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)

Adult-onset osteomalacia with multiple renal tubular defects and generalized aminoaciduria is uncommon, and where familial it is characteristically an autosomal recessive disorder. This paper describes a kindred in which the syndrome has appeared in four successive generations, apparently inherited in a dominant manner, and possibly associated with diabetes mellitus. The proposita had hypophosphataemia, renal glycosuria, proteinuria and generalized aminoaciduria, and at the age of 22 developed symptoms of osteomalacia which responded to treatment with oral phosphate. Her father had been similarly affected: renal glycosuria was first noted when he was 24, and 12 years later he developed diabetes mellitus from which he died. One sister, aged 31, has renal glycosuria, aminoaciduria and hypophosphataemia without bone disease. In the three preceding generations at least seven other individuals had crippling bone disease and profound muscle weakness of early adult onset; in four, preterminal polydipsia was recorded, and others had renal glycosuria or diabetes mellitus. Three of the five children in the latest generation have slight proteinuria but not other detectable abnormality. The possible association between these renal tubular defects and diabetes mellitus is discussed.
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PMID:Hypophosphataemic osteomalacia and Fanconi syndrome of adult onset with dominant inheritance. Possible relationship with diabetes mellitus. 94 41

Twenty-two young cows died or were euthanatized after intoxication associated with ingestion of redroot pigweed (Amaranthus retroflexus) growing in marginal grass pasture. After several days of weakness and posterior incoordination, the cattle became recumbent but remained alert. Pertinent clinical laboratory findings included increased blood urea nitrogen content and marked proteinuria. At necropsy, perirenal edema and toxic tubular neprosis were seen.
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PMID:Perirenal edema and toxic nephrosis in cattle, associated with ingestion of pigweed. 118 28

Acetazolamide is a useful prophylactic for acute mountain sickness causing marked reduction in headache, nausea, vomiting, weakness, etc. Improvements correlate with increased arterial oxygen concentrations, reduction in proteinuria and peripheral oedema and other objective measures of acute mountain sickness. Evidence that Acetazolamide is beneficial for pulmonary oedema or cerebral oedema is scanty because of the lower frequency of these severe forms of mountain sickness. Dexamethasone, used prophylactically, also reduces the symptoms of acute mountain sickness partly due to its euphoric effect. Use of Acetazolamide as a treatment for established acute mountain sickness has been investigated. Large doses of Acetazolamide increase arterial oxygen levels over a few hours and this leads to a reduction of symptoms but data is limited and faster acting carbonic anhydrides inhibitors such as Methazolamide may be preferable in an emergency situation. There is no comparison of the effectiveness of Acetazolamide with other drugs used for treating acute mountain sickness such as steroids and calcium channel blocking drugs. Also, there is no data on drug combinations which could have additive effects and thereby be more beneficial than individual drugs.
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PMID:Acetazolamide and high altitude diseases. 148 96

This paper describes the clinical symptoms and signs of Balkan endemic nephropathy (BEN). The initial asymptomatic period followed by weakness and lassitude during renal insufficiency is emphasized. Non-characteristic lumbar pain may be present and episodes of macrohaematuria may occur. There is no fever, no severe dysuria, and no general disease preceding the symptoms. No oedema of the nephrotic type is recognized. Working capacity is unaffected until the late stage of the disease. In the advanced stages pallor of the skin and xantochromia of palms and soles are noticeable. Blood pressure is normal, but in the advanced phase may be elevated. In the uraemic phase a full uraemic syndrome is found. Urothelial tumours are frequent, occurring in 2-47% of cases; tumour cells may be found in the urine. Proteinuria of tubular type may be found early; in the uraemic phase it is constant. In the urinary sediment there are scarce white and red blood cells (the latter episodically abundant). Bacteriuria is present in about 20% of women patients. Glucosuria (less than 10%) and aminoaciduria (less than 10%) have been reported. In the early stages of BEN the urine concentration capacity is impaired earlier than renal blood flow and glomerular filtration rate. Enzymuria is present in the early phases. Tamm-Horsfall protein may be increased in the urine. Normo- or hypochromic normocytic hyporegenerative anaemia is a frequent finding. Bone marrow and leucocytes are normal. Serum proteins and immunoglobulins are not altered. Complement is normal; anti-glomerular basal membrane and anti-tubular basal membrane are negative. On radiography, kidney size varies from normal to the size of a small contracted kidney. The clinical picture of the disease is that of a slowly progressing tubulo-interstitial chronic nephritis.
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PMID:Clinical features of Balkan endemic nephropathy. 161 41

