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

A 36 year old man, who had been proteinuric for 14 years due to immunoglobulin A (IgA) nephropathy, was admitted because of an acute exacerbation in renal dysfunction with hypercalcemia. He had presented with aortic regurgitation and increased pulmonary marking by chest X-ray, but laboratory examinations had failed to make an exact diagnosis. On admission, noncaseating epithelioid granulomas were disclosed by muscle and skin biopsies. Ophthalmological evaluation revealed old uveitis and retinal changes consistent with sarcoidosis. In this case, IgA nephropathy was thought to be the initial manifestation of sarcoidosis that developed latently. Sarcoidosis should be considered in a differential diagnosis of IgA nephropathy.
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PMID:A case of sarcoidosis revealed in the course of IgA nephropathy. 804 8

This is a retrospective, clinical study evaluating the long-term outcome of subtotal parathyroidectomy (PTX) in 60 patients with chronic renal failure and severe secondary hyperparathyroidism. Patients were 41 +/- 2 years old (mean +/- SE) at the time of PTX, and followed for 69 +/- 6 months since the procedure. At the time of PTX, three patients had chronic renal failure, 53 had been on chronic hemodialysis, and four had received successful kidney transplants. In more than 80 per cent of patients, symptoms of hyperparathyroidism (bone pain and muscle weakness) resolved within weeks, and biochemical signs (hypercalcemia, and high plasma alkaline phosphatase and parathyroid hormone concentrations) returned to normal ranges within a year. Subperiosteal resorption, bone fractures, and soft tissue calcification frequently improved. Osteosclerosis (rugger-jersey spine), cystic bone changes, osteopenia, and vascular calcifications were, however, often unchanged or progressive. Five patients (8%) who had either persistent or recurrent hyperparathyroidism required additional surgical procedures, and two had subsequent improvement. Twelve patients who had aluminum associated bone disease diagnosed later continued to progress with a high incidence of bone fractures and severe osteopenia. Cystic bone changes, especially of the carpal bones, in association with carpal tunnel syndrome, probably representing amyloid bone disease, also did not respond to PTX. In conclusion, PTX is an effective surgical procedure to reverse complications of hyperparathyroidism in patients with end-stage renal disease, provided that other causes of osteodystrophy, such as aluminum or amyloid-associated bone diseases, are adequately excluded. We feel that subtotal PTX, leaving a small remnant in place, is the procedure of choice.
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PMID:Long term results of subtotal parathyroidectomy in patients with end-stage renal disease. 806 33

Abnormalities of calcium homeostasis are a recognized feature of end-stage renal disease. The treatment of choice is renal transplantation, but this does not always result in normalization of the biochemical profile. Persistent hypercalcaemia is well documented and our study was undertaken to investigate the status of the calcium regulating hormones in renal patients post-transplantation. Serum calcium, parathyroid hormone, 1,25-dihydroxyvitamin D (1,25(OH)2D) and osteocalcin concentrations were measured in post-transplant patients. Twenty per cent of the patients had subnormal 1,25(OH)2D concentrations while 55% had biochemical evidence of hyperparathyroidism but only 5% were hypercalcaemic. Time elapsed since transplantation was not correlated with any of the analytes investigated and there was no relationship between persistent impairment of renal function and abnormalities of calcium homeostasis.
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PMID:Calcium metabolism following renal transplantation. 788 84

Advances over the last several years have led to a better understanding of the etiology of hyperparathyroidism in renal disease and to more effective means of medical prevention and therapy. Thus, in most dialysis populations, many of the serious complications, such as bone fractures, refractory hypercalcemia, and hyperphosphatemia with vascular and other extraskeletal calcifications, have diminished. Furthermore, more aggressive medical management has decreased the requirement for parathyroidectomy. Unfortunately, not all patients respond to medical management and few still develop refractory hyperparathyroidism with associated morbidity. Of the many complications of refractory hyperparathyroidism in dialysis patients, the development of life-threatening hypocalcemia has not been described. We describe a patient with severe secondary hyperparathyroidism who presented with the acute development of hypocalcemia. To our knowledge, this represents the fourth case, the first reported in a patient with end-stage renal disease, of parathyroid autoinfarction presenting as acute hypocalcemia.
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PMID:Hypocalcemia in end-stage renal disease: a consequence of spontaneous parathyroid gland infarction. 807 80

