Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The anti-tumor therapy followed by tumor lysis syndrome may cause the metabolic disorders including hyperkalemia, hyperphosphatemia and hyperuricemia. It should be known that it occurs frequently in lymphoproliferative diseases, especially in Burkitt's lymphoma. Two cases of T-ALL accompanied by this syndrome, from which the patients were recovered, at the induction therapy of the first complete remission are reported here. Case 1. A 28-year-old man received VP therapy under the diagnosis of T-ALL with massive hepatosplenomegaly and bilateral enlarged kidneys. During the therapy, metabolic disorders with both renal failure and ventricular tachycardia happened. They were resolved by certain series of treatments. The patient was brought to a complete remission with normal size of liver, spleen and kidneys. Case 2. A boy aged 15 having received the intrasubarachnoidal infusion of MTX and 1-Ad-VP therapy under the diagnosis of T-ALL accompanied by this syndrome which was improved by an appropriate treatment, and the patient was lead to the remission. The risk factors of this syndrome, such as 1-high drug sensitivity of the tumor; 2-renal dysfunction; 3-rapid cytokinetics of the tumor cell; 4-bigger size of the tumor, as well as the preventive treatment of this syndrome are reviewed.
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PMID:[Tumor lysis syndrome at the induction therapy of the first remission in two cases of T-ALL]. 218 70

Renal osteodystrophy is a complex disorder which can be divided into five distinct bone histologic subtypes: mild bone disease, hyperparathyroid bone disease, mixed bone disease, osteomalacia, and low-turnover bone disease. Hyperparathyroidism develops in renal failure due to two principal abnormalities: 1,25(OH)2D3 deficiency and hyperphosphatemia. Treatment of these problems is important in order to prevent hyperparathyroidism. Most cases of osteomalacia, mixed bone disease, and low-turnover bone disease are influenced by aluminum status and parathyroid hormone. Aluminum-associated bone disease can be treated with termination of aluminum exposure and/or deferoxamine therapy. Numerous diagnostic pitfalls exist in the evaluation of renal osteodystrophy, and the bone biopsy is extremely important to avoid these problems and plan proper therapy.
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PMID:Renal osteodystrophy. 219 69

Renal amyloidosis was diagnosed in 14 young Chinese Shar Pei dogs, all of which were related. Clinical signs were those of renal failure and included vomiting, anorexia, lethargy, polydipsia, polyuria, weight loss, and dehydration. Some dogs had a history of intermittent fever and joint swelling. Laboratory findings also were compatible with renal failure and included azotemia, hyperphosphatemia, low total CO2 content in serum, isosthenuria, proteinuria, and hypercholesterolemia. All dogs had medullary deposition of amyloid, and 9 of 14 (64%) had glomerular involvement. The remaining renal lesions were typical of end-stage renal disease. In some dogs, amyloid deposits were found in other tissues (eg, liver, spleen, stomach, small intestine, myocardium, lymph node, prostate gland, thyroid gland, and pancreas). Amyloid deposits were sensitive to potassium permanganate oxidation, suggesting the presence of amyloid protein AA.
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PMID:Familial renal amyloidosis in Chinese Shar Pei dogs. 221 Dec 93

Hypocalcemia based on total calcium measurement is frequent in certain cancers (especially prostate) in association with osteosclerotic bone metastases. In a majority of these patients hypocalcemia is related to the low serum albumin and/or renal failure. True ionized hypocalcemia may be seen as a toxic effect of certain chemotherapeutic agents or as a consequence of hyperphosphatemia due to rapid tumor lysis. In addition, tumors may produce osteoblast-stimulating factor(s) which cause massive accretion of calcium by the skeleton. Isolation and purification of these factors may provide us with unique osteoblast-stimulating factors which may have therapeutic applications.
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PMID:Hypocalcemia in cancer. 222 3

Four sequential Tc-99m pyrophosphate (PYP) imaging studies were performed in a 28-year-old man with high fever and exudate pharyngitis associated with renal failure. Radiotracer localization in the left ventricle (LV), lungs, kidneys, and skeletal muscles were seen in two, initial imaging studies. In the second and third imaging studies, area of increase in activity was seen in the left-sided bowel. In studies done two months later (in the third study), the radioactivity in the skeletal muscles was no longer seen. Studies obtained nine months (in the fourth study) after the first imaging showed less radiotracer localization in the LV, lungs, and kidneys as compared to that seen in the initial study. Myocardial necrosis and microcalcification were proved by LV biopsy. The exact mechanism of extraosseous bone-imaging agent localization is unknown. However, this phenomenon may be related to renal failure, rhabdomyolysis, hypercalcemia, hyperphosphatemia, or elevated parathyroid hormone. The Tc-99m PYP imaging study is useful and sensitive in the detection of extraosseous tissue calcification and monitoring of the disease process.
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PMID:Extensive extraosseous localization of bone imaging agent in a patient with renal failure and rhabdomyolysis accompanied by combined hypercalcemia and hyperphosphatemia. 254 39

Hyperphosphatemia and secondary hyperparathyroidism are regular complications in patients suffering from end-stage renal failure. Aluminum-containing drugs are widely used to control serum phosphate, but this therapy carries the well-known risk of aluminum toxicity. Previously we demonstrated that a mixture of ketoacids is very effective in lowering increased serum phosphate and serum PTH levels. Recent studies to clarify the underlying mechanisms whereby these compounds lower serum phosphate revealed that ketoacids act as intestinal phosphate binders. In balance studies we demonstrated that intestinal phosphorus uptake decreased in normal subjects (decrease of absorption during ingestion: 0.7-3.14 mmol/day). Additional in vitro studies not only confirmed the in vivo results but also showed that ketoacids are as efficient as calcium carbonate although they provide less calcium. It is of further interest that ketoacids reached their greatest binding efficiency when the pH is 7.0, whereas calcium carbonate binds phosphate predominantly when the pH is 2.0 or 5.0. Ketoacids represent a further therapy to lower serum phosphate in uremia. As they provide less calcium than calcium carbonate, they could be considered as an advantageous, less dangerous alternative.
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PMID:Calcium salts of ketoacids as a new treatment strategy for uremic hyperphosphatemia. 263 49

