Aim: To assess the prevalence of chronic kidney disease (CKD) and its potential utility as an early indicator of neuroretinal damage in diabetic retinopathy and hepatic damage in individuals with type 1 diabetes. Methods: We conducted a retrospective cross-sectional study of subjects diagnosed with type 1 diabetes and undergoing either continuous subcutaneous insulin infusion (CSII) or multiple daily injection (MDI) therapy, using either intermittent or continuous glucose monitoring for glycaemic detection. Hepatic steatosis index (HSI) and fibrosis index (FIB-4) were calculated for each subject to non-invasively detect liver damage (defined by HSI>36 or FIB-4≥1.3). Comprehensive ophthalmic examinations, ultra-widefield colour fundus photography and optical coherence tomography (OCT) of the macula and optic nerve were performed. Renal function was assessed by glomerular filtration rate (eGFR)<60 mL/min/1.73 m2 and/or the presence of diabetic nephropathy (CKD) by the presence or absence of microalbuminuria. Adult Treatment Panel III (ATP III) criteria were used to define the presence of metabolic syndrome (MS). Glycaemic variability indices were extrapolated from the last 14 days using the AGP obtained by downloading the glucose monitoring systems used by the patients. Results: The mean age of the patients was 48.8 +/- 13 years, with a mean duration of diabetes of 22 +/- 13 years. Of the patients, 23% had metabolic syndrome. Significant correlations were observed in the whole population (with and without DR): macular ganglion cell complex (GCC) and temporal nerve fibre layer (NFL) thinning with eGFR (p<0.05). There was also a significant inverse correlation between eGFR and FIB-4 (p<0.001), but no significant correlations were found between eGFR and HSI (p=0.502) or between glycaemic variability and FIB-4. Conclusions: The present data show how renal function significantly correlates with incipient liver damage in the studied population and can also be considered as a predictor of early neuroretinal changes. However, further research is needed to understand the complex relationship between eGFR and early diabetic metabolic complications.