Osteomalacia induced by vitamin D deficiency in hemodialysis patients: the crucial role of vitamin D correction

Vitamin D deficiency/insufficiency is significantly prevalent in chronic kidney disease. Data in the literature are however scarce about the effects of this deficiency on bone metabolism in hemodialysis (HD) patients. Moreover, it is still debated whether low vitamin D levels should be normalized in HD patients. In this paper, we report two cases showing the deleterious consequences of vitamin D deficiency in HD patients which is characterised by hypophosphatemia, hypocalcemia and osteomalacia (OM) leading to bone fractures. As vitamin D repletion is an easy way to treat OM, this report underlines the importance of monitoring and correction of vitamin D deficiency in this population.     

Effect of vitamins on the lipid profile of patients on regular hemodialysis

OBJECTIVE: The aim of this study was to investigate the lipid-lowering effect of vitamins compared to placebo and their short-term supplementation safety in patients on hemodialysis. MATERIAL AND METHODS: Eighty-four hemodialysis patients were randomly allocated to four therapeutic groups. Each group (n = 21) received one of the following treatments: vitamin C (200 mg), E (200 mg), D3 (50,000 IU) or placebo daily. Serum triglyceride, total cholesterol, low-density lipoprotein cholesterol (LDL-c), and high-density lipoprotein cholesterol (HDL-c) were measured before and following 3 months of vitamin therapy. RESULTS: LDL-c and total cholesterol levels as well as the ratios of LDL-c to HDL-c and cholesterol to HDL-c significantly decreased after vitamin C therapy. Triglyceride and the ratio of triglyceride to HDL-c significantly decreased following vitamin D3 therapy. HDL-c increased and the ratio of LDL-c to HDL-c decreased significantly after vitamin E therapy. No major side-effects were encountered during the 3 months' trial. CONCLUSIONS: Short-term supplementary vitamins are safe and beneficial for treatment of lipid abnormalities in hemodialysis patients.     

Beyond minerals and parathyroid hormone: role of active vitamin D in end-stage renal disease

Secondary hyperparathyroidism is a common complication of end-stage renal disease (ESRD) that is often treated with activated forms of intravenous vitamin D. The natural course and treatment of secondary hyperparathyroidism in hemodialysis patients is punctuated by episodes of hypercalcemia, hyperphosphatemia, and increased calcium-phosphate product, which in previous studies were linked to increased mortality. Historically these episodes have been attributed to vitamin D, leading some authorities to favor decreased vitamin D use. However, the studies that examined the impact of mineral levels and parathyroid hormone (PTH) on survival did not consistently account for vitamin D therapy itself on hemodialysis patient survival. The current review examines in detail two recent large-scale studies of hemodialysis patients: one that demonstrated a survival advantage of paricalcitol over calcitriol and a second that demonstrated a significant survival advantage of any intravenous vitamin D formulation versus none. In both studies, the effects were independent of mineral and PTH levels, suggesting "nontraditional" actions of vitamin D contributed to the observed survival advantage. Several of these nontraditional actions are reviewed with an emphasis on those that might impact hemodialysis outcomes.     

Postoperative PTH Measurement Is Not a Reliable Predictor for Hypocalcemia After Total Thyroidectomy in Vitamin D Deficiency: Prospective Study of 203 Cases

Background

Several factors have been used to predict post total thyroidectomy (TT) hypocalcemia. Serum intact PTH (PTH) levels <10 pg/mL after TT is considered to be the most accurate predictor. The aim of the present study was to evaluate the accuracy of PTH as a predictor of post-TT hypocalcemia in patients with vitamin D deficiency.

Materials and methods

The present prospective study was conducted from 2009 to 2011 and included patients undergoing TT for benign goiter. The PTH levels 8 h after TT in patients who were vitamin D sufficient (group A; S Vit D >20 ng/mL) versus those who were vitamin D deficient (group B) were compared. Comparison was also performed between patients belonging to group A and group B who developed hypocalcemia. Appropriate statistical tests were applied.

