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14:00
15:30
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Chung-Kuan Wu
Speaker
SGLT-2 抑制劑於慢性腎臟病之臨床應用與保護機轉 The role of SGLT2 inhibitors in the treatment of diabetic and non-diabetic kidney disease
Diabetic kidney disease is a major cause of chronic kidney disease and end-stage kidney disease. In addition to hyperglycemia and metabolic abnormalities, its pathophysiology involves glomerular hyperfiltration, increased intraglomerular pressure, excessive tubular workload, and renal inflammation. Sodium-glucose cotransporter-2 inhibitors (SGLT2 inhibitors) reduce glucose and sodium reabsorption in the proximal tubule, restore tubuloglomerular feedback, lower intraglomerular pressure, decrease tubular workload, and may attenuate renal inflammation. These mechanisms contribute to cardiovascular and kidney protection beyond their glucose-lowering effects. In addition, the sustained beneficial effects extend to non-diabetic kidney disease. Large clinical trials and meta-analyses have demonstrated that SGLT2 inhibitors reduce albuminuria, slow kidney function decline, and decrease cardiovascular and renal adverse events. These benefits were observed in addition to standard treatment with renin–angiotensin system inhibitors.
Key topics of the presentation include:
1. The physiological roles of SGLT1 and SGLT2 in the intestine and proximal renal tubule
2. The mechanisms by which SGLT2 inhibition reduces intraglomerular pressure, tubular workload, and renal inflammation
3. Cardiovascular and renal outcomes from the clinical trial, and relevant meta-analyses
4. The role of SGLT2 inhibitors in the comprehensive management of patients with type 2 diabetes and chronic kidney disease according to the KDIGO guideline
Overall, SGLT2 inhibitors have evolved from glucose-lowering agents into a fundamental component of cardiovascular and kidney risk management in diabetic kidney disease. Their timely use, based on kidney function, albuminuria, cardiovascular risk, and the overall comorbidity profile, may help delay kidney disease progression and improve long-term clinical outcomes.
The role of SGLT2 inhibitors in the treatment of diabetic and non-diabetic kidney disease
Diabetic kidney disease is a major cause of chronic kidney disease and end-stage kidney disease. In addition to hyperglycemia and metabolic abnormalities, its pathophysiology involves glomerular hyperfiltration, increased intraglomerular pressure, excessive tubular workload, and renal inflammation. Sodium-glucose cotransporter-2 inhibitors (SGLT2 inhibitors) reduce glucose and sodium reabsorption in the proximal tubule, restore tubuloglomerular feedback, lower intraglomerular pressure, decrease tubular workload, and may attenuate renal inflammation. These mechanisms contribute to cardiovascular and kidney protection beyond their glucose-lowering effects. In addition, the sustained beneficial effects extend to non-diabetic kidney disease. Large clinical trials and meta-analyses have demonstrated that SGLT2 inhibitors reduce albuminuria, slow kidney function decline, and decrease cardiovascular and renal adverse events. These benefits were observed in addition to standard treatment with renin–angiotensin system inhibitors.
Key topics of the presentation include:
1. The physiological roles of SGLT1 and SGLT2 in the intestine and proximal renal tubule
2. The mechanisms by which SGLT2 inhibition reduces intraglomerular pressure, tubular workload, and renal inflammation
3. Cardiovascular and renal outcomes from the clinical trial, and relevant meta-analyses
4. The role of SGLT2 inhibitors in the comprehensive management of patients with type 2 diabetes and chronic kidney disease according to the KDIGO guideline
Overall, SGLT2 inhibitors have evolved from glucose-lowering agents into a fundamental component of cardiovascular and kidney risk management in diabetic kidney disease. Their timely use, based on kidney function, albuminuria, cardiovascular risk, and the overall comorbidity profile, may help delay kidney disease progression and improve long-term clinical outcomes.
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Kuang-Yu Wei
Speaker
新型鉀離子結合劑 Lokelma 的應用Over the past decade, treatment of chronic kidney disease (CKD) and heart failure has evolved towards an integrated approach to cardiorenal protection that includes renin–angiotensin–aldosterone system (RAAS) inhibitors, mineralocorticoid receptor antagonists (MRAs), sodium–glucose cotransporter 2 (SGLT2) inhibitors and more individualized strategies for dietary potassium intake. RAAS inhibitors remain a cornerstone of treatment, and clinical trials have generally demonstrated the greatest benefits when these drugs are prescribed at maximally tolerated doses. However, the risk of hyperkalaemia frequently limits their initiation, dose optimization and continued use, thereby reducing the potential kidney and cardiovascular benefits of treatment.
Hyperkalaemia should therefore be regarded as a manageable complication of cardiorenal therapy rather than an automatic indication to reduce or discontinue RAAS inhibition. Contemporary management includes correction of reversible causes together with individualized dietary interventions, diuretics, SGLT2 inhibitors and potassium-lowering therapies. The aim of these strategies is not merely to achieve a transient reduction in blood potassium, but to enable patients to initiate and maintain guideline-directed treatment. When further inhibition of the RAAS pathway is indicated, an MRA can be added to a maximally tolerated angiotensin-converting enzyme inhibitor or angiotensin receptor blocker. In individuals at increased risk of hyperkalemia, the non-steroidal MRA may offer a more favorable potassium profile than steroidal MRAs.
Beyond their established cardiorenal benefits, SGLT2 inhibitors reduce the risk of serious hyperkalemia and could therefore facilitate continued treatment with RAAS inhibitors and MRAs. Novel potassium binders, including sodium zirconium cyclosilicate and patiromer, effectively reduce blood potassium levels and prevent recurrent hyperkalaemia, thereby enabling sustained or intensified RAAS inhibitor therapy in patients with CKD and heart failure. Sodium zirconium cyclosilicate has also been shown to control predialysis hyperkalaemia in patients receiving haemodialysis. Emerging evidence suggests that potassium binders may have additional effects, including reductions in aldosterone levels, systolic blood pressure and urinary albumin excretion with patiromer, and increased serum bicarbonate concentrations with sodium zirconium cyclosilicate. By mitigating the risk of hyperkalemia, potassium binders could also enable some patients with CKD to adopt healthier potassium-rich, plant-predominant dietary patterns.
Room 6
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