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 7-year-old boy was referred to the children's hospital because of gross oedema and tiredness. Massive proteinuria was found and the condition was diagnosed as a childhood nephrotic syndrome. Concomitantly, pathologically low levels of serum alkaline phosphatase were recorded, and this, together with generalized osteoporosis and premature synostosis of cranial sutures, led to a second diagnosis: hypophosphatasia. The patient's family history further confirmed this condition of a heritable defect of metabolism. Dental inspection revealed very carious teeth with characteristically enlarged pulp chambers in molars. Histological examination of an extracted tooth revealed an unusually wide zone of predentine with some other dentinal irregularities. No cement layer was found. The skeletal age and exfoliation of primary teeth, however, were normal, unlike most reported cases of hypophosphatasia. The patient's renal disease was treated mainly with corticosteroids. There is no treatment for hypophosphatasia.
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PMID:Cranial manifestations of hypophosphatasia in childhood nephrotic syndrome. 643 Aug 33

The effect of nickel on cadmium nephro-toxicity and hepato-toxicity in rats was investigated. The administration of nickel (6 mg per kg, i.p., three days) or cadmium (6 mg per kg, i.m., once) significantly enhanced the urinary excretion of alkaline phosphatase (ALP), lactate dehydrogenase (LDH), glutamate oxaloacetate transaminase (GOT), amino acids, and proteins. In addition, it increased the activity of serum ALP, GOT, and glutamate pyruvate transaminase (GPT). These biochemical alterations in urine and serum were used as a measure of kidney and liver damage. Cadmium-induced enzymuria, proteinuria, amino aciduria and increase in the activity of serum enzymes were significantly less marked in animals pretreated with nickel than in controls. However, the accumulation of cadmium in kidneys and liver and its urinary excretion were unaffected by nickel pretreatment. The results suggest protection by nickel against cadmium nephro- and hepato-toxicity.
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PMID:Preventive effects of nickel on cadmium hepatotoxicity and nephrotoxicity. 647 83

I treated a patient who had amyloidosis with predominantly hepatic involvement and portal hypertension. The main clinical features were hepatomegaly, gross ascites, proteinuria, and elevated alkaline phosphatase levels. Despite permanganate-sensitive AA protein being present in the biopsy specimen, none of the recognized disease entities associated with secondary amyloidosis were found. A review of the literature and the mechanism of portal hypertension in amyloidosis is given. It is suggested that elevated portal pressures may be of greater importance in the pathogenesis of ascites in amyloidosis than has been appreciated.
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PMID:Hepatic amyloidosis. An unusual cause of ascites and portal hypertension. 649 30

Patients with the nephrotic syndrome and normal renal function have low levels of 25(OH)D in serum presumably due to the loss of this metabolite in the urine. Osteomalacia and hyperparathyroidism have been recently reported to occur as a consequence of those low levels of 25-hydroxyvitamin D (25OHD). We studied six patients (aged 26-52 yr) with the nephrotic syndrome (mean duration, 6.7 yr; range, 2-12 yr) and normal renal function, and evaluated their calcium, phosphorus, PTH, and vitamin D metabolite levels. Bone biopsies were obtained in all patients. The creatinine clearance ranged from 83-134 ml/min . 1.73 m2 of body surface, serum albumin was 2.65 +/- 0.42 (+/- SD) g/100 ml, and proteinuria ranged from 3.5-13.2 g/24 h. All patients had normal serum magnesium, phosphorus, ionized calcium, and alkaline phosphatase (total and bone fraction), and normal roentgenographic metabolic bone survey. Serum PTH, measured by the carboxy-terminal RIA, was 5.1 +/- 2.3 mu leq/ml (normal, 2-10), serum 250HD was 8.8 +/- 4.0 ng/ml (normal, 15-30), and 1,25-dihydroxyvitamin D3 was 38 +/- 25 pg/ml (normal, 17-58). Serum vitamin D-binding protein was 420 +/- 42 micrograms/ml (normal, 400-800). The histological appearance of bone biopsies obtained in these patients was not different from that in a group of sex- and age-matched controls. Specifically, there was no increase in the volume of osteoid (unmineralized bone), the percentage of trabecular surface covered by osteoid, or the number of osteoclasts. The cellular rate of mineralization was normal in all six patients. Thus, these data indicate that low serum levels of 250HD in patients with the nephrotic syndrome and normal renal function do not necessarily result in the development of osteomalacia and/or hyperparathyroidism.
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PMID:Absence of metabolic bone disease in adult patients with the nephrotic syndrome and normal renal function. 682 51

