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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Leukemic infiltration of the kidneys is a very rare cause of renal failure. A woman with acute lymphoblastic leukemia presented with nonliguric renal failure and was found to have massively enlarged kidneys. The size of the kidneys was dramatically reduced through the combined effects of local radiation therapy and systemic chemotherapy. Because this rapid shrinkage of the kidneys was associated with improvement in renal function, the uremia was ascribed to leukemic infiltration. As a consequence of rapid tumor lysis in the presence of renal failure, marked hyperphosphatemia and hypocalcemia developed. The literature experience with renal failure secondary to leukemic infiltration of the kidneys is reviewed.
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PMID:Renal failure secondary to leukemic infiltration of the kidneys. 26 82

This study has confirmed previous experiments which indicated that inorganic phosphate concentrations rise in body fluids after intestinal infarction. The phosphate clearance ratio is elevated in dogs after occlusion of the superior mesenteric artery, but is not as sensitive as indicator of the presence of a necrotic intestine as the serum or peritoneal fluid phosphate levels. The rise and fall of phosphate levels occur within the first 24 hours after infarction, similar to amylase levels in acute pancreatitis. The renal failure observed in dogs after ligation of the superior mesenteric vein is likely on the basis of hypovolemia and does not seem to result from hyperphosphatemia. Intestinal infarction should be suspected with laboratory evidence of hemo-concentration, marked leukocytosis, an inappropriate metabolic acidosis and elevated serum and peritoneal fluid phosphate levels. In dogs with normal renal function, an elevated urinary phosphate clearance ratio of greater than 0.20, as measured on a spot sample of urine and serum, is also highly suggestive of the presence of this condition, but its absence, by no means, excludes the diagnosis. With these simple laboratory tests, possibly an earlier diagnosis can be made, and timely operation can be an entirely intestine-saving procedure.
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PMID:The significance of urine phosphate measurements in the early diagnosis of intestinal infarction. 41 30

Renal osteodystrophy has many skeletal pathologic features, eg, fibroosteoclasia (osteitis fibrosa), osteomalacia, osteopenia, pseudofracture, cyst formation, and osteosclerosis. Many of these are caused by the secondary hyperparathyroidism that usually accompanies renal failure. Derangements in parathyroid hormone secretion, calcium and phosphate metabolism, and renal production of 1,25-dihydroxycholecalciferol (the most active form of vitamin D) are all interrelated and pathogenetic features of renal osteodystrophy. Types of abnormalities detected radiologically vary with patient age, type of management, and duration of hemodialysis, as well as with techniques and type of film used and interest of the radiologist. An x-ray film of the hands should always be made--it will show subperiosteal resorption in a large number of patients on dialysis. Prevention and management of renal osteodystrophy hinge on control of hyperphosphatemia and hypocalcemia.
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PMID:Renal osteodystrophy in end-stage renal failure. 71 29

In early chronic renal failure, the state of the bones resembles that of type II primary hyperparathyroidism. Cortical bone becomes thinner and more porous, and there is increased extent of surface remodeling. These changes are followed in turn by osteomalacia and osteitis fibrosa, although sometimes these may be alternate rather than successive stages. Bone turnover is less than would be expected for the elevation of PTH level, probably because of 1,25 (OH)2D3 deficiency. The resorption velocity and lamellar bone appositional rates are depressed, but woven bone appositional rate may be increased, possibly because of hyperphosphatemia. Bone mass reflects the summation of three independent processes: loss of lamellar bone due to hyperparathyroidism (depending on the extent of insulation by osteoid); accumulation of partly mineralized osteoid because of osteomalacia; accumulation of woven bone because of osteitis fibrosa. Osteosclerosis may be growth-related metaphyseal, subchondral or diffuse axial, and periosteal neostosis may also occur. Some patients on hemodialysis lose bone because of planing rather than lacunar or dissecting resorption, combined with depression of both lamellar and woven bone formation. Hyperparathyroid bone disease tends to improve slowly after renal transplantation. Persistent hypocalcemia reflects a defect in the calcium homeostatic system and cannot be explained solely by the known stimuli to secondary hyperparathyroidism. The increment in plasma calcium in response to PTH infusion is subnormal, both in early chronic and in acute renal failure, probably because of 1,25(OH)2D3 deficiency. This is also the most likely explanation for the depressed level of blood-bone equilibrium. The activity of all three of the PTH responsive cell systems in bone is depressed in renal failure, probably because all three require 1,25(OH)2D3 in order to function normally. In pseudohypoparathyroidism, as in chronic renal failure, hypocalcemia results from a defect in the regulation of the blood-bone equilibrium. The bone-remodeling system shows all gradations of response, from slight depression of bone turnover to overt osteitis fibrosa, but bone turnover is never as low as in PTH deficiency. These differences may reflect the presence or absence of resistance to PTH of the osteoprogenitor cell as well as of the calcium homeostatic system, or may be due to varying degrees of 1,25(OH)2D3 deficiency, as in chronic renal failure. An increase in plasma calcium in response to PTH can occur either in the untreated state or after treatment with vitamin D because either the error-correcting or remodeling system remains responsive to PTH. Pseudohypoparathyroidism may be subdivided into three types, depending on whether the urinary cyclic-AMP response to PTH remains defective despite treatment with vitamin D, improves with treatment, or is normal before treatment. Only the former is associated with the genetic syndrome of Albright's hereditary osteodystrophy...
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PMID:The actions of parathyroid hormone on bone: relation to bone remodeling and turnover, calcium homeostasis, and metabolic bone disease. Part IV of IV parts: The state of the bones in uremic hyperaparathyroidism--the mechanisms of skeletal resistance to PTH in renal failure and pseudohypoparathyroidism and the role of PTH in osteoporosis, osteopetrosis, and osteofluorosis. 78 23

