Table 1.

Therapeutic strategies in the DKD with potential anti-inflammatory properties.

Drug	Primary target	Main outcomes in DKD	Anti-inflammatory effects	References
RAS blockers	Inhibition of ACE or blockade of angiotensin II receptor.	Reduce proteinuria and the progression of nephropathy.	Inhibition of NF-κB, MCP1 gene expression, and macrophage infiltration.	(68, 69)
SGLT2 inhibitors	Blockade of glucose reabsorption by SGLT2 at the proximal tubule.	Improved glycemic control. Slower progression of kidney disease and lower rates of clinically relevant renal events.	Reduction of inflammation by targeting the IL1ß and reduction of hsCRP, TNFα, IL6, and IFNγ.	(70–90)
DPP4 inhibitors and GLP-1 receptor agonists	Stimulation of glucose-dependent insulin release.	Improved glycemic control and body weight reductions. Renoprotective actions	Reduction in levels of inflammatory markers including CRP, TNFα, IL6, and IL18.	(91–97)
Pentoxifylline	Inhibition of phosphodiesterases.	Reduced progression of renal disease and proteinuria.	Downregulation of NF-κB signaling and reduction of inflammatory biomarkers.	(98–114)

RAAS, Renin-Angiotensin Aldosterone System; ACEI, angiotensin converting enzyme; NF-κB, nuclear factor-κB; MCP1, monocyte chemoattractant protein 1; SGLT2, type 2 sodium-glucose cotransporter; IL, interleukin; hsCRP, high sensitivity C reactive protein; TNFα, tumor necrosis factor α; IFN-γ, interferon γ; DPP4, dipeptidyl-peptidase-4; GLP-1, glucagon-like peptide-1.