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)

Even in specific risk groups, the relation between exposure to organic solvents and chronic renal diseases remains controversial. Thus, in a collaborative European study, we assessed the renal effects of occupational exposure to perchloroethylene (PCE) in dry-cleaners compared with matched controls who were simultaneously examined. Single high and low molecular weight proteins, kidney-derived antigens and enzymes, and prostanoids were measured in urine. beta 2-microglobulin, creatinine, laminin fragments, and anti-glomerular basement membrane antibodies were also measured in serum. A canonical function based on 23 such variables correctly classified 93% of individuals as either PCE-exposed or controls; with 13 markers, group membership was identified in 87% of subjects. Increased high molecular weight protein in urine was frequently (17/50 vs 1/50, p less than 0.0001) associated with tubular alterations. Changes were consistent with diffuse abnormalities along the nephron in workers exposed to low levels of PCE (median 15 parts per million). Generalised membrane disturbances might account for the increased release of laminin fragments, fibronectin, and glycosaminoglycans, for high molecular weight proteinuria, and for the increased shedding of epithelial membrane components from tubular cells with different location along the nephron (brush-border antigens and Tamm-Horsfall glycoprotein). These findings of early renal changes indicate that solvent-exposed subjects, especially dry-cleaners, need to be monitored for the possible development of chronic renal diseases.
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PMID:Nephropathies and exposure to perchloroethylene in dry-cleaners. 135 33

Proteinaceous cast formation in the distal nephron of the kidney from low molecular weight proteinuria is a significant, but poorly characterized, cause of renal failure. To study this phenomenon, we: (a) microperfused the loop segment (LS) of rats in vivo with artificial tubule fluid (ATF) containing four different low molecular weight proteins, 0.01-50 mg/ml, to detect alterations in LS function, and (b) examined the interaction between several proteins and Tamm-Horsfall glycoprotein (THP) in vitro with turbidity and dynamic light-scattering measurements. Perfusion of the LS for less than 2 min with cast-forming proteins (Bence Jones protein [BJP3] and myoglobin) decreased chloride absorption and elevated early distal tubule fluid (ED) [Cl-], compared with results obtained with control perfusions that used ATF alone. BJP3 decreased chloride absorption in a concentration-dependent fashion. Perfusion with non-cast-forming proteins (albumin and BJP1) enhanced chloride absorption and decreased ED [Cl-]. In vitro, proteins that had isoelectric points (pI) greater than 5.1 aggregated with THP. Aggregation was enhanced with increasing [NaCl] or [CaCl2]. Albumin (pI 4.8) and beta-lactoglobulin (pI 5.1) did not coprecipitate. The molecular size of THP alone increased when [NaCl] greater than 80 mM. Thus, cast-forming proteins aggregated with THP in vitro and caused in vivo LS dysfunction, which elevated ED [Cl-], facilitating aggregation. In contrast, non-cast-forming proteins either did not interact with THP or lowered ED [Cl-], which did not provide an environment for aggregation. Altered LS function and interaction of some proteins with THP were related to different physicochemical properties of the proteins and independently contributed to the formation of proteinaceous casts in the kidney.
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PMID:Mechanisms of intranephronal proteinaceous cast formation by low molecular weight proteins. 229 21

Five children with end-stage reflux nephropathy underwent kidney transplantation at our clinic. Reflux nephropathy was studied clinically and histologically. All children had proteinuria before starting hemodialysis, and hypertension was present in 2 cases. Three children underwent antireflux operations prior to transplantation. The original kidneys exhibiting reflux were removed during renal transplantation. All original kidneys exhibited atrophy and scarring. Focal and segmental glomerulosclerosis was found in 4 cases. PAS deposition in the interstitium, suggestive of Tamm-Horsfall glycoprotein, was found in all cases. No recurrent signs of focal and segmental glomerulosclerosis have been found in the children who have been followed up from 1 to 6 years after transplantation.
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PMID:Clinicopathological study on end-stage reflux nephropathy in renal-transplanted children. 233 Jun 60

A recently developed, simple and sensitive radioimmunoassay has been used to examine 24 h excretion and plasma levels of Tamm-Horsfall glycoprotein (THG) in normal subjects, stone formers and patients with stable chronic renal disease. In normal subjects THG excretion ranged from 22 to 66 mg/24 h, with no sex difference and no correlation with creatinine clearance or body surface area. There was no correlation between 24 h THG excretion and urine volume, pH or osmolality, excretion of Na+, K+ or Ca2+ or free-water clearance. There was a small significant correlation between plasma THG concentration and urinary THG excretion. A good correlation was obtained between the THG/creatinine ratio in 24 h and random samples. This made possible the use of random samples to establish a reference range for THG excretion of 0.15-0.50 micrograms/ml of creatinine clearance which did not depend on sex or age. The excretion rate of THG in stone formers was generally within the reference range. It was not significantly different in those who were hypercalciuric or in those taking thiazides. In patients with chronic renal disease there was a good correlation between 24 h THG excretion, plasma THG concentration and creatinine clearance. The range of excretion of THG per ml of creatinine clearance was greater than in normal subjects, independent of the type of renal disease and unrelated to proteinuria. In patients with glomerulonephritis the excretion of THG per ml of creatinine clearance was significantly higher in those with well-preserved tubules compared with those with tubular atrophy.
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PMID:Human Tamm-Horsfall glycoprotein: urinary and plasma levels in normal subjects and patients with renal disease determined by a fully validated radioimmunoassay. 397 15

