Table 3.
Mechanism of nephroprotection by SGLT2 inhibitors and RAAS-based agents
| Nephroprotective effects | SGLT2-based agents | RAAS-based agents | |
|---|---|---|---|
| SGLT2 inhibitor | ACE inhibitor | ARB | |
| Metabolic effects | |||
| HbA1c | Reduced | ||
| Body weight | Reduced | ||
| Serum uric acid | Reduced | ||
| Renal effects | |||
| Glomerular | |||
| Glucose reabsorption | Inhibited | ||
| Glomerular hyperfiltration | Reduced | ||
| Systemic and intraglomerular pressure | Reduced | Reduced | Reduced |
| Albuminuria | Reduced | Reduced | Reduced |
| Tubular | |||
| Proximal Na + reabsorption | Reduced | ||
| Tubular inflammation and fibrosis | Reduced | ||
| Tubular apoptosis | Reduced | ||
| Glomerular and tubular | |||
| Tubule-glomerular feedback | Inhibited | ||
| Glomerular and tubulointerstitial damage | Reduced | ||
| Effects on RAAS | |||
| Production of angiotensin II | Reduced | Reduced | |
| Secretion of aldosterone | Reduced | ||
| Sodium and water retention | Reduced | ||
| Peripheral vascular resistance | Reduced | ||
| Bradykinin activation | Inhibited | ||
| Other effects | |||
| Chronic hypoxia | Corrected | ||
| Abnormal iron deposition in the interstitium | Prevented | ||
| Plasminogen activator inhibitor-I | Inhibited | ||
| Formation of advanced glycation end products | Inhibited | ||
| Hydroxyl radical scavenging | Increased | ||
| Expression of hemoxygenase-1 and NADPH oxidase | Reduced | ||
| Inflammatory cell infiltration | Ameliorated | ||
ACE angiotensin-converting enzyme, ARB angiotensin receptor blocker, HbA1c glycosylated hemoglobin, Na sodium, NADPH nicotinamide adenine dinucleotide phosphate, RAAS renin-angiotensin-aldosterone system, SGLT2 sodium-glucose cotransporter-2