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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute renal failure following angiography with contrast agents is known to occur, but the circumstances and frequency of its occurrence are not well described. A retrospective review of consecutive angiographic procedures performed over a six month interval revealed a 12 per cent incidence of renal failure following angiography. The degree of failure was severe in approximately 30 per cent of these cases and was associated with a significant mortality even though renal function usually recovered. The occurrence of renal failure was associated with the presence of renal insufficiency, impaired liver function, diabetes mellitus, hypoalbuminemia and proteinuria at the time of angiography to a statistically significant level. Furthermore, combinations of these factors, particularly preexisting combined renal insufficiency and impaired liver function, were associated with an increased incidence of acute renal failure. It is concluded that angiography poses a significant hazard to patients with underlying medical problems, particularly those involving the excretory routes of the contrast agent.
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PMID:Renal failure following major angiography. 68 98

The hemolytic-uremic syndrome consists of microangiopathic hemolytic anemia, acute renal failure, and thrombocytopenia following a prodromal illness of gastroenteritis or upper respiratory infection. The syndrome can present in dramatic fashion with severe abdominal pain and signs of peritonitis suggesting an acute surgical crisis. In a series of 25 patients, 40% had abdominal pain, 25% had abdominal tenderness, and 20% had peritoneal signs. Clues to diagnosis in the early stages of the acute illness were mild to moderate hypertension, abnormal peripheral blood smear, anemia despite dehydration, and proteinuria. Significant abdominal pain and x-ray evidence of colitis may occur before development of typical laboratory findings, and these were evident in at least one case. Three patients underwent laparotomy for suspected bowel perforation. Colitis without perforation was found in all cases. In the absence of documented perforation, toxic megacolon, or intussusception, the decision to perform laparotomy in patients with hemolytic-uremic syndrome who have signs of peritonitis must be individualized. Failure to recognize the underlying renal problem can lead to serious errors in fluid and electrolyte management and delay of appropriate therapy.
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PMID:Hemolytic-uremic syndrome: a diagnostic and therapeutic dilemma for the surgeon. 73 58

Association of membranous glomerulonephropathy with crescentic glomerulonephritis is apparently extremely rare. We report three patients who had this combination. One patient had biopsy-proven membranous glomerulonephropathy thirteen months prior to sudden and rapid decline in renal function necessitating hemodialysis. A repeat renal biopsy showed a superimposed crescentic nephritis and antiglomerular (GBM) antibodies were demonstrable in the serum. A second patient had proteinuria of unknown duration and then developed renal failure. Renal biopsy showed crescentic nephritis with a fine granular glomerular immunofluorescence for IgG typical of membranous glomerulonephropathy. Anti-GBM antibodies were present in this patient's serum. The third patient presented with acute renal failure of moderate severity. A renal biopsy revealed crescentic nephritis, granular deposits of immunoglobulins, and epimembranous electron-dense deposits typical of membranous glomerulonephropathy. Although his creatinine clearance improved spontaneously, nephrotic syndrome has persisted and a repeat renal biopsy showed a progression of the membranous glomerulonephropathy with the disappearance of the crescentic lesions. The reason for this peculiar association of membranous glomerulonephropathy and crescentic glomerulonephritis is unclear. It is possible that deposition of immune-complexes along glomerular basement membrane may render the glomerulus more susceptible to additional injury from a variety of other agents. Alternatively, depostis formed in one disease could initiate release of normal or altered basement membrane material and lead to formation of anti-GBM antibodies and subsequent development.
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PMID:Association of crescentic glomerulonephritis with membranous glomerulonephropathy: a report of three cases. 78 51

Five patients are described in whom only gentamicin sulfate appeared responsible for acute renal failure. Subjects received 1.2 to 2.88 gm over 12 to 18 days. All were over 45 years of age, and premorbid kidney abnormalities may have enhanced susceptibility to toxic effects of the drug. Renal failure appeared 8 to 17 days after beginning gentamicin therapy and was characterized by creatinine clearances 4 to 10 ml/min, urine to plasma creatinine ratios less than 20, urinary sodium concentrations 16 to 60 mEq/liter, proteinuria, and cylindruria. Oliguria was not observed and this feature may impair recognition of kidney damage. Clinical recovery required an average of 42 days and was complete in four of five patients. Gentamicin alone may be nephrotoxic and should be given with particular caution to the elderly and those with even mild kidney abnormalities.
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PMID:Gentamicin-associated acute renal failure. 78 66

In order to define the possible effects of gentamicin on the course of experimental acute renal failure, the interaction between gentamicin and mercuric chloride was studied in rats. Acute renal failure was induced with 1 mg. of HgCl2 per kilogram intravenously. When given alone, HgCl2 produced a uniform, reproducible, nonoliguric, acute renal failure with a low mortality rate. Animals receiving gentamicin over the course of HgCl2-induced acute renal failure, in doses sufficient to produce a 1 hour postinjection serum concentration of 10 mug/ml., recovered glomerular filtration in a fashion similar to animals receiving only HgCl2(p greater than 0.05). Animals that recovered from HgCl2-induced acute renal failure were given 10 mg./Kg. of gentamicin every 4 hours for 15 days and developed proteinuria and decline in urine osmolality to the same degree as animals given gentamicin alone, but failed to develop azotemia. Nevertheless, morphological changes associated with gentamicin nephrotoxicity were found which were similar in severity to those seen with gentamicin alone. Animals pretreated with 10 mg./Kg. of gentamicin every 4 hours for 7 days were then given HgCl2. Acute renal failure in these animals was more severe than in animals receiving HgCl2 alone, as manifest by a greater degree of azotemia and death (p less than 0.05). The data indicate that in the rat the concomitant administration of gentamicin did not interfere with recovery from HgCl2-induced renal failure. Rats recovering from HgCl2-induced acute renal failure were resistant to a depression in glomerular filtration when given gentamicin. The prior administration of gentamicin enhanced the nephrotoxicity of HgCl2.
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PMID:The effect of concomitant mercuric chloride and gentamicin on kidney function and structure in the rat. 83 19

