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 5-year-old mixed breed dog was presented with a history of depression and anorexia. Physical examination revealed a pharyngeal tumour and a neurological examination indicated the presence of a possible space-occupying lesion in the brain. Investigative procedures included a bloodsmear, impression smears and cytology of the pharyngeal tumour, haematology, chemical pathology, faecal analysis, urinalysis, electrocardiography, cerebrospinal fluid analysis, hormone assays and a computerised axial tomography scan. Results of these investigations revealed a round cell tumour in the pharynx, hypergammaglobulinaemia (34 g l-1), azotaemia (urea 8.6 mmol l-1 and creatinine 170 mumol l-1), hypoalbuminaemia (20 g l-1), proteinuria, sinus bradycardia (heart rate 60 beats per min), increased concentration of protein in the CSF (1.1 g l-1), hypoadrenocorticism (base line cortisol less than 55 nmol l-1) and hypothyroidism (T4 less than 13 nmol l-1). The computerised axial tomography scan revealed a brain tumour in the region of the hypophysis. The dog was euthanased and a post mortem examination confirmed the presence of a pharyngeal tumour with apparent direct extension of the tumour into the brain. Both tumours were confirmed histologically as mastocytomas.
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PMID:An expansile secondary hypophyseal mastocytoma in a dog. 251 66

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

A case of alpha-fetoprotein (AFP) producing primary intracranial embryonal carcinoma was reported with special reference to the chemotherapy. The patient was a 14-year-old male who had suffered from vomiting and disturbance of consciousness. CT scan revealed a tumor originating in the anterior part of the third ventricle and expanding into both lateral ventricles. Right frontotemporal craniotomy was performed and the tumor was totally removed under the microscope. The histological diagnosis was embryonal carcinoma. Inspite of the elevated amount of AFP in the serum, we could not verify the yolk sac element in the surgical specimen. Three months later, he became drowsy and another CT scan revealed recurrence of the tumor. Ommaya's reservoir was placed and CSF was drained to control the intracranial hypertension. But the disturbance of consciousness did not improve. We then started a combination chemotherapy with cis-platinum, vinblastine and bleomycin. Cis-platinum was given in a dosage of 20 mg/m2 body surface area as a 15 min. intravenous infusion for 5 consecutive days every 3 weeks for three courses. Vinblastine was given in a dosage of 0.4 mg/kg body weight intravenously for 2 consecutive days every 3 weeks for three courses. Bleomycin was given in a dosage of 30 mg intravenously 6 hours after vinblastine weekly for a total of 12 weeks. The AFP level of the serum and CSF was monitored every several days. After the chemotherapy, the AFP level of the serum and CSF decreased. Repeated CT scan revealed no evidence of tumor. His clinical condition improved remarkably. Toxicity was vomiting, proteinuria and leukopenia, but not so severe. Proteinuria continued after the chemotherapy, but BUN and creatinine did not elevate. It was emphasized that the combination chemotherapy with cis-platinum, vinblastine and bleomycin is effective remission-induction treatment for AFP producing primary intracranial embryonal carcinoma.
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PMID:[A case of alpha-fetoprotein producing primary intracranial embryonal carcinoma treated with combination chemotherapy with cis-platinum, vinblastine and bleomycin (author's transl)]. 616 18

Five patients aged 1.1 - 4.3 years, affected by nephritis secondary to infection of ventriculo-atrial shunt are presented. The time lag between the occurrence of shunt infection and diagnosis of nephropathy varied from 1 to 12 months. In four patients "Staphylococcus epidermidis" was isolated from blood and CSF cultures, and "Staphylococcus aureus" in another one. Renal lesion presented as hematuria and proteinuria, and two patients developed a nephrotic syndrome. Hypertension was present in three patients. C'2 and D'4 hypocomplementemia was a constant feature in the acute stage of the disease. Endocapillary glomerulonephritis was observed in three patients and endo-extracapillary glomerulonephritis in one (70% of crescent formations). After shunt removal and antibiotic administration a favorable clinical course was followed in three patients, with remission of nephropathy signs. The fifth patient (non biopsied) died in the course of a septic process, having kept until then a good renal function.
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PMID:[Shunt nephritis (author's transl)]. 621 Nov 17

