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

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

Hypercalcemia in malignant lymphoma is not common. Our case of malignant lymphoma with multiple bony lesions showed hypercalcemia (13 mg/dl) at the time of bone marrow relapse. The serum level of parathyroid hormone-related peptide increased to 142 pmol/l, which may be secreted by malignant lymphoma cells. The course of the patient was aggressive and she died from bone marrow relapse after 6 months of treatment including high-dose methotrexate, which caused acute nonoliguric renal failure. At autopsy there was extensive calcium deposition in the lungs, kidneys and pancreas and prominent tubular damage of kidneys.
Nephron 2002 Jan
PMID:Report of a patient with a high level of parathyroid hormone-related peptide associated with malignant lymphoma involving multiple bony lesions. 1174 12

The low calcium (Ca(2+)) dialysate have been developed to diminish the risk of hypercalcemia with the administration of active vitamin D and Ca(2+) carbonate as phosphate binder. Today, increasing numbers of hemodialysis (HD) patients have been on the low Ca(2+) dialysate (Ca(2+) = 2.5 mEq/l). However, the clinical consequences of a negative calcium net-balance which may be induced by the use of low Ca dialysate are not well evaluated. In the present study, we explored the effects of low Ca(2+) dialysate on the calcium balance and the PTH secretion. Eighty one chronic HD patients (male/female: 47/34; mean age: 60.2 +/- 1.5 years; mean HD periods: 11.1 +/- 0.8 years) who had been dialyzed with 3.0 mEq/l Ca(2+) dialysate were studied. All patients were transferred to the low Ca dialysate, which actually brought about a negative net-balance in Ca (mean: -94.5 mg) and an increase in serum intact PTH levels (mean: +23.7%: p = 0.03) during a single HD session. However, no changes in serum ionized Ca(2+) were found in spite of negative Ca(2+) balance. One month after change to the low Ca(2+) dialysate (total 12 sessions in each case), serum intact PTH levels increased significantly (186.7 +/- 19.5 vs. 216.2 +/- 21.9 pg/ml: p = 0.01) in spite of the fact that no changes were found in serum ionized Ca(2+), Pi and Mg. This result indicates that the negative Ca(2+) balance during low-Ca(2+) hemodialysis-stimulated PTH secretion, which offset the decrease of serum Ca(2+); a trade-off phenomenon between negative Ca balance and PTH. This suggests that low Ca(2+) dialysate may exaggerate the progression of secondary hyperparathyroidism.
Nephron 2002 Sep
PMID:The negative Ca(2+) balance is involved in the stimulation of PTH secretion. 1218 89

The human body is equipped with an efficient protection system against hypocalcemia. This system is composed of parathyroid glands, bone, kidney, and intestine. By appropriate actions of parathyroid hormone (PTH) and active vitamin D (1,25-dihydroxyvitamin D), a small fall of extracellular calcium ion concentration is instantly corrected. Thus, a defect of any step in this system results in the development of hypocalcemia. Overloaded calcium either from bone or intestine is efficiently excreted into the urine. Thus, hypercalcemia develops almost exclusively when a greater amount of calcium than the kidney can excrete is loaded. In chronic dialysis patients, either hypocalcemia or hypercalcemia may develop because of defects in these two defense systems against calcium imbalance.
Nephron 2002
PMID:Calcium homeostasis and imbalance. 1242 29

The prevalence and extent of vascular calcification (VC) increases rapidly with time on dialysis. There is increasing evidence that medial calcification of conduit arteries, without intimal disease, is associated with important abnormalities of vascular compliance and increased risk of cardiovascular death. Coronary artery calcification is also common in end-stage renal disease, but further research is required to determine how much of this calcification is in the form of calcified intimal atherosclerotic plaque and how much in the tunica media. Calcific uraemic arteriolopathy causes a syndrome of ischaemic necrosis of the skin and subcutaneous tissue and appears to be increasing in incidence. At all sites, arterial calcification is a biologically controlled process, with expression in vascular smooth muscle cells of genes usually expressed in osteoblasts and the formation of hydroxyapatite. High extracellular phosphate concentration induces these phenotypic changes in vitro, and much of the clinical evidence supports hyperphosphataemia as the major driver of VC. Whether warfarin treatment plays a role, by inhibiting production of vitamin-K-dependent inhibitors of calcification in humans, remains uncertain but possible. High doses of prescribed calcium-based phosphate binders are associated with VC, whereas use of sevelamer to achieve the same serum phosphate level greatly retards progression of coronary and aortic calcification. The biological mechanism by which positive calcium balance and/or episodes of hypercalcaemia promotes VC remains unclear. Treatment of established calcific uraemic arteriolopathy consists of aggressive reduction of serum calcium x phosphate product; the roles of hyperbaric oxygen, steroid therapy, and non-warfarin anticoagulation remain uncertain.
Nephron Clin Pract 2003
PMID:Vascular calcification in chronic renal failure. 1275 80

