Interaction between phosphorus and parathyroid hormone in non-dialysis CKD patients under nephrology care.

BACKGROUND: Whether the traditional treatment of chronic kidney disease (CKD)-mineral and bone disorder is effective in the setting of tertiary nephrology care is an unexplored question. We evaluated phosphate, calcium and PTH levels during the first year of nephrology care and the prognostic role of month-12 levels in non-dialysis patients referred prior to availability of the novel P binders. METHODS: We studied a historical cohort of consecutive patients with CKD stage 3-5 at referral (baseline), and after 6 and 12 months of nephrology care; thereafter, patients were followed for renal survival (time to death or end-stage renal disease). RESULTS: At month 12, versus baseline, we detected a larger implementation of dietary protein restriction (P = 0.001), vitamin D and P binder (P < 0.0001 for both). Mean serum P remained unchanged (4.02 ± 0.77, 4.01 ± 0.79, 4.10 ± 0.85 mg/dL at baseline, month 6 and 12, respectively) with only 18, 16 and 21 % patients showing uncontrolled serum P at the three study visits. Similarly, calcium levels were unchanged and within the target in most cases. Conversely, intact PTH increased from 102 pg/mL (interquartile range 67-139) to 113 (68-179), P = 0.015, with 59, 60 and 53 % patients showing high values at the three study visits. During the subsequent follow-up (31 months), 96 renal deaths occurred. Cox analysis evidenced a significant prognostic role of the interaction P × PTH (P = 0.002), that is, the risk of renal death associated with serum P increased in the presence of higher PTH. CONCLUSIONS: In patients under nephrology care, P and PTH should be considered in concert to optimize risk stratification for renal death.

[Amino acid loss during dialysis treatment]. / Perdita di aminoacidi nel corso di terapia emodialitica extracorporea.

Protein-calorie malnutrition is a widespread complication in hemodialysis (HD) patients and is associated with increased mortality. The pathogenesis of malnutrition is multifactorial. Intradialytic amino acid (AA) loss is considered one of the cofactors in the complex mechanisms that lead to malnutrition in HD patients. It has been documented that in each dialysis session there is a 6-8 gram loss of AA into the dialysate, which worsens with the use of high-flux membranes. The intradialytic AA loss is variably compensated by reduction of liver synthesis and increased AA release from muscle stores. In malnourished HD patients the serum AA concentration, especially branched-chain AA (BCAA), is correlated with nutritional status and anorexia, whereas BCAA supplementation improves the nutritional parameters and increases appetite. Further studies are necessary to clarify the role of alterations of AA metabolism in the pathogenesis of malnutrition and the potential beneficial effects of BCAA supplementation or alternative treatments in malnourished patients.

[Role of paracalcitol in the management of non-dialysis CKD: state of art and... Unmet needs]. / Ruolo del paracalcitolo nella terapia conservativa della malattia renale cronica: stato dell'arte e... Unmet needs.

Chronic kidney disease (CKD) is associated with a high risk of cardiovascular morbidity and mortality due to the high prevalence of traditional risk factors and the presence of factors specific to CKD. Vitamin D deficiency and secondary hyperparathyroidism are the earliest complications in CKD, and observational data show that low plasma vitamin D is an independent predictor of death in patients with CKD. Oral supplementation with active oral vitamin D appears to be associated with greater survival but a significant improvement in renal outcome has not been demonstrated, probably because of its unwanted side effects (increase in plasma calcium and phosphate levels). Oral paracalcitol, a new vitamin D receptor activator, is now available for CKD patients not yet on dialysis. It suppresses PTH with a low incidence of increased serum calcium and phosphate levels in patients treated with dialysis and when high doses are administered. Furthermore, recent data show that paracalcitol treatment in CKD patients also results in a significant reduction of albuminuria, which is a major risk factor for cardiorenal outcome. The antiproteinuric effect of paracalcitol appears to be the result of intrarenal suppression of the renin-angiotensin system (RAS). Therefore, paracalcitol may be mostly effective in reducing albuminuria in patients already treated with RAS inhibitors who show compensatory increments of RAS components. Studies in large patients series and with adequate follow-up are needed to evaluate the effects of long-term paracalcitol treatment in CKD and its potential role in improving renal outcome in comparison not only with placebo but also other vitamin D metabolites and analogues.