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)

Rats with established progressive passive Heymann nephritis (PPHN) were stimulated with tubular nephritogenic antigen derived from rat kidney fraction 3 (rKF3) or heterologous antibody to the eKF3 antigen. Rats stimulated with antigen had elevated levels of circulating autoantibody and increased amounts of rat IgG in a beaded pattern around the glomerular capillaries. The brush border (BB) region of the proximal convoluted tubules also stained for rat IgG. Rats stimulated with antibody had similar changes, but in addition the injected antibody was demonstrated in the glomerular deposits and in the BB region of the proximal convoluted tubules. Proteinuria was markedly increased in the antibody injected rats. This study indicates that the cells of the 'primed' immune system of rats with PPHN can be stimulated by 'additional' rKF3 antigen or antibody to it, to produce increased levels of circulating autoantibody. It is suggested that the progression of PPHN is dependent on the availability and access of the nephritogenic autoantigen to the immune system and that autoantigen may be released by autoantibody.
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PMID:Stimulation of circulating autoantibody levels in the rat with established progressive passive Heymann nephritis. 353 26

The significance of urinary trehalase as a possible early indicator of renal disorder was examined using Cd-treated rabbits, which received 1 mg/kg Cd thrice weekly for 3 months subcutaneously. The results showed that urinary trehalase increased significantly from 1 week after treatment, earlier than LAP, ALP, proteinuria and glucosuria, with no changes in plasma trehalase level. A marked decrease in trehalase activity in renal brush border membranes prepared from Cd-treated rabbits was observed. It was also confirmed by immunohistological techniques that Cd treatment resulted in a marked decrease in specific fluorescence compared with controls. Ouchterlony double diffusion analysis demonstrated that urine and renal brush border extracts formed precipitation lines against anti-renal trehalase IgG, indicating that urinary trehalase and renal trehalase had the same antigenicity. Therefore, the facts presented here would suggest that urinary trehalase originated from the renal brush border, indicating its superiority as a diagnostic tool over other indicative indicating its superiority as a diagnostic tool over other indicative enzymes like LAP and ALP in detecting injury to renal proximal tubular cells in the early stage.
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PMID:Urinary trehalase as an early indicator of cadmium-induced renal tubular damage in rabbit. 354 50

Passive Heymann nephritis with acute and severe proteinuria was produced in rats by a single injection of heterologous antibody against a purified glycoprotein which consisted of homologous subunits with a molecular weight of 108,000 (gp108). Gp108 was identified as one of the major antigens in rat renal tubular fraction (FX1A) on immunoblotting assay by using total proteins of FX1A and rabbit antiserum against FX1A. A band of gp330, which was identified as a pathogenic antigen of Heymann nephritis by Kerjaschki D and Farquhar MG (Proc Natl Acad Sci USA 79:5557, 1982) was detected as another band by Coomassie blue staining and immunoblotting. Autoantibodies in the sera of FX1A-injected (active Heymann nephritis) rats reacted to the band of gp330 but not to gp108. These results indicate that gp108 is a different glycoprotein from both gp330 and its degradation products. GP108 was subsequently purified to near homogeneity by extraction with Triton X-100, and then DEAE-cellulose and Bio-Gel A-1.5m column chromatographies. On gel permeation chromatography, the purified antigen showed a molecular weight of 310,000, suggesting that it consists of dimer or trimer of gp108. Rabbits immunized with gp108 produced an antibody which showed monospecific binding to gp108. The antibody stained with brush border of proximal renal tubules in addition to the capillary loops in rat glomeruli by indirect immunofluorescence. Injection of rabbit antiserum against gp108 in rats induced severe proteinuria within 2 days. On the 2nd day after the injection, the glomeruli of the animals showed granular immune deposits along the capillary loops in addition to dominant staining of the brush border of the proximal tubules by immunofluorescence. These results indicate that gp108 is a pathogenic antigen in passive Heymann nephritis and that an antibody against gp108 has a nephritogenic and proteinuria-inducing activity.
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PMID:Passive Heymann nephritis with acute and severe proteinuria induced by heterologous antibody against renal tubular brush border glycoprotein gp108. 375 92

