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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intensive training in a humid and warm environment can cause exertional heat stroke (ExHS) and rhabdomolysis (RBD) in military recruits. To investigate the role of vitamin D and monomeric calcitonin (CT) on the calcium metabolism in ExHS with RBD and acute renal failure (ARF), we studied 21 recruits with ExHS (mean age 21.4 years), 7 of which had ARF. Another 11 age-matched recruits with heat exhaustion (HE) and 11 healthy subjects were selected as controls. Our results showed that in 14 ExHS patients without ARF, mean serum creatinine (Cr) levels were significantly higher (151.16 vs. 106.08 mumol/l, p < 0.01), whereas serum osteocalcin (OC) levels were significantly lower (2.22 vs. 4.65 micrograms/l, p < 0.01) than in healthy controls. In 7 patients with ExHS and ARF, the mean serum Cr (774.38 vs. 105.20 mumol/l, p < 0.01), phosphorus (P) (2.26 vs. 1.26 mmol/l, p < 0.05), creatine phosphokinase (CPK) 274,143.97 vs. 85.78 IU/l, p < 0.05), intact parathyroid hormone (I-PTH) (299.81 vs. 18.66 ng/l, p < 0.05) and CT (13.58 vs. 6.63 ng/l, p < 0.01) levels on admission were significantly higher while the mean ionized calcium (iCa) levels were significantly lower than the healthy controls (0.9 vs. 1.18 mmol/l, p < 0.01). The mean serum 25-hydroxyvitamin D [25(OH)D] levels were not significantly different from healthy controls. However, mean serum 1,25-dihydroxyvitamin D [1,25(OH)2D] levels and the ratio of 1,25(OH)2D to 25(OH)D were significantly lower than healthy controls throughout the whole course of ARF. None of the 7 patients with ExHS and ARF developed hypercalcemia during the diuretic phase. Their mean serum I-PTH levels decreased significantly from 299 to 18 ng/l during the recovery phase (p < 0.05). Our study seems to suggest that the abnormal calcium metabolism in this unique patient group is in part caused by persistently decreased renal production of 1,25(OH)2D, although increased monomeric CT levels were associated with hypocalcemia. However, whether or not a causal relationship exists merits further investigation.
Nephron 1995
PMID:A prospective study of calcium metabolism in exertional heat stroke with rhabdomyolysis and acute renal failure. 858 23

We have used high-dose oral pulse therapy with 1 alpha-hydroxycholecalciferol (1 alpha-OH-D3) to treat 40 hemodialysis patients suffering form secondary hyperparathyroidism. Forty patients with intact parathyroid hormone (PTH) levels of > 150 pg/ml were treated with 4 micrograms oral 1 alpha-OH-D3 twice weekly for 1 year. The mean PTH level was 515 +/- 50 pg/ml prior to treatment, which fell to 191 +/- 42 pg/ml after 6 months of treatment (p < 0.00001), and to 164 +/- 39 pg/ml after 12 months of treatment. Patients with very high PTH levels (> 800 pg/ml) suppressed less well than patients with lower levels (150-300 pg/ml). The therapeutic end point of PTH < 100 pg/ml was achieved in 23 patients (58%). The main side effect of the treatment was hypercalcemia, but this was symptomatic in only 3 patients, all above the age of 70 years. In summary, oral high-dose pulse therapy with 1 alpha-OH-D3 was highly effective in suppressing PTH levels in hyperparathyroid hemodialysis patients, and side effects were relatively few.
Nephron 1996
PMID:Successful treatment of secondary hyperparathyroidism in hemodialysis patients with oral pulse 1-alpha-hydroxy-cholecalciferol therapy. 868 18