In 6 of 24 courses of a disease a nephrotic syndrome appeared under the application of penicillamine. An acute renal failure with exitus letalis developed under the penicillamine therapy of a scleroderma. In the treatment of a mercurial poisoning by penicillamine the nephrotic syndrome increased to a proteinuria of 50 g/24 hours which receded after discontinuation of the remedy. In one group of patients with chronic pyelonephritis could be demonstrated that penicillamine in a primarily damaged kidney must not lead to a secondary glomerular lesion. These findings led to the conclusion that in the appearance of a proteinuria under penicillamine a strong observation of the renal function is necessary, if a continution of the therapy is given from vital indication.
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PMID:[Penicillamine-induced glomerulonephritis]. 84 41

The occurrence of renal manifestations of Hodgkin's disease may result from multiple physio-pathological processes: mechanical, by obstruction of the vessels or excretory systems of the kidneys; specific, by lymphogranulomatous infiltration of the parenchyma; immunological, as immunune complex glomerulonephritis or, more frequently, as amyloid disease; infective or metabolic as a complication of long term corticosteroid or immunodepressive therapy. These various causes of renal problems during Hodgkin's disease lead to the observation of three principal clinical pictures: acute renal failure, chronic renal failure and permanent proteinuria with or without nephrotic syndrome. Acute renal failure generally results from a severe infection with toxi-infective shock. More rarely it is related to thrombosis of the renal veins, with a grave prognosis, or to unreteral compression with anatomical or functional exclusion of the contralateral kidney. Chronic renal failure may be caused either by distension of the excretory pathways, progressively obstructed or invaded by the Hodgkin's process and requiring specific therapy to relieve the obstruction (cobaltotherapy, chemotherapy), by specific infiltration of the renal parenchyma or by amyloid disease. Permanent proteinuria, with or without nephrotic syndrome, may be the presenting feature of renal vein thrombosis, amyloidosis or paraneoplastic nephrotic syndrome.
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PMID:[Renal manifestations of Hodgkin's disease]. 96 42

1. The clinical manifestations, laboratory data and renal histologic features of acute renal failure occurring in 14 patients with multiple myeloma are reviewed and contrasted with the data from 29 previously reported cases. 2. Whereas other reports have stressed the role of intravenous pyelography and dehydration in the development of acute renal failure in multiple myeloma, the most common etiologic factor in our experience was hypercalcemia (7 patients). Other factors included potentially nephrotoxic antibiotics (3 patients) and volume depletion (2 patients). Intravenous pyelography could be clearly implicated in ony one patient. 3. The unusually high incidence of Bence Jones proteinuria in these patients is consistent with the possibility that Bence Jones protein excretion is associated with an increased susceptibility to renal injury. This could be due to an adverse effect of Bence Jones proteins on the renal tubules or their tendency to precipitate in tubular lumina during periods of reduced tubular flow. 4. The prognosis of patients with multiple myeloma who develop acute renal failure is poor; only 5 of our 14 patients survived the early period of acutely impaired renal function, and 4 of these subsequently died within 2 months. Preventive measures particularly the prompt correction of hypercalcemia and volume depletion, are the most important aspects of patient management.
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PMID:Acute renal failure in multiple myeloma. 114 86

Numerous plasma cells were transiently found in the urine of a patient with multiple myeloma. The patient was in acute renal failure, and she had K-type Bence-Jones proteinemia and proteinuria. A slide of stained urine sediment showed cells with freatures characteristic of plasma cells. Their cytoplasm was highly reactive with anti-K antiserum on immunofluorescence, suggesting that these were myeloma cells.
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PMID:Plasma cells in urine: occurrence in multiple myeloma. 116 26

To define interstitial nephritis without preselection bias, 25 consecutive renal biopsy specimens from patients with tubular damage, interstitial damage and interstitial inflammation were analyzed in detail. In four patients (all with acute renal failure), tubulitis, and interstitial eosinophil and lymphocyte infiltration were found, but no glomerular abnormalities. In four others, the findings were similar but some glomerular abnormalities were noted. Two patients had probable healed interstitial nephritis. The clinical presentation varied from transient renal insufficincy to oliguric renal failure. Three of the patients with glomerular abnormalities had significant proteinuria. When the 10 patients with interstitial nephritis were compared with the other 15 serving as controls, striking features in the former group were skin rash, eosinophilia, the absence of hypertension and the frequency of administration of penicillin and its analogs. Serum immunoglobulin E (IgE) levels were elevated in three of the patients. The striking eosinophilia, interstitial eosinophil infiltration and increased IgE levels suggest that allergen-reaginic complexes may be involved in the pathogenesis of the lesion.
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PMID:Acute interstitial nephritis. A clinical and pathologic study based on renal biopsies. 120 34


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