Results

A total of 203 patients (19 males, 184 females) underwent TT; 58.6 % (n = 119) belonged to group A and 41.4 % (n = 84) to group B. Their mean age was 36.81 ± 12.9 years, and the mean duration of goiter was 45.35 ± 54.6 months. Hypocalcemia occurred in 41 patients (20.2 %). Among them 15 belonged to group A and 26 to group B (p = 0.002). The mean PTH in patients who developed hypocalcemia was 12.75 ± 8.91 versus 22.58 ± 15.38 in those who did not develop hypocalcemia (p = 0.00). Furthermore it was seen that the mean PTH in vitamin D sufficient hypocalcemic patients (n = 15) was 7.12 ± 1.79 and that in vitamin D deficient hypocalcemic patients (n = 26) was 16 ± 9.77 (p = 0.001)

Conclusions

Our findings suggest that the fall in PTH after TT in vitamin D deficient patients is unreliable in predicting hypocalcemia and should not be relied on to plan early postoperative discharge.     

Hypercalcemic and hypocalcemic disorders: diagnosis and treatment.

Current concepts concerning the mechanisms, diagnosis and means of treatment of a number of the major causes of hypercalcemia and hypocalcemia are reviewed. In particular, the role of abnormalities in metabolism of vitamin D including (1) excessive hepatic production of 25-hydroxyvitamin D (vitamin D intoxication), (2) increased production of 1 alpha, 25-dihydroxyvitamin D (hyperparathyroidism and sarcoidosis), (3) impaired production of 1 alpha, 25-dihydroxyvitamin D (hypoparathyroidism, renal failure, vitamin-D-dependent rickets type I, pseudohypoparathyroidism) and (4) resistance to 1 alpha, 25-dihydroxyvitamin D; the use of vitamin D and its metabolites therapeutically is discussed.     

Activated injectable vitamin D and hemodialysis survival: a historical cohort study

Patients with ESRD commonly experience secondary hyperparathyroidism, a condition primarily managed with activated injectable vitamin D. The biologic effects of vitamin D, however, are widespread, and it is possible that activated injectable vitamin D alters survival in ESRD. This hypothesis was tested in a historical cohort study of incident hemodialysis patients who lived throughout the United States between January 1996 and December 1999. The primary outcome was 2-yr survival among those who survived for at least 90 d after initiation of chronic hemodialysis. During this period, 51,037 chronic hemodialysis patients survived for at least 90 d from the initiation of hemodialysis, and in the ensuing 2 yr, 37,173 received activated injectable vitamin D and 13,864 did not. At 2 yr, mortality rates were 13.8/100 person-years in the group that received injectable vitamin D compared with 28.6/100 person-years in the group that did not (P < 0.001). Cox proportional hazards analyses adjusting for several potential confounders and examining injectable vitamin D therapy as a time-dependent exposure suggested that compared with patients who did not receive injectable vitamin D, the 2-yr survival advantage associated with the group that did receive injectable vitamin D was 20% (hazard ratio, 0.80; 95% confidence interval, 0.76 to 0.83). The incidence of cardiovascular-related mortality was 7.6/100 person-years in the injectable vitamin D group, compared with 14.6/100 person-years in the non-vitamin D group (P < 0.001). The benefit of injectable vitamin D was evident in 48 of 49 strata examined, including those with low serum levels of intact parathyroid hormone and elevated levels of serum calcium and phosphorus, situations in which injectable vitamin D is often withheld. Repeating the entire analysis using marginal structural models to adjust for time-dependent confounding by indication yielded a survival advantage of 26% (hazard ratio, 0.74; 95% confidence interval, 0.71 to 0.79) associated with the injectable vitamin D group. In this historical cohort study, chronic hemodialysis patients in the group that received injectable vitamin D had a significant survival advantage over patients who did not. Randomized clinical trials would permit definitive conclusions.     

