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 mutant strain of mice manifesting high proteinuria, wasting syndrome, and kidney glomerular defect was established from the F5 offspring of an interstrain cross of CBA/Nga and RFM/Nga mice. Affected mice had high levels of proteinuria after 40 days of age. The body weight of about 22.6% of affected mice decreased rapidly and they died between 3 and 5 months of age. We learned that this abnormality is controlled by two pairs of autosomal recessive genes; the mutant strain of mice is designated FGS/Nga. The mutant strain has been characterized by high proteinuria and renal lesions with focal sclerosis of glomeruli and tubular atrophy with interstitial nephritis in the kidney resembling the human disease. The FGS/Nga mouse strain is a potential animal model for studying kidney glomerular defect in humans.
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PMID:A new mouse strain manifesting high proteinuria and kidney glomerular defect. 166 45

Focal sclerosing glomerulopathy and especially focal segmental glomerulosclerosis (FSGS) have been recognized as a distinct clinical entity, however, there still exist controversies in terms of prognostic risk factors of progression and optimal mode of treatment. A total of 32 patients (2 with focal global sclerosis; FGS, the remainder with FSGS) were followed up for a mean period of 82 months (3-240 months). Fourteen presented with nephrotic syndrome and 18 had proteinuria with or without hypertension. Thirteen patients, all of whom except 1 were nephrotic, received steroid treatment with or without other immunosuppressive agents (cyclophosphamide/cyclosporin A/azathioprine). Three of the steroid-treated remained stable in complete remission; 5 nephrotic non-responders had renal death. The mean slope of 1/creatinine versus time for steroid-treated and non-treated groups was -0.23 and -0.043, respectively (p = 0.04), suggesting that nephrotic range proteinuria might be prognostically important. However, for the population of FSGS/FGS as a whole, only the initial serum creatinine predicted renal survival (p = 0.001 by Cox's regression model). Hypertension and hypercholesterolaemia were not important variables by themselves. Nevertheless, we found that the 9 patients treated with antihyperlipidaemics (gemfibrozil/probucol/cholestyramine/maxEPA) fared better, mean slope being -0.023 versus -0.103 for non-treated, though not reaching statistical significance (p = 0.96). Controlled prospective study involving a larger number of patients might be worthwhile.
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PMID:Focal sclerosing glomerulopathy. Risk factors of progression and optimal mode of treatment. 176 95

Forty seven renal allografts performed over a period of 12 years in 43 recipients with chronic renal failure due to biopsy-proved focal glomerulosclerosis (FGS, 5.34% from 888 cadaveric renal transplantations) were reviewed. Recurrence of the disease was suspected in 14 grafts (29.8%) on the basis of immediate proteinuria, but recurrence of FGS lesions was demonstrated in only 7 patients. The remaining 7 patients had minimal-change nephropathy or mesangial hyperplasia. The duration of renal disease before transplantation was a clear predictive risk factor of FGS recurrence, and mesangial hyperplasia in the native kidneys was associated with 50% risk of FGS recurrence. Some reports have suggested that plasma exchange may be beneficial in the treatment of FGS recurrence. Our experience, in 9 patients, indicates that plasma exchange initiated early in the course of recurrent proteinuria leads to transient but significant disappearance (2 cases) or decrease (5 cases) of proteinuria, with a return to pre-plasma exchange levels within 2 weeks after the end of treatment. In 2 cases, there was no beneficial effect on proteinuria. Plasma exchange efficacy was correlated with proteinuria levels relative to disease severity. Although plasma exchange does not seem to improve the outcome of FGS recurrence, it demonstrates the possible presence of circulating factor(s) and argues for the characterization of humoral mediator(s).
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PMID:Recurrent nephrotic syndrome following renal transplantation in patients with focal glomerulosclerosis. A one-center study of plasma exchange effects. 194 68

