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)

A 4-year-old Japanese girl had a congenital disorder that was characterized by recurrent thrombocytopenia, hemolytic anemia, hematuria, and proteinuria, which were repeatedly improved by the infusion of factor VIII concentrate. She developed the similar symptoms within 1 h after 1-desamino-8-D-arginine vasopressin (DDAVP) administration. Coagulation studies 30 and 60 min after DDAVP infusion showed a disappearance of large factor VIII:von Willebrand factor (VIII:vWF) multimers, which was the same abnormality that was observed at acute episodes. There were no significant changes in the plasma levels of 6-keto-prostaglandin F1 alpha and thromboxane B2 before and after DDAVP infusion. These results provide further support that VIII:vWF is directly involved in the pathogenesis of this congenital disorder.
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PMID:Factor VIII concentrate-responsive thrombocytopenia, hemolytic anemia, and nephropathy. Evidence that factor VIII:von Willebrand factor is involved in its pathogenesis. 309 91

Seventy-nine children with haemolytic uraemic syndrome (mean age 28 months) were randomly assigned either to a group receiving plasma infusions (plasma group, n = 39) or to a group treated conservatively (control group, n = 40). The duration of haemolysis, thrombocytopenia and anuria was similar in the two groups. Serum creatinine levels were similar in the two groups at the 1-month follow-up but were higher in the control group at 3 months (plasma group 49 +/- 14, control group 66 +/- 28 mumol/l; P less than 0.02) and at 6 months (plasma group 48 +/- 13, control group 63 +/- 21 mumol/l; P less than 0.005). The prevalence of proteinuria was also higher in the control group at the 6-month follow-up (plasma group 17%, control group 46%; P less than 0.02). However, differences were no longer significant after 1 year. Renal tissue was examined in 54 cases (plasma group, n = 27; control group, n = 27). Diffuse cortical necrosis was present in 7 cases in the control group but was absent in the plasma group (P less than 0.02). Taking into consideration the higher serum creatinine levels, the higher prevalence of proteinuria during the first 6 months of follow-up in the control group and the presence of diffuse cortical necrosis in this group compared with the plasma group, we conclude that plasma infusions should be regarded as beneficial. Further study is needed to determine which plasma fraction is involved.
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PMID:Treatment of the childhood haemolytic uraemic syndrome with plasma. A multicentre randomized controlled trial. The French Society of Paediatric Nephrology. 264 3

A phase I trial of chlorozotocin was completed for a weekly times four dose schedule repeated every 8 weeks. Thrombocytopenia was the acute dose limiting toxicity. Nausea and vomiting were moderate to severe and dose related. Two cases of possible drug related irreversible nephrotoxicity were seen. Transient elevations of serum creatinine and mild proteinuria were noted. Also, transient elevations in SGOT were observed. One patient with a carcinoid tumor had a 60% reduction in his 5HIAA level after one course of therapy. The recommended dose for phase II clinical studies of chlorozotocin is 40 mg/m2 IV weekly for four weeks, repeated every 8 weeks.
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PMID:Phase I evaluation of chlorozotocin (NSC-178248): weekly schedule. 315 61

Visceral leishmaniasis was diagnosed in a 5-year-old English Foxhound born and housed in an Ohio research colony. Physical examination revealed pyrexia, hematochezia, panuveitis, splenomegaly, and lymphadenopathy. Hematologic and serum biochemical abnormalities consisted of anemia, thrombocytopenia, hypoalbuminemia, hyperglobulinemia, azotemia, and proteinuria. Postmortem examination revealed widely disseminated (spleen, bone marrow, lymph node, liver, kidney, lungs) Leishmania amastigotes within macrophages.
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PMID:Visceral leishmaniasis in an English foxhound from an Ohio research colony. 319 62

Auranofin (triethylphosphine gold), an oral gold preparation, has recently been made available, and along with injectable gold preparations, is of therapeutic value for rheumatoid arthritis. Serious gold toxicity is uncommon, and drug-related deaths rare. Many potential adverse reactions are similar, including dermatitis, stomatitis, thrombocytopenia, leucopenia, and proteinuria, generally with increased incidence in the injectable gold-treated patients. Oral gold is associated with benign lower gastrointestinal side effects, including diarrhoea, loose stools and abdominal cramps that are often dose-related and resolve spontaneously. The incidence of severe reactions such as thrombocytopenia, aplastic anaemia and exfoliative dermatitis is lower with oral gold than injectable preparations, and contributes to a superior risk-benefit ratio. The treatment of gold toxicity depends on the type and extent of organ involvement.
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PMID:Adverse reactions with oral and parenteral gold preparations. 329 22

