Altered serum levels of FGF-23 and magnesium are independent risk factors for an increased albumin-to-creatinine ratio in type 2 diabetics with chronic kidney disease

Abstract Background We compared the effects of sodium–glucose cotransporter 2 (SGLT2) inhibitors on renal function in participants with type 2 diabetes and chronic kidney disease (CKD) classified by degree of albuminuria. Methods A retrospective review of the clinical records of Japanese participants with type 2 diabetes (age > 20 years; SGLT2 inhibitor treatment > 2 years; estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m2) was conducted. Based on the urinary albumin-to-creatinine ratio (UACR) or urinary protein-to-creatinine ratio (UPCR) at the start of SGLT2 inhibitor administration, participants were categorized into three groups: normoalbuminuria (A1; UACR < 30 mg/g Cr or UPCR < 0.15 g/g Cr), microalbuminuria (A2; UACR 30 to < 300 mg/g Cr or UPCR 0.15 to < 0.50 g/g Cr), and macroalbuminuria (A3; UACR ≥ 300 mg/g Cr or UPCR ≥ 0.50 g/g Cr). The study outcome was a comparison of the rates of change in renal function evaluated by eGFR at 2 years after starting SGLT2 inhibitor among the three groups. Results A total of 87 participants (40 females, 47 males) were categorized into three groups: A1 (n = 46), A2 (n = 25), and A3 (n = 16). eGFR was similarly decreased at 2 years before starting SGLT2 inhibitor in all three groups. However, the decline in eGFR was ameliorated at 2 years after starting SGLT2 inhibitor, and eGFR was rather increased in the A1 and A2 groups. Interestingly, the rate of change in eGFR at 2 years after starting SGLT2 inhibitor in the A1 group was significantly higher than that in the A3 group. Conclusions These results demonstrate that more favorable effects of SGLT2 inhibitors on renal function were observed in participants with type 2 diabetes and CKD with normoalbuminuria compared with those with macroalbuminuria. Trial registration UMIN-CTR: UMIN000035263. Registered 15 December 2018

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A Pilot Randomized Crossover Trial Assessing the Safety and Short-Term Effects of Walnut Consumption by Patients with Chronic Kidney Disease

Nutrients ◽

10.3390/nu12010063 ◽

2019 ◽

Vol 12 (1) ◽

pp. 63 ◽

Cited By ~ 1

Author(s):

Pilar Sanchis ◽

Marilisa Molina ◽

Francisco Berga ◽

Elena Muñoz ◽

Regina Fortuny ◽

...

Keyword(s):

Risk Factors ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Inositol Phosphates ◽

Control Diet ◽

Fibroblast Growth Factor 23 ◽

Serum Levels ◽

Short Term ◽

Daily Consumption ◽

Randomized Crossover Trial

The aim of this study of patients with chronic kidney disease (CKD) is to assess the safety of daily consumption of walnuts on the physiological levels of phosphorous, potassium, parathyroid hormone (PTH), and fibroblast growth factor 23 (FGF23), and to assess the short-term benefits of this intervention on risk factors associated with cardiovascular events. This led us to perform a prospective, randomized, crossover, pilot clinical trial examined 13 patients with CKD. Subjects were randomly assigned to a diet of 30 g of walnuts per day or the control diet. After 30 days, each group was given a 30-day washout period, and then switched to the alternate diet for 30 days. Urinary and serum levels of phosphorous and potassium, multiple vascular risk factors, and urinary inositol phosphates (InsPs) were measured at baseline and at the end of the intervention period. Our results showed that the walnut dietary supplement led to reduced blood pressure, LDL cholesterol, and albumin excretion, but had no effect on the physiological levels of phosphorous, potassium, PTH, and FGF23. This is the first report to show that daily consumption of walnuts by patients with CKD does not alter their physiological levels of phosphorous, potassium, PTH, and FGF23 when included in a sodium-, protein-, phosphate-, and potassium-controlled diet, and it could be an effective strategy for reducing cardiovascular risk in patients with CKD.

