Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From 1974 to 1989, 18 patients underwent surgical treatment for isolated dissection of the renal artery causing high grade stenosis, including 2 patients with bilateral renal involvement. The causes of renal artery dissection were blunt trauma (1 patient), unsuccessful percutaneous transluminal angioplasty (5) and atherosclerosis (5) or intimal fibroplasia (7) of the renal artery. The most common presenting signs or symptoms of a dissection were hypertension (94%), an abdominal bruit (44%), headache (44%), minimal proteinuria (44%), microscopic hematuria (38%) and flank pain (38%). Renal artery dissection led to segmental or total renal infarction in 8 of 20 involved kidneys (40%). Seventeen patients underwent unilateral surgical revascularization with amelioration of hypertension and preservation of renal function. Three kidneys were lost due to irreversible ischemic damage from an occlusive dissection. Isolated renal artery dissection is an uncommon lesion that can cause hypertension and threaten renal function.
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PMID:Surgical treatment for isolated dissection of the renal artery. 214 39

Hantaviruses, the causative agents of HFRS, have become more widely recognized. Epidemiologic evidence indicates that these pathogens are distributed worldwide. People who come into close contact with infected rodents in urban, rural and laboratory environments are at particular risk. Transmission to man occurs mainly via the respiratory tract. The epidemiology of the hantaviruses is intimately linked to the ecology of their principal vertebrate hosts. Four distinct viruses are now recognized within the hantavirus genus and that number is likely to increase to six very soon; however, further investigations are necessary. Much more work is still needed before we fully understand the wide spectrum of clinical signs and symptoms of HFRS as well as the pathogenicity of the different viruses in the hantavirus genus of the Bunyaviridae family. HFRS is difficult to diagnose on clinical grounds alone and serological evidence is often needed. A fourfold rise in IgG antibody titer in a 1-week interval, and the presence of the IgM type of antibodies against hantaviruses are good evidence for an acute hantavirus infection. Physicians should be alert for HFRS each time they deal with patients with acute febrile flu-like illness, renal failure of unknown origin and sometimes hepatic dysfunction. Especially the mild form of HFRS is difficult to diagnose. Acute onset, headache, fever, increased serum creatinine, proteinuria and polyuria are signs and symptoms compatible with a mild form of HFRS. Differential diagnosis should be considered for the following diseases in the endemic areas of HFRS: acute renal failure, hemorrhagic scarlet fever, acute abdomen, leptospirosis, scrub typhus, murine typhus, spotted fevers, non-A, non-B hepatitis, Colorado tick fever, septicemia, dengue, heartstroke and DIC. Treatment of HFRS is mainly supportive. Recently, however, treatment of HFRS patients with ribavirin in China and Korea, within 7 days after onset of fever, resulted in a reduced mortality as well as shortened course of illness.
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PMID:Hemorrhagic fever with renal syndrome. 257 14

Clinical symptoms and laboratory measures of renal and liver function, coagulation, and inflammatory parameters were prospectively studied in 74 hospitalized patients (14-74 years of age) with serologic evidence of nephropathia epidemica. The most common clinical findings were acute onset of symptoms, fever (greater than or equal to 38 degrees C), thirst, headache, nausea, back pain, vomiting, myalgia, and abdominal pain. Twenty-seven patients (37%) had hemorrhagic manifestations, i.e., epistaxis, melena, hematemesis, petechial bleeding, macroscopic hematuria, or metrorrhagia. Disseminated intravascular coagulation developed in four patients. Fifty-one percent had thrombocytopenia. Proteinuria was recorded for all patients, while hematuria and glucosuria were noted for 85% and 58%, respectively. Serum creatinine levels were elevated in 71 (96%) of the patients. Levels of C-reactive protein or erythrocyte sedimentation rates were elevated in all cases, usually to levels found in serious bacterial diseases. Sixty-six (89%) of the patients were followed for up to 7 months, at which time all had recovered clinically. No patient died or required dialysis. We conclude that nephropathia epidemica in Sweden has a clinical picture similar to that of hemorrhagic fevers in other parts of the world, but with a milder course and a better prognosis.
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PMID:Clinical characteristics of nephropathia epidemica in Sweden: prospective study of 74 cases. 257 3