A patient with multiple myeloma was initially seen with Bence Jones-type kappa proteinemia and intermittent Bence Jones proteinuria. In the late stage of the disease, involvement of the CNS was observed, and abnormal plasma cells were found in the CSF. Chromosomal analysis of these plasma cells showed an accessory chromosome in the A2 group and an abnormal chromosome in the D13 group. In addition to Bence Jones-type kappa protein similar to that in the serum, the CSF contained IgA-kappa M component. Immunoquantitation detected 250 mg/dL of IgA in the CSF and only 33 mg/dL in the serum. T our knowledge, such discordance of M components has never been described before.
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PMID:Multiple myeloma with discordant M components in the serum and CSF. 679 5

We describe a patient with acute myeloblastic leukemia (AML) who developed nephrotic syndrome after receiving several courses of chemotherapy, including macrophage-colony-stimulating factor (M-CSF). At the onset of nephrotic syndrome, the patient remained in a hematological remission. A renal biopsy showed diffuse mesangial proliferation with marked glomerular infiltration of macrophages and massive subendothelial and mesangial deposits. After the institution of the combined therapy with corticosteroid, anticoagulant, and dipyridamole, urinary protein excretion was attenuated to less than 1.0 g/day. It should be emphasized that the recurrence of nephrotic syndrome was observed after the following chemotherapy, including M-CSF, whereas the bone marrow still remained completely remitted. In contrast, after the last course of chemotherapy, which did not include M-CSF, urinary protein excretion was not enhanced. Of note is that the renal histology at autopsy showed a remarkable improvement of mesangial hypercellularity with concomitant reduction in the number of glomerular macrophages. These evolutional changes in both proteinuria and glomerular histology suggest a close linkage between the M-CSF treatment and macrophage-related glomerular injury. The possibility can be raised that M-CSF accelerated the underlying renal disease in this case through enhancing macrophage accumulation into the glomerulus, leading to the development of nephrotic syndrome.
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PMID:Development of nephrotic syndrome in a patient with acute myeloblastic leukemia after treatment with macrophage-colony-stimulating factor. 865 Dec 54

DOCA-NaCl treatment causes hypertension, accelerates development of proteinuria, and leads to glomerulosclerosis in rats with autoimmune Heymann nephritis. To study the mechanisms of kidney injury induced by renal haemodynamic load in chronic nephritis, we studied by immunohistochemistry the local expression of various cytokines, growth factors and adhesion molecules in the kidneys of Heymann nephritic rats with or without DOCA-NaCl-induced hypertension. The DOCA-NaCl-nephritis group developed hypertension and marked renal enlargement as compared with the nephritis group, the DOCA-NaCl group, and the controls. Albuminuria appeared earlier and was heavier in the DOCA-NaCl-nephritis group compared with the nephritic rats without DOCA-NaCl. Expression of IL-6, TNF-alpha, GM-CSF, b-FGF, NGF, TGF-beta, and ICAM-1 was enhanced in the kidneys of the DOCA-NaCl-nephritis group as compared with other groups, localized mainly in the glomerular mesangium (IL-6, GM-CSF, TGF-beta), glomerular and peritubular endothelium (ICAM-1), and collecting ducts (TNF-alpha, b-FGF, NGF, TGF-beta), possibly associated with the observed tubulointerstitial mononuclear cellular infiltration. Thus in autoimmune Heymann nephritis, DOCA-NaCl treatment causes hypertension and increased renal mass together with upregulation of local cytokine and growth factor production, which may further aggravate hypertension and accelerate progression of renal damage.
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PMID:Increased renal expression of cytokines and growth factors induced by DOCA-NaCl treatment in Heymann nephritis. 880 10

In this study, we examined the effects of macrophage-colony stimulating factor (M-CSF) on glomerular macrophages in lipopolysaccharide (LPS)-induced murine nephritis. Mice injected intraperitoneally with either M-CSF plus LPS, LPS alone, M-CSF alone or saline every day for 8 days were examined for the degree of urine albumin excretion and lymphocyte-function associated antigen-1-positive (LFA-1+) cells in peripheral blood as well as renal pathology. From our results, LPS or M-CSF combined with LPS emphasized the degree of proteinuria, glomerular deposition of immunoglobulins and mesangial proliferation, associated with accumulation of macrophages in the glomeruli. However, in immunohistological examination of kidneys from these nephritic mice, neither intercellular adhesion molecule-1 (ICAM-1), which may play an important role in the recruitment of macrophages into glomeruli, M-CSF receptor nor the number of LFA-1+ cells in peripheral blood was enhanced by M-CSF. On the other hand, M-CSF alone induced neither proteinuria nor any pathological changes and did not increase the number of glomerular Mac-1+ cells above that in saline-treated controls. These results indicate that M-CSF does not directly cause glomerulonephritis but might participate in accelerating the glomerular inflammatory process by stimulating a potent chemoattractant to recruit monocytes-macrophages into the glomeruli.
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PMID:Macrophage-colony stimulating factor (M-CSF) enhances proteinuria and recruitment of macrophages into the glomerulus in experimental murine nephritis. 891 75