Phensuximide is a succinimide antiepileptic drug useful in the treatment of petit mal epilepsy. Phensuximide has been reported to be nephrotoxic in man but not in animals. In the present study, the effects of single and subacute administration for seven days of phensuximide on renal function and urinary tract morphology were evaluated in Sprague-Dawley and Fischer 344 rats. Single administration of phensuximide (1.25 mmol/kg, ip) induced mild changes in renal function (trace hematuria, increased proteinuria and decreased p-aminohippurate uptake). No morphological changes were observed at 24 hr. Subacute administration of phensuximide (0.6 mmol/kg/day, ip) produced diuresis in the Sprague-Dawley rat, but little functional evidence of nephrotoxicity. Renal morphological changes in Sprague-Dawley rats were seen primarily in distal segments of the nephrons. These changes were characterized by distensions of the basal infoldings, apical protrusions, and occlusion of some lumen. In the Fischer 344 rat, subacute phensuximide administration (0.3 or 0.6 mmol/kg/day, ip) resulted in transient hematuria and proteinuria, but no change in the other renal function parameters studied. Renal morphological changes observed in Fischer 344 rats occurred primarily in proximal tubular cells. Damaged cells were characterized by large vacuoles at the basal infoldings, accumulations of opaque granules, migration of nuclei to the lumenal membranes, occlusion of the lumen and/or loss of the brush border. Morphological damage was more widespread in Fischer 344 rats than in Sprague-Dawley rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urinary tract effects of phensuximide in the Sprague-Dawley and Fischer 344 rat. 377 11

The progression of changes in rabbit kidney function following dosing with the nephrotoxin S-(1,2-dichlorovinyl)-L-cysteine (DCVC, 20-50 mg/kg) was determined. Proteinuria was observed 0.5-1 hr after administration of DCVC at doses of 20-50 mg/kg. Blood urea nitrogen levels, glomerular filtration rates, urinary glucose excretion, and urine volume were also altered following DCVC dosing; however, these parameters were less sensitive than proteinuria as markers of early renal dysfunction. None of these latter four indicators were affected by low DCVC doses, nor were they altered by high DCVC doses until 1.5-2.5 hr after dosing. Dose-dependent morphological changes to kidney structure were also observed 5 hr after DCVC administration. Low doses caused damage restricted to brush border membranes in the pars recta, while higher doses produced a necrotic lesion encompassing all regions of the proximal tubule. This study indicates that DCVC can cause rapid renal dysfunctional changes which are first detected by elevated urinary protein excretion.
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PMID:Early biological indicators of S-(1,2-dichlorovinyl)-L-cysteine nephrotoxicity in the rabbit. 381 16

Alterations in kidney function were assessed early in the course of Heymann nephritis that was induced in rats by immunization with Fx1A, an extract prepared from rat kidney cortex. Whole kidney and single nephron function were evaluated by clearance and micropuncture techniques. Kidney function was studied in stage 1 of Heymann nephritis, before the onset of proteinuria, and in stage 2, when antibodies are deposited along the brush border of proximal tubules. Although overall kidney function was similar in rats in stage 1 and normal controls, glucose reabsorption was somewhat depressed in the first part of the proximal convoluted tubule in stage 1. Both whole kidney and single nephron glomerular filtration rates were depressed in stage 2. Proteinuria in stage 2 was characterized by an increased albumin sieving coefficient, which resulted in an elevated excretion of albumin. Furthermore, several proximal tubule functions (glucose and fluid reabsorption and PAH extraction) were substantially depressed in stage 2. These findings demonstrate that immunological injury to the proximal tubules in stage 2 of Heymann nephritis produces a significant impairment of proximal function.
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PMID:Pathophysiology of the kidney in rats with Heymann nephritis. 387 41

Deposits of C3 but not of C1q and C4 were detected on the proximal tubules of kidneys from nephrotic patients with non-selective proteinuria. The incidence of tubular C3 deposits was significantly higher in patients with membranous glomerulonephritis, focal glomerulosclerosis, membrano-proliferative glomerulonephritis and non-selective proteinuria than in patients with minimal change disease, nephrotic syndrome and selective proteinuria or in patients with glomerular disease, but without nephrotic syndrome. The occurrence of tubular C3 deposits was positively correlated with the amount of urinary C3 excretion. In vitro studies showed that the human normal kidney as well as pathologic specimens negative for in vivo tubular C3 deposits were able to bind C3 on the brush border of proximal tubules when incubated with fresh heterologous serum. In contrast, in patients with non-selective proteinuria and in vivo tubular C3 deposits, the binding of heterologous C3 to the brush border of proximal tubules was markedly reduced. The positive correlation between the occurrence of tubular C3 deposits and the urinary complement excretion, together with the detection of the C3 breakdown products in the urines further supported the hypothesis that complement components, once filtrated through the glomerular barrier, might be activated by the brush border of the proximal tubule.
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PMID:In vivo localization of C3 on the brush border of proximal tubules of kidneys from nephrotic patients. 388 30

