Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a patient recovering from acute renal failure, hypercalcemia abruptly developed at a time when the serum creatinine level remained high (5 mg/dl) but well after the serum phosphate level had been restored to normal by oral aluminum hydroxide therapy. The renal damage had been severe, with oliguria lasting six weeks. Parathyroid hormone (PTH) immunoreactivity was measured with two different "carboxyterminal" PTH assays, giving high-normal or slightly mild renal failure could have accounted for the increased immunoreactivity. After five months of hypercalcemia, prednisone was administered and produced a prompt and sustained normalization of serum calcium. This prolonged variant of hypercalcemia after renal failure is not well recognized in the literature. The response to glucocorticoids suggests that abnormal metabolism of vitamin D or osteoclast activating factor might be involved in its genesis.
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PMID:Hypercalcemia after acute renal failure. 744 7

Acute renal failure may be caused by a failure of renal perfusion (pre-renal failure), damage to the renal parenchyma (intrinsic renal failure) or obstruction of the urinary tract (post-renal failure). Most cases of intrinsic renal failure in the newborn are due to asphyxia, often in combination with sepsis and nephrotoxic drugs. Persistent elevation of the plasma creatinine concentration above 132.5 micromol/l (1.5mg/dl) is widely accepted as a diagnostic criterion. Oliguria or anuria may occur but is not always present. Post-renal failure is diagnosed by renal ultrasonography and is treated by relief of the obstruction. Pre-renal and post-renal failure can be distinguished by an analysis of urinary indices, especially the fractional sodium excretion, and by the response to fluid replacement. The conservative management of intrinsic renal failure includes careful attention to fluid balance, maintenance of adequate nutrition and prevention or correction of hyperkalemia, acidosis and hyperphosphatemia. Severe cases may require dialysis: peritoneal dialysis is used in most cases, but extracorporeal methods, including intermittent hemodialysis, hemofiltration and hemodiafiltration, are possible. Congenital chronic renal failure, usually caused by renal dysplasia with or without obstruction, presents in a manner similar to that of acute renal failure, with a progressive deterioration of plasma biochemical values. Dialysis is rarely necessary in the newborn period. The conservative management of chronic renal failure is similar to that of acute renal failure, with particular emphasis on nutrition, control of acidosis and the prevention of renal osteodystrophy by the use of dietary phosphate binders and vitamin D analogs.
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PMID:Management of acute and chronic renal failure in the newborn. 1500 Nov 36

The toxicity of serpentine phosphate and superphosphate for non-pregnant dry ewes, pregnant ewes and lactating ewes was investigated by oral dosing. An attempt was made to reproduce a natural episode of poisoning by exposing pregnant and lactating ewes to topdressed pasture. A total dose in the range of 1200 to 1800 g of serpentine phosphate was required to kill two ewes and it was concluded that natural episodes of poisoning with this material are unlikely. The toxic process was similar to that caused by superphosphate. The LD50 of superphosphate was estimated to be in the range of 5 to 6 g/kg and a dose in the range of 200 to 300 g was sufficient to kill most sheep. The apparently greater susceptibility of pregnant and lactating sheep to poisoning suggested by the study of natural outbreaks was not demonstrated in these experiments, but the numbers of experimental animals may have been too small to detect differing susceptibility. The clinical disease resembled that seen in natural episodes; anorexia, diarrhoea, progressive depression and death in a period of 5 to 8 days after the start of dosing. Sublethal doses produced a transient diarrhoea and, in two sheep, a severe wool-break. The principal biochemical changes were hyperphosphataemia and evidence of renal failure (oliguria, uraemia, azotaemia). Gross lesions were not consistently present but included abomasal ulceration and renal cortical swelling and pallor. The histopathological evidence of renal tubular obstruction by flocculant eosinophilic casts was characteristic.
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PMID:Phosphatic fertiliser poisoning of sheep: experimental studies. 1603 Aug 36

Hyperkalemia is common soon after birth in extremely premature infants and often occurs in the absence of oliguria or renal failure. Our objective was to examine the early biochemical indicators, clinical risk factors, and incidence of early-onset nonoliguric hyperkalemia in a cohort of extremely premature infants. We studied clinical and biochemical data from 154 consecutive premature infants < or = 28 weeks of gestation admitted to a tertiary neonatal unit over a 3-year period. Hyperkalemia (> 7 mmol/L) was found in 33 (21%) of patients during the first 4 days of life, with peak potassium levels occurring at 3 days of age. Hyperkalemic patients had similar birthweight, gestation, creatinine and sodium levels as normokalemic infants, but they had higher phosphate and urea levels, with lower calcium levels. The combination of a high phosphate (> 2.0 mmol/L) and a high potassium (> 5.6 mmol/L) within 6 hours of birth predicted later development of hyperkalemia, with a positive likelihood ratio of 8.3 (post-test probability, 70%). Potassium level of < 5.6 mmol/L at birth indicates subsequent hyperkalemia is unlikely (likelihood ratio, 0.25; post-test probability, 4%). Mildly elevated potassium and phosphate levels within 6 hours after birth may be useful in predicting the development of early-onset hyperkalemia.
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PMID:Can early-onset nonoliguric hyperkalemia be predicted in extremely premature infants? 1826 46

Crush injury or traumatic rhabdomyolysis is caused by crushing of large muscule mass, usually of the femoral and gluteal compartment. Crush syndrome is general manifestation of crush injury with renal failure (ARF). ARF is caused by deposition of myoglobin in distal tubules. The concentration of serum creatin phosphokinase is an indicator of the extent of injured muscule. The serum concentration of myoglobin is an indicator of the extent of injured muscule and the main cause of development of crush syndrome. In a prospective study the concentration of myoglobin and CPK was measured in 81 patients with injuries of lower extremities and pelvis as a part of severe trauma. The increase of CPK concentration above 1000 U/L was measured in all patients. The increase of CPK concentration above 2000 U/L was measured in 78 (96.3%) patients. The increase of myoglobin concentration of >700 mcg/L was measured in 19 (23.5%) patients. In the group of 19 patients with CPK concentration of >2000 U/L and myoglobin concentration of >700 mcg/L crush syndrome developed in 6 (7.4%) patients with oliguria (urin output <50 ml/h) and the increase of serum potassium, phosphate and creatinine concentrations. The decrease of CPK and myoglobin concentrations was achieved in 5 patients during 10-12 days and 1 patient with associated craniocrebral injury died.
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PMID:[Crush syndrome in severe trauma]. 1828 95


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