The aetiology of stones in children differs from that in adults. Young children, especially boys, are prone to infective stones, although this type of calculi is decreasing in frequency over time in prosperous countries. Two monogenic causes, cystinuria and hyperoxaluria, each account for 5-15% of paediatric stones. Increased factors for stone formation in children include prematurity, neurological problems, ketogenic diet and reconstructed or augmented bladders. Hypercalciuria is commonly found in paediatric stone formers, is usually idiopathic and is only rarely associated with hypercalcaemia. All children with stones should undergo a metabolic evaluation.
Nephron Clin Pract 2004
PMID:Aetiological factors in paediatric urolithiasis. 1549 5

Cardiovascular disease is a major cause of death among patients with chronic kidney disease and vitamin D deficiency is a common problem also among these patients. Abnormalities in left ventricular size and function are frequent, as they are encountered in 70-80% of incident dialysis patients. These alterations develop early in the course of renal disease and their prevalence progresses in parallel with the decline in renal function. This process of left ventricular dilatation with compensatory hypertrophy continues after the institution of dialysis therapy, especially in the first year. The main factors responsible for the progression of left ventricular hypertrophy (LVH) are considered to be blood pressure and anemia, and in patients receiving hemodialysis, the arteriovenous fistula, volume overload and abnormalities in mineral metabolism. This additional potential set of factors related to LVH - mineral and bone metabolism - is intriguing and begs an immediate question: by what possible mechanism can these factors be linked to cardiac morphology? Recent observational studies have indeed indicated that vitamin D treatment was associated with a significant reduction of cardiovascular death among dialysis patients, and a reduction in LVH; in contrast, other studies suggested that excess vitamin D contributes to risk of hypercalcemia and vascular calcification, which is associated with reduced survival and morbidity. This review examines the evidence linking vitamin D with cardiac structure and function.
Nephron Clin Pract 2010
PMID:The effects of vitamin D therapy on left ventricular structure and function - are these the underlying explanations for improved CKD patient survival? 2060 78

The aim of the present study was to assess the frequency and factors associated with the progression of vascular calcifications (VCs) using a semiquantitative X-ray score. We included all prevalent hemodialysis patients with initial radiological scores ranging from 0 to 3 according to the severity of the VCs. Patients were classified as non-progressors or progressors after 3 years. Among the 85 patients, 44.7% were classified as progressors. Only exhibiting high levels of serum intact parathyroid hormone (PTH, >190 pg/ml) and fibroblast growth factor (FGF)-23 levels (>3,000 RU/ml) is associated with the risk of VC progression (OR 5.8, 95% CI 1.7-19.8, p = 0.004). Calcitriol analogs (38%), cinacalcet (15%), dialysate calcium (mean 1.48 mmol/l), dialysis session time (4-8 h) and calcium- (10%) and non-calcium-based phosphate binders (38%) were prescribed on an individual basis. Hyperphosphatemia (<10%) and, especially, hypercalcemia (1%) and hyperparathyroidism (>585 pg/ml = 0%) were infrequently observed. In conclusion, the main factor associated with VC progression was the association of higher serum PTH and FGF-23 levels. It remains to be seen whether patients should be treated to lower their PTH value, even within the target range, using calcitriol analogs, calcimimetics, parathyroidectomy, or by modifying the Klotho-FGF-23 axis.
Nephron Clin Pract 2012
PMID:Increased levels of serum parathyroid hormone and fibroblast growth factor-23 are the main factors associated with the progression of vascular calcification in long-hour hemodialysis patients. 2258 63

Bisphosphonates are commonly used for the treatment of osteoporosis, Paget's disease, multiple myeloma and hypercalcemia. Collapsing focal segmental glomerulosclerosis (FSGS) is known to occur uncommonly with exposure to bisphosphonates, specifically pamidronate and alendronate; it has rarely and equivocally been reported with zoledronate therapy. We describe the case of a 36-year-old African American female with metastatic breast cancer who presented with nephrotic-range proteinuria and acute kidney injury within 2 weeks of exposure to a single dose of zoledronate. The patient had a partial recovery of her renal function and showed improved proteinuria to a subnephrotic level after discontinuing zoledronate. In contrast to 2 prior reports of zoledronate-induced collapsing FSGS, the causative role of the exposure described here is certain. Our case necessitates the addition of zoledronate to the list of known causes of collapsing FSGS. Furthermore, it highlights the importance of periodically monitoring renal function and urine protein excretion with the use of zoledronate, which allows prompt diagnosis and withdrawal of the drug to increase the probability of renal recovery.
Nephron Extra 2014 Sep
PMID:Collapsing focal segmental glomerulosclerosis resulting from a single dose of zoledronate. 2547 6


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