Cases reported "Oliguria"

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1/5. Transient paradoxical renal vasoconstriction following cardiac operation. Treatment with volume depletion.

    Following cardiac operation complicated by inferior myocardial injury, a patient developed normal cardiac output congestive heart failure associated with severe renal vasoconstriction, oliguria and azotemia. The patient's renal dysfunction responded to volume depletion with hemofiltration. These paradoxical renal responses to volume changes may be caused by transiently altered cardiac volume receptor thresholds or afferent signals resulting in cardiorenal dysfunction.
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ranking = 1
keywords = azotemia
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2/5. Muscular, renal, and metabolic complications of acute arterial occlusions: myonephropathic-metabolic syndrome.

    Acute arterial occlusions of the extremities may result, in approximately 7.5% of cases, in a severe and complex metabolic syndrome which often leads to loss of limb and life. The manifestations of this syndrome are divided into two stages: (1) the ischemic or devascularization phase, and (2) the revascularization phase. The ischemic phase includes severe clinical manifestations, of which the rigidity of the limb ("rigor mortis") is an outstanding sign, as are nephropathic-metabolic changes (oliguria, acidosis, myoglobinuria, azotemia, hyperkalemia). Their identification and correction at this phase may minimize their impact on the revascularization syndrome. The clinical and metabolic manifestations during the latter phase are more severe and may determine the outcome of the viability of the limb and the survival of the patient. amputation rates are quite high (40% to 50%) and mortality rates range between 30% and 80%. The ischemic rhabdomyolysis appears to be the initiating event which leads to the biochemical and metabolic alterations that dominate the prognosis as to limb and life. The guiding principles of the management in these severe ischemic cases consist of early revascularization with emphasis on concurrent fasciotomy, alkalinization of the patient, reestablishment of acid-base balance, hemodialysis for renal shutdown, and often early amputation for better control of the metabolic omplications.
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ranking = 1
keywords = azotemia
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3/5. Acute oliguric renal failure induced by indomethacin: possible mechanism.

    A patient with compensated congestive heart failure suffered acute deterioration of her renal function and cardiac status, requiring peritoneal dialysis, in association with indomethacin therapy. Discontinuation of this inhibitor of prostaglandin synthesis led to a prompt improvement in both her renal function and cardiac status. The patient was rechallenged with indomethacin and again developed acute reduction of her glomerular filtration rate and severe volume retention, which were again totally reversed when the drug was stopped. Urinary prostaglandin E was measured by radioimmunoassay in this patient and five additional patients with congestive heart failure and prerenal azotemia. All patients were found to have elevated levels of urinary prostaglandin E. The possible role for renal prostaglandin E as a compensatory mechanism to the vasoconstrictive stimuli present in congestive heart failure is discussed. The potential danger of inhibitors of prostaglandin synthesis in patients with congestive heart failure and prerenal azotemia is emphasized.
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ranking = 2
keywords = azotemia
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4/5. Perinatal asphyxia and renal failure in neonatal patients.

    Herein we discuss oliguria and azotemia in neonatal patients associated with perinatal complications, including difficult labor and delivery, and respiratory asphyxia. Renal failure in these patients is accompanied by proteinuria, microscopic hematuria and red blood cell casts, and it generally resolves in 7 to 10 days. Umbilical aortography can be helpful in determining the presence of normal kidneys in these patients.
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ranking = 1
keywords = azotemia
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5/5. Lipoid nephrosis appearing as acute oliguric renal failure.

    Acute oliguric renal failure previously was reported to develop in patients with preexisting idiopathic nephrotic syndrome in association with clinical evidence of vascular volume depletion. We describe an 81-year-old man without recent proteinuria or evidence of preexisting nephrotic syndrome in whom acute oliguric renal failure developed. Renal biopsy disclosed minimal change disease. Nephrotic range proteinuria without severe hypoalbuminemia was detected during the 25-day course of oliguric renal failure. Renal vein thrombosis was excluded. urine sodium concentration and fractional sodium excretion were reduced, yet left ventricular filling pressure was not subnormal and could be increased to supernormal levels without improvement in glomerular filtration rate. oliguria and azotemia were corrected following initiation of glucocorticoid therapy. This case suggests that lipoid nephrosis can appear as acute oliguric renal failure without historical or physical evidence of preexisting nephrotic syndrome.
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ranking = 1
keywords = azotemia
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