It has been shown that calcium carbonate (CaCO3) is an effective phosphate binder which is less toxic than Al(OH)3. However, given that its use with standard calcium dialysate (CaD) levels may lead to hypercalcemia, a decrease in CaD levels has been proposed. The aim of the present study was to elevate the acute clinical and biochemical consequences of a lowering of CaD in HD patients. Dialysate composition was otherwise the same. (1) Blood pressure levels (BP) during short hemodialysis were measured in a group of 12 patients who underwent alternate hemodialyses with dialysate calcium of 1.75 and 1.25 mmol/l. (2) Ca2+ and PTH kinetics during short hemodialysis were studied in a group of 6 patients who were sequentially treated with 1.75 and 1.25 mmol/l CaD. The results show: (1) that cardiovascular stability in chronic HD patients during short HD sessions with low CaD (LCaD) may be good; (2) that a single treatment with standard CaD (SCaD) produces positive calcium balances (JCa2+) with Ca2+ plasma increase and PTHi inhibition at the end of HD sessions; during HD with LCaD there were neutral mean JCa2+ and no changes in post-dialysis mean Ca2+ and PTHi plasma levels; furthermore 2 patients showed a small PTHi increase during HD with LCaD and neutral JCa2+ because of a high positive bicarbonate balance during HD. In conclusion, as with several aspects of dialysis treatment, dialysate calcium levels should also be individualized to avoid hypercalcemic crises or PTHi stimulation.
Nephron 1996
PMID:Intradialytic calcium balances with different calcium dialysate levels. Effects on cardiovascular stability and parathyroid function. 945 16

The drug therapies for hypercalcemia of malignancy have been known to be associated with either limited efficacy or cumulative toxicity in patients with advanced renal failure. To establish the guidelines for the use of dialysis and to determine its optimal prescription for hypercalcemia, calcium-free hemodialysis was performed in 6 hypercalcemic patients with renal failure not responding enough to forced saline diuresis. Calcium-free dialysate contained sodium 135, potassium 2.5, chloride 108, magnesium 0.75, bicarbonate 30 mmol/l. Mean hemodialysis time was 160 +/- 27 min and mean Kt/V urea was 0.75 +/- 0.2. Plasma calcium concentrations fell from a mean value of 2.92 +/- 0.21 mmol/l (range 2.55-3.25) to 2.58 +/- 0.16 mmol/l at 1 h of hemodialysis and to 2.16 +/- 0.33 mmol/l (range 1.63-2.53) following 2-3 h of hemodialysis. The ionized calcium (n = 4) decreased from 1.44 +/- 0.14 mmol/l to 0.99 +/- 0.2 mmol/l. No patient showed any hypocalcemic symptoms and signs during hemodialysis. The rate of decrease in plasma calcium did not appear to produce adverse effects in any of the patients. There was a significant positive correlation between the decrease in plasma calcium concentration and the Kt/V urea (y = 1.4x - 0.29, r = 0.92, p < 0.01). We conclude that calcium-free hemodialysis is indicated when the presence of severe renal failure prevents the administration of large volumes of intravenous fluids to hypercalcemic patients. The amount of dialysis (Kt/V urea) can be used to predict the decrease in plasma calcium concentration during calcium-free hemodialysis.
Nephron 1996
PMID:Calcium-free hemodialysis for the management of hypercalcemia. 885 91

