This study aimed to assess whether routine nephrology examinations could predict renal amyloidosis in kidney disease patients with monoclonal gammopathy. A total of 356 consecutive hospitalized patients in the nephrology department with monoclonal gammopathy performed renal biopsies, including 50 renal amyloidosis patients and 306 non-renal amyloidosis patients, were included after strict filtering. Laboratory and imaging data were collected for each patient. Renal amyloidosis patients exhibited significantly higher 24-h proteinuria and estimated glomerular filtration rate and decreased serum creatinine (SCr), albumin and immunoglobin M, with lower κ light chain and κ/λ ratio in urine and serum. Higher 24-h proteinuria and 24-h microalbuminuria and lower random urine κ/λ ratio, serum κ light chain, serum κ/λ ratio and SCr were significant risk factors for renal amyloidosis. Nomogram model identified albumin, 24-h urinary microalbumin excretion rate, 24-h urine κ light chain, 24-h urine κ/λ ratio and serum IgM as combined predictors of renal amyloidosis (area under the curve 0.781, 95% CI 0.718-0.854). Combined biomarkers (albumin, 24-h urinary microalbumin excretion rate, 24 h urine κ light chain, 24-h urine κ/λ ratio and serum IgM) effectively predicted renal amyloidosis in kidney disease patients with monoclonal gammopathy.

Retinal microvascular impairments are recognized as a non-invasive measure of systemic vascular injury in patients with diabetes. Change in retinal structure and function may serve as markers of renal and cardiovascular microvascular pathology, thereby providing a potential source of prognostic information for predicting outcomes of diabetic kidney disease (DKD), chronic kidney disease (CKD), and cardiovascular disease (CVD). The study design of a comprehensive literature review was selected. The literature review was conducted using the systematic approach of PRISMA 2020 guidelines. However, the study design is a literature review. The literature review aimed to synthesize the current evidence using a narrative approach to the relationship between retinal microvascular parameters and renal and cardiovascular outcomes in patients with diabetes. Cross-sectional, case-control, randomized controlled, and prospective cohort studies published between January 1, 2000, and December 31, 2025, were included after the literature search. We conducted the literature search and screening in compliance with the PRISMA 2020 guidelines to ensure transparency and reproducibility. The review indicates that broader retinal venules, constriction of arterioles, decreased fractal dimension, failed circulation inside the fovea, and expanded foveal avascular zone were considerably associated with the augmented danger of DKD, albuminuria, and lost estimated glomerular filtration rate (eGFR). In several longitudinal cohort studies, diabetic retinopathy at moderate-to-severe levels, but not at mild, fully explained incident CVD and stroke, as well as coronary events and all-cause mortality. Synergistic outcomes were a development of the coexistence of retinal abnormalities and microalbuminuria, with a risk of up to seven times that of cardiovascular events. Nonetheless, certain studies identified no or weak correlations when traditional risk factors were adjusted, underscoring the variability in predictive efficacy. The study concluded that retinal microvascular predictors, particularly diabetic retinopathy severity and imaging parameters, have strong potential to predict non-invasive renal and cardiovascular outcomes in diabetes. These results support the notion of the retina as a window into microvascular health within the systemic circulation. Future, large-scale studies using standardized imaging modalities are warranted to determine the additional prognostic value of retinal biomarkers in risk-stratification models for diabetic complications.

Diabetic kidney disease (DKD) persists as the leading cause of chronic kidney disease (CKD) and often leads to end-stage renal disease (ESRD). Worldwide, 30-50% of patients with diabetes are affected by DKD, while DKD contributes to about half of ESRD. Previously, DKD had been defined based on overt proteinuria-that is, a urine albumin-to-creatinine ratio (UACR) above 300 mg/g-after a stage of microalbuminuria (UACR 30-300 mg/g). However, emerging data suggest that a significant number of patients develop renal functional decline without albuminuria, suggesting that DKD can occur in the absence of protein excretion. This phenotype of normoalbuminuric or non-proteinuric DKD (NA-DKD or NP-DKD) is emerging as an important clinical entity. It is characterized by a gradual decline in renal function, commonly with an annual reduction in estimated glomerular filtration rate (eGFR) > 3 mL/min/1.73 m[2] or an eGFR < 60 mL/min/1.73 m[2], while the UACR remains < 30 mg/g. Growing rates of NP-DKD expose limitations inherent in traditional models of DKD pathogenesis and underscore the need for diagnostic and therapeutic paradigms that are not reliant on albuminuria-only criteria. Here, we present a comprehensive review of the NP-DKD to guide a more inclusive model of DKD pathogenesis, its diagnosis, and therapy.