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Query: UMLS:C0028961 (oliguria)
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In a retrospective study we analyzed the clinical and blood chemical data of 12 patients with severe tropical malaria in the intensive care units of the University Hospital Zurich and the Stadtspital Triemli, Zurich, between 1991 and 1994. None of the 12 patients had been exposed to malaria before or had taken drugs for chemoprophylaxis. 7 patients survived, 5 died from complications of malaria. According to the criteria of severe tropical malaria defined by the WHO, the following pathological clinical and blood chemical parameters were noted on admission: cerebral coma (2/12); blood hemoglobin < 5 g/dl (0/12), < 8 g/dl (2/12); serum creatinine > 265 mumol/l (3/12); blood glucose < 2.2 mmol/l (0.12); circulatory collapse/shock (0/12); bleeding/signs of disseminated intravascular coagulation in laboratory tests (4/12); acidosis with pH < 7.25 (1/12). Further signs of severe tropical malaria were: hyperparasitemia > 5% (9/12); qualitative and quantitative disturbances of consciousness (6/12); thrombocytopenia < 30 x 10(9)/l (9/12); hyponatremia 125-135 mmol/l (9/12), < 125 mmol/l (2/12); rhabdomyolysis with creatine kinase > 1000 U/l (4/12). The basic treatment consisted of parenteral quinine hydrochloride in all patients; doxycycline was added in 8 cases, clindamycin in 3. Adjuvant therapy with desferrioxamin was given in 3 cases. 6 patients had exchange transfusions. Parasitemia cleared in all patients within 5 to 6 days. Later in the course, 5 patients developed acute respiratory distress syndrome, 6 required hemofiltration due to oliguria, and one became comatose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Intensive care aspects in severe tropical malaria: clinical aspects, therapy and prognostic factors]. 777 Jul 59

Fluid loading with balanced salt solution (BSS) was carried out in 200 patients with extensive soft tissue injuries from severe beatings. Urinary volume and dipstick specific gravity testing were used to monitor renal function with administration of furosemide for persistent oliguria. Acute intrinsic renal failure (AIRF) occurred in 21 patients (10.5%) and five patients died (2.5%); two of hyperkalemia, two of sepsis and one of multiple organ failure. Significantly increased rates of AIRF and death were associated with injury-admission intervals of more than 12 hours, severe metabolic acidosis, low initial hemoglobin, heavy pigmenturia, and high serum creatine kinase (CK) levels. An increased serum creatinine/BUN ratio was noted in four of the five patients who died. An average of 7.5 L fluids was needed in non-AIRF patients to achieve adequate diuresis with a mean positive fluid balance of 4.7 L. No patient without pigmenturia developed AIRF. Balanced salt solution volume diuresis supplemented with furosemide as necessary appears to be safe and effective in preventing AIRF in soft tissue injuries sustained in beatings.
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PMID:Traumatic rhabdomyolysis from severe beating--experience of volume diuresis in 200 patients. 806 19

Urological laparoscopy has gained increasing acceptance recently. Alterations in renal water and electrolyte homeostasis by carbon dioxide peritoneal insufflation, retroperitoneal insufflation and abdominal wall lifting were measured in 30 well-hydrated pigs over a 2-h period. Oliguria was observed after gaseous insufflation but not alter lifting the abdominal wall. Return to normal urinary output was observed at 30 min after release of pneumoretroperitoneum, and 60 min after pneumoperitoneum. Creatinine clearance declined, while the clearance rates of potassium, sodium and urea remained unchanged during peritoneal and retroperitoneal insufflation. An elevated serum aldosterone concentration was found which may mediate the increased urinary excretion of potassium and decreased urinary excretion of sodium found during peritoneal insufflation. Renal function remained stable, despite an elevation of serum creatine kinase being elicited after lifting the abdominal wall. In conclusion, significant changes in water and electrolyte homeostasis occurred gaseous, not gasless, laparoscopy in pigs.
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PMID:Changes in urinary output and electrolytes during gaseous and gasless laparoscopy. 900 30

