Expression and Release of Kidney Injury Molecule-1 in Response to Glucose Variations Initiates Kidney Injury in Early Diabetes

2021 ◽  
Author(s):  
Josephine M. Forbes ◽  
Domenica A. McCarthy ◽  
Andrew J. Kassianos ◽  
Tracey Baskerville ◽  
Amelia J. Fotheringham ◽  
...  
Keyword(s):  
T Cells ◽  
Type 1 Diabetes ◽  
T Cell ◽  
High Risk ◽  
Kidney Disease ◽  
Kidney Injury ◽  
Glycemic Variability ◽  
Low Risk ◽  
Kidney Injury Molecule 1

Half of the mortality in diabetes is seen in individuals <50 years of age and commonly predicted by the early onset of kidney disease (DKD). In Type 1 diabetes, increased uACR (urinary albumin-creatinine ratio) during adolescence defines this risk, but the pathological factors responsible remain unknown. We postulated that early in diabetes, glucose variations contribute to kidney injury molecule- 1 (KIM-1) release from circulating T cells, elevating uACR and DKD risk. <p>DKD risk was assigned in youth with type 1 diabetes [n=100; 20.0±2.8 yrs; M:F-54:46, HbA<sub>1C</sub>-66.1(12.3) mmol/mol; diabetes duration-10.7±5.2 yrs; BMI-24.5(5.3) kg.m<sup>-2</sup>] and 10 year historical uACR, HbA<sub>1C</sub> and random blood glucose concentrations collected retrospectively. Glucose fluctuations in the absence of diabetes were also compared to streptozotocin diabetes in <i>Apolipoprotein E-/-</i> mice. Kidney biopsies were used to examine infiltration of KIM-1 expressing T cells in DKD and compared with other chronic kidney disease.</p> <p>Individuals at high risk for DKD had persistent elevations in uACR (uACR<sub>AUC0-10yrs</sub>, 29.7±8.8 vs 4.5±0.5; <i>P</i><0.01 vs low risk) and early kidney dysfunction including ~8.3ml.min<sup>-1</sup>.1.73m<sup>-2</sup> higher estimated glomerular filtration rates (eGFR<sub>SCHWARTZ</sub>; <i>P<sub>adj</sub></i> <0.031 vs low risk) and plasma KIM-1 concentrations (~15% higher vs low risk;<i> P</i><0.034). High risk individuals had greater glycemic variability and increased peripheral blood T cell KIM-1 expression, particularly on CD8+ T cells. These findings were confirmed in a murine model of glycemic variability both in the presence and absence of diabetes. KIM-1+ T cells were also infiltrating kidney biopsies from individuals with DKD. Healthy primary human proximal tubule epithelial cells exposed to plasma from high risk youth with diabetes showed elevated collagen IV and SGLT2 expression, alleviated with KIM-1 blockade. Taken together, these studies suggest that glycemic variations confer risk for DKD in diabetes via increased CD8+ T cell production of KIM-1.<b><br> </b></p>

scholarly journals Evaluation of kidney injury molecule-1 as a disease progression biomarker in diabetic nephropathy

2019 ◽  
Vol 35 (4) ◽  
Author(s):  
Fatima Abid Khan ◽  
Syeda Sadia Fatima ◽  
Ghulam Mustafa Khan ◽  
Sana Shahid
Keyword(s):  
Diabetic Nephropathy ◽  
Disease Progression ◽  
Kidney Function ◽  
Kidney Injury ◽  
Positive Association ◽  
Kidney Damage ◽  
Control Group ◽  
Diabetic Patients ◽  
Kidney Injury Molecule 1

Background & Objective: Kidney Injury Molecule-1 (KIM-1) is a peptide whose release into circulation is specific to tubular injury. This study aimed to estimate levels of kidney injury molecule-1 in diabetic patients with and without kidney disease. And evaluate the role of KIM-1 as an early screening marker of progressive kidney injury. Methods: This follow-up study included n=85 subjects from the diabetic clinic of Jinnah Post Graduate Medical Center (JPMC) in collaboration with Aga Khan University from November 2016 till September 2017 They were divided as: i) Group A1 (n=30) participants with diabetes for <5 years without microalbuminuria ii) Group A2 (n= 30) subjects with diabetes for 6-10 years with microalbuminuria; iii) Group B (n=25) subjects as healthy control group. All study participants were followed for 6 months and their blood glucose, urea, creatinine, electrolytes, albuminuria and serum KIM-1 were assayed. Results: High KIM-1 at baseline was present in group A2 patients as compared to controls and group A1 (p<0.001). Higher levels were seen after six months in group A1 along with the presence of micro albuminuria (p<0.001) suggesting kidney damage. Moderate positive association were seen for KIM1 with creatinine levels (r=0.530; p<0.001), and HbA1c (r=0.576; p<0.001) in all patients. While a strong positive association was seen for blood urea nitrogen as a marker for kidney function both at baseline (r= 0.728; p=0.000) and follow up (r=0.747; p=0.001). Multiple logistic regression controlling for age showed that KIM1 was independently associated with BUN (r=0.727; p<0.001), creatinine (r=0.510; p<0.001) and HbA1c (r=0.401; p=0.008) in all groups. Conclusion: Rising KIM-1 levels with progressive kidney damage with or without derangement of kidney function is reported in this study. This finding may pave a way towards identifying KIM1 as a prognostic marker for kidney injury. doi: https://doi.org/10.12669/pjms.35.4.154 How to cite this:Khan FA, Fatima SS, Khan GM, Shahid S. Evaluation of kidney injury molecule-1 as a disease progression biomarker in diabetic nephropathy. Pak J Med Sci. 2019;35(4):---------. doi: https://doi.org/10.12669/pjms.35.4.154 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