Multiclinic controlled studies have shown that enalapril alone 10 to 40 mg/day orally is effective in lowering blood pressure in patients with essential hypertension. Enalapril has been compared with thiazides and beta-blockers (propranolol, metoprolol and atenolol). The effect on systolic blood pressure has been greater with enalapril than with beta-blockers. The proportion of patients who respond to enalapril alone with a decrease in diastolic blood pressure (greater than or equal to 10mm Hg) is around 70%. When a thiazide is added to the treatment, the proportion is above 90%. Enalapril improves the signs and symptoms associated with congestive heart failure. Patients increased their exercise tolerance by an average of 148 sec and improved in their NYHA cardiac status and prognosis classification. The overall incidence of side effects is similar to that seen in the placebo control groups. Side effects such as agranulocytosis, taste loss, rash, proteinuria were not characteristic of enalapril. This supports the hypothesis that the improved safety profile of enalapril is the result of being a nonsulphydryl angiotensin-converting enzyme (ACE) inhibitor. The most common side effects reported were dizziness, headache and asthenia. Abnormalities in electrolytes, uric acid, glucose or in lipids have generally not been associated with enalapril.
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PMID:Enalapril in hypertension and congestive heart failure. Overall review of efficacy and safety. 286 29

Thirteen cases of hemorrhagic fever with renal syndrome (HFRS) have been observed in the Nancy area. Ten occurred during the summer of 1983 and three in April and May 1985. The clinical characteristics were in each case very typical: abrupt onset with high fever, myalgia, intense lumbar and abdominal pain, pulsatile headache, inflammatory syndrome, WBC count increase and thrombocytopenia. Acute renal failure occurred a few days later with oliguria (9 cases out of 13), massive proteinuria (9/13) and hematuria (6/13). All patients recovered without sequelae within 8-10 days. Renal biopsy performed in 8 patients showed slight tubular lesions with interstitial mononuclear cell infiltrate, congestion and diffuse interstitial edema, and in 2 cases hemorrhagic extravasation. No glomerular lesions were observed. Clinical, histological and epidemiological characteristics of these 13 French cases are highly similar to those of the Scandinavian Nephropathia Epidemica reports. The epidemiology of HFRS remains unclear as do its pathophysiological mechanisms.
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PMID:[Hemorrhagic fever with renal syndrome. Apropos of 13 cases observed in Lorraine]. 287 52

Haemorrhagic fever with renal syndrome (HFRS) is caused by a group of RNA viruses within the family of Bunyaviridae known as hantaviruses. The classical, severe form of HFRS is characterized by fever, headache, abdominal and lumbar pain, proteinuria, haemorrhagic phenomena, shock and renal failure. The disease is associated with the prototype Hantaan virus and occurs in rural areas of Korea and China with Apodemus mice as reservoir hosts. A clinically less severe form of HFRS, which is caused by Seoul virus, occurs in urban areas with the house rat Rattus novegicus as the main reservoir host. The disease in nonendemic areas may be atypical and patients with symptoms the hepatitis and minimal renal involvement have been observed in Malaysia. Outbreaks of HFRS in humans involving infected laboratory rat colonies have occurred in several medical centres in various countries. Hantaviruses cause a chronic, asymptomatic infection in rodents which excrete the virus in their lungs, saliva and urine. Man becomes infected mainly by inhalation of infected droplets from healthy rodent carriers. Seroepidemiological studies using mainly the indirect immunoflourescent antibody test of sera from humans and rats showed that hantaviruses have a worldwide distribution.
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PMID:Haemorrhagic fever with renal syndrome: clinical, virological and epidemiological perspectives. 289 3

A 34-year-old quadripara was hospitalized in the 33rd gestational week due to an acute hypertensive crisis, headache, upper abdominal pain, icterus, and proteinuria. Laboratory testing revealed hemolysis, hepatic dysfunction, and thrombopenia. The values returned toward normal after delivery by cesarean section. Diffuse bleeding in the surgical wound and acute renal failure necessitated two relaparotomies, intensive hemotherapy, and hemodialysis. Mother and child were released in good condition. Anesthesiological and obstetrical aspects of the HELLP syndrome are discussed.
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PMID:[The HELLP syndrome--a rare form of preeclampsia. Anesthesiologic and obstetric aspects]. 291 50

