Chronic kidney disease (CKD) is a growing global health burden, strongly associated with cardiovascular disease, the leading cause of mortality in this population. Dyslipidemia is a key metabolic abnormality in CKD, but traditional lipid measures such as total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides often fail to capture the complexity of lipid disturbances in CKD and after kidney transplantation. Apolipoproteins have emerged as more reliable markers of cardiovascular and renal risk. Elevated apolipoprotein B (ApoB), reduced apolipoprotein A1 (ApoA1), and a higher ApoB/ApoA1 ratio are linked to CKD progression, cardiovascular events, and post-transplant complications, including post-transplant diabetes mellitus. Lipoprotein(a), a genetically determined atherogenic lipoprotein, accumulates in CKD due to impaired clearance and further increases cardiovascular risk. Other apolipoproteins, such as APOL1 and APOE, modulate CKD susceptibility through lipid-dependent and independent mechanisms. In addition, proprotein convertase subtilisin/kexin type 9 (PCSK9) has been identified as an important regulator of lipid metabolism, and PCSK9 inhibitors may represent a promising therapeutic option, though evidence in advanced CKD and transplant recipients is still limited, especially regarding their effects on apolipoproteins. This review summarizes current evidence on apolipoproteins and PCSK9 in CKD and transplantation, with attention to their potential as biomarkers and therapeutic targets.

Magnesium (Mg²⁺) is essential for cardiovascular and metabolic health, yet hypomagnesemia is common in kidney transplant recipients (KTRs) due to immunosuppressive therapy and renal dysfunction. Oral Mg²⁺ supplementation is often ineffective due to poor absorption and side effects. Sodium-glucose cotransporter 2 inhibitors (SGLT2i) have been shown to increase serum Mg²⁺ in chronic kidney disease, but their effects in KTRs, particularly patients without diabetes, remain unclear. This observational study assessed 63 KTRs treated with dapagliflozin, analyzing the serum Mg²⁺ levels at baseline and after 3 and 6 months. The hypomagnesemia prevalence, associations with oral supplementation, diabetes status, and diuretic use were evaluated. The results showed a significant Mg²⁺ increase with SGLT2i therapy, reducing hypomagnesemia regardless of the diabetes status. Oral supplementation did not correlate with improved Mg²⁺ levels, reinforcing its limited efficacy. Additional benefits included reductions in the body weight, blood pressure, and serum urate without compromising graft function. SGLT2i may offer a novel approach to managing hypomagnesemia in KTRs, potentially reducing the reliance on ineffective supplements while providing renal and cardiovascular benefits. Further research is needed to confirm these findings and elucidate the underlying mechanisms.

Background: SGLT2 inhibitors (SGLT2is) lower glucose and have renoprotective effects, including reducing proteinuria. In kidney transplant recipients (KTRs), proteinuria impacts graft and patient survival. While SGLT2is benefits have been reported in diabetic KTRs, the data on non-diabetic KTRs are poor, and no data are available for albuminuria and non-albumin proteinuria. This study assessed the effects of dapagliflozin on urinary protein excretion in KTRs with and without diabetes. Methods: This analysis, from the Salerno CKD Cohort Study, included 66 KTRs (≥1 year post-transplant) with proteinuria despite renin–angiotensin system inhibitor therapy. The patients received dapagliflozin (10 mg/day) for six months, with assessments at the baseline (T0), three months (T1), and six months (T2); adverse events were monitored. The primary outcomes were changes in the urinary total, albumin, and non-albumin proteins. The secondary outcomes included weight, blood pressure, and eGFR. Results: At T1, the urinary total, albumin, and non-albumin proteins were significantly decreased, with a greater reduction in the non-albumin proteins vs. albumin (−27% vs. −9.4%, p = 0.001). No further changes occurred at T2. The patients’ weight and blood pressure also declined, while their eGFR and glucose remained stable. The non-albumin protein reduction was correlated with weight loss and diastolic blood pressure changes. Two patients discontinued use due to adverse events (one with a urinary tract infection, one with hypotension). Conclusions: Dapagliflozin reduces proteinuria, particularly non-albumin proteins, in KTRs with and without diabetes, with a low incidence of adverse effects. Further studies are needed to confirm the long-term benefits, especially in non-diabetic recipients.

Proteinuria is a strong predictor of graft failure in kidney transplant recipients (KTRs). While non-steroidal mineralocorticoid receptor antagonists (NS-MRAs), particularly finerenone, have demonstrated renoprotective benefits in chronic kidney disease, KTRs were excluded from pivotal trials. Evidence on finerenone’s safety and antiproteinuric effects in this population remains limited. This retrospective observational study evaluated 13 diabetic KTRs with persistent proteinuria despite optimized renin–angiotensin system blockade and sodium–glucose cotransporter 2 inhibitor therapy. Finerenone (10 mg/day) was added to standard care. Clinical and laboratory parameters, including estimated glomerular filtration rate (eGFR), serum electrolytes, total proteinuria, albuminuria, and their creatinine ratios, were assessed at baseline, 3 months, and 6 months. Safety outcomes focused on hyperkalemia and eGFR. Finerenone was discontinued in one patient due to hyperkalemia. In the remaining 12, 24-h proteinuria and urinary protein-to-creatinine ratio declined at 3 months and stabilized by 6 months. Conversely, no statistically significant changes were observed in albuminuria or the albumin-to-creatinine ratio. No clinically relevant changes occurred in eGFR, blood pressure, body weight, or serum electrolytes. This is the first study assessing finerenone in diabetic KTRs. Finerenone was well tolerated, was associated with an early reduction in proteinuria, and showed no adverse effects on graft function. These findings provide novel insights into the safety and potential role of finerenone in kidney transplant recipients.