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)

Fourty four patients suffering non traumatic rhabdomyolysis (RM) are studied. The most frequently encountered etiologies were neurologic abnormalities in 26 patients, followed by infections in 7 patients and metabolic abnormalities in four cases. Eleven patients (25%) presented several associated factors. The clinical manifestations of RM were not very significant, with only 18% of patients presenting muscle pain, 38.6% proteinuria and 36.4% hematuria. A significant increase in K, CPK, LDH, and ASAT values was observed after the RM episode (p less than 0.05). Those patients with an infectious RM were older (p less than 0.05) and presented higher urea (p less than 0.01) and creatinine (p less than 0.05) values. Only two patients presented renal failure. One patient with septic shock died. RM is a relatively common condition, often secondary to multiple systemic processes, which can go unnoticed due to the underlying disease.
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PMID:[Acute rhabdomyolysis. A study of 44 cases]. 227 Mar 37

A 73-year-old male was admitted to our hospital in October 1987 because of severe anemia, anorexia, and loss of weight. The hemoglobin level was 5.7 g/dl, the white blood cell count 2,500/microliters with 5% myeloblasts positive for peroxidase, and the platelet count 8.6 x 10(4)/microliters. The LDH was 656 mU/ml, the total protein in the serum 7.4 g/dl, IgG 419 mg/dl, IgA 104 mg/dl, IgM 10 mg/dl, and urine Bence Jones (BJ) protein 8.8 g/day. The X-ray survey of the bones showed multiple osteolytic lesions. A bone marrow aspirate was hypercellular with 91.4% plasma cells, and was cultured a whole day for chromosome study. It revealed an abnormal karyotype of 46, XY, -15, t(6; 14) (p21.1; q32.3), +der(15)t(1; 15) (q23; q24). Immunoelectrophoresis demonstrated lambda type BJ protein. He was treated with melphalan and prednisolone. Proteinuria and marrow plasma cells decreased in amount. In December a white cell count was 6,030/microliters with 80% myeloblasts. A bone marrow aspirate revealed an increase of 82.6% myeloblasts or promyelocytes. The patient was refractory to chemotherapy and died of sepsis in April 1988. An unrelated abnormal karyotype; 48, XY, +8, +13 appeared concomitant with an increase of the leukemic cells, but no cells showed the t(6; 14). We cytogenetically discussed the simultaneous presence of multiple myeloma with acute myelogenous leukemia.
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PMID:[Acute myelogenous leukemia (M2) simultaneously associated with multiple myeloma with special reference to chromosome abnormality of t(6; 14) (p21.1; q32.3)]. 236 41

A 6-year-old girl with cerebral palsy developed conscious disturbance and generalized convulsion after one-hour hot herb drug bath. Physical examination on admission revealed rectal temperature 41 degrees C, hot skin, respiration 46/min, regular heart beat 98/min, BP 130/60 mmHg, Glascow coma scale 4 (E2M1V1), soft and flat abdomen, no hepatosplenomegaly, no skin rash, no focal neurological sign, increased generalized muscle ton. Laboratory data showed CBC: WBC 20400 cumm (Neutrophils 31%, Lymphocytes 69%), Hb 11.6gm%, ESR 11 mm/hr, arterial blood gas: PH 7.077, PO2 43mmHg, PCO2 57.1mmHg, HCO3- 16 mEq/L, BE-11.5mEq/L, serum sodium 143 mEq./L, potassium 5.2 mEq/L, chloride 101 mEq/L, free calcium ion 3.8mg%, GOT 63IU/L, GPT 263 IU/L, amylase 193 IU/L, alkaline phosphatase 388 IU/L, LDH 1245 IU/L, CPK 677 IU/L, total bilirubin 0.8 mg/dl, direct type 0.1 mg/dl, BUN 18 mg/dl, Glucose 35 mg/dl. Urinalysis revealed proteinuria( ) trace hematuria and pyuria, but no cast. Lumbar puncture is within normal limits. Bacteriology including blood and CSF are normal. Multiple organ failure was noted at that time. Intensive cooling methods were performed including central and peripheral cooling. We used luminal and valium to control the seizure. Condition didn't improve. Afterwards cardiopulmonary arrest developed. Patient expired 8 hours after admission despite of resuscitation. Heat stroke in infancy and childhood is different from that in adulthood. The predisposing factors are high ambient temperature, dehydration, very young baby, sweat gland dysfunction, or ectodermal dysplasia. Definition of heat stroke includes 1) rectal temperature above 41 degrees C, 2) behavioral change, 3) warm skin, wet or dry.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Status epilepticus induced by prolonged immersion in hot herb bath: report of one case]. 263 19