Hyperphosphatemia, hypocalcemia and acute oliguric renal failure resulting from uric acid nephropathy developed in a patient with Burkitt's lymphoma and Burkitt cell leukemia after effective chemotherapy. A review of other reported cases in which the patients had similar metabolic abnormalities is presented, and the pathophysiology is discussed. The clinical setting in which these metabolic developments are most likely to occur is defined, and an approach for their prevention and management is presented.
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PMID:Hyperphosphatermia and hypocalcemia accompanying rapid cell lysis in a patient with Burkitt's lymphoma and Burkitt cell leukemia. 83 6

Decreased production of 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) by the kidney may be responsible for vitamin D resistance in renal failure and contribute to renal osteodystrophy. The present studies investigate the effect of reduced renal mass and reduced renal function on conversion of 3H-25-hydroxycholecalciferol to 3H-1,25-(OH)2D3 in vitamin D-deficient rats. Renal mass was reduced by partial or total nephrectomy. Renal function was reduced by ureteral ligation. At comparable degrees of renal function, reducing renal mass decreased 1,25-(OH)2D3 formation approximately proportional to the amount of renal tissue removed. Ureteral ligation without reduction of renal mass also reduced production within the first 24 hours. This may have been caused by the marked hyperphosphatemia which occurred with ureteral ligation. When partial nephrectomy and ureteral ligation were done together the results were additive. The decreased 1,25-(OH)2D3 formation produced by unilateral nephrectomy was not improved 4 weeks after surgery, although renal function had returned to normal.
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PMID:The effect of decreased renal function with and without reduction in renal mass on 1,25-dihydroxycholecalciferol production in rats. 86

Serum phosphorus concentrations are maintained within narrow limits in humans. In the extracellular fluid most of the phosphorus is present in the inorganic form and at the level of the glomerulus greater than 90% of PO4 is ultrafilterable. The kidney plays a key role in PO4 homeostasis. Micropuncture experiments have demonstrated that 60 to 70% of the filtered PO4 is reabsorbed in the proximal tubule; however, there is evidence that a significant amount of PO4 is reabsorbed in the distal tubule. Phosphate secretion probably plays a minor role in the overall renal regulation of phosphate. In normal individuals the amount of PO4 ingested plays a key role in the amount that ultimately will be excreted in the urine. The reabsorption of PO4 along the nephron is regulated by a series of factors of which parathyroid hormone is the most important one. Hyperphosphatemia is seen frequently in clinical medicine and by far, the most common cause is a decrease in urinary PO4 excretion secondary to renal failure. From the practical point of view, the most effective way to treat hyperphosphatemia is to decrease PO4 absorption in the GI tract by the use of PO4 binders.
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PMID:Hyperphosphatemia. 87 Feb 69

The ingestion of a sodium phosphate laxative preparation (Phosphosoda, Fleed) in a patient who had acute renal failure resulted in hypocalcemic tetany primarily due to severe hyperphosphatemia. Hypernatremia and a marked anion gap were present and attributable in part to the sodium phosphate ingestion of this preparation in the presence of renal failure.
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PMID:Hypocalcemic tetany due to sodium phosphate ingestion in acute renal failure. 113 13

Hyperuricemia, due to inborn errors of metabolism, dehydration, or tumor lysis, may cause renal insufficiency. Hyperuricemia from tumor lysis syndrome in malignancy is usually associated with electrolyte disturbances such as hyperkalemia, hyperphosphatemia or hyper or hypocalcemia. Tumor infiltration into the kidneys can occur, yet this accounts for renal insufficiency in only 1% of patients. This infiltration of tumor cells into the kidneys is usually associated with evidence of malignancy elsewhere as identified by physical exam, radiographic studies, and examination of the peripheral smear or bone marrow. We report an unusual presentation of a child with acute lymphocytic leukemia presenting with acute renal failure, nephromegaly and hyperuricemia without electrolyte disturbances or systemic evidence of tumor elsewhere. We stress the importance of kidney biopsy in order to identify the etiology of the renal failure and hyperuricemia.
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PMID:Renal biopsy diagnosis of acute lymphocytic leukemia. 139 66

A retrospective review of 25 patients who underwent orthotopic liver transplantation was performed to relate the prevalence and preferred sites of microscopic calcium deposition seen at autopsy to clinical parameters, namely, hypercalcemia, hypercalcemia, hyperphosphatemia, and renal failure. Microscopic foci of calcification were noted in 84% of patients, and hypercalcemia was noted in 68%. Multiple regression analysis demonstrated that the number of microscopically calcified organs depended in part on the peak total serum calcium level and the duration of hypercalcemia and that the peak total serum calcium level depended in part on the peak phosphorus level and the quantity of calcium administered intraoperatively. Univariate analysis showed that peak phosphorus level was partially dependent on the peak creatinine level. The data suggest that hypercalcemia and postoperative ectopic calcification are common and related occurrences following hepatic transplantation and that intraoperative manipulations of serum calcium levels and renal failure partially, but not entirely, account for this phenomenon.
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PMID:Tissue calcification after orthotopic liver transplantation. An autopsy study. 152 56


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