Although hypoalbuminemia is a fundamental characteristic of nephrotic syndrome (NS), there are many patients with massive proteinuria that do not develop hypoalbuminemia. We have studied the clinical and biochemical characteristics of 19 patients with persistent massive proteinuria (greater than 5 g/d) and normal serum albumin (group I) in comparison with 16 patients with similar proteinuria excretion, but persistent hypoalbuminemia (group II). Most of group I patients had diagnoses suggesting glomerular hyperfiltration (focal glomerulosclerosis [FGS] associated with vesicoureteral reflux [VUR], reduction of renal mass, proteinuria associated with obesity, sclerotic phase of idiopathic crescentic glomerulonephritis [GN] in contrast with those of group II, in which membranous GN was the most frequent diagnosis. We prospectively investigated differences in the antiproteinuric effect of captopril, an antiotensin-converting enzyme inhibitor (ACEI); after 6 months of treatment, proteinuria decreased clearly in group I (7.1 +/- 1.7 to 3.7 +/- 1.7 g/d; P less than 0.001), whereas no significant changes were observed in group II (8.1 +/- 2.4 to 8.8 +/- 4 g/d). Serum creatinine (Scr) remained stable during captopril treatment in group I, whereas three patients in group II showed a worsening of renal function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nephrotic proteinuria without hypoalbuminemia: clinical characteristics and response to angiotensin-converting enzyme inhibition. 199 78

This study deals with the quantification of mRNA of basement membrane components (laminin, type IV collagen, heparan sulfate proteoglycan) and type I collagen in focal glomerular sclerosis induced by the aminonucleoside of puromycin (PAN) in rats. PAN (15 mg/100 g B.W.) was injected intraperitoneally to male Sprague-Dawley rats on day 0. On day 22, the right kidney was removed from group II and III. Rats in group III received injections of PAN (5 mg/100 g B.W.) on day 27, 34 and 41. Rats in group II received injections of 0.9% NaCl instead of PAN. Remnant kidneys were removed on days 48, 60 and 80 and processed for RNA isolation and histopathological study. Glomerular RNAs were isolated using guanidinium thiocyanate and then dotted onto nylon membrane. Filters were hybridized with specific cDNA probes and exposed to film for analysis by densitometer. FGS was detected in 70% of glomeruli on day 80 in group II. All the basement membrane components and type I collagen were accumulated in the sclerotic areas. The mRNA coding for laminin and type IV collagen continued to increase in group III till day 80. The mRNA for HSPG decreased when the urinary protein excretion was maximum on day 48, then increased with the remission of proteinuria. The type I collagen mRNA also increased during the course of the FGS. We suggest that decrease of mRNA for HSPG may play an important role in the development of proteinuria in PAN nephrosis and increase of mRNA coding for laminin, type IV collagen and type I collagen may be involved in focal glomerular sclerosis.
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PMID:[Changes in the expression of basement membrane and type I collagen gene in focal glomerular sclerosis (FGS)]. 208 58

In this study we evaluated the incidence of chronic renal failure in children with asymptomatic proteinuria and/or hematuria detected by a mass screening program in school and kindergarten. A total of four thousand and three children, aged from 2 to 18 years old was referred to our institute between 1977 and 1990. Of them, 4 cases were AGN, 8 cases Alports' syndrome, 7 cases FGN, 7 cases F(s)GS, 3 cases HSPN, 148 cases IgA nephropathy, 12 cases MN, 24 cases MPGN (including 7 cases of focal type MPGN), 1 case lupus nephritis, and others. Of these children 2 of 8 cases of Alports' syndrome, one of 7 cases of FGS, 6 of 148 cases of IgA nephropathy and none of 24 cases of MPGN developed chronic renal failure. It is true that the incidence of chronic renal failure in children with various kinds of renal disease detected by a mass screening program is lower than that of symptomatic children. However, since we do not have yet any specific treatment in most cases and also since the follow-up period is not long enough, the definite conclusion that a mass screening program can alter the prognosis of children with renal diseases cannot be drawn except for some particular lesions such as MPGN, especially the focal type. Further study including a much larger population of patients is necessary.
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PMID:Screening for proteinuria and hematuria in school children--is it possible to reduce the incidence of chronic renal failure in children and adolescents? 208 74