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

Pretreatment with nickel has earlier been shown to protect against cadmium intoxication. The effect of cadmium pretreatment on the nephro- and hepatotoxicity of nickel has been investigated. The administration of cadmium (6 mg/kg, i.m., once) to rats significantly enhanced urinary excretion of ALP, LDH, GOT, amino acids and proteins and increased the activity of serum ALP, GOT, and GPT, while the administration of nickel (6 mg/kg, i.p., 3 days) altered these parameters less significantly. These changes in urine and serum were used as a measure of renal and hepatic damage. The administration of nickel for three days, one week after cadmium treatment, caused significantly more marked enzymuria, aminoaciduria, proteinuria and an increase in the activity of serum enzymes than induced by either of them individually. However, cadmium pretreatment had no influence on urinary excretion or hepatic uptake of nickel, but increased renal uptake of nickel on the fourth day. The results suggest that cadmium enhances the nephro- and hepatotoxicity of nickel.
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PMID:Effect of cadmium pretreatment on nickel toxicity. 653 85

The effects on the neonate of severe maternal hypertension originating before the thirty-sixth week of gestation were determined by comparing data obtained on 28 preterm infants born of hypertensive mothers with data from 28 gestational age-matched controls. All hypertensive mothers had diastolic blood pressure greater than or equal to 110 mm Hg, proteinuria, and systemic symptoms of their disease; over half had thrombocytopenia and significant elevations of LDH and SGOT. All hypertensive mothers had been treated intravenously with magnesium sulfate, and 79% received other antihypertensive agents. When compared to control infants, the infants of hypertensive mothers had a significantly higher incidence of somatic growth retardation, microcephaly, thrombocytopenia, leukopenia, neutropenia, low Apgar scores, delayed adaptation, patent ductus arteriosus, hypotonia, and gastrointestinal hypomotility. Apgar scores, platelet count, WBC count, neutrophil count, and weight percentile correlated with the severity of maternal platelet and enzyme abnormalities. The occurrence of gastrointestinal hypomotility, hypotonia, and patent ductus arteriosus may be related to transplacental passage of maternally administered drugs.
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PMID:Neonatal manifestations of severe maternal hypertension occurring before the thirty-sixth week of pregnancy. 705 37

Abnormal myoglobinemia (above 77 microgram/l) and free hemoglobin in plasma were found in 16 runners and in nine non runners immediately following distance running. The same abnormalities were found iun six elite rowers following rowing. In parallel with the rise in myoglobin and free hemoglobin a rise was found in serum concentrations of cellular enzymes (LDH, CK, ASAT, alkaline phosphatase) and of various metabolites. We found no proteinuria nor casts in the urine. Non runners had a higher rise in serum myoglobin than runners. Competitive running caused a rise in the serum concentration of the heart specific fraction of creatine kinase in seven of the nine (healthy) elite runners. The abnormal findings are only explainable on the basis of leakage of proteins from muscle cells to the circulation in otherwise healthy, well trained persons. Myoglobinemia and a transient rhabdomyolysis is a common phenomenon in long distance running, but evidently also occurs in distance rowing. Three months of running training prevented most of the muscle damage from relaxed jogging in the nine previous non runners. Neither the observed myoglobinemia nor the hemoglobinemia resulted in any significant loss of iron in the urine.
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PMID:Muscle cell leakage due to long distance training. 720 6