We examined the circulating levels of the proinflammatory cytokines tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 alpha, IL-6, granulocyte macrophage-colony stimulating factor (GM-CSF), and the anti-inflammatory cytokine IL-10, and their expression in kidneys acutely infected with murine malaria parasite P. berghei ANKA in C57BL/6J mice. Groups of six mice sacrificed on days 5, 10, 15, and 20, and normal controls were used for cytokine analysis. High concentrations of TNF-alpha and IL-10 were detected in plasma as shown by ELISA, and elevated levels of mRNA specific for TNF-alpha and IL-10 in infected kidneys were demonstrated by reverse transcription-polymerase chain reaction (RT-PCR) analysis. Kidney sections stained with antibodies against TNF-alpha, IL-1 alpha, IL-6, GM-CSF and IL-10 for immunohistochemistry showed markedly enhanced staining for TNF-alpha, and progressively increased staining for IL-1 alpha and IL-6 both in the tubules and the walls of arteries during the course of infection. The endothelia of blood vessels and inflammatory cells located around small arteries showed positive staining for GM-CSF from day 10 onwards. Unlike the staining for proinflammatory cytokines, the anti-inflammatory cytokine IL-10 showed strongly positive staining in normal tubules and walls of arteries, especially in the brush border of proximal tubules, but the staining intensity decreased dramatically after day 15 post-infection. A strongly positive correlation was found between the antibody staining for TNF-alpha/IL-1 alpha in tubules, and the severity of proteinuria. In contrast, there was an inverse correlation between the staining for IL-10 with TNF-alpha/IL-1 alpha, and the degree of proteinuria. Plenty of pigmented macrophages showed positive staining both for proinflammatory and anti-inflammatory cytokines in the tubulointerstitium. Our findings imply that the up-regulation of proinflammatory cytokines and the dysregulation of anti-inflammatory cytokines are involved in the pathogenesis of tubulointerstitial nephritis associated with malaria.
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PMID:Dysregulation of cytokine expression in tubulointerstitial nephritis associated with murine malaria. 955 90

Malaria infections often cause glomerulonephritis (GN), and multiple factors have been implicated in the pathogenesis of glomerular injury. The role of cytokines in malaria associated glomerulonephritis has not been clearly defined. To study the importance of cytokines in malarial nephritis, we investigated the expression of tumour necrosis factor-alpha (TNF-alpha), interleukin-1alpha (IL-1alpha), IL-6, IL-10 and granulocyte macrophage-colony stimulating factor (GM-CSF) in kidneys acutely infected with murine malaria parasite Plasmodium berghei ANKA in C57BL/6 J mice. Groups of six mice sacrificed on days 5, 8-10, 15, and 20 postinfection, and normal controls were used for cytokine analysis. Elevated levels of messenger RNA (mRNA) specific for these cytokines in infected kidneys after day 5 postinfection were demonstrated by reverse transcription-polymerase chain reaction (RT-PCR) analysis. Kidney sections stained with specific antibodies against TNF-alpha, IL-1alpha, IL-6, IL-10 and GM-CSF by immunohistochemistry showed that the staining for these cytokines on the glomeruli was positive from day 10 postinfection, and increased progressively, mainly in the infiltrating macrophages and the glomerular mesangium. Strong correlation was found between the expression of TNF-alpha with IL-6, and IL-1alpha with IL-6. The expression of TNF-alpha, IL-1alpha, IL-6, and IL-10 also strongly correlated with the severity of proteinuria. Our findings show that there is up-regulation of cytokines in the pathogenesis of glomerulonephritis associated with murine malaria infection.
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PMID:Up-regulation of cytokines in glomerulonephritis associated with murine malaria infection. 1046 63


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