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Introduction: Secondary hyperparathyroidism (SHPT) represents a complication of chronic kidney disease (CKD). Vitamin D system is altered since early CKD, and vitamin D deficiency is an established trigger of SHPT. Although untreated SHPT may degenerate into tertiary hyperparathyroidism with detrimental consequences in advanced CKD, best treatments for counteracting SHPT from stage 3 CKD are still debated. Enthusiasm on prescription of vitamin D receptor activators (VDRA) in non-dialysis renal patients, has been mitigated by the risk of low bone turnover and positive calcium-phosphate balance. Nutritional vitamin D is now suggested as first-line therapy to treat SHPT with low 25(OH)D insufficiency. However, no high-grade evidence supports the best choice between ergocalciferol, cholecalciferol, and calcifediol (in its immediate or extended-release formulation).Areas covered: The review discusses available data on safety and efficacy of nutritional vitamin D, VDRA and nutritional therapy in replenishing 25(OH)D deficiency and counteracting SHPT in non-dialysis CKD patients.Expert opinion: Best treatment for low 25(OH)D and SHPT remains unknown, due to incomplete understanding of the best homeostatic, as mutable, adaptation of mineral metabolism to CKD progression. Nutritional vitamin D and nutritional therapy appear safest interventions, whenever contextualized with single-patient characteristics. VDRA should be restricted to uncontrolled SHPT by first-line therapy.

Monitoring venous congestion by ultrasound assessment of hepatic venogram allowed individualized fluid management in severe cardiorenal syndrome type 5 due to light chain myeloma, preserving residual renal function and avoiding heart failure.

Secondary hyperparathyroidism (SHPT) is a major complication of chronic kidney disease (CKD), responsible for skeletal and vascular damage with increased risk of bone fractures, cardiovascular events, and mortality. However, the optimal serum parathormone (PTH) levels for improving clinical outcomes remain uncertain. Treatment of SHPT is based on nutritional therapy, phosphate binders, vitamin D, and calcimimetics, but none of these interventions has ever been tested against placebo in randomized controlled trials. Treatment of SHPT in the elderly should consider the many peculiarities of aging in terms of physiopathology, quality of life, symptoms, subjective perception of disease, drug load, and the modifying effect of treatment on disease-related outcomes. Unfortunately, peculiarities of SHPT among elderly CKD patients are mainly unexplored. The present review aims to provide a reasonable merging of evidence regarding the management of SHPT in CKD, with more actual concepts on how to care for older patients.

Background and Aims The variable deterioration of patients with chronic kidney disease poses an omnipresent need for improved renal care management. At present, renal function in CKD patients is measured or estimated using the glomerular filtration rate (mGFR and eGFR). While mGFR affords the most objective and accurate evaluation of kidney function, it is not routinely used for repeated assessment due to its expense and difficulty to execute. Although eGFR provides the most diffuse approach for the monitoring of renal function, its commonality does not come without limitations: above 60mL/min*1.73m2, serum creatinine, and therefore eGFR variability are increasingly impacted by muscle metabolism/mass, age, gender, diet and fluid imbalances. eGFR can neither anticipate nor predict kidney damage. In CKD, deficiency of 1,25-dihydroxyvitamin D (1,25(OH)2D) develops during the progression of kidney failure, due to the decreased capability of renal proximal tubule cells to mediate the final hydroxylation step of 25-hydroxyvitamin D to 1,25(OH)2D. While not measured routinely in the clinic, new methods make the measurement of 1,25(OH)2D possible and reliable, and data on its performance as a biomarker are emerging. The aim of this study is to describe the ability of the LIAISON® XL 1,25 Dihydroxyvitamin D measurement to predict worsening renal function in conjunction with other relevant analytes. Method This monocentric study was observational, prospective and descriptive, with a longitudinal approach. 71 patients were assessed for mGFR determination by 99mTc-diethylenetriamine-pentaacetic acid at baseline. Twenty percent worsening of renal function, based on eGFR, provided the primary endpoint which was evaluated at 3 and 6 months. In addition, serum levels of 1,25(OH)2D, 25(OH)D, 1-84 PTH, intact FGF23, sclerostin, alkaline phosphatase (bone-specific and total) and calcium/phosphorus along with 24h urine levels of creatinine, phosphorus, calcium and sodium were measured. Endpoint analyses were performed by receiver operating characteristics, univariate, and multivariate logistic regressions. Results ROC analyses of 1,25(OH)2D and the 1,25(OH)2D/1-84PTH ratio for patients with early CKD (stage 3) showed very good performance in predicting worsening of renal function with AUCs of 0.916 (p Conclusion 1,25(OH)2D and the ratio of 1,25(OH)2D/1-84PTH are strong predictors of outcome in CKD3 patients, and thus these measurements may indicate improved clinical care for this important class of patients. Further research of these biomarkers is needed to expand the observations to larger numbers and more diverse populations.

Chronic kidney disease is a condition in which parathyroid are affected by a combination of elevated extracellular phosphate concentration, decreased extracellular ionized calcium concentration, and markedly reduced serum calcitriol, leading to increased PTH synthesis and release. At early stages in the development of hyperparathyroidism, these changes are compounded of variable down-regulation of the calcium-sensing receptor (CaSR) and vitamin D receptor (VDR), making the parathyroid cells unable to respond appropriately to calcium and/or calcitriol. The resulting increase in proliferative activity in the parathyroid glands leads to parathyroid hyperplasia.