No abstract

The traditional chronic kidney disease (CKD) biomarkers (eGFR based on serum creatinine, sex and age and albuminuria) cannot predict a patient’s individual risk for developing progressive CKD. For this reason, it is necessary to identify novel CKD biomarkers that will be able to predict which patients are prone to develop progressive disease and discriminate between disease processes in different parts of the nephron (glomeruli or tubules). A good biomarker should change before or simultaneously with lesion development and its changes should correlate strongly with lesion development. Also, there should be a close relationship between severity of injury and amount of detectable biomarker and its levels should decrease with diminishing injury. Among the large number of molecules under investigation, we have reviewed the most promising ones: NGAL and KIM-1, MCP-1, MMP-9, clusterin, MMP-9, TIMP-1, Procollagen I alpha 1 and suPAR. All these, have been studied as biomarkers for prediction of CKD progression in cohorts of patients with chronic kidney disease of different stages and various aetiologies (proteinuric and non-proteinuric, glomerulonephritides, diabetic, hypertensive and polycystic kidney disease). There is evidence that these molecules could be useful as biomarkers for progressive chronic kidney disease, however, the available data are not enough to draw final conclusions. Further studies with large cohorts and long follow-up are required to identify appropriate biomarkers, that will be able to accurately and reliably define the risk for progressive chronic kidney disease.

Objectives: Persistent secondary hyperparathyroidism is common after successful kidney transplant, with concomitant hypercalcemia and hypophosphatemia potentially leading to reduced graft survival and increased cardiovascular risk. Cinacalcet, a calcimimetic agent that activates the calcium-sensing receptors in parathyroid glands, is a therapeutic option. In this study, we assessed the long-term treatment effects of cinacalcet for a period of up to 5 years in a cohort of kidney transplant recipients. Key words: Hypophosphatemia, Kidney function, Renal transplant IntroductionSecondary hyperparathyroidism is a frequent complication of end-stage renal disease. After successful kidney transplant, secondary hyperparathyroidism usually remits; however, it persists in 30% to 50% of patients 1 year after transplant. [1][2][3] Risk factors for the development of persistent secondary hyperparathyroidism after kidney transplant include the duration of renal replacement therapy and the severity of secondary hyperparathyroidism before transplant. 1,4 In kidney transplant recipients, persistent secondary hyperparathyroidism is characterized by elevated serum parathyroid hormone (PTH) and/or hypercalcemia and hypophosphatemia. 2,5 Parathyroid hormone increases bone resorption, inhibits fractional renal calcium excretion, and promotes calcitriol production by the kidney allograft. Calcitriol, in turn, increases calcium absorption from the intestinal tract.

No abstract

No abstract