The administration of ethacrynic acid and frusemide to healthy volunteers was regularly followed by the excretion of hyaline casts, without any concomitant proteinuria. Hydrochlorothiazide and chlorthalidone did not themselves induce cylindruria but augmented that provoked by acidifying agents. It was shown by the indirect immunofluorescence method that the casts were composed of uromucoid (Tamm-Horsfall mucoprotein), which is always present in the urine, usually in solution, and originates predominantly from the tubule cells of the ascending limb of Henle's loop. The urinary excretion of Tamm-Horsfall mucoprotein was not increased after the administration of ethacrynic acid. This mucoprotein is precipitated and forms aggregates when the concentration of electrolytes increases and when the pH of the urine declines. The casts that appear in the urine after strenuous physical exertion are of essentially the same composition. Casts produced by patients with kidney diseases, on the other hand, contain various protein fractions derived from the blood as well as mucoprotein. Cylindruria occurring during diuretic therapy and physical exertion is of no pathological significance, and the diagnostic value of byaline casts is very much limited if their exact composition cannot be determined.
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PMID:Excretion of urinary casts after the administration of diuretics. 455 42

Urinary Tamm-Horsfall glycoprotein (TH) excretion was measured by radioimmunoassay in 98 patients (55 men), aged 43.8 +/- 13.5 years, with renal disease. The radioimmunoassay was not affected by the urinary protein concentrations encountered. TH excretion (19 +/- 18 mg/24 h) was significantly lower than that in normals (39 +/- 13 mg/24 h; p less than 0.001) and was not related to age, sex or urine volume (1867 +/- 848 ml). TH excretion was not influenced directly by the degree of proteinuria (0.1-20.3 g/24 h), nor by variations in proteinuria with changes in disease activity or albumin infusions. There was a positive correlation between TH excretion and creatinine clearance less than 80 ml/min (r = 0.69, p less than 0.001). Patients with polycystic kidney disease had a disproportionate reduction in TH excretion with reduction in creatinine clearance. A major factor for the lessened excretion of TH in renal disease is probably a reduction in the number of functional distal tubular cells.
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PMID:Excretion of Tamm-Horsfall glycoprotein in renal disease. 651 75

The nephrotoxicity associated with mercury may be manifested as either acute tubular necrosis or an immune complex glomerulonephritis, depending upon the conditions under which the patient is exposed to the metal. Two patients with industrial exposure to mercury developed the nephrotic syndrome due to membranous glomerulonephritis. A multidisciplinary approach was used to define more precisely the pathogenetic mechanisms involved in the production of the glomerular lesion. Although glomeruli were normal by light microscopy, immunohistochemical studies demonstrated confluent finely granular epimembranous deposits of IgG and C3. This distribution was confirmed at the ultrastructural level with immunoelectron microscopy. High resolution elemental analysis of electron dense inclusions in tubular epithelial phagolysosomes demonstrated energy dispersion spectra characteristic of coexisting mercury and selenium. Eluates from the biopsy material were not immunoreactive against normal rat or human kidney. There was no immunoreactivity of epimembranous deposits with antibodies having renal tubular epithelial antigen or urinary uromucoid specificity. These observations suggest that a distinctive immunopathologic lesion is associated with mercury-associated membraneous glomerulonephritis, that the role of the metal itself may only be coincidental, and that the involved antigen remains unknown. Prednisone therapy had no documented persistent beneficial influence upon the level of proteinuria in one patient who has been lost to follow-up. In one patient not treated with steroid therapy, withdrawal of exposure to the metal resulted in disappearance of mercury from body fluids and clinical remission.
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PMID:Membranous glomerulonephritis associated with industrial mercury exposure. Study of pathogenetic mechanisms. 704 18

1. Tamm-Horsfall glycoprotein was determined, by radioimmunoassay, in samples of urine from normal individuals under a variety of physiological conditions. 2. The amount of glycoprotein excreted in 24 h by our population (39 +/- 13 mg, corrected for body surface area) was found not to be influenced by sex, age (19-60 years) or amounts of Ca2+, Mg2+ and Na+ excreted. 3. Urine samples collected at 2 h intervals over 24 h from individuals drinking in response to thirst, contained quantities of the glycoprotein which showed high positive correlations with urine volumes, but not with Ca2+, Mg2+ or Na+ excretion. 4. The amounts of urine and of the glycoprotein were correlated for individuals in antidiuresis, induced by restriction of water intake. Relatively small amounts of glycoprotein were excreted by individuals in states of water-induced diuresis. 5. The amounts of glycoprotein excreted after exercise were positively correlated with the small volumes of urine voided, but they were uninfluenced by the degree of proteinuria or of hyaline cast formation. 6. The half-life for turnover of the glycoprotein in a given individual is highly variable, from a minimum of 3-7 to a maximum of 168 h.
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PMID:Factors affecting excretion of human urinary Tamm-Horsfall glycoprotein. 719 48