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)

Quantitative estimation of proteinuria done by the refractometric method was compared with that done by the sulphosalycilic acid method and biuret method in 102 urine samples. The analysis of results by students' t test showed no statistically significant difference between the three methods. It is concluded that quantitative estimation of urinary protein excretion by refractometric method is a simple cheap and reliable method and can be performed easily in the outpatient clinic. The instrument is quite handy and can be carried in the pocket.
J Assoc Physicians India 1992 Sep
PMID:Quantitative estimation of urinary protein excretion by refractometry. 130 25

Hantavirus infection was confirmed by history, symptoms and biochemical changes, as well as immunofluorescence test in 29 patients (24 men, 5 women; mean age 36.9 +/- 11.5 years) with nontraumatic renal failure (ANF), retrospectively in 15 patients. Cardinal symptoms were acute onset (n = 29), fever (n = 27), pain in the flanks, abdomen or head (n = 27), reduced glomerular filtration rate (n = 29), proteinuria (n = 25) and thrombocytopenia (n = 16). Normal renal function was restored in all patients. Follow-up examination of 15 patients 6-7 years after the acute illness revealed normal blood pressure, normal serum creatinine, absent proteinuria and normal inulin clearance in all, thus confirming the favourable prognosis of the infection in Western Europe. Nonetheless, because Hantavirus infection is by no means rare, it should be included in the differential diagnosis of acute renal failure.
Dtsch Med Wochenschr 1992 Sep 18
PMID:[Hantavirus infection with acute kidney failure]. 135 86

Hyperoxaluria is frequently seen in patients with inflammatory bowel disease, or after resection of the ileum. It is assumed to be responsible for the development of nephrolithiasis, nephrocalcinosis (oxalate nephrosis) and progressive renal impairment in these patients. Steatorrhea may aggravate the severity of hyperoxaluria. A 60-year-old male underwent massive resection of the jejunum and ileum 10 years prior to admission, due to strangulation of the small bowel, with occlusion of the superior mesenteric artery. He remained well except for steatorrhea which developed two-and-a-half years prior to admission, when microhematuria, proteinuria and oxaluria developed progressively. Since that time, the nephrolithiasis, nephrocalcinosis and renal failure have continued to worsen despite therapy with oxalate restriction and oxalate-binding agents. A renal biopsy, performed late in the clinical course, showed severe changes in the renal parenchyma. The decline in renal function proved irreversible. The unusual metabolic consequences of massive resection of the small intestine and their mechanisms are discussed.
J Formos Med Assoc 1992 Sep
PMID:Hyperoxaluria, nephrolithiasis, nephrocalcinosis and renal failure after massive resection of the small intestine: report of a case. 136 95

1. Aprotinin (Trasylol) is a cationic 6500 Da polypeptide that inhibits proteolytic enzymes, and when labelled with 99mTc it is a reproducible marker for the renal tubular turnover of small filtered proteins in man. Lysine potently inhibits tubular peptide uptake, and may thus depress the uptake and metabolism of aprotinin. This was investigated in 14 glomerulonephritic patients with normal renal function and variable proteinuria and in one healthy subject. 2. 99mTc-labelled aprotinin was given intravenously alone, and again 3 days later, immediately after the intravenous administration of 3-6 g of lysine, followed by an infusion over 1 h of 0.3-1.9 g of lysine/kg in individual patients. Activity over kidneys and in urine was measured over 24 h and chromatography was used to separate the undegraded peptide from free isotope. 3. At the low dosage of lysine (< 0.8 g/kg) given to six patients, kidney activity (representing tubular uptake) was unchanged, but early urine samples contained some undegraded aprotinin. Urinary excretion of free isotope, representing tubular metabolism, fell from 1.6 +/- 0.2% of dose/h with no lysine to 0.9 +/- 0.1% of dose/h in the 24 h after lysine, suggesting suppression of tubular aprotinin degradation. Corrected fractional degradation was calculated from the mean urinary excretion of free isotope over a given interval, determined by chromatography, divided by the mean cumulative kidney counts over this same interval, and this also fell after lysine from 0.06 +/- 0.006 to 0.03 +/- 0.006 h-1 (P < 0.005) between 3.75 and 24 h.(ABSTRACT TRUNCATED AT 250 WORDS)
Clin Sci (Lond) 1992 Sep
PMID:Effects of lysine infusion on the renal metabolism of aprotinin (Trasylol) in man. 138 15

