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)

Clinical, hematologic, and immunologic findings for 14 dogs with Ehrlichia canis monoclonal gammopathy were studied retrospectively. Epistaxis, anemia, thrombocytopenia, hypoalbuminemia, hypergammaglobulinemia, and proteinuria were documented in the majority of these dogs. The serum protein electrophoresis pattern was characterized by a distinct narrow-base monoclonal spike, by a broad-base monoclonal spike, or by a monoclonal spike superimposed on a polyclonal gammopathy. The monoclonal spike disappeared following tetracycline treatment for ehrlichiosis. The long-term prognosis following treatment was generally good. The diagnostic features of monoclonal gammopathy due to myeloma were compared with those of E. canis monoclonal gammopathy. Owing to numerous similarities in clinical, hematologic, and immunologic findings, we conclude that an E. canis antibody titer should be determined in all dogs in which a diagnosis of benign monoclonal gammopathy is contemplated or definitive evidence of myeloma, leukemia, or macroglobulinemia is lacking.
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PMID:Monoclonal gammopathy associated with naturally occurring canine ehrlichiosis. 350 17

Laboratory findings in an adult bull terrier presented with a history of anorexia and weight loss included the following: severe anaemia, leukocytosis, neutrophilia, lymphopaenia, thrombocytopaenia, Ehrlichia canis morulae in monocytes, hypergammaglo-bulinaemia, a bleeding tendency, icterus and proteinuria. In addition, a high Haemobartonella canis parasitaemia, non-encapsulated yeasts on urinalysis and a localised Demodex canis infestation were present. Treatment for ehrlichiosis was initiated but the dog died. Lesions found were a severe cryptococcal granulomatous pneumonia and cryptococcal colonies in the lungs, bronchial lymph nodes, kidneys, liver, spleen, heart, meninges, eyes and thoracic cavity. In addition, hyphal forms resembling Filobasidiella neoformans, the teleomorph of Cryptococcus neoformans, were seen in lung fine needle aspiration smears, impression smears and lung sections. C. neoformans was cultured from urine, lung and liver. Lung and kidney also yielded Salmonella typhimureum. Cortical atrophy with T-cell depletion of lymph nodes as well as splenic lymphoid follicular atrophy, typical of chronic ehrlichiosis-induced cell mediated immunosuppression, could have predisposed to the fatal disseminated cryptococcis.
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PMID:Fatal disseminated cryptococcosis and concurrent ehrlichiosis in a dog. 350 65

Six women without hypertension or proteinuria, admitted for severe upper abdominal pain in the third trimester of pregnancy had elevated serum liver enzymes (SGOT, SGPT), markedly increased serum LDH levels, thrombocytopenia and abnormal blood coagulation tests, in particular low antithrombin III levels, indicating disseminated intravascular coagulation (DIC). Liver biopsies showed periportal and/or focal parenchymal lesions with large fibrin deposits, comparable to the liver lesions in eclampsia. Immunofluorescence (IF) showed microthrombi and large fibrin deposits. Three of the six women recovered spontaneously before delivery; in the remaining three all signs and symptoms rapidly disappeared after delivery. Perinatal outcome was poor. Seven women with pregnancy-induced hypertension and elevated serum liver enzymes constituted a reference series. Histopathological examination of liver biopsies in the reference group revealed periportal and/or focal parenchymal lesions in three whereas IF showed fibrin deposition in all seven, but less extensive than in the study group. The present findings indicate that upper abdominal pain in the last trimester of pregnancy can be caused by a syndrome of (pre)-eclamptic liver damage and DIC, even when hypertension and proteinuria are lacking.
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PMID:A syndrome of liver damage and intravascular coagulation in the last trimester of normotensive pregnancy. A clinical and histopathological study. 351 56

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

To understand the role of neutrophil leukocytosis in hemolytic uremic syndrome, we studied the changes in neutrophil function in the modified generalized Shwartzman reaction in rabbits. This model resembles hemolytic uremic syndrome associated with endotoxemia. At the end of an endotoxin infusion, we observed leukopenia, thrombocytopenia, and a decrease in hematocrit associated with schistocytosis. Plasma B-glucuronidase levels increased and this was associated with a decrease in neutrophil content of the enzyme. The chemotactic index and neutrophil aggregation to zymosan-activated serum were impaired compared to controls. The neutrophil procoagulant content increased after endotoxin infusion. The serum creatinine concentration and proteinuria increased in the endotoxin-treated animals. The changes returned to normal by 48 h. Renal cortical malondialdehyde, a reflection of lipid peroxidation, was higher in the endotoxin-treated animals than in the controls. We have shown enzyme release by neutrophils, impairment of chemotaxis and aggregation, increased procoagulant content in neutrophils, and evidence of lipid peroxidation in renal cortical tissue in this model. These observations raise the possibility that leukocytes may have a role in the pathogenesis of the hemolytic uremic syndrome.
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PMID:Neutrophil function in an experimental model of hemolytic uremic syndrome. 355 Jun 73

