Role of magnetic resonance diffusion weighted imaging in diagnosis of diabetic nephropathy in children living with type 1 diabetes mellitus

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Eman Nabil Wahba ◽  
Ashraf Elsharkawy ◽  
Mohammad Hosny Awad ◽  
Ashraf Abdel Rahman ◽  
Amr Sarhan
Keyword(s):  
Type 1 Diabetes ◽  
Diabetic Nephropathy ◽  
Glomerular Filtration Rate ◽  
Magnetic Resonance ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Estimated Glomerular Filtration Rate ◽  
Apparent Diffusion

Abstract Objectives Diabetic nephropathy is a serious and a common complication of diabetes that can lead to end stage renal disease among children living with type 1 diabetes, thus an early and accurate method of diagnosis that allows timely intervention is of high importance. This study aimed to evaluate the role of magnetic resonance diffusion weighted imaging in diagnosis of diabetic nephropathy in children with type 1 diabetes. Methods This prospective, observational, case control study included 30 children with type 1 diabetes and 30 matched healthy controls attending the outpatient clinics in Mansoura University Children’s Hospital. All were subjected to magnetic resonance DWI of the renal parenchyma and their glomerular filtration rate (GFR) was estimated, along with micro albumin in 24 h urine collection and HbA1c in patients with diabetes. Results Children with diabetes who were positive for microalbuminuria had significantly lower apparent diffusion coefficient value compared to Children with diabetes who were negative for microalbuminuria (p = 0.034) as well as controls (p = 0.001). Among children with type 1 diabetes, apparent diffusion coefficient had significant positive correlation with estimated glomerular filtration rate (r = 0.491, p = 0.006) and negative correlation with microalbuminuria (r = −0.437, p = 0.016). Conclusion Magnetic resonance DWI of the renal parenchyma is correlated with estimated glomerular filtration rate (eGFR) in children with type 1 diabetes and can detect GFR deterioration even in presence of normal albumin excretion.

1695-P: Genetic Determinants of Estimated Glomerular Filtration Rate (eGFR) in Type 1 Diabetes

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1695-P
Author(s):  
STUART MCGURNAGHAN ◽  
ATHINA SPILIOPOULOU ◽  
HELEN M. COLHOUN ◽  
PAUL M. MCKEIGUE
Keyword(s):  
Type 1 Diabetes ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Estimated Glomerular Filtration Rate ◽  
Genetic Determinants

Early Glomerular Filtration Rate Loss as a Marker of Diabetic Nephropathy

2012 ◽  
Vol 08 (01) ◽  
pp. 40 ◽  
Author(s):  
George Jerums ◽  
Elif Ekinci ◽  
Sianna Panagiotopoulos ◽  
Richard J MacIsaac ◽  
◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Type 1 Diabetes ◽  
Diabetic Nephropathy ◽  
Glomerular Filtration Rate ◽  
Kidney Disease ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Clinical Level ◽  
Ckd Stage

In the early 1980s, studies in type 1 diabetes suggested that glomerular filtration rate (GFR) loss begins with the onset of macroalbuminuria. However, recent evidence indicates that up to one-quarter of subjects with diabetes reach a GFR of less than 60 ml/min/1.73 m2(chronic kidney disease [CKD] stage 3) before developing micro- or macroalbuminuria. Furthermore, the prospective loss of GFR can be detected in early diabetic nephropathy (DN) well before CKD stage 3. Early GFR loss usually reflects DN in type 1 diabetes but, in older patients with type 2 diabetes, the assessment of early GFR loss needs to take into account the effects of aging. The assessment of GFR is now feasible at clinical level, using formulas based on serum creatinine, age, gender, and ethnicity. Overall, the estimation of early GFR loss is more accurate with the Chronic Kidney Disease Epidemiology (CKD–EPI) formula than with the Modification of Diet in Renal Disease (MDRD) study formula, but there is some evidence that the CKD-EPI formula does not exhibit better performance than the MDRD formula for estimating GFR in diabetes. Both formulas underestimate GFR in the hyperfiltration range. Formulas based on the reciprocal of cystatin C can also be used to estimate GFR, but their cost and lack of assay standardization have delayed their use at clinical level. In summary, early GFR loss is an important marker of DN as well as a potentially reversible target for interventions in DN.

