Cases reported "Oliguria"

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1/20. antimony excretion in a patient with renal impairment during meglumine antimoniate therapy.

    meglumine antimoniate was administered to a patient with visceral leishmaniasis with normal renal function. Soon after the first intramuscular administration of meglumine antimoniate 20 mg/kg, equivalent to 510 mg antimony (Sb), the patient developed septic shock with oliguria. creatinine clearance decreased to 23 ml/minute. Treatment was discontinued, and Sb urinary excretion was measured. After the initial dose, 500.25 mg Sb was recovered in urine over 8 days, corresponding to 98% of the amount of Sb given intramuscularly (66% eliminated within first 48 hrs). Nine days after the dose, meglumine antimoniate was reintroduced at a dosage of 11.7 mg/kg (equivalent to 300 mg Sb) every 48 hours with good tolerance. At that time creatinine clearance had returned to 87.8 ml/minute. By day 14 of therapy the interval was reduced to daily administration of the same dose; the dosage was increased to 16.6 mg/kg/day (equivalent to 425 mg Sb) from day 17 to day 31. The patient eventually completely recovered and was discharged with normal renal function. Although no specific guidelines exist for dosage adjustment in renal failure, monitoring of Sb urinary excretion indicates that the kidneys are the almost exclusive route of elimination.
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2/20. Care of the critically ill parturient: oliguria and renal failure.

    The incidence of acute renal failure in pregnancy has decreased. This decrease is less marked in developing countries in which resources are more scarce. The clinical diagnosis of acute renal failure is crude due to the variability of clinical signs and the late occurrence of basic biochemical abnormalities. Obstetric and gynaecological diseases are found among the traditional pre-renal, intra-renal and post-renal causes of acute renal failure. The cornerstone of management is the identification of high-risk cases and the prevention of acute renal failure by maintaining intravascular volume. The evidence for the efficacy of other prophylactic medical interventions, such as the use of loop diuretics, mannitol, low-dose dopamine and others, is poor. Management of established acute renal failure includes restoration of intravascular volume, treatment of any reversible causes, especially pregnancy complications such as pre-eclampsia, strict fluid balance and correction of any electrolyte abnormality or metabolic acidosis. dialysis is a supportive measure until the kidneys recover.
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3/20. Oliguric acute renal failure in mycosis fungoides with lymphomatous infiltrates in the kidneys.

    OBJECTIVE: To present the clinical picture of acute renal failure in patients with mycosis fungoides (MF) and renal lymphomatous infiltrates. To analyze the pathogenesis of renal failure. methods: Correlation of clinical picture, urinary findings, imaging reports and autopsy findings in two patients with long-standing MF who died with renal failure. CASE SUMMARIES: Both subjects had sustained oliguria in the last 2 weeks. One patient had persistent hypotension, normal urinalysis, normal renal sonogram, and scarce interstitial lymphomatous infiltrates with preservation of renal parenchymal architecture. He was thought to have ischemic acute renal failure not directly linked to the lymphomatous infiltrates. The second patient developed hypertension one month prior to death, and had moderate proteinuria, hematuria, pyuria, grossly enlarged kidneys with hypoechoic masses, and extensive replacement of the renal parenchyma by lymphomatous infiltrates. This picture is typical of renal failure secondary to lymphomatous replacement of the kidneys. CONCLUSIONS: The development of oliguric renal failure in MF with renal lymphomatous infiltrates may have varying clinical and imaging manifestations and pathogeneses. Potentially reversible pathogenic mechanisms should be systematically investigated, particularly if the overall clinical picture is not characteristic of renal failure secondary to lymphomatous replacement of the parenchyma.
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4/20. A large renal pelvic diverticulum, presenting incomplete excretion during tc-99m MAG-3 scintigraphy and tracer accumulation on tc-99m DMSA scintigraphy; a case report.

    This case report illustrates the dynamic and static renal scintigraphic images of a patient with an unusual large diverticulum of the renal pelvis. The initial diagnosis by intravenous pyelography (IVP) and ultrasonographic (US) examination was a renal pelvic diverticulum of the left kidney, and the patient was referred to the nuclear medicine department for exploration of the effect of the pelvic diverticulum on renal functions. We performed dynamic renal scintigraphy with technetium-99m (Tc-99m) labeled mercaptoacetyl triglycine (MAG-3) and static renal scintigraphy with Tc-99m labeled dimercaptosuccinic acid (DMSA). In dynamic renal scintigraphy, bilaterally normal concentration function was observed. While right kidney excretion function was normal, an incomplete excretion pattern was seen on the left side. Complete urinary flow obstruction occurred approximately at the 10th minute of the acquisition, which did not seem to respond to the i.v. furosemide application. However, when only the renal cortex was included in the region of interest, the obstructive pattern disappeared. In static renal scintigraphy, a large renal pelvic diverticulum localized antero-medially was clearly visualized in the left-anterior oblique projection, most probably due to accumulation of radiopharmaceutical inside it. This case showed that a renal pelvic diverticulum should be thought of when an incomplete excretion pattern is seen on dynamic renal scintigraphy. Using only a cortical region of interest may also help to distinguish other types of obstructive pattern from diverticulum. Additionally, Tc-99m DMSA scintigraphy may show diverticulum localization with antero-oblique projections in addition to routine projections.
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5/20. life-threatening tertiary hyperparathyroidism in the critically ill.

