The importance of FH as a complement regulator and conveyor of host protection is highlighted in cases where its function is perturbed leading to a number of non-ocular diseases, for example in the kidney conditions including atypical hemolytic uremic syndrome (aHUS) and Membranoproliferative Glomerulonephritis Type II (MPGNII—also referred to as dense deposit disease). This evidence concerns the gene FH and dense deposit disease.