The present communication describes a 22 year-old male with clinical, biochemical and histopathological signs of Fabry's disease (FD). This is the second case of FD reported in Mexico. The main clinical manifestations of this patient were during puberty: intermittent weakness, acroparesthesias and hypohidrosis. At age 21 he developed heavy proteinuria (7-12 g/day) systemic hypertension and moderate renal failure. The kidney biopsy showed the typical alterations described in FD. On light microscopy, the renal pathology showed numerous vacuolated epithelial cells in the glomerular wall, giving them a "foamy" appearance; vacuolization was due to the presence of lipid material within these cells and in the interstitium. In electron microscopy, dense, irregularly shaped osmiophilic, laminated bodies with myelinlike configuration, were seen within the glomerular epithelial cells and in the urinary spaces. The low alfa-galactosidase activity in serum (0.18 nmol/h/mL normal values: 12.8) confirmed the diagnosis. Our findings in this case indicate that patients with FD may start with renal symptoms alone, which were full blown nephrotic syndrome, hypertension and moderate renal failure.
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PMID:[Nephropathy in a case of Fabry's disease]. 166 22

The patient was a left handed 25-year-old man who had worked in a vinyl chloride resin factory since July 1987 using lead stearate as a stabilizer. During the two years preceding hospitalization, he had been admitted three times for colicky abdominal pain with constipation and nausea. Anemia and proteinuria without causative diseases were pointed out. Because of progressive muscle weakness of hands which began since January 1989, he was admitted to our neurologic clinic on October 2 1989. Neurological examination showed severe atrophy of both small hand muscles without sensory disturbances. Left hand was predominantly affected, especially in interossei muscles. Laboratory findings are as follows; RBC 3.25 million/cu.mm: Hb 9.7 g/dl:blood lead concentration 100 micrograms/dl: urinary coproporphyrin 4503 micrograms/l: urinary delta-ALA 138 mg/l: and urinary lead excretion after 1 g CaEDTA infusion: 3938 micrograms/day. Electromyography of extensor carpi radialis, flexor carpi ulnaris and opponens showed increased polyphasic, long duration MUPs. Electromyography of dorsal interossei showed fibrillation. Nerve conduction study showed mildly decreased motor and sensory conduction velocities and markedly reduced amplitude of compound muscle action potentials (CAMPs). Investigation by inching method revealed conduction block of left ulnar nerve across elbow. After CaEDTA chelating therapy, 1 g once a week, steady improvement of muscular weakness was observed within a few months. Serial nerve condition studies revealed constant recovery of nerve conduction velocities, amplitude of CMAPs and diminution of conduction block across the left elbow. Conduction block across left elbow without sensory disturbances implies that subclinical cubital tunnel syndrome might have existed in this patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of lead neuropathy--importance of subclinical entrapment of nerves in lead neuropathy]. 178 56

A 13-year-old boy was admitted to this hospital for evaluation of pitting edema of both legs. Three years ago, he had been diagnosed to have nephrotic syndrome. Two and half years ago, because of persistent heavy proteinuria, poor response to steroids and frequent relapse of disease, a renal biopsy was done; characteristics of IgM nephropathy was shown. About a year previously, the patient felt dizziness and weakness of the left side of his body upon awakening one morning. Neurologic examination showed loss of muscle tone, muscle power and deep tendon reflexes. Sensory and cranial nerve function were intact. Blood pressure was normal. The CT scan of brain showed a patch of low attenuation area in the right temporal region, obliteration of the right cortical sulci and mild compression of right lateral ventricle. A diagnosis of nephrotic syndrome with right cerebral infarction was made. The patient's condition became stable two days later after mannitol infusion, correction of electrolytes, and supportive therapy. According to literature, most cases of nephrotic syndrome complicate with renal thrombosis, pulmonary emboli, and deep vein thrombosis. Few cases complicate with cerebral thrombosis and infarction. If patient have low plasma albumin and anti-thrombin III level, hyperfunction of platelet aggregability and use long-term diuretic therapy, they may be at higher risk of thromboembolic complications. If thromboembolic complications exist, anticoagulation treatment should be instituted. Prophylactic therapy with aspirin or dicumarol is not currently recommended.
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PMID:[Nephrotic syndrome complicated with cerebral infarction: report of one case]. 182 17

