Table 1.

Clinical manifestations and initiators of APOL1 nephropathies

Clinical pathologic syndrome	Proposed initiating factors
Primary FSGS, manifesting as various histologic subtypes	Presumed plasma factor(s) associated with recurrent FSGS; possible role of chronic microvascular inflammation (e.g. chronic HIV infection with effective anti-retroviral therapy)
Adaptive FSGS, the most characteristic histologic manifestation being perihilar FSGS	Imbalance between glomerular load and glomerular capacity
	Sickle cell disease
Medication-associated FSGS, particularly collapsing variant	Interferon therapy
HIV-associated nephropathy, particularly FSGS collapsing variant with uncontrolled HIV infection	Interferon
	Podocyte infection with HIV
	HIV accessory proteins Tat, Vpr and Nef
Collapsing glomerulopathy associated with lupus nephritis	Possibly interferon
Arterionephrosclerosis	Chronic microvascular inflammation, driven by smoking, obesity, hyperlipidemia, chronic viral infection (e.g. HIV)
Accelerated kidney allograft loss	Possibly drivers of chronic allograft nephropathy