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)

We analyzed biochemical data derived from 911 patients with renal insufficiency observed at our institution for periods up to 7 years. During early renal failure (RF) (creatinine less than 5 mg/dL), the rate of change of hematocrit, total CO2 (tCO2) and urea per unit change of creatinine was significantly higher than during moderate (creatinine between 5 and 10 mg/dL) or advanced (creatinine greater than 10 mg/dL) RF. For example, the rate of change of hematocrit (%, volume/volume [v/v]) was (mean +/- SEM) -2.15 +/- 0.15% for each 1 mg/dL increase in creatinine in the range of creatinine less than 5 mg/dL, whereas for the range of creatinine greater than 10 mg/dL, the rate of change was only -0.48 +/- 0.06% (P less than 0.001). Similarly, the rate of change of tCO2 was -1.68 +/- 0.09 mEq/L for each 1 mg/dL increment in creatinine concentration during early RF, and -0.19 +/- 0.09 mEq/L per unit increase in creatinine during advanced RF (P less than 0.001). Chloride concentration initially increased as a function of creatinine in early RF, but decreased in advanced RF, whereas the anion gap increased throughout the course of RF. Mean serum phosphate concentration also increased steadily, but remained below the upper range of normal (4.7 mg/dL) during early RF without the use of phosphate binders. These data suggest that different biochemical parameters change at different rates as a function of the severity of renal dysfunction, and that although phosphate retention may occur, hyperphosphatemia is not a hallmark of early RF.
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PMID:Biochemical parameters in chronic renal failure. 312 41

We report the cases of two children presenting with tumor lysis syndrome responsible for major hyperphosphatemia, hypocalcemia and acute renal failure and treated by hemodialysis. Twenty similar cases have been reported in the literature. Hyperphosphatemia responsible for hypocalcemia and renal failure occurs within 24 to 48 hours after the onset of chemotherapy, is maximal on the 2nd or 3rd day and is, on the average, of 7 days duration. Short-term functional renal prognosis is good but long-term studies are lacking. The usual preventive measures are not always sufficient to prevent these accidents. A dialysis is appropriate when phosphatemia rises rapidly and exceeds 5 mmol/l, when the creatinine plasma level exceeds 200 mumol/l and kaliemia 6 mmol/l and when hyperphosphatemia is associated with severe clinical signs.
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PMID:[Acute kidney failure caused by hyperphosphoremia in tumor lysis]. 316 15

Hyperphosphatemia and secondary hyperparathyroidism are regular complications in patients suffering from advanced renal failure. As aluminum-containing drugs carry the well-known risk of aluminum intoxication, we were interested in testing in a prospective study a mixture of ketoanalogues and amino acids which have been shown to lower the serum phosphate and parathyroid hormone in uremic patients. For 3 months, in addition to their diet, 17 uremic patients and 12 hemodialysis patients received a daily supplement of this mixture. Although no additional phosphate binders were administered, serum phosphate decreased significantly in the former group and was slightly lower in the latter. The serum parathyroid hormone level was consistently lowered when the initial concentration was not higher than 20 times normal.
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PMID:The beneficial effect of ketoacids on serum phosphate and parathyroid hormone in patients with chronic uremia. 318 May 19

It has been postulated that hyperparathyroidism in chronic renal failure results from hypocalcemia, occurring, in part, from phosphate retention and/or deficient 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] synthesis. However, many studies have failed to demonstrate hyperphosphatemia or low 1,25-(OH)2D levels in patients with mild renal failure. We measured creatinine clearance (CCr), fractional excretion of phosphorus (FEP), and serum phosphorus, ionized calcium, and plasma N-terminal PTH, and 1,25-(OH)2D concentrations in 21 normal subjects and 51 patients with renal failure. Patients with mild renal failure (Ccr, greater than 40 mL/min.1.73 m2) had normal mean serum phosphorus and ionized calcium and decreased mean 1,25-(OH)2D levels compared with those in normal subjects. In patients with moderate renal failure (CCr, 20-40), the mean ionized calcium level was normal, plasma PTH levels and FEP were elevated, and the decrement in 1,25-(OH)2D was more pronounced. The mean ionized calcium level was decreased only in the group of patients with severe renal failure (CCr, less than 20). The 1,25-(OH)2D values correlated positively with CCr and negatively with the log of plasma PTH and serum phosphorus concentrations. Log of plasma PTH correlated negatively with CCr and positively with FEP. The ionized calcium concentration correlated very weakly with CCr and the log of the plasma PTH level. These data demonstrate the presence of hyperparathyroidism, normocalcemia, and 1,25-(OH)2D deficiency in renal failure and are consistent with a role for 1,25-(OH)2D in the suppression of parathyroid activity through as yet unidentified mechanisms.
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PMID:Hyperparathyroidism and 1,25-dihydroxyvitamin D deficiency in mild, moderate, and severe renal failure. 318 62