The effects of intravenous administration of 1 alpha-hydroxycholecalciferol [1 alpha (OH)D3] in combination with CaCO3 and 'low-calcium dialysis' (1.25 mmol/l) on plasma (p) parathyroid hormone (PTH) and biochemical bone markers (osteocalcin, alkaline phosphatase, procollagen type 1 c-terminal extension peptide) were examined in 54 patients on chronic hemodialysis with either normal or elevated PTH. Increasing doses of 1 alpha (OH)D3 were administered intravenously under careful control of p-Ca2+ and inorganic phosphate. Blood samples were obtained 1 week before the start of treatment and then every 2nd week. 20 patients with initially normal PTH levels (23.5 +/- 4.17 pg/ml) and 34 patients with initially elevated PTH levels (301 +/- 45 pg/ml) were followed for up to 88 weeks. The present investigation: demonstrated: (1) 'Low-calcium hemodialysis' (1.25 mmol/l) made it possible to use larger doses of CaCO3 and to reduce the doses of an aluminium-containing oral phosphate binder. A decrease in p-Ca2+ during dialysis was induced, and special care had to focus on the compliance to CaCO3, in order not to aggravate the secondary hyperparathyroidism. (2) The combination of 'low-calcium hemodialysis', CaCO3, and pulse intravenous 1 alpha (OH)D3 prevented the development of secondary hyperparathyroidism in patients with normal PTH levels and induced a long-term suppression of p-PTH (106 +/- 25 pg/ml, 88 weeks) in the patients with secondary hyperparathyroidism. By careful monitoring, severe hypercalcemia and hyperphosphatemia were avoided. There were no indications, clinically or biochemically, of development of adynamic bone disease. (3) Bone lesions were healed and a decrease of the bone mineral content in lumbar spine and femoral neck of patients with both normal and elevated PTH levels prevented. (4) The present results may suggest that PTH might be of influence on that regulation of procollagen type 1 c-terminal extension peptide.
Nephron 1996
PMID:Long-term effects of intravenous 1 alpha (OH)D3 combined with CaCO3 and low-calcium dialysis on secondary hyperparathyroidism and biochemical bone markers in patients on chronic hemodialysis. 888 25

Phosphate binders are necessary to control hyperphosphataemia in the majority of dialysis patients. Whilst aluminium salts are efficient phosphate binders, their use is associated with toxic side effects. Calcium salts are a widely used alternative, but hypercalcaemia is a common side effect, limiting their use and raising concern about metastatic calcification. Reduction of the dialysis fluid calcium concentration has been shown to reduce hypercalcaemia in haemodialysis patients, with an associated decrease in serum PTH. We analysed the effect of reduced calcium/magnesium (1.25/0.25 mmol/l), 40 mmol/l lactate, PD fluid (PD4) on 11 CAPD patients with uncontrollable hypercalcaemia (> 2.65 mmol/l) and hyperphosphataemia (> 1.80 mmol/l). Only 1 patient remained hypercalcaemic, while phosphate fell in 6 patients (2.23 +/- 0.16 on no binder, to 1.68 +/- 0.08 mmol/l at 6 months (p < 0.05), but was unchanged in 5 (2.10 +/- 0.15 to 2.48 +/- 0.14 mmol/l [p = NS]). Overall mean calcium x phosphate product changed little. However, in a subgroup it fell significantly (p < 0.05). Geometric mean iPTH rose, but not significantly. The subgroup of patients whose calcium x phosphate product fell, exhibited a much smaller rise in iPTH than the others (57.3-73.2 vs. 52.8-167.1 pg/ml). 1.25-Dihydroxyvitamin D3 was subnormal in all patients. Mean serum magnesium fell from 1.24 +/- 0.06 to 0.89 +/- 0.04 mmol/l (p < 0.001), whilst mean serum bicarbonate rose significantly (25.2 +/- 0.4 to 28.9 +/- 1.2 mmol/l; p < 0.01). Withdrawal of aluminium-containing phosphate binders resulted in mean serum aluminium falling significantly from 31.1 +/- 5.7 at start of PD4 to 15.4 +/- 2.7 mu g/l at 6 months (p < 0.05). In summary, in around 50% of CAPD patients with persistent hypercalcaemia and hyperphosphataemia, reduction in PD fluid calcium can produce significant improvement in phosphate, reduction of calcium x phosphate product, and enable avoidance of aluminium-containing phosphate binders. Patients whose calcium and phosphate control remains poor, still benefit from the reduction, or cessation, of oral aluminium intake.
Nephron 1996
PMID:Hypercalcaemia, hypermagnesaemia, hyperphosphataemia and hyperaluminaemia in CAPD: improvement in serum biochemistry by reduction in dialysate calcium and magnesium concentrations. 890 61

