Secondary hyperparathyroidism in chronic renal disease - etiopathogenesis, diagnosis and treatment.

Chronic renal failure (CRF) is usually slowly progressive and irreversible impairment of the functional unit of the kidney – the nephron. According to the agreed and established criteria (National Kidney Foundation / Kidney Disease Outcomes Quality Initiative – NKF / KDOQI) there is a five-stage classification, so that in I stage glomerular filtration rate (GFR) > 90 mL/min/1.73m and morphological and functional abnormalities may exist. Mild, moderate and pronounced reductions in GFR correspond with the stages II–IV, and GFR < 15 mL/min/1.73m means end-stage renal failure . Progressive decrease in GFR leads to a number of adaptive changes on tubular processes which maintain the external balance of substances and water. Biological ‘price’ of exhausted compensatory mechanisms is expressed as the disorder of internal balance – homeostasis along with the development of azotemia, hyperkalemia, hypocalcemia, hyperphosphatemia, and a number of consequential changes in all organs 2, . Mineral and bone disorder (MBD) related to renal osteodystrophy (ROD), occurs relatively early in the course of chronic kidney disease (CKD-MBD) and includes: abnormal levels of serum calcium (Ca), phosphate (P), parathyroid hormone (PTH) and vitamin D; lower rates of bone turnover, mineralization, structure, strength and linear growth; vascular and soft tissue calcification . Secondary hyperparathyroidism (SHPT) is a disorder of increased bone turnover, which is pathophysiological and can combine all the above mentioned disorders.