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

By means of immunonephelometry, determinations of a number of high molecular weight (HMW) and low molecular weight (LMW) proteins in urine and serum were undertaken in 42 consecutive patients, who had been subjected to jejuno-ileal bypass surgery for treatment of massive obesity two to six years before the study. Five patients demonstrated a distinct LWM proteinuira, ie excessive excretion of free-light lamdba and kappa chains of immunoglobulin and beta-2-microglobulin. The creatinine clearance was normal in four of these five patients. This LMW-proteinuria group differed from the remaining 37 patients in several respects. First, they had lost weight more effectively (P less than 0.01); secondly, they exhibited secondary hyperparathyroidism (P less than 0.05), increased levels of alkaline phosphatase and low serum concentrations of bicarbonate (P less than 0.001). It is suggested that LMW proteinuria may be a manifestation of secondary hyperparathyroidism.
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PMID:Tubular proteinuria following jejuno-ileal bypass surgery. 722 72

Anti-rat glomerular basement membrane (GBM) rabbit serum was produced by immunizing rabbits with the supernatant substance of trypsin-digested rat GBM. Nephritis was induced in rats by a single intravenous administration of 0.25 ml of anti-serum and changes in pathohistological and biochemical parameters during the process of the disease were investigated in comparison with those of Masugi nephritis and the modified type of Masugi nephritis previously reported. In light microscopic studies, histological changes seen in the kidneys closely resembled those of typical human glomerulonephritis. Changes such as hypercellularity, adhesion between capillary wall and Bowman's capsule, crescent formation and hyalinization in glomeruli and interstitial infiltration were the most pronounced on the 30th day after the anti-serum injection. In immunofluorescent studies, a linear fixation of rabbit IgG was observed along the GBM from the 1st day and the staining of a certain intensity was preserved throughout the experimental periods. A linear staining with anti-rat IgG serum was recognized from the 10th day. The fixation of fibrinogen was also seen in not only the glomerular capillary walls, but also in Bowman's space after the 10th day. Proteinuria significantly increased from the 1st day, reached a peak of 12 times the control level, and thereafter gradually decreased. The patterns of progress of urinary alkaline phosphatase and N-acetyl-beta-glucosaminidase activities were much the same as those seen in cases of proteinuria and the levels at their peak times were about 10 and 3 times control levels, respectively. Plasma urea nitrogen level transiently increased on the 5th day and then reverted to the control level by the 30th day. Plasma cholesterol levels were significantly high from the 5th to the 20th days. It is concluded that glomerular damages in this model are more severe, so-called, "nephritic type" and continue for longer periods than in cases of Masugi nephritis, however, do not differ in degree and duration from findings in the modified type of Masugi nephritis.
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PMID:[Pharmacological studies on experimental nephritic rats (11). Changes in pathohistological and biochemical parameters in anti-rat GBM rabbit serum-induced nephritis (author's transl)]. 728 45

