Ah, you must mean secondary hyperPARAthyroidism. 😉
Read up on normal phosphate homeostasis/metabolism, PTH, vitamin D, Ca, and how the kidney is involved in the process. First understand the normal, then look at the pathophysiology in these systems (i.e., PTH, vitamin D, Ca, and kidneys), such as with secondary hyper-PTH in CRF and how it differs from primary hyper-PTH.
In essence, because your kidney is in chronic failure, you can't clear the phosphate due to insufficient active Vitamin D (read about the metabolism of Vitamin D and how the kidneys are involved), so you get hyperphosphatemia, which binds to calcium, forming calcium phosphate, which is insoluble. You have less available calcium in your blood, so you have hypocalcemia (what are the consequences of low serum calcium?), which your parathyroid responds to by increasing PTH to try to compensate, resulting in the hyper-PTH that you see.
In regard to your second question: there are several sequele of secondary hyper-PTH. Straight from little Robbins & Coltran (p. 582), you may see hyperplasia of your parathyroid glands, low serum calcium levels, osteitis fibrosa cystica (and bone pain or pathological fractures secondary to it), osteomalacia, and metastatic calcifications.