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 43-year-old woman with a history of systemic lupus erythematosus manifested severe diarrhea, generalized gastrointestinal polyposis, pigmentation, and onychodystrophy, which were typical of Canada-Cronkhite syndrome. The exacerbation of systemic lupus erythematosus, presenting with hemolytic anemia and subsequently with profound proteinuria, was seen during the course of this syndrome. The patient achieved complete symptomatic remissions of both entities for more than four years following prednisolone therapy; the resolution of the gastrointestinal polyps was confirmed histologically. This case showed that this syndrome could be completely reversible in its course and that it might have an exogenous cause, as previously suggested.
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PMID:Canada-Cronkhite syndrome associated with systemic lupus erythematosus. 396 88

The concentration of serum fibrinogen-fibrin-related antigen (F.R.-antigen) was measured in a group of 142 patients with various renal disorders, in 38 of whom urine F.R.-antigen was also estimated. Raised serum F.R.-antigen levels were present in 48% of the patients, with no particular preponderance in any diagnostic category apart from acute reversible intrinsic renal failure in which high levels were invariably present. Significantly-raised serum levels were also present in the patients with microangiopathic haemolytic anaemia and in those with the more severe degrees of renal impairment. Urine F.R.-antigen was increased in 34 of the 38 patients. The amount of F.R.-antigen in the urine correlated with the degree of proteinuria but not with the serum F.R.-antigen levels. The evidence relating to intravascular coagulation in renal disease is reviewed, and it is suggested that there is a high incidence of localized fibrinogen or fibrin degradation in the kidney, which is related more to factors such as the presence of uraemia and microangiopathic haemolytic anaemia rather than to the diagnostic category.
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PMID:Serum and urine fibrinogen-fibrin-related antigen (F.R.-antigen) levels in renal disease. 507 72

The chronic administration of captopril to Sprague-Dawley rats was performed under the barrier system by feeding ad libitum with mixed diet in various concentrations of captopril with 3 months recovery period. The number of animals was 180 female and 180 male including 5 groups of control, 30, 100, 300 and 900 mg/kg/day. The maximum nontoxic dose was estimated as about 30 mg/kg/day for male but a little more than this for female rats. Body weight increase was significantly reduced in male but for the first 3 months in female rats. No death was ascribed to the toxic effect of captopril. Polydipsia and polyuria in male, and the significant increase in values of BUN and inorganic phosphate in both sexes were observed. The reduction in erythrocyte count, values of hemoglobin and hematocrit, hemosiderosis in reticulum cells of the spleen and Kupffer cells in the liver and the increase of erythropoieses indicated hemolytic anemia. Heart weight reduced while kidney weight increased. Pathological examination revealed hypertrophia and hyperplasia of JG cells and thickening of walls of afferent arterioles with hyperplasia of vascular smooth muscle cells and increase of collagen fibers. Thickening of walls extended to walls of the interlobular arteries which remained after withdrawal of captopril for 3 months though JG granules attenuated. The age-related increases of incidences of proteinuria and myocardial fibrosis were attenuated dose-dependently which are probably due to hypotension induced by captopril.
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PMID:[Twelve month studies on the chronic toxicity of captopril in rats]. 627 84

This report describes a patient with thrombocytopenia, microangiopathic hemolytic anemia, proteinuria, and microscopic hematuria that could be transiently improved by the infusion of plasma or various plasma components. An increase in platelet count following the transfusion of normal plasma was predictable and reproducible. In therapeutic trials with commercially available plasma components, factor VIII preparations were effective for inducing an increase in the platelet count and improving hemolytic anemia, but albumin, gamma-globulin, factor IX, and fibronectin preparations were ineffective. Serum from normal donors also relieved the symptoms of this condition in our patient. Partial plasma exchange (1,000 ml/m2 of body surface area) was performed with albumin instead of normal plasma, but there was no significant effect on platelet count or anemia. Large, multimeric von Willebrand factor components of the factor VIII complex (VIII/vWF) were found in the patient's plasma when his platelet count was normal, but their levels were reduced when the platelet count was decreased. The multimers of the patient's plasma were larger than those in normal plasma, but smaller than those in normal platelet lysate. Although the pathogenesis of this disease remains unknown, we conclude that transfusions of normal plasma, serum or factor VIII concentrate provide a factor that causes significant improvement in the thrombocytopenia and hemolytic anemia. Furthermore, large VIII/vWF multimers are possibly directly involved in pathogenesis of this disease.
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PMID:Efficacy of several plasma components in a young boy with chronic thrombocytopenia and hemolytic anemia who responds repeatedly to normal plasma infusions. 643 3

We describe a 25-year-old male with juvenile onset diabetes mellitus who developed severe pseudomembranous enterocolitis with intractable diarrhea for which he was maintained on total parenteral nutrition. Subsequently, he developed clinical signs and typical radiological manifestations of hypertrophic osteoarthropathy (HOA) associated with hemolytic anemia, proteinuria and immunoglobulin deficiency. Immune complexes were not detected in either sera and synovial fluid.
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PMID:Hypertrophic osteoarthropathy and pseudomembranous enterocolitis. 679 83