Aggressive therapeutic maneuvers to reduce the risk for acute renal failure are routine in the management of children receiving therapy for advanced stage Burkitt lymphoma and B cell acute lymphoblastic leukemia. The case histories of 40 children entered into a prospective treatment protocol for high-risk disease revealed that ten of 40 patients (25%) had acute renal failure, two at the time of hospital admission and eight in whom renal insufficiency developed 12 to 132 hours following initiation of cytotoxic chemotherapy. Admission values for serum lactic dehydrogenase and serum uric acid were not statistically different between patients with and without subsequent renal failure. Urine output in the 12 hours prior to antineoplastic therapy was 2.9 +/- 0.8 mL/kg/h in the eight children in whom renal failure developed and 5.3 +/- 0.4 mL/kg/h in the patients who did not (P less than .01). The urinary flow rate in the 24 hours following initiation of chemotherapy was significantly lower in children in whom renal impairment developed (1.0 +/- 0.2 mL/kg/h, mean +/- SE) compared with those who did not (3.7 +/- 0.3 mL/kg/h, P less than .001). Renal failure could not be attributed to hyperuricemia or hyperphosphatemia in the majority of patients with renal failure. One to four hemodialysis treatments (2.5 +/- 0.3) were required for the ten patients. Serum creatinine concentrations returned to normal in the nine survivors. Response to initial antineoplastic therapy was not affected by the presence of renal failure. Renal failure continues to be a major clinical problem in children with Burkitt lymphoma and B cell lymphoblastic leukemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute renal failure at onset of therapy for advanced stage Burkitt lymphoma and B cell acute lymphoblastic lymphoma. 318 76

Acute renal failure during treatment of lymphoblastic malignancies is usually due to drug toxicity or acute uric nephropathy. Observations were recently reported where extreme hyperphosphatemia may represent another pathophysiological mechanism. We describe 2 cases, in 36- and 77-year-old women, with acute lymphoblastic leukemia. Acute renal failure was observed 2 days after cytotoxic treatment. Maximal blood creatinine values were 860 and 550 mumol/l respectively, and for phosphate 6.3 and 7.5 mmol/l. With oral phosphate binders, and after four peritoneal exchanges for the second patient, renal function gradually returned to normal values within 4 weeks. Tumor lysis syndrome with associated hyperphosphatemia is described exclusively in lymphoblastic malignancies and renal failure is probably a consequence of intratubular calcium phosphate precipitation. In this situation prophylactic administration of phosphate binders and attentive monitoring of phosphatemia are necessary.
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PMID:[Hyperphosphatemia and transient renal insufficiency following chemotherapy of acute lymphoblastic leukemia]. 321 26

Because the kidneys are primarily responsible for the regulation of fluid and electrolyte balance, acute or chronic changes in renal function can result in multiple imbalances. Acutely, the rapidity of onset of renal deterioration makes nursing assessment and intervention critical to the prevention of complications and potentially fatal outcomes. For patients with chronic renal failure, nursing assessment and intervention are equally significant, since there is an absence of renal regulatory mechanisms. In renal failure, acute or chronic, one most commonly sees patients who have a tendency to develop hypervolemia, hyperkalemia, hyperphosphatemia, hypocalcemia, and bicarbonate deficiency (metabolic acidosis). Sodium is generally retained, but may appear normal, or hyponatremic, because of dilution from fluid retention. Following the relief of a urinary tract obstruction, hypovolemia, hyponatremia (true loss of sodium), hypokalemia, hypocalcemia, hypomagnesemia, and bicarbonate loss are most apt to occur. Electrolyte imbalances after urinary diversion vary depending on the site of urine diversion.
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PMID:Fluid and electrolyte problems in renal and urologic disorders. 331 87