Renal transplantation is usually accompanied by an improvement in reproductive function. The possibility of conception in women of childbearing age emphasizes the need for counseling, and couples who want a child should be encouraged to discuss all implications, with the advice based on strict guidelines. If a recipient becomes pregnant, she must be monitored as a high-risk patient. Management requires particular attention to BP control, renal function, and all infection, as well as fetal surveillance. Just under 40% of conceptions do not go beyond the first trimester, but of those that do, greater than 90% end successfully. In most patients, renal hemodynamics improve during gestation, but permanent impairment occurs in 15% of pregnancies. Other patients may experience transient deterioration in late pregnancy (with or without proteinuria). Patients have a 30% chance of developing hypertension, preeclampsia, or both. Despite its pelvic location, the transplanted kidney rarely produces dystocia and experiences no apparent mechanical injury during vaginal delivery. Thus, cesarean section should be reserved for obstetric reasons only. Aseptic technique, bacterial prophylaxis even for trivial surgery, and steroid augmentation are necessary. Preterm deliveries occur in 45% to 60%, and intrauterine growth retardation in at least 20%, of gestations. Neonatal complications include respiratory distress syndrome, leukopenia, thrombocytopenia, adrenocortical insufficiency, and infection. No predominant or frequent developmental abnormalities have been described, and data on infancy and childhood are encouraging. Future goals should be to improve prepregnancy assessment criteria, to reassess the rationale and implications of immunosuppression during pregnancy, and to monitor the remote effects of pregnancy on both renal prognosis and the offspring.
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PMID:Renal transplantation and pregnancy. 355 13

The diagnosis of preeclampsia near term is seldom difficult, even when complicated by altered liver function, hemolysis and thrombocytopenia. Three patients recently presented before term with thrombocytopenia, abnormal liver function tests and hemolytic anemia (two cases), with development of hypertension and proteinuria after days to weeks. Numerous disease processes during pregnancy are characterized by a similar presentation. Many of these cases may represent severe preeclampsia, previously unrecognized.
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PMID:Hepatic dysfunction, thrombocytopenia and late-onset preeclampsia. A report of three cases. 368 63

A 28-year-old female, who suffered from thrombotic thrombocytopenic purpura (TTP) in the 14th week of her first pregnancy, recovered after a plasma exchange followed by an induced abortion. From six months after the abortion, she no longer required plasma infusions every 3-4 weeks to prevent a relapse of TTP manifested as thrombocytopenia, and complete remission continued until her next pregnancy. In her second pregnancy, she had an immediate relapse of TTP and responded to plasma infusion until the 24th week. However, the TTP gradually became resistant to plasma infusion, and developed into toxemia with edema, hypertension and proteinuria in the 27th week. Although the TTP was alleviated by the infusion of large amounts of plasma, the placenta failed as the result of numerous white infarcts. She delivered a 948 g live baby by cesarean section in the 33rd week. The baby had transient thrombocytopenia but did not suffer from TTP. The mother required plasma infusions every 3-4 weeks for about five months, and she has continued in remission.
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PMID:Successful delivery in a female with thrombotic thrombocytopenic purpura. 369 21

A very rare, but severe complication, occurring together with preeclampsia, is the so-called HELLP syndrome (H for haemolysis, EL for elevated liver enzymes and LP for low platelet counts). Perinatal mortality for this syndrome is estimated at 9.5% up to 60%, maternal mortality at 3.5%. We examined retrospectively 11 patients of the last 5 years, presenting not only hypertension, proteinuria and oedema, but also pathologically elevated data concerning transaminases, indirect bilirubin and thrombocytopenia; the mean value for GI in this group was 7.7 (3-11). Thrombocyte counts showed mean values of 71,000 +/- 28,500. In 9 cases the patients suffered from severe upper abdominal pain. Liver enzymes and bilirubin were clearly elevated. Time interval between onset of therapy and delivery was 3 days on the average, the mean gestational age at time of delivery was 34 weeks (27-39), average infant weight amounted to 1,960 g (580-3,700 g). 7 of the 11 women delivered by Caesarian section (64%); perinatal, respectively neonatal 3 babies died (27%). In two cases one Caesarian section did not produce maternal complications; 3 women had to undergo a hysterectomy. This syndrome is associated with a very problematic obstetrical situation in respect of differential diagnosis, foetal outcome and the high frequency of postoperative maternal complications.
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PMID:[HELLP syndrome: a rare, threatening complication in pre-eclampsia]. 377 Apr 12

Carboplatin has been developed for clinical trials as a less nephrotoxic, less emetogenic analog of cisplatin. In preclinical tumor models it was less potent than the parent compound on a molar basis, but reduced toxicity allowed comparable antitumor doses to be given. In phase I studies its dose-limiting toxicities were reversible myelosuppression, especially thrombocytopenia. Leucopenia and anemia occurred to a lesser degree. Other reported toxicities included nausea, vomiting, malaise, myalgia, arthralgia, ototoxicity, hypomagnesemia, and proteinuria. Nausea and vomiting occurred frequently, but was much less severe than that observed with cisplatin. The incidence of serum creatinine elevations was low. The increase was usually reversible and occurred only in association with administration of aminoglycosides, or abnormal pretreatment renal function. Recommended phase II doses by schedule are: bolus every 4 weeks, 400-500 mg/m2 (560 mg/m2 in children); 24 hour continuous infusion every 4 weeks, 320-400 mg/m2; weekly bolus for 4 consecutive weeks with 2 weeks rest, 100-125 mg/m2 (175 mg/m2 in children); bolus for 5 consecutive days every 4 weeks, 77-95 mg/m2. Objective responses were observed during these phase I studies in adult patients (head and neck, breast, renal carcinomas) and children (osteosarcoma, brain stem lesions). In addition to phase II evaluations in all major tumor types, plans for phase III studies in selected tumors are underway.
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PMID:Results of NCI-sponsored phase I trials with carboplatin. 391 Feb 21


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