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Differences in Risk Factors for Diabetic Retinopathy in Type 1 and Type 2 Diabetes Mellitus Patients in North-East Poland

Medicina ◽

10.3390/medicina56040177 ◽

2020 ◽

Vol 56 (4) ◽

pp. 177

Author(s):

Wojciech Matuszewski ◽

Magdalena M. Stefanowicz-Rutkowska ◽

Magdalena Szychlińska ◽

Elżbieta Bandurska-Stankiewicz

Keyword(s):

Diabetes Mellitus ◽

Risk Factors ◽

Type 2 Diabetes ◽

Chronic Kidney Disease ◽

Type 2 Diabetes Mellitus ◽

Diabetic Retinopathy ◽

Kidney Disease ◽

Study Group

Background and Objective: Nowadays, diabetes is one of the main causes of blindness in the world. Identification and differentiation of risk factors for diabetic retinopathy depending on the type of diabetes gives us the opportunity to fight and prevent this complication. Aim of the research: To assess differences in the risk factors for diabetic retinopathy in type 1 and type 2 diabetes mellitus patients in Warmia and Mazury Region, Poland. Materials and Methods: Risk factors for diabetic retinopathy (DR) were assessed on the basis of an original questionnaire, which included: personal data, clinical history of diabetes and eye disease. Elements of clinical examination: blood pressure, BMI, waist circumference. Indicators of diabetes metabolic control: mean glycemia, glycated hemoglobin (HbA1c), total cholesterol and triglycerides, creatinine, glomerular filtration rate (GFR), albumin–creatinine ratio in urine. Results: The study group included 315 (26%) patients with DM1 and 894 (74%) patients with DM2. Risk factors were estimated on the basis of logistic regression and verified with Student’s t-test. Statistically significant dependencies were found in both groups between the occurrence of diabetic retinopathy and diabetes duration, HbA1c, triglyceride concentrations, indicators of kidney function and cigarette smoking status. In the DM2 group, the development of DR was significantly influenced by the implemented models of diabetic treatment. Conclusions: In the whole study group, the risk of DR was associated with the duration of diabetes, HbA1c, triglyceride concentrations and smoking. In DM1 patients, the risk of DR was associated with diabetic kidney disease in the G1A1/A2 stage of chronic kidney disease, and in DM2 patients with the G2 stage of chronic kidney disease. An important risk factor for DR in DM2 patients was associated with late introduction of insulin therapy.

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Serum Carnosinase-1 and Albuminuria Rather than the CNDP1 Genotype Correlate with Urinary Carnosinase-1 in Diabetic and Nondiabetic Patients with Chronic Kidney Disease

Journal of Diabetes Research ◽

10.1155/2019/6850628 ◽

2019 ◽

Vol 2019 ◽

pp. 1-12 ◽

Cited By ~ 1

Author(s):

Angelica Rodriguez-Niño ◽

Sibylle J. Hauske ◽

Anna Herold ◽

Jiedong Qiu ◽

Jacob van den Born ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Healthy Subjects ◽

Linear Regression Analysis ◽

Multivariate Linear Regression Analysis ◽

Creatinine Ratio ◽

Healthy Individuals ◽

Albumin Creatinine Ratio ◽

Spot Urine

Background. Carnosinase-1 (CN-1) can be detected in 24 h urine of healthy individuals and patients with type 2 diabetes (T2DM). We aimed to assess whether urinary CN-1 is also reliably measured in spot urine and investigated its association with renal function and the albumin/creatinine ratio (ACR). We also assessed associations between the CNDP1 (CTG)n genotype and CN-1 concentrations in serum and urine. Methods. Patients with T2DM (n=85) and nondiabetic patients with chronic kidney disease (CKD) (n=26) stratified by albuminuria (ACR≤300 mg/g or ACR>300 mg/g) recruited from the nephrology clinic and healthy subjects (n=24) were studied. Results. Urinary CN-1 was more frequently detected and displayed higher concentrations in patients with ACR>300 mg/g as compared to those with ACR≤300 mg/g irrespective of the baseline disease (T2DM: 554 ng/ml [IQR 212-934 ng/ml] vs. 31 ng/ml [IQR 31-63 ng/ml] (p<0.0001) and nondiabetic CKD: 197 ng/ml [IQR 112-739] vs. 31 ng/ml [IQR 31-226 ng/ml] (p=0.015)). A positive correlation between urinary CN-1 and ACR was found (r=0.68, p<0.0001). Multivariate linear regression analysis revealed that ACR and serum CN-1 concentrations but not eGFR or the CNDP1 genotype are independent predictors of urinary CN-1, explaining 47% of variation of urinary CN-1 concentrations (R2=0.47, p<0.0001). Conclusion. These results confirm and extend previous findings on urinary CN-1 concentrations, suggesting that assessment of CN-1 in spot urine is as reliable as in 24 h urine and may indicate that urinary CN-1 in macroalbuminuric patients is primarily serum-derived and not locally produced.

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