scholarly journals Regression of microalbuminuria in type 1 diabetes is associated with lower levels of urinary tubular injury biomarkers, kidney injury molecule-1, and N-acetyl-β-D-glucosaminidase

2011 ◽  
Vol 79 (4) ◽  
pp. 464-470 ◽  
Author(s):  
Vishal S. Vaidya ◽  
Monika A. Niewczas ◽  
Linda H. Ficociello ◽  
Amanda C. Johnson ◽  
Fitz B. Collings ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Kidney Injury ◽  
Tubular Injury ◽  
Kidney Injury Molecule 1

scholarly journals T Cell Expression and Release of Kidney Injury Molecule-1 in Response to Glucose Variations Initiates Kidney Injury in Early Diabetes

2021 ◽  
Author(s):  
Josephine M. Forbes ◽  
Domenica A. McCarthy ◽  
Andrew J. Kassianos ◽  
Tracey Baskerville ◽  
Amelia J. Fotheringham ◽  
...  
Keyword(s):  
T Cells ◽  
Type 1 Diabetes ◽  
T Cell ◽  
High Risk ◽  
Kidney Disease ◽  
Kidney Injury ◽  
Glycemic Variability ◽  
Low Risk ◽  
Kidney Injury Molecule 1

Half of the mortality in diabetes is seen in individuals <50 years of age and commonly predicted by the early onset of kidney disease (DKD). In Type 1 diabetes, increased uACR (urinary albumin-creatinine ratio) during adolescence defines this risk, but the pathological factors responsible remain unknown. We postulated that early in diabetes, glucose variations contribute to kidney injury molecule- 1 (KIM-1) release from circulating T cells, elevating uACR and DKD risk. <p>DKD risk was assigned in youth with type 1 diabetes [n=100; 20.0±2.8 yrs; M:F-54:46, HbA<sub>1C</sub>-66.1(12.3) mmol/mol; diabetes duration-10.7±5.2 yrs; BMI-24.5(5.3) kg.m<sup>-2</sup>] and 10 year historical uACR, HbA<sub>1C</sub> and random blood glucose concentrations collected retrospectively. Glucose fluctuations in the absence of diabetes were also compared to streptozotocin diabetes in <i>Apolipoprotein E-/-</i> mice. Kidney biopsies were used to examine infiltration of KIM-1 expressing T cells in DKD and compared with other chronic kidney disease.</p> <p>Individuals at high risk for DKD had persistent elevations in uACR (uACR<sub>AUC0-10yrs</sub>, 29.7±8.8 vs 4.5±0.5; <i>P</i><0.01 vs low risk) and early kidney dysfunction including ~8.3ml.min<sup>-1</sup>.1.73m<sup>-2</sup> higher estimated glomerular filtration rates (eGFR<sub>SCHWARTZ</sub>; <i>P<sub>adj</sub></i> <0.031 vs low risk) and plasma KIM-1 concentrations (~15% higher vs low risk;<i> P</i><0.034). High risk individuals had greater glycemic variability and increased peripheral blood T cell KIM-1 expression, particularly on CD8+ T cells. These findings were confirmed in a murine model of glycemic variability both in the presence and absence of diabetes. KIM-1+ T cells were also infiltrating kidney biopsies from individuals with DKD. Healthy primary human proximal tubule epithelial cells exposed to plasma from high risk youth with diabetes showed elevated collagen IV and SGLT2 expression, alleviated with KIM-1 blockade. Taken together, these studies suggest that glycemic variations confer risk for DKD in diabetes via increased CD8+ T cell production of KIM-1.<b><br> </b></p>

scholarly journals Kidney Function After Islet Transplant Alone in Type 1 Diabetes: Impact of immunosuppressive therapy on progression of diabetic nephropathy

Diabetes Care ◽  
2007 ◽  
Vol 30 (5) ◽  
pp. 1150-1155 ◽  
Author(s):  
P. Maffi ◽  
F. Bertuzzi ◽  
F. De Taddeo ◽  
P. Magistretti ◽  
R. Nano ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Diabetic Nephropathy ◽  
Immunosuppressive Therapy ◽  
Kidney Function ◽  
Islet Transplant
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