Severe rhabdomyolysis following an influenza B infection developed in a previously well 13-year-old girl. There was no history of trauma. Her course was complicated by episodes of severe hyperkalemia, hypocalcemia, hyperphosphatemia, and myoglobinuria. Renal failure, hypertension, and life-threatening arrhythmias developed; she died. Muscle biopsy revealed that this girl had carnitine palmityl transferase deficiency. An asymptomatic sister was demonstrated to have the same disorder. Although carnitine palmityl transferase deficiency is usually associated with mild bouts of rhabdomyolysis that become apparent only in adulthood, severe forms of this disorder may be seen in children. Life-threatening rhabdomyolysis and myoglobinuria may follow any infection associated with decreased intake. If carnitine palmityl transferase deficiency is diagnosed in a proband, other siblings should be evaluated so that proper preventative measures can be undertaken to help prevent the development of symptoms in susceptible individuals who have not been recognized to have the disease.
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PMID:Fatal rhabdomyolysis following influenza infection in a girl with familial carnitine palmityl transferase deficiency. 274 60

We report a case of a calcium phosphate bezoar resulting in colonic intussusception in a boy with chronic renal failure who received calcium carbonate to control hyperphosphatemia. Because of concerns about aluminum-related disease in patients receiving aluminum hydroxide phosphate binders, calcium carbonate is being used more frequently to manage phosphate retention in renal failure. The development of bezoars may complicate this new form of therapy.
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PMID:Colonic intussusception secondary to a calcium phosphate bezoar in a child receiving calcium carbonate for hyperphosphatemia. 280 98

Renal failure is frequently associated with osteodystrophia due to secondary hyperparathyreoidism and/or increased aluminum intake. The problem of hypercalcemia and hyperphosphatemia can more easily controlled by CAPD than by hemodialysis. Total serum and ionized calcium levels are rapidly normalized by a CAPD regime of four 2-1 exchanges with 1.75 mmol/l Ca. Under the same CAPD regime 250-300 mg phosphate are removed per day. Depending on the ingestion of phosphate, 100-200 mg phosphate per day remain to be removed by phosphate binding agents. Since the main source of aluminum in CAPD patients is oral ingestion of aluminum-containing phosphate binders, serum levels should be regulated by diet and calcium carbonate. To suppress PTH secretion serum ionized calcium levels need to be maintained at the upper limit of normal. This can also be achieved by the use of oral calcium carbonate. Vitamin D or analogs should be prescribed only when clinically indicated by persistent hypocalcemia, osteitis fibrosa or non-aluminum related osteomalacia.
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PMID:Renal osteodystrophy and aluminum bone disease in CAPD patients. 305 62

Phosphorus is the sixth most abundant element in the body after oxygen, hydrogen, carbon, nitrogen, and calcium. It comprises about 1% of the total body weight of humans. Eighty-five percent of it is stored in the bone in the form of hydroxyapatite crystal; 14% is in the soft tissues in the form of energy-storing bonds with nucleotides (ATP, GTP), nucleic acids in chromosomes and ribosomes, 2,3-DPG in the red blood cells, and phospholipids in the cells' membranes. Less than 1% is in the extracellular fluids. Phosphate balance is maintained by multiple systems. The gut is responsible for the absorption of two thirds of the 4-30 mg/kg/day of phosphate intake. Absorption sites are all along the gut; in humans the most active site is the jejunum. The kidney filters 90% of the plasma phosphate and reabsorbs it in the tubuli. In states of hypophosphatemia the kidney can reabsorb the filtered phosphates very efficiently, reducing the amount excreted in the urine virtually to zero. The healthy kidney can excrete high loads of phosphate and rid the body of phosphate overload. Through the vitamin D-PTH axis the endocrine system regulates the phosphate balance by influencing the kidney, gut, and bone. Other hormones, including thyroid, insulin, glucagon, glucocorticosteroid, and thyrocalcitonin, play a lesser role in regulation of phosphate metabolism. Because of the complex control of phosphate homeostasis, various clinical conditions may lead to hypophosphatemia. These include nutritional repletion, gastrointestinal malabsorption, use of phosphate binders, starvation, diabetes mellitus, and increased urinary losses due to tubular dysfunction. The clinical picture of phosphate depletion is manifested in different organs and is due mainly to the fall in intracellular levels of ATP and decreased availability of oxygen to the tissues, secondary to 2,3-DPG depletion. The various manifestations of phosphate depletion are listed in Table 2. The treatment of hypophosphatemia consists of administering enteral or parenteral phosphate salts. An important aspect of dealing with the potentially serious effects of phosphate depletion is to prevent the depletion from happening in the first place. Hyperphosphatemia can occur in renal failure, hemolysis, tumor lysis syndrome, and rhabdomyolysis. The treatment of hyperphosphatemia usually consists of fluid administration (in the absence of kidney failure). In chronic hyperphosphatemia, phosphate binders such as aluminum and magnesium salts can reduce the phosphate load. The use of these phosphate binders is limited by their potential side effects.
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PMID:Consequences of phosphate imbalance. 306 Jan 61


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