Chronic progressive membranous nephropathy (MN) in humans is characterized by thickening of the glomerular basement membrane (GBM) with formation of spikes which contain laminin and other extracellular matrix (ECM) proteins. We have utilized two models of MN in the rat (active and passive Heymann nephritis, AICN, PHN) to define the sequential changes in composition of GBM as they relate to changes in glomerular gene expression for ECM components, altered permeability and morphological changes. Renal biopsies obtained during the course of AICN and PHN were immunostained for various ECM proteins and total glomerular RNA was hybridized with cDNA probes specific for laminin B2-chain, s-laminin, and types I and IV collagen. In addition, the ability of anti-glomerular epithelial cell (GEC) antibody and complement on rat GEC in culture to induce laminin release or laminin and s-laminin mRNA expression was determined. The results demonstrate that at weeks 12, 16, and 20 of AICN, immunostaining for laminin, s-laminin, fibronectin, entactin, and heparan sulfate proteoglycan increased in the GBM in a spike-like pattern. Concomitantly, glomerular mRNA levels of laminin B2-chain and of s-laminin increased. Type IV collagen protein and gene expression remained unchanged or decreased. No glomerular immunostaining for type I collagen occurred during AICN despite increased expression of mRNA for this collagen type. In contrast to AICN, in PHN no pronounced changes of the glomerular ECM occurred, except for transient expression of type I collagen mRNA in whole glomerular RNA and type I collagen protein the GEC cytoplasm. Stimulation of GEC in culture with anti-GEC antibody and complement also failed to induce transcription of laminin or s-laminin mRNA or the release of laminin protein. These findings suggest that the polyantigenic expansion of GBM which occurs in chronic experimental MN may be stimulated by factors different from the C5b-9 mediated processes that cause the initial proteinuria.
Kidney Int 1992 Sep
PMID:Altered glomerular extracellular matrix synthesis in experimental membranous nephropathy. 138 96

We studied three patients with late onset, chronic sensorimotor and autonomic neuropathy in course of plasma cell dyscrasia with Bence Jones proteinuria. Histopathological findings of nerve biopsies consisted in diffuse loss of myelinated and unmyelinated fibers associated with perivascular deposits of amorphous material with physico-chemical and ultrastructural features of amyloid. By immunohistochemistry, light chains of the same type as Bence Jones protein, components of the classic and lytic pathways of the complement and vitronectin were detected at the level of amyloid nodules. The colocalization of complement neoantigen and vitronectin suggests that this complex derives from the circulation. The elucidation of the chemical composition of amyloid might shed some light in the pathogenesis of these disorders.
Ital J Neurol Sci 1992 Sep
PMID:Complement neoantigen and vitronectin are components of plaques in amyloid AL neuropathy. 138 57

Several renal and renal-related disturbances have been described in patients with AIDS (acquired immune deficiency syndrome), in adults and children as well. These are mainly electrolyte and acid-base imbalance, acute renal failure and nephrotic syndrome. The latter is usually steroid non-responder. The renal histopathological lesions described more commonly are minimal change, mesangial hyperplasia and focal segmental glomerulosclerosis. Herein, we describe a 5 year-old with AIDS, that developed nephrotic syndrome, characterized by edema, ascites, hypoalbuminemia and massive proteinuria. A percutaneous renal biopsy showed mesangial proliferation. She did not respond to a 6 week treatment with prednisone. She died with sepsis after several viral and bacterial infections.
Bol Med Hosp Infant Mex 1992 Sep
PMID:[Nephrotic syndrome associated with AIDS in children]. 138 85