The renal concern in a multiple myeloma (MM) case has a frequency of 50% and causes a worsening of the disease with a survival average of about 12 months. The monoclonal light free chains (CLL) produced in excess by the plasmacytes are present in the urine as proteinuria of Bence Jones (PBJ) in 60-70% of patients affected by MM. They represent the major pathogenetic factor of the nephropathy in course of MM as they can deposit in shape of intratubular "casts" in the myeloma casts nephropathy (MCN). In some worse cases, dehydration or hypercalcaemia can cause an irreversible acute renal insufficiency (RI). It is therefore important in a patient affected with MM with PBJ to prevent, locate and opportunely treat these situations which worsen the nephropathy. Beside the tubular cast nephropathy, the CLL "accumulate" in the kidney even though with a lower frequency compared to MCN, in the light chains deposition disease (LCDD) and in the amyloidosis AL (AL). LCDD is characterized by a deposit of nodular amorphous materials PAS positive in the glomerulus and sometimes even in the tubulus. It usually presents itself as a chronic RI and a proteinuria causing nephrotic syndrome (NS). This quickly evolves into uraemia and its evolution can be lessened by the MM treatment. AL in course of MM also reveals with a chronic RI and NS. CLLs deposit in the typical fibrillar structure, on the vessel walls, in the glomerulus, in the mesangium and can be marked out with the Congo red colouring and the subsequent green birefringence through microscope with polarized light. Prognosis of AL is extremely severe and no benefit is given by the treatment of the hematological illness. It is therefore absolutely necessary to study the renal histology through biopsy when MM is grade B, that is, with serumal creatinine above 2 mg/dl as: MCN imposes the MM treatment programme in order to reduce the tubular excess of PBJ and to attempt to make RI reversible; MCN with tubular atrophy and interstitial fibrosis results in an unfavourable prognosis as it expresses a nephropathic irreversibility due to the loss nephrons. It will therefore necessary to start on a renal substitutional treatment programme. Renal damage in course of MM is not always tubular, rather an unexpected glomerular damage of LCDD or amyloidosis AL type can be found.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The kidney in multiple myeloma. The physiopathological and clinical aspects]. 818 90

We present two cases of hypercalcemic nephropathy associated with primary hyperparathyroidism. Case 1 is a 37-year-old man who had repeated bone fractures and recurrent ureteral stones, which led to the diagnosis of primary hyperparathyroidism. Case 2 is a 35-year-old man in whom parathyroid carcinoma was discovered because of secondary nephrogenic diabetes insipidus, resulting from severe hypercalcemia. Both patients developed mild renal dysfunction during the course of hyperparathyroidism. In the renal biopsy materials obtained from case 1, the renal interstitium showed chronic inflammatory changes. The tubules were partly damaged (focal necrosis). Deposition of calcium was sometimes noted within the mitochondria of the tubular epithelial cells. Some glomeruli showed glomerular sclerosis. In biopsy materials obtained from case 2 after resection of the carcinoma, similar histological features were observed, but tubular atrophy and necrosis were advanced. Polyuria and hypercalcemia were ameliorated after resection. These findings indicate that severe hypercalcemia might induce tubular dysfunction as well as organized changes.
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PMID:[Two cases of hypercalcemic nephropathy associated with primary hyperparathyroidism]. 826 8

In a population of 716 patients with end-stage renal disease (ESRD), 46 patients (6.4%) were identified as having pancreatitis. Pancreatitis was significantly more common in those with alcohol abuse, systemic lupus erythematosus (SLE), and polycystic kidney disease. It was not significantly associated with hyperlipidemia, biliary tract disease, or hypercalcemia. Acute pancreatitis occurring before the patient developed ESRD was mainly alcohol-related and did not appear to be a significant risk factor for future episodes of pancreatitis during dialysis. Chronic calcific pancreatitis diagnosed before ESRD was almost invariably due to alcohol abuse, and tended to be a marker for recurrent acute exacerbation after development of ESRD, whether alcohol consumption continued or not. Pancreatitis occurring for the first time after ESRD in patients on dialysis was generally benign, and was usually accompanied by an uneventful recovery and few recurrent episodes. However, a significant elevation of the calcium x phosphate product was observed in these patients, occurring in about half the patients without any known precipitating factor. After kidney transplantation, the development of pancreatitis was associated with higher morbidity and mortality. Chronic calcific pancreatitis diagnosed after ESRD occurred only in patients with SLE; reported here for the first time, it may be a manifestation of long-standing disease, chronic steroid therapy, or both.
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PMID:Pancreatitis in patients with end-stage renal disease. 830 63