Rhabdomyolysis is a severe clinical symptom of variable etiology. Acquired factors of exogenous origin such as traumata and endogenous metabolic disturbances have to be separated from hereditary disease as causative mechanism. Most frequently, exertional stress during hyperthermia, traumatic damage or ethanol abuse are observed. Almost independent of the diverse initial events, the pathogenesis follows a common final pathway with intracellular calcium accumulation and ATP depletion. Clinical symptoms vary. Seldom, the classical triad of muscle pain, weakness, and dark urine is observed. Recurrent episodes should raise suspicion of an inherited disorder. Severe complications are hypovolemia, electrolyte disorders with hyperkalemia and hypocalcemia resulting in life threatening arrhythmias, a compartment syndrome, disseminated intravascular coagulation and acute renal failure, which is frequently oligo-anuric. In combination with often severe underlying disease, renal failure causes death in 1/5 of the patients. The diagnosis is made with the determination of serum creatine kinase and the myoglobin levels in plasma and urine. Therapeutic options are to correct the hypovolemia with sufficient fluid supply, the prevention of oliguria using loop diuretics, alkalinization of the urine, normalization of serum electrolytes with reduction of hyperkaemia, and decompression of compartment syndromes. An underlying disease should be evaluated to initiate specific therapeutical and preventative steps. Avoiding pre-disposing factors by identifying the mechanisms of disease will reduce the occurrence of rhabdomyolysis with its still high mortality.
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PMID:[Rhabdomyolysis]. 1295 32

A 64-year-old man was admitted to our hospital because of general fatigue and drowsiness. On admission, a physical examination disclosed dehydration and a laboratory investigation revealed the following values: plasma glucose, 1309 mg/dl; serum sodium, 160 mmol/l; potassium, 3.0 mmol/l; urea nitrogen, 65 mg/dl; creatinine, 2.73 mg/dl; and plasma osmolarity, 403 mOsm/kg. Urine ketone bodies were negative. A diagnosis of hyperosmolar non-ketotic diabetic syndrome was made, and hydration with an infusion of hypotonic saline (0.45%) and insulin therapy were immediately started. However, despite adequate rehydration and correction of blood glucose, his serum creatinine level increased to 3.1 mg/dl, while oliguria and myoglobinuria developed on the 4th hospital day, with serum creatine kinase increasing up to a maximum level of 16,749 IU/l, suggesting rhabdomyolysis. A final diagnosis of hyperosmolar non-ketotic diabetic syndrome associated with rhabdomyolysis and acute renal failure was made. His renal function gradually improved without hemodialysis, though acute renal failure due to rhabdomyolysis with hyperosmolar non-ketotic diabetic syndrome can sometimes be fatal. This rare case is presented along with a review of literature.
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PMID:Hyperosmolar non-ketotic diabetic syndrome associated with rhabdomyolysis and acute renal failure: a case report and review of literature. 1500 Apr 44

A 46-year-old man with no previous history of abnormal urinalysis findings or renal dysfunction was admitted to a local hospital because of a motor vehicle crash. An open laparotomy was performed to treat a perforation of the small intestine. After operation, oliguria and renal dysfunction developed, and he was admitted to our hospital because of acute renal failure after trauma. Acute renal failure was assumed to be due to rhabdomyolysis with elevated serum creatinine, blood urea nitrogen, and creatine kinase levels and myoglobinemia. Left flank pain occurred several days after admission, and the serum alkaline phosphatase level increased between days 5 and 12 following admission. Although hemodialysis was performed 9 times and the urine output was satisfactory, the creatinine clearance levels increased only to about 50 mL/min/1.73 m2 (0.84 mL/s/m2) at 6 weeks following admission. As a result, a diagnosis of renal infarction due to acute renal artery occlusion was considered. The left kidney was atrophic on an abdominal computed tomographic scan and was nonfunctioning on a renogram. This case shows the importance of not overlooking the possibility of a renal infarction associated with rhabdomyolysis after a motor vehicle crash. In particular, the changes in the serum alkaline phosphatase levels were important in making a correct diagnosis in this case.
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PMID:Rhabdomyolysis and unilateral renal infarction after a motor vehicle crash. 1787 63