An immunoblotting procedure for the sensitive detection of Bence Jones proteinuria following agarose gel electrophoresis was developed. After immunonephelometric determination of urinary kappa and lambda light chains [employing antisera to human kappa and lambda light chains (free + bound)], urine samples (diluted to 2.5 mg/l kappa and lambda light chains, respectively) were electrophoretically separated using the Paragon system and blotted by capillary diffusion onto nitrocellulose. Rabbit anti-human kappa and lambda light chains reacted to kappa and lambda light chains attached to the membrane. Goat anti-rabbit IgG alkaline phosphatase conjugate was employed as detection system. The detection limit of the immunoblotting procedure (monoclonal component, as determined by serial dilutions) was 0.3 mg/l urine. Among 65 urine specimens received for routine testing for Bence Jones proteinuria, 32 monoclonal components (in 20 urine samples) were found by immunoblotting compared with 10 monoclonal components (in 9 urine samples) detected by immunofixation. In only 5 out of these 65 urine samples a kappa/lambda ratio (as determined immunonephelometrically) < 1 or > 5.2 (decision limits for discriminating between monoclonal and polyclonal urinary light chains; Boege F, Koehler B, Liebermann F. Eur J Clin Chem Clin Biochem 1990; 28:37-42) was observed. In conclusion, the immunoblotting method is superior to both immunofixation and immunonephelometry with respect to the diagnostic sensitivity for detection of Bence Jones proteinuria.
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PMID:An immunoblotting procedure following agarose gel electrophoresis for detection of Bence Jones proteinuria compared with immunofixation and quantitative light chain determination. 760 25

Analysis of 2,547 cases of multiple myeloma (MM) reported in China in 1980s showed that the clinical manifestations are characterized by multipliey. High misdiagnosis rate (69%) and multiple complications. While the monoclonal protein had more than 25 immunological type, IgG myeloma was the commonest (43.1%). Light chain subgroup trended to have higher incidence of renal damage (76.9%). Plasma cell leukemia eventually developed in 30 cases. In order to improve diagnosis and avoid misdiagnosis, the key points are 1, to better the recognition of clinical features of MM. 2. patient should receive urine Bence-Jones protein, immunoglobulins, immunoeletrophresis, bone X-ray and multiple site bone marrow puncture whenever one of such manifestations as unexplained anemia, skeletal pain, proteinuria, elevation of ESR, hyperviscosity syndrome, hypercalcemia, hyperuricemia, elevation of alkaline phosphatase, pathological fractures and diffuse osteoporosis. 3. immuno-binding electrophoresis and immunofluorence antibody detection should be done for suspected cases with normal immunoglobulin level.
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PMID:[On the diagnosis of multiple myeloma an analysis of 2,547 domestic cases]. 765 87

Aminoglycosides, among the most commonly used antibiotics in neonates, have frequently been implicated in nephrotoxic reaction. Studies in adults have indicated that phospholipiduria (PLU) is rapidly increased during aminoglycoside therapy, in relation to the renal phospholipidosis these drugs are known to induce in renal cortex. We studied the effect of amikacin (AK) on PLU in male prematurely-born neonates (gestational age > 34 weeks; postnatal age < or = 2 days) by assessing the urinary excretion of 4 enzymes (N-acetyl-beta-D-glucosaminidase [NAG], alkaline phosphatase, tau-glutamyltransferase and alanine aminopeptidase) and 4 low-molecular-weight proteins (beta-2-microglobulin, clara cell protein, microalbumin and retinol-binding protein) which are currently used to monitor the development and extent of renal tubular damage. Twenty-two patients and 8 healthy (as control) neonates were enrolled in the study. Patients were treated with AK (15 mg/kg per day) given in one (qd, n = 10) or two equal injections (b.i.d., n = 12) for durations of 7-11 days. PLU and proteinuria were determined in 24-h urine sample collections, and enzymes were assessed in spot urine collected at 9 a.m. We found that in neonates, AK causes a significant increase in PLU, and in enzymuria except for NAG in the qd group. Proteinuria showed no significant change due to AK treatment. No significant differences were observed between qd and b.i.d. administrations of AK for all parameters tested. We conclude that PLU could be used in neonates as well as in adults as a non-invasive method to monitor the development of the renal phospholipidosis during aminoglycoside therapy.
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PMID:Urinary phospholipids excretion in neonates treated with amikacin. 767 71


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