Two new cases of hereditary lecithin-cholesterol acyltransferase (LCAT) deficiency in a brother and sister born to consanguinous parents are reported. Both have corneal opacity, splenomegaly and mild hemolytic anemia. The brother, the older of the 2, also has significant proteinuria. The literature dealing with reported cases of hereditary LCAT deficiency and the clinical, pathological, diagnostic and management aspects of the disorder are reviewed.
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PMID:Hereditary lecithin-cholesterol acyltransferase deficiency. Report of 2 new cases and review of the literature. 683 94

Our experience with 61 episodes of the hemolytic-uremic syndrome in 60 patients showed a mean patient age of 3 years and a higher incidence of the disease during the summer months. Diarrhea, often bloody, preceded the other features of the illness in 93 percent of the cases. Hemolytic anemia, hematuria and proteinuria occurred in all of the patients. Thrombocytopenia and severe azotemia (blood urea nitrogen greater than 100 mg per dl) occurred in 74 percent and 72 percent of the children, respectively. Blood transfusions were necessary in 64 percent and dialysis was required in 54 percent of the cases. Mortality was low (5 percent) and 85 percent of the children had a complete recovery.
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PMID:The hemolytic-uremic syndrome. 726 54

Microangiopathic hemolytic anemia and thrombocytopenia secondary to disseminated intravascular coagulation is a well-described complication of widely metastatic carcinoma. The authors report four cases of gastric carcinoma, one case of colon cancer, and one case of adenocarcinoma of unknown primary in which the patient developed a syndrome analogous to thrombotic thrombocytopenic purpura, consisting of microangiopathic hemolytic anemia, thrombocytopenia, and renal failure without definite evidence of disseminated intravascular coagulation. In contrast to previous reports, postmortem examination in three of the cases revealed no recurrence or only microscopic foci of residual tumor. In the remaining three, there was clinical and pathologic evidence of grossly disseminated carcinoma. Also in contrast to previous cases, all patients evidenced azotemia and proteinuria at the onset of the syndrome and ultimately uremia was a contributing cause of death. Coagulation profiles showed prolonged thrombin times and elevated fibrin degradation products in four instances and did not distinguish the patients with grossly metastatic disease from those with no tumor or only microscopic residua. Circulating immune complexes containing carcinoembryonic antigen were found in the patient with metastatic colon carcinoma. The syndrome was clinically identical whether or not grossly metastatic tumor was present, and it should not be attributed to advanced disease without definite clinical or pathologic evidence of a recurrence.
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PMID:Microangiopathic hemolytic anemia, thrombocytopenia, and renal failure in patients treated for adenocarcinoma. 728 73

We describe a patient with POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin changes) who was found to have renal involvement with particular renal pathological findings. So far, 17 other cases, most of them from Japan, of POEMS syndrome with renal involvement, have been published. Clinical features are variable: acute renal failure with anasarca or moderate chronic renal insufficiency with mild proteinuria. This latter presentation often passes unnoticed. There is no severe hypertension, no microangiopathic hemolytic anemia. Renal biopsy shows prominent glomerular changes which are unusual and distinct from membranoproliferative glomerulonephritis (MPGN) and from glomerular thrombotic microangiopathy (TMA). Mesangial proliferation and thickening of the capillary wall with double contour on light microscopy suggest an MPGN. By immunofluorescent microscopy, no immunoglobulins or complement deposits were found. The occurrence of mesangiolytic lesions has led to the term of "mesangiolytic glomerulonephritis". The presence, on electron microscopy, of lucent subendothelial spaces could indicate TMA. But there are neither thrombi nor arteriolar changes. We are inclined to consider that the microangiopathic lesions are due to chronic injury of glomerular endothelial cells, exacerbated at outbreaks of the disease. Increased production of IL 6 could support the efficacy of corticosteroid therapy, particularly in acute clinical situations.
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PMID:Renal involvement in POEMS syndrome. 763 52

A 34-year-old female patient was admitted to our hospital with a 1-year history of chronic congestive heart failure, massive proteinuria and tibial edema. On admission, she presented with hemolytic anemia, hepatomegaly, splenomegaly and renal impairment. Furthermore, the skin of her face, hand, forearm, lower extremities showed crust and bulla. Laboratory examination revealed a large amount of protoporphyrin in her blood and feces, but no increase in urine. Light microscopy of renal biopsy showed moderate chronic tubulointerstitinal disease and mild proliferation of mesangial cells. The prophyians are a group of compounds associated with involving the disturbance of various biosynthetic heme pathwas. Until now, the regulation of porphyrin and heme metabolism in the kidney have received relatively little attention as compared with those in liver and erythropoietic tissue. However, some recent reports have confirmed that proximal tubular cells may contribute to heme biosynthesis. It was strongly suggested that chronic tubulointerstitinal injury in this case might be directly induced by the disturbance of the biosynthetic heme pathway in the tubules.
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PMID:[A case of erythropoietic protoporphyria associated with tubulointerstitial disease and dilated cardiomyopathy]. 773 Nov 9


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