Cases reported "Proteinuria"

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1/12. Congenital nephrotic syndrome with clinical hypothyroidism.

    A 15 month old boy with typical features of congenital nephrotic syndrome (CNS) is reported, who in addition to the renal pathology had an associated clinical hypothyroidism with low levels of total and free thyroxine and triiodothyronine and an elevated serum TSH. Improvement in the physical parameters and mental status from thyroid hormone replacement therapy is documented.
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2/12. A 14-year-old girl with recumbent proteinuria.

    We describe a 14-year-old female who presented with persistently elevated nighttime urinary protein excretion without additional clinical symptoms. She had no evidence of intrinsic renal disease on physical examination or laboratory studies. Ultrasound examination of the abdomen revealed a large cyst arising from the spleen. CT scan showed compression of the left renal vein by the splenic cyst. Removal of the cyst resulted in resolution of her proteinuria. Entrapment of the left renal vein (nutcracker syndrome) remains a rare but important cause of elevated protein excretion.
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3/12. hypercalciuria in osteogenesis imperfecta type I.

    BACKGROUND: In osteogenesis imperfecta severity of disease and reduced physical activity have been considered the main factors contributing to hypercalciuria; however, its pathogenesis in osteogenesis imperfecta Type I, in which mobility is normal, is still unclear. PATIENT, methods AND RESULTS: We describe a patient with osteogenesis imperfecta Type I and hypercalciuria, in whom measurement of calcium intake, plasma 1 - 25(OH) (2) vitamin d, fasting calciuria and tubular proteinuria led us to exclude an absorptive or renal component in the pathogenesis of hypercalciuria. CONCLUSIONS: We believe that hypercalciuria is determined by bone disease in osteogenesis imperfecta Type I. This condition should be added to the causes of normocalcemic hypercalciuria in children and the mildest forms should be differentiated from Idiopathic hypercalciuria.
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4/12. Long-lasting fever of unknown origin preceding the diagnosis of intravascular lymphomatosis: a further case stimulates some remarks.

    Neurological and skin involvements usually dominate the clinical presentation of intravascular lymphomatosis (IL), while fever is the most frequent general sign. However, an onset only characterized by fever of unknown origin (FUO) has been rarely reported. We would like to describe a further case of IL, which presented a long-lasting FUO before the diagnosis. At admission, physical examination detected hepatosplenomegaly without lymph nodes enlargement or dermatological or neurological abnormalities. Significant laboratory data included severe anemia, leukopenia, thrombocytopenia, and increased serum LDH. Moreover, a chest CT evidenced bilateral multiple pulmonary infiltrates and pleural effusion. After the development of proteinuria, a diagnosis of large B-cell intravascular lymphoma was made with a renal biopsy 10 months after the onset of the clinical manifestations. So far, more than 100 cases of IL have been reported and the diagnosis often turned out to be difficult, as clinical signs did not point to a lymphoproliferative disorder. This report confirms that FUO is not only frequently associated with IL but that it even marks the real onset of the disease. We are then tempted to conclude that undiagnosed fever is not so rare in IL and if we call it FUO, it is only because diagnosis is necessarily elusive and hence time-consuming.
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5/12. Development of IgA nephritis following cat scratch disease in a 13-year-old boy.

    We describe a 13-year-old boy who presented with hematuria and intermittent low-grade proteinuria at the time when he was diagnosed with cat scratch disease. Two months before presentation, he had a negative urinalysis during a routine physical evaluation. He continued to have microscopic hematuria for the next 6 months, when he developed gross hematuria and recurrence of low-grade proteinuria. The renal biopsy showed evidence of mild/moderate IgA nephropathy. We speculate that the immunological changes associated with cat scratch disease in this patient may have triggered the development of IgA nephropathy. A history or serological evidence of infection with bartonella henselae may need to be sought in patients presenting with IgA nephritis.
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6/12. Acute alcohol intoxication in a two-month-old baby.

    A 2-month-old, well developed, healthy boy, weighing 5.55 kg, was fed 200 ml of bottle-milk containing 65 ml of sake. So-called kanzamashi (sake boiled in the evening and remaining in a bottle overnight,) was mistaken for yuzamashi (water boiled and left to cool), and used to prepare a 15% formula milk. About 10 minutes later, the baby became flushed, began to breath hard, and lose consciousness, and an alcoholic odor was noticed. He was brought to our clinic, where gastric lavage and parenteral fluid therapy were started. On admission, his main physical signs were, whole body had become red, unconsciousness, alcoholic odor, tachycardia and tachypnea, without low body temperature, while his remarked laboratory findings were metabolic acidosis, hyperglycemia, and high A/G ratio. Moreover, a transient proteinuria, alternately followed by a transient glycosuria, appeared within the course. About 10 hours later, he showed an obvious improvement in both physical and laboratory findings. As an explanation of these changes in his condition due to alcohol ingestion, we speculated that a metabolic acidosis with hyperglycemia caused the disturbed reabsorption in his renal tubulus, which revealed alternating proteinuria and glycosuria.
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7/12. urinalysis and clinical renal disease.

    urinalysis is a simple, efficient, and accurate guide in the diagnosis of renal disease. By determining a patient's history and obtaining a physical examination, the physician is very often able to diagnose a patient's renal lesion. Heavy proteinuria and a microscopic sediment containing red cells and red cell casts strongly suggest acute glomerulonephritis. The causes of this nephropathy are legion. On the other hand, mild proteinuria and a lack of microscopic findings suggest nephrosclerosis, interstitial nephritis, or acute tubular necrosis in the proper clinical setting. When glomerular disease produces nephrotic syndrome, the various types of glomerular disease can be diagnosed accurately without biopsy in a high percentage of cases.
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8/12. Severe energy restriction in treatment of toxemia of pregnancy.

    A total of 78 patients with toxemia pregnancy were treated for over a week before delivery. The treatment was characterized by (1) mental and physical rest, (2) disuse of hypotonic, diuretic, and antispasmodic agents, and (3) a diet with reduced salt and energy (200-1200 Cal/day). Except for one fetal death, which occurred during delivery, all mothers and their babies left the hospital in good condition. No fetal or neonatal deaths that were related to the maternal condition or severity of toxemia were encountered. The long-lasting complications of toxemia were lower than those reported by others. No critical accident was noted. Our treatment proved to be efficient in the treatment of toxemia.
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9/12. A six-year-old girl with Turner's syndrome and proteinuria.

    A 6-year-old girl with Turner's syndrome presented with recent onset of proteinuria and pedal edema. There was no history of arthritis, fever, or abdominal pain. A physical examination revealed the stigmata of Turner's syndrome, hepatomegaly, and pedal edema. The urine contained 4 protein without red blood cells or casts, and the BUN and creatinine were mildly elevated. The serum lipids were normal. An excretory urogram showed bilaterally enlarged, smooth kidneys without calyceal distortion. Because the proteinuria failed to respond after 1 month of steroid therapy, a diagnostic procedure was performed.
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10/12. 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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