Fibric acid derivatives and statins have been increasingly recognized as causes of rhabdomyolysis and acute renal failure. We report severe rhabdomyolysis and acute renal failure associated to combination treatment with statin and fenofibrate in two patients with underlying coronary artery disease. Both patients developed rhabdomyolysis-induced acute renal failure after their hyperlipidemia treatment was changed from statin to statin plus fenofibrate. Both patients experienced intense muscle symptoms, hemoglobinuria, oliguria, and elevation of blood urea nitrogen and serum creatinine. Their serum creatine kinase levels were markedly elevated (case 1; 97,392 IU/l and case 2; 96,639 IU/l). Rhabdomyolysis induced acute renal failure was diagnosed in both patients. Both patients were managed with cessation of the statin-fibrate combination, adequate fluid resuscitation and forced alkaline-mannitol diuresis. Although both patients required hemodialysis, their renal function recovered. Fenofibrate initiation is associated with an increased risk for rhabdomyolysis in patients receiving statin therapy. To prevent future events, it is crucial that clinicians recognize the interaction risk associated with concurrent use of statin and fenofibrate. We recommend careful monitoring when fenofibrate is given to patients receiving statin therapy.
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PMID:Fenofibrate-induced acute renal failure due to massive rhabdomyolysis after coadministration of statin in two patients. 1852 Jan 13

Pigment nephropathy accounts for approximately 3% of all cases of acute renal failure (ARF) in children. Studies of risk factors associated with ARF and the need for renal replacement therapy (RRT) in children with rhabdomyolysis-associated pigment nephropathy consist of retrospective case series with variable inclusion criteria. Our objective was to evaluate clinical and laboratory characteristics, etiology, initial fluid therapy, prevalence of ARF and the requirement for RRT in pediatric patients with acute rhabdomyolysis. Twenty-eight patients (19 male) with a mean age of 11.1 +/- 5.6 years were studied. Acute renal failure occurred in 11 patients (39%), seven of whom (64%) required RRT. Features associated with the need for RRT included history of fever, persistent oliguria, admission blood urea nitrogen level, creatinine, Ca(2+), K(+), bicarbonate and aspartate aminotransferase. Most of these factors are related to the level of renal insufficiency and degree of muscle injury. There was no difference in admission and peak creatine kinase (CK) levels between those who did or did not require RRT. However, all who required RRT had a peak CK level > 5000 U/L.
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PMID:Factors associated with acute renal failure in children with rhabdomyolysis. 1860 38

Familial renal hypouricemia is a hereditary disease characterized by extraordinary high renal uric acid clearance and is associated with acute renal failure (ARF). An 18-year-old sumo wrestler developed ARF after anaerobic exercise. Several hours after the exercise, he had a pain in the loins with oliguria, headache, and nausea. On admission, his serum uric acid was decreased despite the elevation of serum creatinine (9.5 mg/dL). The level of creatine kinase was normal and there was no myoglobinuria or urolithiasis. Magnetic resonance imaging showed no significant abnormality. Renal function improved completely within 2 weeks of hydration treatment. After remission, hypouricemia became obvious (1.0 mg/dL) from the initial level of uric acid (6.1 mg/dL) and fractional excretion of uric acid was 49%. Polymerase chain reaction of a urate anion exchanger known to regulate blood urate level (SLC22A12 gene: URAT1) demonstrated that homozygous mutations in exon 4 (W258X). Both parents showed heterozygous mutation of the URAT1 gene, but both siblings showed no mutation. Thus, we describe a Japanese sumo wrestler of familial renal hypouricemia complicated with anaerobic exercise-induced ARF, with definite demonstration of genetic abnormality in the responsible gene, URAT1.
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PMID:Acute renal failure after exercise in a Japanese sumo wrestler with renal hypouricemia. 1909 27

A 52-year-old Indian woman with underlying diabetes mellitus and hyperlipidemia, presented with generalized musculoskeletal pain and oliguria for three days. The patient was taking 80 mg of simvastatin initiated 20 days earlier after cardiac catheterization for an inferior myocardial infarction. Laboratory investigations revealed the following serum levels: creatine kinase 81,620 U/L, aspartate aminotransferase 2497 U/L, alanine aminotransferase 1304 U/L, blood urea nitrogen 21.7 mmol/L, creatinine 447 micromol/L, Free T4 12.6 pmol/L, and thyroid stimulating hormone (TSH) 22.7 microIU/L. Simvastatin was discontinued and the patient received forced alkaline diuresis. Her hypothyroidism was treated with thyroxin, which was continued upon discharge, and her renal function recovered within two months. This case report discusses the incidence of rhabdomyolysis in a patient with primary hypothyroidism receiving large doses of simvastatin.
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PMID:Severe rhabdomyolysis and acute renal failure secondary to use of simvastatin in undiagnosed hypothyroidism. 1911 32


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