Two dialysis patients with markedly elevated plasma silicon (Si) levels (3,849 and 2,350 micrograms/l, respectively) and a presumed Si-related syndrome are described in this report. One patient presented with transient hypercalcemia in the face of low PTH, vitamin D and plasma A1 levels. Both patients had painful, nodular skin eruptions and aberrant hair growth, characterized as perforating folliculitis on skin biopsy, compatible with known effects of organosilicon compounds in man and animals. Plasma Si was found to be moderately elevated in 30 dialysis patients studied at random (710 +/- 53 micrograms/l, dialysis, vs. 152 +/- 9 micrograms/l, normal control), but there was no significant difference between the arterial values before and after dialysis, implying that the source of Si was ingested foods and fluids rather than dialysate. In these patients, plasma Si was weakly correlated with serum calcium as well as with serum calcium corrected for serum albumen, indicating that Si, like aluminum, may affect calcium metabolism.
Nephron 1997
PMID:Silicon-related syndrome in dialysis patients. 938 Feb 38

Pamidronate constitutes a major advance in the treatment of tumor-associated hypercalcemia. However, transient electrolyte abnormalities have been reported after pamidronate administration. We describe here a patient with multiple myeloma and severe hypercalcemia who developed transient but significant electrolyte disturbances (mainly hypophosphatemia and hypomagnesemia) after a single dose of 90 mg of pamidronate, focusing on the underlying pathophysiological mechanisms.
Nephron 1998
PMID:Multiple electrolyte abnormalities after pamidronate administration. 967 36

Calciphylaxis is a rapidly developing, fatal process of vascular calcium deposition with prominent cutaneous manifestation. We treated a long-term haemodialysis patient who developed an analogous disorder limited to the lungs. A 57-year-old man was admitted for initiation of peritoneal dialysis because limited cardiac reserve precluded further haemodialysis. He was treated successfully for pneumonia until hypoxia and progressive hypercalcaemia developed. (99m)Tc-methylene disphosphonate scintigraphy showed diffusely increased pulmonary uptake. Death supervened despite aggressive and successful treatment of hypercalcaemia. Autopsy studies included immunohistochemistry and morphometric studies of bone. Alveolar capillary walls showed diffuse calcium deposition. Both gross and microscopical findings differed from those of typical metastatic calcification in dialysis patients. Immunoreactivity for parathyroid hormone-related protein was present in the lesions. Bone histomorphometry indicated mild osteitis fibrosa. Pneumonia is believed to have caused local synthesis of parathyroid hormone-related protein that, along with high calcium x phosphorus product, contributed to calcium deposition. By analogy with the cutaneous process we termed the deposition "pulmonary calciphylaxis".
Nephron 2001 Jan
PMID:Acute respiratory failure due to "pulmonary calciphylaxis" in a maintenance haemodialysis patient. 1117 29

Hyperparathyroidism is a common problem for patients on renal replacement therapy programs. Many long-term dialysis patients require parathyroidectomy while on dialysis. Some patients, however, despite severe renal osteodystrophy, are transplanted, and in these a large proportion show a slow resolution of bony problems, in the context of the removal of the uremic stimulus to abnormal bone metabolism. A proportion of these patients become hypercalcaemic after renal transplantation, sometimes with symptoms. There is not a consensus on how these patients should be managed, with opinions varying from early parathyroidectomy to later parathyroidectomy and to conservative treatment. We present the case of a lady who underwent 23 years of conservative management of her post-transplant hyperparathyroidism. She was hypercalcaemic for almost all of that period, despite excellent renal transplant function. Finally, after 23 years she underwent surgical parathyroidectomy with autografting with prompt sustained resolution of her symptomatic hypercalcaemia.
Nephron 2001 Sep
PMID:Persistent post-transplant autonomous hyperparathyroidism despite 23 years of excellent renal allograft function. 1152 40


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