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)

Twenty-one patients in severe diabetic coma were treated with small doses of insulin at a rate of 4.1 units per hour (total dose about 100 units per 24 hours). Using single doses of 4 to 10 units by the intravenous or intramuscular routes the fall of blood glucose was steady in all cases. In the treatment of diabetic coma this regimen of insulin administration has proved simple, safe and effective since 1946. Main dangers during recompensation of diabetic coma are: hypovolaemia with oliguria -- anuria, dysequilibrium syndrome with cerebral edema and hypokalaemia. Therefore early intensive and adequate intravenous fluid and electrolyte replacement is the most important part of treatment. Most of the cases in this study were undiagnosed diabetics (14) and elderly patients (9). Three patients older than 65 years and a 56-year old diabetic died. In this context the most important aspects of treatment to avoid death are: prevention of diabetic coma and adequate fluid and electrolyte replacement especially in geriatric patients.
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PMID:Treatment of diabetic coma with low-dose injections of insulin. 95 92

The occurrence of rhabdomyolysis and acute renal failure associated with cytomegaloviral infection is rare. A 27-year-old housewife was admitted to our hospital with complaints of thirst, muscle weakness, abdominal pain and oliguria. There was no past history of diabetes, drinking, fever or drug habituation and a negative family history. Laboratory tests revealed myoglobinuria, hyper-pancreatic type amylaseuria, hyperglycemia, azotemia and highly increased creatine phosphokinase in the plasma. She was treated with hemodialysis and insulin therapy. Serological studies showed a 4-fold increase in cytomegalovirus antibody titers 4 weeks after admission. Muscle biopsy specimens showed hyaline degeneration and infiltration of T cell lymphocytes in the muscle. Renal biopsy specimens showed acute tubular necrosis and some myoglobin casts. No cytomegalovirus antigen was found in renal specimens by immunofluorescence study. From these results, it was determined that a systemic cytomegalovirus infection triggered pancreatitis which caused diabetic ketoacidosis, rhabdomyolysis and acute renal failure.
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PMID:Cytomegalovirus infection associated with acute pancreatitis, rhabdomyolysis and renal failure. 131 48

The renin-aldosterone system and plasma insulin were studied in 19 patients with familial Mediterranean fever (FMF). Their relationships to serum potassium level at rest and before and after oral glucose loading are described. An interesting finding is the occurrence of hyperkalemia in the absence of oliguria, in the advanced stages of renal failure. No differences were found in the activity of the renin-angiotensin-aldosterone system to explain these variations in serum potassium found in some of the patients. The response of the renin-aldosterone system to glucose loading showed no abnormality, and the regular relationship between serum potassium, plasma renin activity (PRA), aldosterone, insulin, and plasma pH is maintained. Levels of insulin, potassium, and bicarbonate in serum or plasma pH were found similar in FMF patients with normal renal function with and without proteinuria. Further decrease in renal function due to the progression of the underlying disease is manifested by an increase in FENa+ and FEK+ and a hyperchloremic metabolic acidosis, as is the case in other patients with chronic renal failure.
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PMID:Normal renin-aldosterone-insulin and potassium interrelationship in FMF patients and amyloid nephropathy. 146 7

HFRS-related oliguria brings about hyperactivity of the system hypothalamus-hypophysis-adrenals and hyperfunction of the pancreas; glucose, urea and creatinine plasma levels are elevated. Prednisolone treatment leads to diminution of ACTH and cortisol levels, elevation of glucose, insulin and C-peptide concentrations in plasma compared to prednisolone-untreated patients, producing insignificant effect on plasma levels of STH, vasopressin, aldosterone, area and creatinine. Therefore, a course administration of glucocorticoids to HFRS patients is justified only in severe collapses and hypopituitary coma confirmed by the laboratory methods.
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PMID:[Effect of glucocorticoid hormones on the status of the hypothalamo-hypophyseal-adrenal system and endocrine function of the pancreas in patients with hemorrhagic fever with renal syndrome]. 197 53

In two cases with drug-related hyperkalemia, potassium homeostasis, causes, symptoms and therapy are discussed. Iatrogenic and therefore avoidable hyperkalemia occurs most often when potassium, ACE-inhibitors, nonsteroidal antiinflammatory drugs or potassium-sparing diuretics are administered in patients with impaired renal function or diabetes mellitus. The emergency treatment in patients with severe hyperkalemia consists of intravenous calcium injections, infusion of glucose with insulin and, more recently, salbutamol. With acidotic patients administration of sodium-bicarbonate can be tried. Ion-exchange drugs and furosemide have a more delayed effect. With oliguria and anuria hemodialysis is often necessary.
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PMID:[Hyperkalemia]. 199

Severe hyperkalemia due to acute renal failure occurred in a preterm infant of a diabetic mother. Despite infusions of calcium gluconate, sodium bicarbonate, glucose, and insulin, the rapidly increasing serum potassium concentration resulted in ventricular flutter. After cardiac resuscitation, continuous arteriovenous hemofiltration was started for potassium elimination. Within 3 h of extracorporeal renal replacement therapy, serum potassium was lowered from 9.4 to below 7 mEq/l. Because of persisting oliguria continuous arteriovenous hemofiltration was continued for 60 h. The infant was discharged from the hospital at the age of 4 weeks with normal physical and neurological findings.
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PMID:Continuous arteriovenous hemofiltration as emergency procedure in severe hyperkalemia. 325 87