    BACKGROUND: Tertiary hyperparathyroidism typically occurs in patients who have recovered from renal failure after renal transplantation. This report describes a syndrome of tertiary hyperparathyroidism after recovery from multiple organ failure (MOF) with acute oliguric renal failure (AORF). methods: Six patients with MOF including AORF are presented. Increased parathyroid hormone (PTH) levels were documented as early as 3 weeks after injury or septic insult and remained increased in some patients for several weeks. RESULTS: The resultant increase in calcium levels led to recurrent bouts of bradycardia, often leading to asystole requiring cardiopulmonary resuscitation. Hypercalcemic-induced bradycardia was refractory to hydration, loop diuresis, atropine, and external pacing. Definitive treatment requires bisphosphonate therapy, which must be repeated until organ function has returned to normal. CONCLUSIONS: A new syndrome of life-threatening tertiary hyperparathyroidism is described in patients with critical illness. This syndrome probably is being overlooked frequently in critical care units. early diagnosis and prophylactic treatment with bisphosphonate may preclude the life-threatening cardiac arrhythmias.
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6/20. Paradoxic activation of the renin-angiotensin system in twin-twin transfusion syndrome: an explanation for cardiovascular disturbances in the recipient.

    Despite advances in treatment, twin-to-twin transfusion syndrome (TTTS) still carries a high risk for perinatal mortality and morbidity. Simple blood transfer from the donor to the recipient twin cannot explain all of the features of this disease, in particular the recipient's hypertensive cardiomyopathy. We report a case in which TTTS resulted in preterm delivery with early neonatal death of both twins, allowing assessment of the renin angiotensin system (RAS) status of each fetus, both by cord blood renin and aldosterone assay and by renal immunohistochemistry. The donor had severe oliguria/oligohydramnios, whereas the recipient, in addition to severe polyuria/polyhydramnios, had cardiomyopathy, atrioventricular regurgitation, and ascites. Although immunohistochemistry demonstrated that renal secretion of renin was up-regulated in the donor and down-regulated in the recipient, cord blood levels of renin and aldosterone were similar, with high renin levels in both twins. This observation supports the hypothesis that despite renal RAS down-regulation, the recipient is exposed to RAS effectors elaborated in the donor and transferred via placental shunts. This may contribute to cardiomyopathy and hypertension in the recipient, which cannot be accounted for by hypervolemia alone. We thus hypothesized that in TTTS, the recipient's hypertensive cardiomyopathy could be due to a mechanism similar to the classical model of hypertension referred to as "2 kidneys-1 clip." Thus the hypovolemic donor twin, comparable to the clipped kidney, produces vasoactive hormones that compromise the recipient, comparable to the normal kidney, causing hypertension and cardiomyopathy.
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7/20. Oliguric acute renal failure due to glue-sniffing. Case report.

    A 38-year-old male developed acute oliguric renal failure following repeated glue sniffing for about 8 hours. In addition, he had severe liver cell injury, mild myonecrosis and bone marrow depression indicating generalized tissue toxicity. The high urinary spot sodium during the oliguric phase and the total renal functional recovery after a period of oliguria followed by polyuria favoured a diagnosis of acute toxic tubular necrosis causing acute renal failure. toluene which is used as the solvent is presumably the toxic agent involved in glue sniffing. It is advised that toluene inhalation be considered in the differential diagnosis of acute renal failure especially in the young. literature on the renal toxicity of toluene is briefly reviewed.
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8/20. 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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9/20. 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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10/20. Nonoliguric acute renal failure after captopril therapy.

    In a patient with severe renovascular hypertension, nonoliguric acute renal failure developed after she received captopril treatment. We believe this to be a previously unreported complication. urine volume ranged from 1,640 to 2,260 mL/24 hr, and serum creatinine level rose from 2.3 to 8.3 mg/dL. There was no evidence of renal hypoperfusion or interstitial nephritis. Acute renal failure most likely was secondary to the nephrotoxic effect of captopril on chronically hypoperfused kidneys. Renal function improved rapidly after withdrawal of the drug therapy.
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