Oral active vitamin D is associated with improved survival in hemodialysis patients

Injection of active vitamin D is associated with better survival of patients receiving chronic hemodialysis. Since in many countries oral active vitamin D administration is the most common form of treatment for secondary hyperparathyroidism we determined the survival benefit of oral active vitamin D in hemodialysis patients from six Latin America countries (FME Register as part of the CORES study) followed for a median of 16 months. Time-dependent Cox regression models, after adjustment for potential confounders, showed that the 7,203 patients who received oral active vitamin D had significant reductions in overall, cardiovascular, infectious and neoplastic mortality compared to the 8,801 patients that had not received vitamin D. Stratified analyses found a survival advantage in the group that had received oral active vitamin D in 36 of the 37 strata studied including that with the highest levels of serum calcium, phosphorus and parathyroid hormone. The survival benefit of oral active vitamin D was seen in those patients receiving mean daily doses of less than 1 microg with the highest reduction associated with the lowest dose. Our study shows that hemodialysis patients receiving oral active vitamin D had a survival advantage inversely related to the vitamin dose.     

Vitamin D and its analogues: do they protect against cardiovascular disease in patients with kidney disease?

BACKGROUND: Patients with chronic kidney disease (CKD) are at high risk for cardiovascular disease, and despite recent advances in hypertension control, anemia management, and dialysis adequacy, mortality remains high. Improved understanding of nontraditional risk factors, including those present at early phases in CKD, may lead to novel therapeutic strategies. CKD has been demonstrated to be an independent risk factor for cardiovascular disease in the general population, but data are lacking as to the associated potential abnormalities that occur in association with reduced glomerular filtration rate (GFR), which may contribute to this increased risk. Data are accumulating regarding the role of abnormalities of calcium, phosphorus, vitamin D, and parathyroid hormone (PTH) in cardiovascular disease. Vitamin D deficiency is present even in the early stages of CKD. Vitamin D plays a central role in calcium-phosphorus homeostasis, regulation of PTH, and formation and maintenance of bone. However, until recently, vitamin D has not been considered to have a biologic role in CKD beyond mineral regulation, or has been considered as a negative factor contributing to soft tissue and cardiovascular calcification. In light of recent observational studies showing an association of vitamin D therapy and survival benefit in hemodialysis patients, the effects of vitamin D on cardiovascular system have become a heavily debated issue. METHODS: A Medline search was performed to identify relevant literature describing the role of vitamin D in the pathogenesis of cardiovascular disease. Both the experimental and clinical literatures in English were reviewed. RESULTS: The accumulating published data demonstrate both associative relationships and mechanisms for biologic plausibility. The following three potential mechanisms may be important for the protective effects of vitamin D against cardiovascular disease mortality: vitamin D can inhibit various aspects of inflammation, which have been established as a key pathogenic mechanism in atherosclerosis; vitamin D exerts an antiproliferative effect on myocardial cell hypertrophy and proliferation, which underlies the pathogenesis of congestive heart failure; and vitamin D acts as a negative endocrine regulator for the renin-angiotensin system, which itself plays an important independent role in hypertension and cardiovascular health. CONCLUSION: Vitamin D deficiency might be an underestimated nonclassical risk factor for cardiovascular disease in CKD. Based on a review of the evidence, from both basic science and clinical studies, this article supports the possible protective role of vitamin D beyond its effect on mineral metabolism, and suggests the need for ongoing evaluation of the role of vitamin D in cardiovascular health in the CKD population.     

Vitamin D levels and early mortality among incident hemodialysis patients

Vitamin D deficiency is associated with cardiovascular disease, the most common cause of mortality in hemodialysis patients. To investigate the relation between blood levels of 25-hydroxyvitamin D (25D) and 1,25-dihydroxyvitamin D (1,25D) with hemodialysis outcomes, we measured baseline vitamin D levels in a cross-sectional analysis of 825 consecutive patients from within a prospective cohort of incident US hemodialysis patients. Of these patients, 78% were considered vitamin D deficient with 18% considered severely deficient. Calcium, phosphorus, and parathyroid hormone levels correlated poorly with 25D and 1,25D concentrations. To test the association between baseline vitamin D levels and 90-day mortality, we selected the next 175 consecutive participants who died within 90 days and compared them to the 750 patients who survived in a nested case-control analysis. While low vitamin D levels were associated with increased mortality, significant interaction was noted between vitamin D levels, subsequent active vitamin D therapy, and survival. Compared to patients with the highest 25D or 1,25D levels who received therapy, untreated deficient patients were at significantly increased risk for early mortality. Our study shows that among incident hemodialysis patients, vitamin D deficiency is common, correlates poorly with other components of mineral metabolism and is associated with increased early mortality.     

