Table 1.

Effects of spleen tyrosine kinase (Syk) inhibitors on glomerulonephritis.

Clinical disease	Model	Treatment	Results	Reference
Lupus nephritis	NZB/W	Fostamatinib	As prophylactic treatment Delayed proteinuria and azotemia Reduced renal pathology and prolonged survival Did not affect serum anti-DNA autoantibodies In full-blown disease Decreased the incidence and severity of renal pathology	[22]
	MRL/lpr	Fostamatinib	As prophylactic treatment Prevented development of proteinuria and suppressed pathologic changes In full-blown disease Improved proteinuria Decreased lymphadenopathy Did not affect serum anti-DNA autoantibodies	[23]
Antiglomerular basement membrane nephritis	NTN	Fostamatinib	As prophylactic treatment Improved proteinuria Reduced glomerular fibrinoid necrosis and infiltration of inflammatory cells Increased exogenous antibody deposition in glomeruli Suppressed levels of both circulating and glomerulus-deposited endogenous antibodies In full-blown disease Improved proteinuria and serum creatinine levels Increased exogenous antibody deposition in glomeruli Reduced renal MCP-1 and IL-1β production	[24]
	NTN	SYK inhibitor (Celgene Corp.)	As prophylactic treatment Prevented proteinuria, thrombosis, and platelet activation Inhibited JNK and p38 MAPK activation Reduced glomerular inflammation leukocyte recruitment	[25]
IgA nephropathy	In vitro	R406; siRNA	In vitro study  Decreased heat-aggregated IgA1-induced IL-6, IL-8, IFN-γ, IP-10, RANTES, and PDGF-BB production by human mesangial cells Inhibited heat-aggregated IgA1-induced human mesangial cell proliferation	[26]