Metastatic renal cell carcinoma in a hemodialysis patient with acquired renal cystic disease.
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Biomedical subjects
Publications and source records attributed to J Montoliu.
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A 36-year-old man with ankylosing spondylitis, amyloidosis and chronic renal failure on maintenance hemodialysis developed severe hypoglycemia while being treated with propoxyphene. Upon discontinuation of the drug blood glucose levels returned to normal and hypoglycemia did not recur. Simultaneously with hypoglycemia, plasma glucagon and growth hormone levels were appropriately raised and serum insulin levels were adequately suppressed, thus ruling out hyperinsulinemia as the cause of hypoglycemia. A review of the literature disclosed four similar cases of propoxyphene-induced hypoglycemia, two of them with renal dysfunction. Propoxyphene should be remembered as a potential cause of hypoglycemia, particularly in patients with renal failure.
A 25-year-old drug addict who practices subcutaneous injection of heroin and crushed narcotic tablets, a practice known as 'skin popping', developed nephrotic syndrome secondary to renal amyloidosis. The patient had chronic inflammation of the skin in the form of abscesses and ulcerations. She had practiced subcutaneous drug administration for only 2 years. Amyloidosis had the staining characteristics and tissue distribution of the secondary type, and was directly related to chronic skin suppuration. To our knowledge, this represents the first reported case of renal amyloidosis in a subcutaneous drug abuser residing in Europe.
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A 60-year-old man with long-term exposure to toluene presented with both myelofibrosis and focal segmental glomerulosclerosis. There was also evidence of other toluene-related complications to support the diagnosis of toluene toxicity. The toxic effects of toluene, particularly kidney disorders and haematotoxicity, suggest a relationship between toluene, myelofibrosis and focal segmental glomerulosclerosis.
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We report 5 cases of acute visual and auditory neurotoxicity in patients with end-stage renal disease receiving desferrioxamine. Four patients complained of visual toxicity characterized by a decrease in visual acuity, loss of color vision and night blindness. In these patients there was a decrease in visual acuity, and the Farnsworth's test revealed a tritanopy (yellow-blue axis impairment); 1 patient also showed retinal pigmentary changes. A fifth patient complained of bilateral and severe neurosensorial deafness. Patients improved clinically upon drug-withdrawal. We recommend careful monitoring of audiovisual toxicity in patients with end-stage renal disease receiving this drug.
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A 21-year-old heroin addict with right-sided staphylococcal endocarditis developed skin purpura, abdominal pain, bloody diarrhea, proteinuria and microscopic hematuria. Skin biopsy showed leukocytoclastic vasculitis with IgA deposits in dermal vessels and renal biopsy disclosed proliferative glomerulonephritis with granular mesangial IgA and fibrinogen deposition. These features are typical of Henoch-Schönlein purpura. Symptoms abated spontaneously. Since the syndrome appeared during cloxacillin therapy, both this drug or the infectious disease itself could have triggered the immune response. Henoch-Schönlein purpura is a distinct clinical entity that can complicate the course of staphylococcal endocarditis.
Carpal tunnel syndrome, peripheral arthropathy, erosive spondyloarthropathy and lytic bone lesions have all been associated with dialysis amyloidosis. Recent studies indicate that beta 2-microglobulin is the major constituent protein in this new form of amyloidosis. Dialysis amyloidosis was reported to have a local rather than a systemic involvement, although its full extent is yet to be determined. We investigated 3 patients on maintenance hemodialysis with bilateral carpal tunnel syndrome and amyloid arthropathy and found amyloid depositions in several organs. These findings suggest that, in contrast to what had been thought previously, dialysis amyloidosis could have systemic as well as visceral distribution. The amyloid deposits found were resistant against potassium permanganate treatment and reacted with anti-human beta 2-microglobulin antibody.
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A retrospective analysis of 66 adult patients diagnosed as having IgA nephropathy by renal biopsy revealed that 24 (36%) were hypertensive when first seen. Of these hypertensive patients, 10 (15%) had malignant or accelerated hypertension. All patients but one were male and had no knowledge of their renal disease and sought medical advice for symptoms due to hypertension. Five patients had no history of gross hematuria. Histological vascular findings showed, in three proliferative endarteritis and fibrinoid necrosis, in five arteriolosclerosis and in two vascular hypertrophy. In spite of good blood pressure control, six patients reached terminal uremia within a maximum of 14 months. In summary, the incidence of malignant hypertension in adults with IgA nephropathy is higher than previously reported, and its true incidence can only be known if more histopathologic studies of patients with malignant hypertension are performed. Patients with this association reach end stage renal failure in a short period of time.
To study the effect of specific beta 2-adrenergic stimulation on potassium metabolism in renal failure, we intravenously administered albuterol (Salbutamol) sulfate, 0.5 mg, to 20 patients with chronic renal failure (glomerular filtration rate, less than 5 mL/min) receiving maintenance hemodialysis. Within 30 minutes after albuterol administration, serum potassium level dropped from 5.6 +/- 0.2 (+/- SEM) to 4.5 +/- 0.2 mEq/L (5.6 +/- 0.2 to 4.5 +/- 0.2 mmol/L). There were no changes in plasma aldosterone levels or arterial pH, but blood glucose and serum insulin levels increased. Albuterol, however, induced similar decreases in serum potassium levels in three diabetic patients while free C peptide levels remained undetectable or subnormal after administration of the drug. Albuterol sulfate alone (0.5 mg intravenously) was also used to treat 24 patients with acute or chronic renal failure and hyperkalemia. Their serum potassium levels dropped from 7 +/- 0.2 mEq/L (7 +/- 0.2 mmol/L) to 5.6 +/- 0.2 mEq/L (5.6 +/- 0.2 mmol/L), 5.6 +/- 0.2 mEq/L (5.6 +/- 0.2 mmol/L), 6 +/- 0.2 mEq/L (6 +/- 0.2 mmol/L), and 6.2 +/- 0.2 mEq/L (6.2 +/- 0.2 mmol/L) at 30, 60, 180, and 360 minutes after receiving albuterol, respectively, and this was accompanied by reversal of the electrocardiographic manifestations of hyperkalemia. Despite inducing transient tachycardia, albuterol was remarkably well tolerated and no serious side effects were observed. beta 2-adrenergic stimulation of intracellular potassium uptake by albuterol is a safe and effective alternative for the treatment of hyperkalemia in renal failure.
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Twelve HBsAg-negative patients with histologically documented cirrhosis of the liver of either alcoholic (8 of 12) or cryptogenic (4 of 12) origin underwent renal biopsy to investigate proteinuria, hematuria and/or renal failure. Immunofluorescence was positive for IgA in 2 patients with mesangiocapillary glomerulonephritis (MCGN) and could not be performed in 2 additional patients with the same diagnosis. However, in the remaining 8 patients, immunofluorescence was negative for IgA and frequently positive for C3, IgG, IgM and/or fibrinogen. These 8 patients without IgA were classified as follows: MCGN with subendothelial electron-dense deposits (2 cases), IgM-IgG cryoglobulinemia with diffuse endocapillary glomerulonephritis (1 case), membranous nephropathy (1 case), diffuse endocapillary proliferative glomerulonephritis (1 case), vasculitis with focal segmental necrotizing glomerulitis and crescentic glomerulonephritis (2 cases). These results show that cirrhosis of the liver can be associated with a wide variety of glomerular disorders. Contrary to previous belief, IgA is absent in two thirds of patients with cirrhosis and glomerulopathy. Therefore, the pathogenetic importance of IgA in the development of glomerular disease in such patients is doubtful.