Impact of activated vitamin D and race on survival among hemodialysis patients

Contrary to most examples of disparities in health outcomes, black patients have improved survival compared with white patients after initiating hemodialysis. Understanding potential explanations for this observation may have important clinical implications for minorities in general. This study tested the hypothesis that greater use of activated vitamin D therapy accounts for the survival advantage observed in black and Hispanic patients on hemodialysis. In a prospective cohort of non-Hispanic white (n = 5110), Hispanic white (n = 979), and black (n = 3214) incident hemodialysis patients, higher parathyroid hormone levels at baseline were the primary determinant of prescribing activated vitamin D therapy. Median parathyroid hormone was highest among black patients, who were most likely to receive activated vitamin D and at the highest dosage. One-year mortality was lower in black and Hispanic patients compared with white patients (16 and 16 versus 23%; P < 0.01), but there was significant interaction between race and ethnicity, activated vitamin D therapy, and survival. In multivariable analyses of patients treated with activated vitamin D, black patients had 16% lower mortality compared with white patients, but the difference was lost when adjusted for vitamin D dosage. In contrast, untreated black patients had 35% higher mortality compared with untreated white patients, an association that persisted in several sensitivity analyses. In conclusion, therapy with activated vitamin D may be one potential explanation for the racial differences in survival among hemodialysis patients. Further studies should determine whether treatment differences based on biologic differences contribute to disparities in other conditions.     

Persistently elevated parathyroid hormone levels after parathyroid surgery

BACKGROUND: Persistent elevation of serum parathyroid hormone (PTH), despite normocalcemia, occurs in 8% to 40% of patients after parathyroidectomy. Explanations have included hypocalcemia owing to vitamin D deficiency or bone remineralization, and persistent hyperparathyroidism. METHODS: A retrospective chart review of 816 consecutive patients who underwent surgery for primary hyperparathyroidism was conducted. RESULTS: One hundred fourteen patients (15%) had persistently elevated PTH levels (PPTH). Patients with PPTH had higher preoperative PTH levels than those with normal PTH levels postoperatively. They also had lower postoperative Ca(++) and vitamin D levels. Multiple gland enlargement was identified in fewer patients with PPTH than in those with normal postoperative PTH levels. In patients with PPTH and a postoperative Ca(++) less than 9.6 mg/dL (group I), there was a greater decrease in IOPTH, a higher initial postoperative PTH level, and a lower postoperative vitamin D level than in PPTH patients whose postoperative Ca(++) was > or =9.6 mg/dL (group II). Postoperative Ca(++) and vitamin D levels were also lower in patients whose PPTH did not ultimately resolve. Three patients in group II had recurrent disease. CONCLUSIONS: Persistent elevation of postoperative serum PTH levels in normocalcemic patients is associated with mild hypocalcemia, probably owing to vitamin D deficiency. In some patients it may also be indicative of mild persistent hyperparathyroidism.     

Vitamin D metabolites and their binding protein in adult diabetic patients

Vitamin D metabolites and vitamin D-binding protein were measured in the serum of nonketotic Bantu and Caucasian insulin-requiring diabetic subjects from Zaire and Belgium, respectively. In Caucasian diabetics, whether untreated (N = 18) or insulin treated (N = 26), no abnormalities were found. The Bantu diabetics (N = 20) were more insulin-deficient and had a poorer glucose control than the Caucasians. They presented, compared with Bantu controls, a significant decrease in the serum concentrations of 25-hydroxyvitamin D3 (26 +/- 10 vs. 35 +/- 14 micrograms/L, P less than .01), 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] (38 +/- 15 vs. 58 +/- 17 ng/L, P less than .001), and vitamin D-binding protein (303 +/- 55 vs. 356 +/- 41 mg/L, P less than .001). The decreased concentrations of vitamin D metabolites in the adult Bantu diabetic patients may be partly explained by a concomitant decrease in the concentration of vitamin D-binding protein, possibly due to insulin deficiency. The ratio between the molar concentrations of 1,25-(OH)2D3 and vitamin D-binding protein, used as an index of the free hormonal level, was also decreased, in association with a decreased serum calcium level. In conclusion, no abnormalities in vitamin D metabolism were found in Caucasian insulin-dependent diabetics, whereas low serum 1,25(OH)2D3 concentrations and hypocalcemia were found in poorly controlled Bantu diabetic subjects.     