In a retrospective analytical study involving 98 children with primary glomerulonephritis who were seen by us at our hospital during a 2-year period from 1984 through 1985 and who had renal biopsy performed previously, attempts were made to correlate pathological findings with both clinical findings and prognosis. The results are summarized as follows: 1) Of 87 patients with asymptomatic chronic glomerulonephritis, glomerular findings were those of minimal change lesion, mesangial proliferative nephritis, MPGN, membranous nephropathy and FGS or sclerosing nephritis in 29.9%, 51.7%, 13.8%, 1.1% and 3.5%, respectively. Among the other 11 patients in whom the diagnosis was made after manifesting the nephritic symptoms, minimal change was noted less frequently and MPGN was detected more frequently than in the aforementioned asymptomatic group. IgA nephropathy was estimated to account for 44.2% of cases of asymptomatic chronic nephritis. 2) Mild mesangial proliferation was observed relatively frequently and severe mesangial proliferation or MPGN rather infrequently in hematuria cases without proteinuria while in those with severe proteinuria minimal change lesion was uncommon and severe mesangial proliferative changes, MPGN or FGS were relatively frequent. 3) In 22 patients with IgA nephropathy and 11 with non-IgA nephritis the severity of glomerular changes was related to the intensity of proteinuria at the time of renal biopsy. 4) A 3 to 5 years' follow-up study of patients with mesangial proliferative nephritis inclusive of IgA nephropathy disclosed that 26-28% of patients became free from urinary abnormalities, 27-37% had persistent hematuria without proteinuria and 24-32% still had proteinuria of 2 plus or above. Patients with milder glomerular changes had a definitely better prognosis than those with severe glomerular lesions.
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PMID:[Clinicopathological correlation of young onset chronic glomerulonephritis]. 273 25

Total serum IgE was measured in 119 cases of primary glomerular diseases and 33 normal healthy persons. Statistically significant higher levels were noted in minimal change disease (MCD; median: 630 U/ml), IgM nephropathy (IgMN; 618 U/ml), focal glomerulosclerosis (FGS; 373 U/ml) and membranous glomerulonephritis (MGN; 144 U/ml). A higher level of serum IgE was noted in association with more frequent relapse or steroid resistance in MCD and IgMN and in FGS with nephrotic syndrome. A small group of IgA nephropathy with nephrotic range proteinuria was also noted to have extraordinarily high serum IgE. These findings suggest that IgE may play an important role in the pathogenesis of MCD, IgMN, and FGS and may serve as a prognostic indicator in terms of steroid responsiveness in MCD and IgMN.
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PMID:Serum IgE in primary glomerular diseases and its clinical significance. 338 Feb 16

The obese Zucker rat is a model of nonimmune glomerular disease characterized by spontaneous proteinuria and focal glomerulosclerosis. Mechanisms important in the pathogenesis of glomerular injury in obese Zucker rats are unknown, but may involve hemodynamic and metabolic factors. Micropuncture studies of superficial nephron function were performed prior to the development of FGS in male obese Zucker rats and lean littermates 9 to 13 weeks of age. Compared with lean littermates, obese Zucker rats demonstrated small increases in superficial nephron glomerular filtration rate (32.3 +/- 2.3 nl/min vs. 27.8 +/- 2.0, P greater than 0.05) and plasma flow (87.1 +/- 7.2 nl/min vs. 79.0 +/- 5.1, P greater than 0.05). Intraglomerular hydraulic pressures were not significantly different between groups. Despite similarities in superficial nephron glomerular function, obese Zucker rats displayed increases in glomerular area and mesangial matrix. These morphologic changes occurred in both superficial and deep nephrons. We conclude that increases in glomerular pressures and flows are not a prerequisite for the initiation of glomerular injury in the obese Zucker rat.
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PMID:Effects of genetic obesity on renal structure and function in the Zucker rat. II. Micropuncture studies. 405 71

The strain of FGS/Nga mouse is reported to develop proteinuria and progressive glomerulosclerosis. We studied the renal pathology of that strain periodically for 1 year. Focal and segmental glomerulosclerosis was observed 3 months after birth and the lesion progressed to the glomerular obsolescence in a year. Electron microscopic study revealed electron dense deposits (DD) in the mesangium and the splitting of glomerular basement membrane. Studies using immunofluorescence and immunoelectron microscopy revealed that these DD were contained IgA, IgM, C3 and the retroviral envelope antigen (gp70). Clinically, proteinuria began at the age of 3 months and the renal function was decreased on time course. No other organs were involved. We studied the renal lesions of FGS mice by the histological and immunohistochemical methods and concluded that this mouse strain provides the tool for studying the mechanisms of the progression of glomerulosclerosis.
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PMID:Renal lesions of the FGS strain of mice: a spontaneous animal model of progressive glomerulosclerosis. 819 Jan 85


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