Renal transplantation is invariably accompanied by improvements in reproductive function. The possibility of conception in women of childbearing age emphasizes the need for compassionate and comprehensive counselling. Couples who want a child should be encouraged to discuss all the implications. Therapeutic abortion is undertaken in 22% of conceptions and the spontaneous abortion rate is about 16%, the same as for the normal population. Of the conceptions that continue beyond the first trimester, over 90% end successfully. In most women, renal function is augmented during pregnancy, but permanent impairment occurs in 15% of pregnancies. In others there may be transient deterioration in late pregnancy (with or without proteinuria). There is a 30% chance of developing hypertension, pre-eclampsia or both. Preterm delivery occurs in 45-60%, and intrauterine growth retardation in at least 20% of pregnancies. Despite its pelvic location, the transplanted kidney rarely produces dystocia and is not injured during vaginal delivery. Caesarean section should be reserved for obstetric reasons only. Neonatal complications include respiratory distress syndrome, leucopaenia, thrombocytopaenia, adrenocortical insufficiency and infection. No predominant or frequent developmental abnormalities have been described and data on infancy and childhood are encouraging. For the future, clinical and laboratory research are essential in order to improve prepregnancy assessment criteria, to understand the mechanisms of gestational renal dysfunction and proteinuria, to assess the side-effects and implications of immunosuppression in pregnancy and to learn more about the remote effects of pregnancy on both renal prognosis and the offspring.
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PMID:Pregnancy in renal allograft recipients: prognosis and management. 333 Apr 84

In addition to its antihypertensive properties, nifedipine inhibits platelet aggregation in vitro. Because increased platelet aggregation is a feature of preeclampsia, we have investigated nifedipine in this condition. Ten women at 31 +/- 2.8 weeks gestation, with blood pressure 162 +/- 18/102 +/- 10 mmHg (despite atenolol 200 mg/day) and proteinuria 2.0 +/- 1.1 g/24 hr, were treated with nifedipine. Pregnancies were prolonged by 17 +/- 15 days (range 5 to 56). Blood pressure was controlled in eight of the ten patients, final values before delivery being 142 +/- 16/89 +/- 12 mmHg (P less than 0.02). Platelet count rose in all women from 190 +/- 80 to 261 +/- 78 X 10(9)/1 (P less than 0.001). Nifedipine appears to reverse the thrombocytopenia of pre-eclampsia, in addition to controlling the blood pressure.
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PMID:Nifedipine and platelets in preeclampsia. 340 56

To assess therapeutic effect and toxicity of D-penicillamine in relation to HLA antigens, 111 consecutive patients with rheumatoid arthritis (RA) were followed for a period of 7-9 years. Side effects occurred in 60% and were the main reason for withdrawal in 52%. HLA typing was performed in 86; overall frequencies were comparable with those found in other studies in patients with RA. Drug induced proteinuria (5 patients) was associated with HLA-B8/DR3 (60 vs 9%), and thrombocytopenia (23 patients) with HLA-DR4 (94 vs 67%). Therapeutic effect was good in 26 (23%), and moderate in 30 (27%). No single variable, including HLA antigens, was predictive of effectiveness. It is concluded that although some of the side effects were associated with HLA antigens, HLA typing is not useful in predicting the outcome of treatment with D-penicillamine.
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PMID:Longterm followup of treatment with D-penicillamine for rheumatoid arthritis: effectivity and toxicity in relation to HLA antigens. 343 18

In 1982 Weinstein described the Hellp-Syndrome in pre-eclampsia. Two personal case histories have led the authors to discuss the need to specify this syndrome. Apart from the classical elements of pre-eclampsia, which are: arterial hypertension, proteinuria and oedema, there are bowel symptoms in 86% of cases and on the biological level there is thrombocytopenia and a rise in the transaminases as well as a haemolytic anaemia. Some cases of rupture of the liver have been described. Treatment is that of pre-eclampsia. This involves treatment with cortisone and sometimes with heparin. Delivery of the fetus is, however, the only really effective treatment. The characteristic three elements of the Hellp-Syndrome seem to be linked to disseminated intravascular coagulation and have long been considered very serious factors in pre-eclampsia. On the other hand it does seem to be useful for the clinician to know about the Hellp-syndrome in order to estimate the seriousness of a case where there are vasculo-renal elements in the syndrome and in order to avoid diagnosis mistakes in cases where the symptoms are often deceptive.
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PMID:[Is it necessary to specify the HELLP syndrome?]. 345 19

In a 3-centre study involving 144 patients with rheumatoid arthritis (RA), a relationship between side effects from D-penicillamine and HLA antigens, allotypic markers of the IgG heavy chain (Gm) and allotypes of complement components Bf, C4A and C4B was sought. There was a significant association between proteinuria induced by D-penicillamine and the antigens DR3 and B8. However, the presence of DR2 seemed to protect against the development of proteinuria. Thrombocytopenia from D-penicillamine was significantly associated with HLA-A1 and DR4; 15 of 23 patients who possessed both antigens developed thrombocytopenia (p less than 0.001 uncorrected, approximate relative risk (RR) = 5.5). A null complement allele located at the C4B locus (C4BQO) was also associated with thrombocytopenia from D-penicillamine (p less than 0.005, RR = 17.3). Our study confirms the findings from other series which indicate that there is a genetic predisposition for the development of proteinuria from D-penicillamine in RA and suggests that this may also be the case in D-penicillamine induced thrombocytopenia.
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PMID:Genetic markers in rheumatoid arthritis relationship to toxicity from D-penicillamine. 345 89


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