<b><i>Background:</i></b> Glycated haemoglobin A_1c (HbA_1c) has limitations as a glycemic marker for patients with diabetes and CKD and for those receiving dialysis. Glycated albumin is an alternative glycemic marker, and some studies have found that glycated albumin more accurately reflects glycemic control than HbA_1c in these groups. However, several factors are known to influence the value of glycated albumin including proteinuria. Continuous glucose monitoring (CGM) is another alternative to HbA_1c. CGM allows one to assess mean glucose, glucose variability, and the time spent in hypo-, normo-, and hyperglycemia. Currently, several different CGM models are approved for use in patients receiving dialysis; CKD (not on dialysis) is not a contraindication in any of these models. Some devices are for blind recording, while others provide real-time data to patients. Small studies suggest that CGM could improve glycemic control in hemodialysis patients, but this has not been studied for individual CKD stages. <b><i>Summary:</i></b> Glycated albumin and CGM avoid the pitfalls of HbA_1c in CKD and dialysis populations. However, the value of glycated albumin may be affected by several factors. CGM provides a precise estimation of the mean glucose. Here, we discuss the strengths and limitations for using HbA1c, glycated albumin, or CGM in CKD and dialysis population. <b><i>Key Messages:</i></b> Glycated albumin is an alternative glycemic marker but is affected by proteinuria. CGM provides a precise estimation of mean glucose and glucose variability. It remains unclear if CGM improves glycemic control in the CKD and dialysis populations.

Background Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease and represents a wide spectrum ranging from mild steatosis over non-alcoholic steatohepatitis with and without fibrosis to overt cirrhosis. Patients with NAFLD have a high risk of developing cardiovascular disease and chronic kidney disease (CKD). So far, there is scarce evidence of the prevalence of NAFLD among patients with CKD. We investigated the prevalence of moderate-to-severe hepatic steatosis graded according to the definition of NAFLD in a cohort of patients with CKD. Methods Hepatic liver fat content was evaluated by computed tomography (CT) scan in 291 patients from the Copenhagen Chronic Kidney Disease Cohort Study and in 866 age- and sex-matched individuals with normal kidney function from the Copenhagen General Population Study. Liver attenuation density &lt;48 Hounsfield units was used as cut-off value for moderate-to-severe hepatic steatosis. Results The prevalence of moderate-to-severe hepatic steatosis was 7.9% and 10.7% (P = 0.177) among patients with CKD and controls, respectively. No association between liver fat content and CKD stage was found. In the pooled data set from both cohorts, adjusted odds ratios for moderate-to-severe hepatic steatosis among persons with diabetes, overweight and obesity amounted to 3.1 (95% confidence interval (CI) 1.6-5.9), 14.8 (95% CI 4.6-47.9) and 42.0 (95% CI 12.9-136.6), respectively. Conclusions In a cohort of 291 patients with CKD, kidney function was not associated with the prevalence of moderate-to-severe hepatic steatosis as assessed by CT scan.

<b><i>Background:</i></b> Nonalcoholic fatty liver disease (NAFLD) is suggested as a risk factor for chronic kidney disease (CKD). The incidence of NAFLD is rising globally in parallel to the increasing incidences of obesity and type 2 diabetes. Diabetes remains the leading cause of CKD, but the co-existence of NAFLD, CKD, and type 2 diabetes is not well elucidated. Here, we evaluated the prevalence of NAFLD in patients with type 2 diabetes with and without CKD. <b><i>Methods:</i></b> This was a cross-sectional study including 50 patients with type 2 diabetes and CKD stages 3–5 (no dialysis), and 50 patients with type 2 diabetes without CKD. Liver fat content was estimated by proton magnetic resonance spectroscopy and magnetic resonance imaging proton density fat fraction. NAFLD was defined as liver fat fraction ≥5.6% according to guidelines. <b><i>Results:</i></b> Mean age was 72 ± 4.9 years in patients with CKD and 65.9 ± 7.8 years in patients without CKD (<i>p</i> &#x3c; 0.0001). Three out of four participants were men. BMI was 28.6 ± 3.5 kg/m² and 27 ± 4.0 kg/m² in patients with and without CKD, respectively (<i>p</i> = 0.0087). NAFLD was identified in 22 (44%) patients with CKD and 19 (38%) patients without CKD (<i>p</i> = 0.6845). Median (IQR) liver fat fraction was 4.7% (3.0–8.5) and 4.1% (2.9–7.7) in patients with and without CKD, respectively (difference in geometric means 5.3%, 95% CI −23; 45, <i>p</i> = 0.7463). <b><i>Conclusion:</i></b> These findings do not support any association between NAFLD and CKD (stages 3–5) in patients with type 2 diabetes.