Dilation of the pulmonary arteries and increased pulmonary blood volume are recorded in sudden infant death syndrome and in infants living at low barometric pressures (high altitude). Low barometric pressure leads to chronic alveolar hypoxia (1,2). There is diversion and loss of body-fluid under conditions of microgravity (near-weightlessness) encountered in human space-travel and prolonged bedrest (3). The condition mimics shock and oligemia (4,5). The human neonate has underdeveloped postural mechanisms and low muscle-power. A transformation begins at about two months of age, which enables the human infant to adapt to the extrauterine environment (6). The neonate resembles the space traveller who, in a near-weightlessness antigravity environment, develops baroreceptor incompetence, visceral and venous congestion and oliguria. The low birthweight infant displays many of the disorders of the space traveller, viz. poor circulation, high blood-glucose, insulin resistance, weak muscles, slow gut absorption and bone demineralization (7-10). These conditions are virtually identical with the internal adjustments the body makes on lying down (negative gravity or near-weightlessness). We discuss the similarities of sudden infant death syndrome to low barometric pressure environment, orthostatic intolerance, the Pickwickian syndrome and X disease.
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PMID:Sudden infant death syndrome: near-weightlessness and delayed neural transformation. 873 69

We report a patient with rhabdomyolysis secondary to hyperosmolar nonketotic diabetic coma (HNKC), who progressed to acute renal failure. A 43-year-old male with diabetes mellitus for three years was admitted to our hospital because of loss of consciousness. The laboratory findings at admission were as follows: serum glucose 1792 mg/dl, serum Na 129 mEq/1, BUN 71 mg/d1, serum creatinine 3.3 mg/d1, CPK 715 IU/1, plasma osmolality 370 mOsm/1, and negative urine ketone bodies. A diagnosis of HNKC was made. On the 2nd day, he had oliguria and the serum creatinine increased despite adequate treatment of HNKC by the administration of intravenous fluid and insulin. On the 4th day, CPK reached 47,300 IU/1, and serum myoglobin was also increased, indicating rhabdomyolysis. His renal function improved gradually and was almost normalized on the 20th day. Renal biopsy on the 23rd day showed myoglobin at the distal renal tubules, which appeared to be involved in the pathogenesis of renal failure by rhabdomyolysis. However, we found little abnormality association with diabetic nephropathy in the renal tissue. Since HNKC is known to induce acute renal failure rarely without diabetic nephropathy, these findings suggested that the acute renal failure was caused mainly by the rhabdomyolysis. Acute renal failure induced by rhabdomyolysis in patients with HNKC is rare, but fatal. The present study showed that the measurement of serum CPK and urine myoglobin was helpful for early diagnosis. Only 12 cases have been reported to have developed renal failure due to rhabdomyolysis among patients with HNKC. To our knowledge, we demonstrated for the first time that myoglobin at the distal renal tubules after renal function was normalized.
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PMID:[Rhabdomyolysis related-acute renal failure in a patient with hyperosmolar nonketotic diabetic coma (HNKC): demonstration of myoglobin casts after normalization of renal function]. 882 59

Fluid retention develops relatively early in the renal insufficiency of patients with diabetic nephropathy. The objective of this study was to clarify the effect of postural change on urine volume and urinary sodium excretion in diabetic nephropathy. Subjects consisted of 16 patients with non-insulin-dependent diabetes mellitus (five with diabetic nephrotic syndrome [DNS], five with nonnephrotic overt diabetic nephropathy [NNODN], and six without overt diabetic nephropathy [ODN]) and 11 patients with nondiabetic renal diseases (five with nondiabetic nephrotic syndrome [NDNS] and six without nephrotic syndrome). Patients were studied during 60 minutes of recumbency, followed by 60 minutes of standing. Mean blood pressure decreased in the standing posture only in patients with DNS and nondiabetic renal diseases. Urine volume decreased in the standing posture in the three groups of diabetic patients. Urine volume showed no changes in the standing posture in nondiabetic patients with and without nephrotic syndrome. The decreases in mean blood pressure and urine volume and the percentage decrease in creatinine clearance were significantly larger in patients with DNS than in those with NDNS and NNODN. The increase in free water clearance was significantly smaller in patients with DNS than in those with NDNS and NNODN. Urinary sodium excretion decreased in the standing posture in diabetic and nondiabetic patients, while no differences in the magnitude of changes were noted among patients with NDNS, NNODN, and DNS. It is concluded that the standing posture causes a greater decrease in urine volume due to orthostatic hypotension in patients with DNS compared with those with NDNS and NNODN, and that the presence of orthostatic hypotension in patients with DNS is likely responsible for the greater fluid retention of this group compared with other nephrotic patients with similar degrees of hypoalbuminemia.
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PMID:Effect of postural change on urine volume and urinary sodium excretion in diabetic nephropathy. 942 50

The authors analyse their experience with the use of peritoneal dialysis (PD) in children with acute renal failure after cardiac surgery. From 1995 through 1998, 1246 children were operated in Pediatric Cardiocenter 38 of them developed acute renal failure and required peritoneal dialysis. Indications for PD were oliguria, anuria, hyperkalemia and fluid overload with generalized tissue oedema. PD was instituted at mean 33.9 (3-132) hours after surgery and lasted mean 53.7 (6-264) hours. None of the patients developed peritoneal infection. Hyperglycaemia developed in 8 patients and was treated with continuous insulin infusion. 5 patients required catheter reposition or reinsertion due to inadequate fluid removal and 1 patient required another renal replacement therapy. 22 (57.9%) patients died due to intractable low cardiac output. 16 survivors recovered their renal functions. In a long-term follow-up, 7 patients had no signs of significant renal dysfunction. In 4 patients, mild elevation of N-acetyl-beta-D-glukozaminidase indicates mild proximal tubular dysfunction. These findings together with aminoaciduria in 5 patients will require a further follow-up. (Tab. 2, Fig. 1, Ref. 16.)
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PMID:[Peritoneal dialysis in children after cardiac surgery]. 1115 67


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