The impact of age and oral calcium and vitamin D supplements on postoperative hypocalcemia after total thyroidectomy. A prospective study

Background

Hypocalcemia caused by transient or definitive hypoparathyroidism is the most frequent complication after total thyroidectomy (TT). We aimed to compare the impact of age and the clinical usefulness of oral calcium and vitamin D supplements on postoperative hypocalcemia after TT, and to determine which risk factors are important for hypocalcemia incidence.

Methods

Two hundred consecutive patients treated by TT were included prospectively in the present study. All patients supplemented oral calcium and vitamin D in the post-operative time. The data concerning symptomatic and laboratoristichypocalcemia were collected.Patients were evaluated according to age, sex, postoperative serum calcium levels, and preoperative serum alkaline phosphatasis levels.

Results

Symptomatic hypocalcemia developed only in 19 patients (9.5%), whereas laboratory hypocalcemia developed in 36 patients (18%). The risk for postoperative hypocalcemia was increate 20-fold for patients older than 50 years.

Conclusions

Age is significantly associated with postoperative hypocalcemia. Implementing oral calcium and vitamin D after total thyroidectomy can reduce the incidence of hypocalcemia related to surgery.

     

Which vitamin D derivative to prescribe for renal patients

PURPOSE OF REVIEW: It is possible to control the secondary hyperparathyroidism and osteitis fibrosa of patients with chronic kidney disease by calcitriol when given early and in appropriate doses. However, this control is often achieved at the price of unacceptably high plasma calcium and phosphorus levels, the induction of adynamic bone disease, and soft tissue calcification. To avoid these side effects, so-called 'nonhypercalcemic' vitamin D analogs have been developed. Their possible advantages and their precise place in the treatment and prevention of secondary hyperparathyroidism remain a matter of debate. RECENT FINDINGS: A large US multicenter study showed that the administration of the vitamin D analog paricalcitol to hemodialysis patients, as compared with calcitriol, was associated with better survival. In a subsequent large US multicenter study paricalcitol-treated hemodialysis patients experienced fewer hospitalizations and hospital days compared with calcitriol-treated patients. In a third, smaller study from Japan, regular alfacalcidol users among hemodialysis patients had better cardiovascular survival than nonusers. Finally, in a recent historical control study the mortality of a large hemodialysis patient cohort was analyzed as a function of previous vitamin D treatment. Patients on active vitamin D compounds at any time had a 2-year survival advantage over vitamin D-naive patients. It must be pointed out, however, that all four studies were retrospective in nature. SUMMARY: The development of vitamin D analogs with less side effects than with calcitriol is of major theoretical interest. Practically speaking, however, we still need to be convinced that this goal can be achieved in chronic kidney disease patients.     

Long-Term Changes in Parathyroid Function After Subtotal Thyroidectomy for Graves’ Disease

BACKGROUND: Transient hypocalcemia is one of the postoperative complications of thyroidectomy for Graves' disease, and perioperative parathyroid hormone (PTH) assays are used to predict postoperative hypocalcemia. We evaluated long-term changes in parathyroid function after surgery for Graves' disease. METHODS: Serum PTH values were measured in Graves' patients with postoperative hypocalcemia, and those patients were followed postoperatively. RESULTS: Subtotal thyroidectomy was performed in 275 patients with Graves' disease. Their serum calcium levels were measured on postoperative day (POD) 1, and patients with transient postoperative hypocalcemia were treated with calcium and vitamin D supplementation and followed up. The amount of calcium and vitamin D supplementation was adjusted to keep the patient's serum calcium level within the normal range. Measurement of their serum intact PTH value on POD 1 revealed normal value in 18 patients, a below normal level in 22, and an above normal level in the other 2. During the follow-up period, the serum iPTH values remained normal in 12 patients, recovered to the normal level in 21 patients, and rose above the normal range in 9 patients. The serum iPTH values of all patients eventually reached the normal range during the follow-up period. A marked difference in preoperative serum alkaline phosphatase concentration was observed between the high-iPTH patients and the normocalcemic patients. CONCLUSIONS: The phenomenon of an elevated serum PTH level after surgery for Graves' disease was observed in 21% of the patients with postoperative hypocalcemia despite the achievement of normal serum calcium levels by calcium and vitamin D supplementation.     