Eighteen patients with solid tumours were treated with human recombinant interferon-gamma at escalating dose levels starting at 1 X 10(6) units/m2 per infusion and rising through 3 X 10(6), 6 X 10(6), 9 X 10(6) and 22 X 10(6) to a maximum of 110 X 10(6) units/m2 per infusion. The IV infusions were given three times a week over a 4-week period. Side effects were seen in all patients, but were mild except at the highest dose. Acute dose-related effects included pyrexia, tiredness, thirst, chills and rigors. Chronic dose-related effects included anorexia, lethargy, weakness, disorientation, a trace of proteinuria and minimal rises in liver enzymes. In addition, effects were observed which were not related to dose. These included headache, nausea and vomiting, backache, myalgia, flatulence and a mild, transient reduction in neutrophils and erythrocytes. At the highest dose level dose-limiting toxicity was observed, consisting in severe tiredness and anorexia, hypotension, disorientation and changes on the electrocardiograph. Overall, toxicity was similar to that seen with preparations of interferon-alpha, except that no tolerance to the effects of interferon-gamma was noted. We observed less hepatic and haematological toxicity, but also recorded flatulence, handcramps and electrocardiograph changes, which have not been reported with interferon-alpha. When given according to this regimen, doses of 22 X 10(6) units/m2 per infusion of recombinant interferon-gamma were generally well tolerated by the patients.
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PMID:A toxicity study of recombinant interferon-gamma given by intravenous infusion to patients with advanced cancer. 309 8

We have prospectively evaluated the clinical and immunological features of serum sickness in 35 patients treated for bone marrow failure with anti-thymocyte globulin (ATG 15 mg/kg/day) and methylprednisolone (1 to 1.5 mg/kg/day). Twenty-one patients were treated for 10 days and 14 were treated for 28 days. Clinical evidence of serum sickness developed in 30 patients (86%) and included fever and malaise (100%), cutaneous eruptions (93%), arthralgias (67%), gastrointestinal complaints (67%), cephalgia (57%), blurring of vision (37%), arthritis, (30%) and lymphadenopathy (13%). Clinical serum sickness began on day 7 +/- 1 (X +/- S.E.M.) and lasted for 10 +/- 2 days in the 18 affected patients receiving the shorter course of ATG. In the 12 affected patients receiving the longer course of ATG, serum sickness began on day 9 +/- 1. The earliest manifestations of serum sickness were fever, malaise, and cutaneous eruptions. Cutaneous findings consisted of morbilliform eruptions (n = 19) and urticaria (n = 1) or a combination (n = 8) that lasted 10 to 14 days. Twenty-one patients (75%) developed a highly characteristic serpiginous band of erythema and purpura along the sides of the fingers, toes, palms and soles 12 to 48 hours before other symptoms of serum sickness. Biopsies of lesional skin during the course of serum sickness revealed immune deposits (IgM, IgE, IgA and C3) in dermal vasculature in 7 of 9 patients. Immunological changes that occurred during the course of serum sickness included increased serum levels of IgG, IgM, IgA, and IgE. Circulating immune complexes, as measured by the C1q-binding assay, increased from a mean value of 12% to 45% on day 13 +/- 1. Complement levels (C3, C4, and CH50) decreased 50 to 80% from their baseline levels on day 10 +/- 2. Acute phase reactants increased: erythrocyte sedimentation rate, C-reactive protein and beta-2 microglobulin. Abnormal urinalysis developed in 17 patients (57%) over the course of serum sickness and included proteinuria, hematuria and hemoglobinuria on day 10 +/- 3. Hematopoietic response occurred in 43%. All 5 patients who did not develop serum sickness recovered from bone marrow failure. Our data document the clinical and immunopathological findings in human serum sickness and suggest that the principles of antigen-antibody interaction, complement activation, and resultant inflammatory response as seen in the previous animal studies are directly applicable to studies of patients with serum sickness.
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PMID:Human serum sickness: a prospective analysis of 35 patients treated with equine anti-thymocyte globulin for bone marrow failure. 325 88

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13


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