Differences in susceptibility to develop parameters of diabetic nephropathy in four mouse strains with type 1 diabetes

2014 ◽  
Vol 306 (10) ◽  
pp. F1171-F1178 ◽  
Author(s):  
Stephanie Franzén ◽  
Malou Friederich-Persson ◽  
Angelica Fasching ◽  
Peter Hansell ◽  
Masaomi Nangaku ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 1 Diabetes ◽  
Diabetic Nephropathy ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Mouse Strains ◽  
Histological Damage ◽  
Glomerular Damage

One-third of diabetes mellitus patients develop diabetic nephropathy, and with underlying mechanisms unknown it is imperative that diabetic animal models resemble human disease. The present study investigated the susceptibility to develop diabetic nephropathy in four commonly used and commercially available mouse strains with type 1 diabetes to determine the suitability of each strain. Type 1 diabetes was induced in C57Bl/6, NMRI, BALB/c, and 129Sv mice by alloxan, and conscious glomerular filtration rate, proteinuria, and oxidative stress levels were measured in control and diabetic animals at baseline and after 5 and 10 wk. Histological alterations were analyzed using periodic acid-Schiff staining. Diabetic C57Bl/6 displayed increased glomerular filtration rate, i.e., hyperfiltration, whereas all other parameters remained unchanged. Diabetic NMRI developed the most pronounced hyperfiltration as well as increased oxidative stress and proteinuria but without glomerular damage. Diabetic BALB/c did not develop hyperfiltration but presented with pronounced proteinuria, increased oxidative stress, and glomerular damage. Diabetic 129Sv displayed proteinuria and increased oxidative stress without glomerular hyperfiltration or damage. However, all strains displayed intrastrain correlation between oxidative stress and proteinuria. In conclusion, diabetic C57Bl/6 and NMRI both developed glomerular hyperfiltration but neither presented with histological damage, although NMRI developed low-degree proteinuria. Thus these strains may be suitable when investigating the mechanism causing hyperfiltration. Neither BALB/c nor 129Sv developed hyperfiltration although both developed pronounced proteinuria. However, only BALB/c developed detectable histological damage. Thus BALB/c may be suitable when studying the roles of proteinuria and histological alterations for the progression of diabetic nephropathy.

Early Glomerular Filtration Rate Loss as a Marker of Diabetic Nephropathy

2010 ◽  
Vol 8 (1) ◽  
pp. 27 ◽  
Author(s):  
George Jerums ◽  
Elif Ekinci ◽  
Sianna Panagiotopoulos ◽  
Richard J MacIsaac ◽  
◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Type 1 Diabetes ◽  
Diabetic Nephropathy ◽  
Glomerular Filtration Rate ◽  
Kidney Disease ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Clinical Level ◽  
Ckd Stage

In the early 1980s, studies in type 1 diabetes suggested that glomerular filtration rate (GFR) loss begins with the onset of macroalbuminuria. However, recent evidence indicates that up to one-quarter of subjects with diabetes reach a GFR of less than 60 ml/min/1.73 m2(chronic kidney disease [CKD] stage 3) before developing micro- or macroalbuminuria. Furthermore, the prospective loss of GFR can be detected in early diabetic nephropathy (DN) well before CKD stage 3. Early GFR loss usually reflects DN in type 1 diabetes but, in older patients with type 2 diabetes, the assessment of early GFR loss needs to take into account the effects of ageing. The assessment of GFR is now feasible at clinical level, using formulas based on serum creatinine, age, gender and ethnicity. Overall, the estimation of early GFR loss is more accurate with the Chronic Kidney Disease Epidemiology (CKD–EPI) formula than with the Modification of Diet in Renal Disease (MDRD) study formula, but there is some evidence that the CKD-EPI formula does not exhibit better performance than the MDRD formula for estimating GFR in diabetes. Both formulas underestimate GFR in the hyperfiltration range. Formulas based on the reciprocal of cystatin C can also be used to estimate GFR, but their cost and lack of assay standardisation have delayed their use at clinical level. In summary, early GFR loss is an important marker of DN as well as a potentially reversible target for interventions in DN.

scholarly journals The Rate of Decline of Glomerular Filtration Rate May Not Be Associated with Polymorphism of the PPARγ2 Gene in Patients with Type 1 Diabetes and Nephropathy

PPAR Research ◽  
2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Bingmei Yang ◽  
Hongxin Zhao ◽  
Beverley Ann Millward ◽  
Andrew Glen Demaine
Keyword(s):  
Type 1 Diabetes ◽  
Diabetic Nephropathy ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Baseline Level ◽  
Filtration Rate ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Rate Of Decline

The aim of the study was to investigate whether a Pro12Ala polymorphism in the peroxisome proliferator-activated receptor gamma 2 (PPARγ2) gene is associated with the progress of diabetic nephropathy in patients with type 1 diabetes. 197 Caucasian patients with type 1 diabetes and ethnically matched 151 normal healthy controls were genotyped for this polymorphism. Results showed that there were no significant differences in the frequencies of the genotypes and alleles of the polymorphism between groups. Multiple regression analysis in 77 patients demonstrated that the rate of decline in renal function in terms of glomerular filtration rate was significantly correlated to the baseline level of cholesterol (P=0.0014), mean diastolic blood pressure during follow-up period (P=0.019), and baseline level of HbA1c (P=0.022) adjusting for the effect of diabetes duration and gender, but no significant association was found between the polymorphism and the progression of diabetic nephropathy in our studied population. In summary, our results show that the PPARγ2 polymorphism is unlikely to be associated with the development and progression of the diabetic nephropathy in patients with type 1 diabetes. Further studies in different populations may be warranted to confirm our findings as the sample size in our study was relatively small.

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