Losses of 1,25- and 24,25-dihydroxycholecalciferol in the peritoneal fluid of patients treated with continuous ambulatory peritoneal dialysis

We measured peritoneal losses of the active vitamin D metabolites 1,25(OH)2D3 and 24,25(OH)2D3 in patients receiving continuous ambulatory peritoneal dialysis (CAPD). The serum concentration of 24,25(OH)2D3 was considerably lower than in hemodialysis patients. The serum concentration of 1,25(OH)2D3 was undetectable and rose to levels similar to those in hemodialysis patients only after loading with much higher oral doses of 1-alpha-vitamin D3 than those received by hemodialysis patients. Losses of both metabolites in peritoneal fluid were considerable, averaging approximately 6-8% of the plasma pool per day. These losses lead to low serum levels of these active vitamin D metabolites in CAPD patients, which may be an important factor in exacerbating renal osteodystrophy. Our results indicate the need for increased replacement doses of vitamin D metabolites in CAPD patients.     

The role of vitamin D in left ventricular hypertrophy and cardiac function

The role of vitamin D in left ventricular hypertrophy and cardiac function. Cardiovascular disease is the leading cause of death among patients with end-stage renal disease (ESRD). Traditional cardiac risk factors, as well as other factors specific to the ESRD population such as hyperphosphatemia, elevated calcium and phosphate product, abnormal lipid metabolism, hyperhomocysteinemia, and chronic inflammation play a role in the excessive risk of cardiovascular death in this population. Left ventricular disorders are proven risk factors for cardiac mortality in hemodialysis patients. These disorders are present in incident ESRD patients at rates far above the general population. There is an accumulating body of evidence that suggests that vitamin D plays a role in cardiovascular disease. Abnormal vitamin metabolism, through deficiency of the active form of 1,25-dihydroxyvitamin D(3), and acquired vitamin D resistance through the uremic state, have been shown to be important in ESRD. Vitamin D deficiency has long been known to affect cardiac contractility, vascular tone, cardiac collagen content, and cardiac tissue maturation. Recent studies using vitamin D receptor deficient mice as a model demonstrate a crucial role of vitamin D in regulation of the renin-angiotensin system. Additionally, there is emerging evidence linking treatment with vitamin D to improved survival on hemodialysis and improvement in cardiac function. The emergence of this data is focusing attention on the previously underappreciated nonmineral homeostatic effects of vitamin D that very likely play an important role in the pathogenesis of cardiac disease in ESRD.     

In vitro and in vivo analysis of the immune system of vitamin D receptor knockout mice.