Aluminum-related osteodystrophy, a crippling disease in patients with renal failure, can develop from the long-term ingestion of aluminum hydroxide gels. We present a diabetic patient treated with continuous ambulatory peritoneal dialysis (CAPD) who developed markedly elevated plasma aluminum levels but no musculoskeletal symptoms. Bone biopsy revealed features of the aplastic form of aluminum-related disease with significant aluminum staining, decreased osteoblastic osteoid, and decreased bone formation by double tetracycline labeling, but no excess accumulation of unmineralized osteoid. Aluminum hydroxide gels were discontinued and the patient received calcium carbonate to control hyperphosphatemia; 9 months later, a bone biopsy showed marked improvement of the aluminum-related bone disease, and at 2 to 10 months, plasma aluminum had decreased from 208.7 +/- 10.3 (SE) to 55.7 +/- 3.9 micrograms/L.
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PMID:Reversal of aluminum-related bone disease after substituting calcium carbonate for aluminum hydroxide. 333 1

A mouse model of renal failure, which is induced by the sequential electrocoagulation of the right renal cortex and left nephrectomy, was examined for the capacity to reproduce the characteristics of chronic uremia. Assessment was conducted six weeks after the second surgical procedure in 13 week old female C57BL/6 inbred mice with renal failure and in normal and sham-operated controls. The surgery, which was well tolerated, was free of local and systemic signs of inflammation or infection. Growth was significantly delayed in all animals post surgery however renal failure mice presented the most severe growth retardation. Biochemical analysis of plasma revealed multiple abnormalities with commensurate elevations of urea and creatinine. In addition to the expected hyperphosphatemia, hyperkalemia and acidosis, a significant increase in cholesterol was present. Furthermore, in contrast to controls, renal failure mice produced large volumes of urine which contained significant levels of protein. Renal failure mice presented profound hematological changes in the red cell series in which anemia was evident. Changes in plasma biochemistry and in bone histology revealed the presence of severe secondary hyperparathyroidism. It was therefore concluded that the described mouse model of chronic renal failure presented characteristics consistent with those observed clinically in end-stage renal disease.
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PMID:Characterization of a mouse model of chronic uremia. 336

Pulmonary calcinosis is a recognized complication of renal failure. The resulting pulmonary compromise may be severe or even fatal. The potential contribution of hypercalcemia, hyperphosphatemia, and increased calcium-phosphorus product to the development of pulmonary calcinosis has been controversial. We describe four patients (ages 2 1/4 to 18 years) who had severe pulmonary calcinosis and respiratory failure within three to five days after renal transplantation. Initial clinical and roentgenographic findings suggested noncardiogenic pulmonary edema. Marked pulmonary hypertension was present in the two patients in whom pulmonary artery pressure data were available. Other clinical features in common included poor allograft function with persistent uremia requiring dialysis and evidence of moderate to severe secondary hyperparathyroidism. In three of the patients, the calcium-phosphorus product increased markedly after transplantation, to peak values of 122 to 147. This increase occurred at the same time as the onset of respiratory failure. Peak serum calcium levels were 10.0 to 11.0 mg/dL and peak serum phosphorus levels were 9.2 to 13.5 mg/dL. All patients died of respiratory failure five to 58 days after transplantation. The posttransplantation period may be a time of increased risk of potentially fatal pulmonary calcinosis in pediatric renal transplant recipients. The diagnosis should be considered in any patient with respiratory failure of unknown cause following renal transplantation.
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PMID:Pulmonary calcinosis after renal transplantation in pediatric patients. 352 Dec 66


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