An 11-month-old male infant with recurrent supraventricular tachycardia (SVT) was treated with oral verapamil. Shortly thereafter he developed marked changes in behavior including lethargy, intensely increased thirst and urination, and irritability when denied fluids. "Primary" polydipsia was diagnosed following an evaluation which showed no evidence of adrenal insufficiency, diabetes insipidus, diabetes mellitus, hypercalcemia, hyperosmolality, or renal disease. The symptoms resolved 1 week after verapamil was discontinued.
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PMID:Verapamil-induced "primary" polydipsia. 852 7

Differences in the regulation of parathyroid hormone (PTH) release by calcium are thought to account for excess PTH secretion in patients with secondary hyperparathyroidism (2 degrees HPTH). To determine whether calcium-regulated PTH release varies with the severity of 2 degrees HPTH in patients with end-stage renal disease, dynamic tests of parathyroid gland function were done using the four-parameter model in 26 patients with 2 degrees HPTH documented by bone biopsy. Estimates of the set point did not differ among patients categorized as mild (basal serum PTH < 400 pg/ml), moderate (basal PTH 400 to 600 pg/ml) or severe (basal PTH > 600 pg/ml) 2 degrees HPTH; values were 1.23 +/- 0.06 mmol/liter, 1.24 +/- 0.06 mmol/liter and 1.23 +/- 0.05 mmol/liter, respectively, and none of these set point estimates differed from results obtained in normal volunteers, 1.21 +/- 0.02 mmol/liter (NS). The slope of the sigmoidal ionized calcium-PTH curve also did not differ among groups. Set point values did not correspond to basal serum PTH levels, to the maximum serum PTH level observed during hypocalcemia or to the minimum serum PTH level seen during hypercalcemia in patients with 2 degrees HPTH. In contrast, basal serum PTH values were positively correlated with both the maximum serum PTH level observed during hypocalcemia (r = 0.76, P < 0.01), and the minimum serum PTH level attained during calcium infusions (r = 0.78, P < 0.01). Calcium-regulated PTH release does not differ with the degree of 2 degrees HPTH, and set point abnormalities do not account for excess PTH secretion in patients with chronic renal failure as judged by in vivo dynamic tests of parathyroid gland function. The results suggest that variations in parathyroid gland size are the major contributor to excessive PTH secretion in patients with chronic renal failure.
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PMID:Calcium-regulated parathyroid hormone release in patients with mild or advanced secondary hyperparathyroidism. 854 13

The introduction of new techniques for the determination of renal parenchymal oxygenation and intrarenal microcirculation has elucidated some important aspects in the pathophysiology of acute renal failure (ARF). Data accumulated over the last decade with these techniques, together with improved morphologic evaluation of the kidney, indicate that medullary damage may play a pivotal role in various forms of acute and chronic renal hypoxic and toxic insults. The outer medulla functions normally under hypoxic conditions, as a result of limited regional oxygen supply and high oxygen consumption for urinary concentration. Outer medullary oxygenation is critically balanced by mechanisms designed to adjust oxygen demand and supply, and their insufficiency may lead to ARF with hypoxic medullary damage. In this article, we outline our current concept of the physiologic control of medullary oxygenation and review the clinical conditions that predispose to hypoxic medullary damage, including rhabdomyolysis, hypercalcemia, or the exposure to endotoxin, nonsteroidal anti-inflammatory drugs, radiologic contrast agents, cyclosporine, FK506, and amphothericin. We shall indicate a possible role for medullary oxygen insufficiency in clinical conditions known to predispose to ARF, such as preexisting renal disease, diabetes mellitus, hypertension, atherosclerosis, effective volume depletion, urinary obstruction, or aging, and suggest potential strategies to preserve medullary oxygenation and integrity.
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PMID:The role of medullary ischemia in acute renal failure. 857 90


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