Manifestations of the human autoimmune disease systemic lupus erythematosus (SLE) include a number of behavioral and cognitive deficits. The present study asks whether neurobehavioral dysfunction is present also in MRL mice that spontaneously develop most of the fundamental immunological aberrations of SLE. There are two congenic substrains of MRL mice that differ in the time of disease onset: MRL-lpr mice develop lupus early and MRL(-)+/+ develop the typical signs of disease relatively late in life. The behavior of these substrains was assessed at 7 to 11 weeks of age, a time that coincides with the onset of disease in MRL-lpr mice and the absence of known lupus symptoms in the MRL(-)+/+ group. When compared to the congenic MRL(-)+/+ control substrain, MRL-lpr mice were spontaneously less active, traversed a crossbeam slower, and ceased responding to the novelty of a new environment sooner. They were also more reluctant to leave their home base or travel far away from it and perseverated in their response bias during extinction and reversal learning. Immunological status was characterized by moderate proteinuria in both substrains and high titers of antinuclear antibodies in MRL-lpr but not MRL(-)+/+ mice. Histological analysis revealed minimal or no signs of joint pathology in MRL-lpr mice. Thus, this study shows the presence of behavioral dysfunction in mice with early stages of autoimmune disease and gives support for the idea that MRL mice may provide a useful model of neurobehavioral dysfunction in SLE. It is suggested that the behavioral profile of MRL-lpr mice may indicate increased "timidity," related to genetics, autoimmunity, or both.
Brain Behav Immun 1992 Sep
PMID:A behavioral profile of autoimmune lupus-prone MRL mice. 139 1

Hemorheological risk factors for thromboembolic disease were evaluated in 25 pediatric patients with idiopathic nephrotic syndrome (NS). In patients with increased proteinuria (greater than 100 mg/m2/24 h) red blood cell (RBC) aggregation and plasma viscosity were significantly increased when compared with patients in remission (less than 100 mg/m2/24 h) and with healthy controls. RBC surface charge was normal during increased proteinuria and remission. RBC aggregation correlated positively with plasma viscosity, fibrinogen, alpha 2-macroglobulin, immunoglobulin M, and the degree of proteinuria, and negatively with plasma albumin levels. RBC aggregation showed no correlation to RBC surface charge. Hematocrit and RBC deformability (rheoscope) were similar in both patient groups and in controls. Increased RBC aggregation and plasma viscosity may contribute to the increased risk of venous thromboembolism in NS.
Clin Nephrol 1992 Sep
PMID:Increased aggregation with normal surface charge and deformability of red blood cells in children with nephrotic syndrome. 139 61

A 35-year-old women was diagnosed as suffering from Hodgkin's disease, lymphocytic predominant, based on a biopsy of an enlarged axillary lymph node. She was classified as stage IIA. Subtotal nodal irradiation resulted in a full remission. Ten months later she presented with a full blown nephrotic syndrome. Renal biopsy disclosed minimal change nephropathy. Despite extensive investigation no evidence of a relapse of the lymphoma was found. Whilst undergoing the investigation her proteinuria began to decrease and during the next 5 months it totally disappeared with no specific treatment being administered. Fourteen months after complete cessation of the proteinuria a left parasternal mass appeared. Biopsy confirmed a relapse of Hodgkin's lymphoma. The patient fully responded to chemotherapy and local irradiation. Noticeably, during the relapse and currently after a 3.5 year follow up period the patient has remained free of proteinuria. A review of the literature yielded altogether 14 cases in which the course of minimal change nephropathy did not run in parallel to that of the lymphoma. These are discussed in detail.
Clin Nephrol 1992 Sep
PMID:Spontaneously remitting minimal change nephropathy preceding a relapse of Hodgkin's disease by 19 months. 139 62


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