Homeostasis of Phosphate Revisited

Wesson, Laurence G.

doi:10.1159/000190285

Cited by 19 publications

(11 citation statements)

References 7 publications

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“…It was shown that hypophosphatemia was the most frequent electrolyte disorder especially in the patients with hyponatremia due to SIADH (22). It can be attributed to volume expansion, since experimental studies clearly showed that volume expansion evoke an inhibition of phosphate uptake by the renal proximal tubules (24). As inappropriate secretion of AVP is thought to contribute to the hyponatremia in our case, this mechanism may also apply.…”

Section: Discussionmentioning

confidence: 48%

Severe Hyponatremia in Association with I131 Therapy in a Patient with Metastatic Thyroid Cancer

et al. 2011

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Hyponatremia is a common clinical problem that results from various causes. Hypothyroidism is known to be one of the causes of this disorder. We report a case of metastatic thyroid cancer presenting with severe hyponatremia in association with hypothyroidism induced by pretreatment of I 131 therapy, such as a low-iodine diet and withdrawal of thyroid hormone. Serum arginine vasopressin (AVP) was elevated and urine osmolality was higher than that of serum. Saline infusion and thyroid hormone replacement normalized serum sodium and AVP. Inappropriate secretion of AVP in hypothyroid state was thought to be one of the causes of this hyponatremia.

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Section: Discussionmentioning

confidence: 48%

Severe Hyponatremia in Association with I131 Therapy in a Patient with Metastatic Thyroid Cancer

et al. 2011

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“…This difference in outcomes between patients with stage 3 and stage 4 CKD is not surprising, as the conversion from 25-vitamin D to 1,25-vitamin D is largely dependent on functional renal mass, which is greater in stage 3 than in stage 4 CKD. Furthermore, renal production of 1,25-vitamin D is inhibited by serum phosphorus and phosphate retention [20], a finding more likely to occur in patients with stage 4 than stage 3 CKD. Interestingly, the decline in calcitriol production begins as early as stage 2 CKD, before notable hypocalcemia or hyperphosphatemia is present [21, 22].…”

Section: Discussionmentioning

confidence: 99%

Impact of Ergocalciferol Treatment of Vitamin D Deficiency on Serum Parathyroid Hormone Concentrations in Chronic Kidney Disease

Zisman¹,

Hristova²,

Ho³

et al. 2007

Am J Nephrol

174

115

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Background: Vitamin D deficiency is highly prevalent and associated with secondary hyperparathyroidism in patients with chronic kidney disease (CKD). The Kidney Disease Outcomes Quality Initiative (K/DOQI) guidelines recommend treatment of vitamin D deficiency starting with CKD stage 3, though no data are available showing an impact on serum parathyroid hormone (PTH) concentrations. The goal of this analysis, therefore, was to determine the effect of ergocalciferol treatment on plasma PTH concentrations in vitamin D-deficient patients with stage 3 and stage 4 CKD. Methods: A prospective, nonrandomized observational analysis was conducted in an academic community hospital CKD clinic. Fifty-two patients with stage 3 or stage 4 CKD with vitamin D deficiency and elevated PTH concentrations received ergocalciferol dosed per a modified K/DOQI guidelines protocol and adjusted every 3 months. Serum PTH, 25-vitamin D, 1,25-vitamin D, calcium, phosphorus, and albumin levels were drawn at initiation of therapy and repeated every 3 months. Results: The mean 25-vitamin D levels normalized in patients with stage 3 and 4 CKD, with values of 31.6 ± 2.2 ng/ml (78.8 ± 5.49 nmol/l) and 35.4 ± 1.9 ng/ml (88.4 ± 4.74 nmol/l), respectively (p < 0.0001). A median decrease in PTH concentrations of 13.1 and 2.0% was noted in patients with stage 3 and stage 4 CKD, respectively (p = 0.041, p = nonsignificant). Conclusions: Ergocalciferol therapy is a reasonable initial therapy for vitamin D deficiency associated with elevated PTH levels in stage 3 CKD. It does not appear to have equivalent benefits in stage 4 CKD.

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“…This volume expansion can also decrease passive magnesium reabsorption and explain the magnesium depletion observed [2]. Hypophosphatemia can be ascribed to volume expansion, since experimental studies clearly showed that volume expansion evoked an inhibition of phosphate uptake by the renal proximal tubules [3]. Interestingly, decreased phosphate levels have been described in SIADH patients, but were related to tumoral hypophosphatemia or to the demeclocycline administration.…”

Section: Discussionmentioning

confidence: 99%

Multiple Metabolic Abnormalities in a Patient with the Syndrome of Inappropriate Antidiuresis

Rizos¹,

Liamis²,

Elisaf³

2002

Nephron

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The syndrome of inappropriate ADH secretion (SIADH) is a common cause of hyponatremia. However, other metabolic abnormalities have infrequently been described in patients with the syndrome of inappropriate antidiuresis. Here, we describe a female patient with hyponatremia due to SIADH who presented with a cluster of metabolic abnormalities and specifically hypouricemia associated with uricosuria, hypokalemia caused by renal potassium wasting, hypomagnesemia with inappropriate magnesiuria, hypophosphatemia with renal phosphate wasting and inappropriate calciuria. These abnormalities could be partly due to the extracellular volume expansion and were corrected with the water restriction-induced increase in serum sodium levels.

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Homeostasis of Phosphate Revisited

Cited by 19 publications

References 7 publications

Severe Hyponatremia in Association with I131 Therapy in a Patient with Metastatic Thyroid Cancer

Severe Hyponatremia in Association with I131 Therapy in a Patient with Metastatic Thyroid Cancer

Impact of Ergocalciferol Treatment of Vitamin D Deficiency on Serum Parathyroid Hormone Concentrations in Chronic Kidney Disease

Multiple Metabolic Abnormalities in a Patient with the Syndrome of Inappropriate Antidiuresis

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