Immune cells carry receptors for 1,25-dihydroxyvitamin D3 [1,25(OH)2D3; vitamin D receptor (VDR)] and individuals with severe vitamin D deficiency have immune abnormalities. The aim of this study was to investigate the role of vitamin D in the immune system by studying VDR-knockout (VDR-KO) mice. VDR-KO mice had the same metabolic phenotype as rachitic animals with severe hypocalcemia. Leukocytosis, lymphocyte subset composition in different immune organs, and splenocyte proliferation to several stimuli were normal, except for a lower response to anti-CD3 stimulation (simulation index [SI] of 13 +/- 4 vs. 24 +/- 9 in wild-type mice; p < 0.01). Macrophage chemotaxis was impaired (41 +/- 19% vs. 60 +/- 18% in wild-type mice; p < 0.01) but phagocytosis and killing were normal. In vivo rejection of allogeneic (31 +/- 12 days vs. 45 +/- 26 days of survival in wild-type mice, NS) or xenogeneic (10 +/- 2 days vs. 16 +/- 9 days of survival in wild-type mice, NS) islet grafts was comparable with wild-type mice. Surprisingly, VDR-KO mice were protected from low-dose streptozotocin-induced diabetes mellitus (LDSDM; 5% vs. 65% in wild-type mice; p < 0.001). Correcting hypocalcemia by use of lactose-rich or polyunsaturated fat-rich diets fully restored the immune abnormalities in vitro and the sensitivity to diabetes in vivo. On the other hand, treatment with 1,25(OH)2D3 protected wild-type mice against diabetes but did not protect normocalcemic VDR-KO mice. We conclude that immune defects observed in VDR-KO mice are an indirect consequence of VDR disruption because they can be restored by calcium homeostasis normalization. This study proves that although 1,25(OH)2D3 is a pharmacologic and probably a physiological immunomodulator, its immune function is redundant. Moreover, we confirm the essential role of calcium in the immune system.     

Opinion: Which of the K/DOQI Guidelines for Bone Disease in Dialysis Patients Should be Changed?

The K‐DOQI guidelines for bone metabolism in chronic kidney disease recommend measuring 25(OH) vitamin D levels and correcting deficiencies in stages 3 and 4 but not in ESRD. Most nephrologists are not concerned with 25(OH) vitamin D deficiency, despite evidence in hemodialysis patients that deficient vitamin D status [as measured by 25(OH) vitamin D levels] plays a role in bone disease. PD patients are often deficient in 25(OH) vitamin D in part because of peritoneal effluent losses, and correction may decrease muscle and bone complaints. Data from other populations are indicative of the importance of vitamin D in cancer surveillance and immune functioning. Randomized controlled trials of correction of 25(OH) vitamin D deficiency in both hemodialysis and peritoneal dialysis patients are urgently needed. vitamin D).     

Anesthesia and postoperative recovery for parathyroid gland surgery

Anesthesia for surgery of primary hyperparathyroidism (HPT) usually concerns asymptomatic elderly women with moderate hypercalcemia. Cardiovascular repercussions of the endocrine disorder are possible, but they are not frequent except for hypertension. Hyperparathyroid crisis is a life-threatening condition with severe hypercalcemia. Intravenous diphosphonates are very effective drugs to control hypercalcemia. The improvement is transient but allows curative parathyroidectomy to be performed with a minimal risk of cardiac arrhythmias. Anesthesia for surgery of secondary HPT concerns patients with chronic renal failure treated by hemodialysis. Cardiovascular disease is frequent and aggravated by the endocrine disorder. In patients with marked aortic stenosis or severe left ventricular dysfunction, parathyroidectomy should be performed by cervicotomy under local anesthesia. Hyperparathyroidism may persist after renal transplantation (tertiary HPT): in this case cardiovascular disease is minimal and the hypercalcemia is moderate. Parathyroidectomy is usually performed by cervicotomy under general anesthesia. Sternotomy is required in the case of an abnormal mediastinal location of a gland. An interaction between myorelaxants and hyperparathyroidism has been observed. Total blood calcium must be systematically assayed postoperatively because postoperative hypocalcemia is constant. Hypocalcemia is moderate in primary and tertiary HPT, due to transient functional hypoparathyroidism, with lowest observed the 2nd or 3rd postoperative day. Hypocalcemia should not be treated when asymptomatic because it resolutes on the 4th or 5th postoperative day. Intravenous calcium infusion may be necessary for 1 or 2 days, if serum calcium is below 1.9 mmol per liter with symptoms of tetany. Persistent hypocalcemia is due to an hungry bone syndrome or organic hypoparathyroidism that should be treated by oral vitamin D and calcium. In secondary HPT, hypocalcemia is early, marked and asymptomatic. Treatment must often be started on the 6th postoperative hour by intravenous calcium infusion, followed by oral vitamin D and calcium. The absence of postoperative hypocalcemia indicate incomplete removal of all abnormal parathyroid tissue. At the third postoperative day, a second cervicotomy may be performed to complete the neck exploration.