In early stages of permanent renal injury or extensive ablation, structural and functional adaptations associated with hypertrophy partially compensate for nephron losses. Glomerulotubular balance is maintained in these conditioned nephrons by intrinsic tubule and peritubular capillary adaptations that parallel single nephron glomerular filtration rate (SNGFR). Studies of Na+-H+ exchange in renal cortical brush border membrane vesicles indicate that tubule functional adaptation is not tied to loss of renal mass per se but rather to factors such as dietary protein content that set the level of SNGFR. Likewise, the structural heterogeneity that follows chronic renal injury or extreme ablation of renal mass is less a consequence of nephron injury than of adaptation linked to dietary protein intake. Indeed, since dietary protein restriction blunts the need for compensatory glomerular hyperfiltration, there is neither a stimulus for nephron hypertrophy nor for enhanced tubule ion and fluid transport. In rats with remnant kidneys, experimentally induced diabetes mellitus, or severe hypertension, increases in glomerular pressures and flows precede proteinuria, glomerular sclerosis, and azotemia. Protein restriction prevents these hemodynamic adaptations as well as the late complications. Similar conclusions appear to be applicable to a wide spectrum of clinical circumstances characterized by reduced nephron number.
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PMID:Nephron adaptation to renal injury or ablation. 389 71

Hypertension has been shown to accelerate the course of experimental nephritis. On the other hand, Heymann nephritic rats undergoing long-term DOCA-NaCl treatment develop hypertension with a malignant course. The present study examined the effect of a short-term DOCA-NaCl load on the development of hypertension and progression of nephritis. Heymann nephritic rats were treated with DOCA-NaCl between weeks 2 and 6 after the first immunization with brush border antigen. Within six weeks, hypertension developed in Heymann nephritis-DOCA-NaCl rats but not in Heymann nephritic rats without DOCA-NaCl treatment whereas DOCA-NaCl-treated rats developed a moderate elevation of blood pressure. During that time, anti-brush border antibodies and immune deposits typical of membranous nephropathy ensued, preceding appearance of proteinuria or histopathologically detectable renal changes in the immunized rats. After discontinuation of DOCA-NaCl treatments at week 6, blood pressure nearly normalized in DOCA-NaCl-treated rats. Within one year, however, blood pressure rose most markedly in nephritic rats treated initially with DOCA-NaCl. The rise in blood pressure at that time correlated with glomerular sclerosis, tubulo-interstitial changes and proteinuria. It is concluded that, during acute nephritis, immunological and hypertensinogenic mechanisms interact, leading to hypertension and aggravated course of nephritis. These experimental observations on nephritis-associated hypertension may have important bearings on human hypertension as well.
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PMID:Hypertension and progression of experimental nephritis. Interaction between immunological and haemodynamic factors. 391 83

We studied the functional effects of intraperitoneal sepsis on systemic hemodynamics in general, and on renal function in particular, in sheep in whom bacterial peritonitis was induced by cecal perforation. In the first group of seven sheep (group 1) fluid was administered throughout the period of sepsis to maintain pulmonary capillary wedge pressure as close to presepsis values as possible. These sheep exhibited hemodynamic changes known to be associated with sepsis in man: increased cardiac output and decreased systemic vascular resistance. In a second group of seven sheep (group 2) fluid intake was restricted; compared with group 1, these sheep demonstrated a smaller increase in cardiac output that did not persist and that was associated with an increase in the systemic vascular resistance during the septic period. Plasma renin levels increased fivefold in group 2 but were unchanged in group 1. Serial renal biopsies during the septic period revealed that all sheep had evidence of tubular cell damage on electron microscopy: cell swelling, loss of the microvillous brush border, and cell necrosis. Both groups of sheep also demonstrated marked tubular proteinuria similar to that found in humans with generalized sepsis. Despite this, sheep in group 1 exhibited no functional renal changes: creatinine clearance levels rose slightly from control values, urine concentrating ability was unimpaired, and fractional excretion of sodium increased appropriately in response to a sodium load. In contrast, group 2 sheep exhibited a fall in creatinine clearance levels but fractional sodium excretion did not fall as would have been expected were renal function entirely normal. The results suggest that generalized "hyperdynamic" sepsis induces tubular cell damage and tubular proteinuria by an unknown mechanism. However, this does not necessarily produce renal impairment since the glomerular filtration rate does not fall unless volume contraction is also allowed to occur.
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PMID:Renal and cardiovascular response to nonhypotensive sepsis in a large animal model with peritonitis. 396 24


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