The presented material consists of 9 postoperative patients' investigations. Interstitial nephritis was diagnosed in them after histological examination. Seven patients had a chronic disease, 2--acute disease. The revealed possible predisposing factors were: a prolonged use of analgetics, contact with formalin and typographical dyes, systematic alcohol usage, frequent catarrhal diseases with long-term fever, a history of acute renal destructive process. The clinical picture of patients with chronic interstitial nephritis was characterized by long periods of temperature elevation, small changes in blood counts, weakness, pain in the lumbar region. In urine analyses: moderate microhematuria, leukocyturia, proteinuria. There were signs of early damaged renal tubular functions. Antiinflammatory therapy was ineffective so the patients were operated on for various indications. During the operations there were severe macroscopic renal cirrhotic deteriorations. 2 patients underwent nephrectomy, 15 intraoperative biopsy. Histologically there were revealed: signs of interstitial tissue various cirrhotic changes in hydrops and lymphoplasmacytic infiltration with tubular compression and dystrophic changes. The following complex therapy including nonsteroid antiinflammatory agents, in some cases corticosteroids, desensitizing and antihistaminic remedy allowed one to achieve alleviation of the process.
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PMID:[Interstitial nephritis in urological practice]. 187 26

We report a case of Castleman's disease of multifocal plasma-cell type revealed by a severe general weakness, associated to a nephrotic syndrome with renal failure. The characteristic aspects of lymphoid hyperplasia with hyalinization of follicles and interfollicular vascular proliferation were observed in mesenteric lymph nodes, the spleen was involved by an infarcted localisation of Castleman's disease. The glomerular lesions were consistent with a proliferative mesangial glomerulonephritis. The removal of the spleen and of the mesenteric nodes involved by the disease, associated with a steroid course was curative. The nephrotic syndrome appears to be etiologically related to the presence of the Castleman's tumor. The removal of the tumor relieves the proteinuria and the renal failure as in other cases reported in the literature.
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PMID:[Castleman's disease and glomerular nephropathy (apropos of 1 case]. 269 15

Eighteen patients with solid tumours were treated with human recombinant interferon-gamma at escalating dose levels starting at 1 X 10(6) units/m2 per infusion and rising through 3 X 10(6), 6 X 10(6), 9 X 10(6) and 22 X 10(6) to a maximum of 110 X 10(6) units/m2 per infusion. The IV infusions were given three times a week over a 4-week period. Side effects were seen in all patients, but were mild except at the highest dose. Acute dose-related effects included pyrexia, tiredness, thirst, chills and rigors. Chronic dose-related effects included anorexia, lethargy, weakness, disorientation, a trace of proteinuria and minimal rises in liver enzymes. In addition, effects were observed which were not related to dose. These included headache, nausea and vomiting, backache, myalgia, flatulence and a mild, transient reduction in neutrophils and erythrocytes. At the highest dose level dose-limiting toxicity was observed, consisting in severe tiredness and anorexia, hypotension, disorientation and changes on the electrocardiograph. Overall, toxicity was similar to that seen with preparations of interferon-alpha, except that no tolerance to the effects of interferon-gamma was noted. We observed less hepatic and haematological toxicity, but also recorded flatulence, handcramps and electrocardiograph changes, which have not been reported with interferon-alpha. When given according to this regimen, doses of 22 X 10(6) units/m2 per infusion of recombinant interferon-gamma were generally well tolerated by the patients.
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PMID:A toxicity study of recombinant interferon-gamma given by intravenous infusion to patients with advanced cancer. 309 8


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