Table 2.

Open questions deserving further research

Are glomerular crescents monoclonal or polyclonal lesions?

How are cellular crescents cleared in those patients where cellular crescent lesions are reversed? Is this achieved by detachment and shedding of cells into the urine or by apoptosis and phagocytic clearance in situ.

Why do parietal epithelial cells start to proliferate in some but not all forms of GN?

Why some patients with IgA nephropathy develop crescents while most other do not?

Do those have concomitant pathogenic variants in complement regulator genes?

In anti-GBM disease, which is the trigger of the disease? Are environmental factors associated with the occurrence in small clusters of unrelated patients?

GBM, glomerular basement membrane; GN, glomerulonephritis.