“…first described the condition in 1967 [ 1 ], several hypotheses have been proposed regarding the pathophysiology of LPHS. These include vascular disease of the kidney, complement activation on arterioles [ 12 , 13 ], coagulopathy [ 14 ], venocalyceal fistula [ 15 ], abnormal ureteral peristalsis [ 16 ], hypersensitivity [ 12 ], psychopathology [ 17 , 18 ], intratubular deposition of calcium [ 2 , 15 , 19 , 20 ] and nephritis [ 16 , 17 ]. Of these, nephritis (usually IgA) is the only one documented [ 21 , 22 ].…”