The nephrotoxicity, pharmacokinetic and therapeutic activity of fosfomycin were investigated in female wistar-rats. Measures of nephrotoxicity were urinary excretion of tubular cells and of the enzymes MDH, LDH, and GOT. Histological investigations and estimation of serum urea concentration and proteinuria were also evaluated. The doses of 500, 1000, 2000, 3000, and 5000 mg/kg/d were administered in 9 single doses with 12 hours interval. The lowest dose which induced a significantly increased tubular cell excretion was 1000 mg/kg/d and therefore in the same range as the tubulotoxic threshold doses of cephalosporins. Chemotherapy of the chronic estrogen induced pyelonephritis revealed equally favourable results for fosfomycin and cefuroxim at dosages of 2 X 150 mg/kg/d. The pharmacokinetics of fosfomycin at a single dose of 150 mg/kg/d were equivalent to those of cefuroxim. These animal experiments showed fosfomycin to be of value as a therapeutic alternative to cephalosporin antibiotics.
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PMID:[Fosfomycin: animal experiments on nephrotoxicity, pharmacokinetics and therapeutic efficacy (author's transl)]. 746 97

Following experimental rhabdomyolysis, animals become resistant to heme protein-induced acute renal failure (ARF). The goals of this study were to: (a) ascertain whether this resistance, previously documented only in vivo, is expressed directly at the proximal tubular cell level; (b) determine whether heme proteinuria (vs. other consequences of rhabdomyolysis) is its trigger; and (c) ascertain some of its subcellular determinants. Rats were injected with a borderline toxic dose of glycerol and 24 hours later proximal tubular segments (PTS) were isolated for study. Their vulnerability to diverse forms of injury (FeSO4-induced oxidant stress, hypoxia, Ca2+ ionophore, cytochalasin D, PLA2) was compared to that found in normal PTS. Post-glycerol PTS manifested significant resistance to each insult (decreased lactate dehydrogenase +/- N-acetyl-beta-D-glucosaminidase release). Protection against FeSO4 was virtually complete and it was associated with a 50% decrease in membrane lipid peroxidation. No decrease in hydroxyl radical generation was noted during the FeSO4 challenge (salicylate trap assessment), suggesting a primary increase in membrane resistance to attack. That PLA2 addition caused less deacylation, plasma membrane enzyme (alanine aminopeptidase) release, and LDH leakage from post-glycerol versus normal tubules supported this hypothesis. To test whether cytoresistance was specifically triggered by heme proteins (vs. being a non-specific filtered protein effect, or a result of endotoxin cascade activation), rats were injected with purified myoglobin, non-heme containing filterable proteins, or endotoxin. Only myoglobin induced cytoresistance. In vivo heme oxygenase inhibition (tin-protoporphyrin) did not block the emergence of cytoresistance and it was expressed despite Na,K-ATPase inhibition (ouabain) or cytoskeletal disruption (cytochalasin D). In vivo heat shock failed to protect. In conclusion, (1) rhabdomyolysis induces broad based proximal tubular cytoresistance; (2) heme proteinuria is its trigger; and (3) it is most easily explained by a primary increase in plasma membrane resistance to attack.
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PMID:Heme protein-induced tubular cytoresistance: expression at the plasma membrane level. 763 63

A twenty-one-year-old male was admitted to our hospital because of hypertension and proteinuria. He had felt general fatigue and low grade fever for one month. Blood pressure was 180/120 mmHg on admission. Laboratory findings showed 3+ proteinuria and 1+ occult blood in urinalysis; an accelerated erythrocyte sedimentation rate (ESR) of 39 mm/hr; elevation of LDH to 755 IU/l. Antinuclear antibody was positive with a titer of 1: 160, with a speckled pattern. Plasma renin activity and serum aldosterone were markedly elevated to 25.8 ng/ml/hr and 585.3 pg/ml, respectively. Renal function had declined mildly; endogenous creatinine clearance was 60 ml/min. Renal arteriogram demonstrated multiple intrarenal aneurysms in the bilateral kidneys. Aneurysms, 5-8 mm in diameter were located in the arteries from the interlobar to interlobular region. He was diagnosed as having polyarteritis nodosa (PN) and was then treated with 20 mg/day of prednisolone and monthly pulse therapy of cyclophosphamide. After steroid, cyclophosphamide and anti-hypertensive therapy, he became well and had normal blood pressure. The patient was considered a rare case of PN with multiple intrarenal aneurysms and accelerated hypertension. We discuss aneurysms in PN and accelerated or malignant hypertension documented in the literature.
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PMID:[A case of polyarteritis nodosa presenting with multiple intrarenal aneurysms and accelerated hypertension]. 769 55


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