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)

Focal glomerular sclerosis was diagnosed in nine patients by renal biopsy. Proteinuria, hematuria, hypertension, and slowly progressive renal insufficiency unresponsive to corticosteroid and immunosuppressive therapy were consistent clinical findings. Focal, segmental, and global glomerular sclerosis with intraluminal deposits of hypereosinophilic and strongly PAS-positive material, intracapillary foam cells, and moderate interstitial involvement were consistent morphologic findings. The importance of this clinicopathologic entity in the spectrum of renal diseases has only recently been appreciated.
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PMID:Focal glomerular sclerosis. 18 92

Rats given N,N'-diacetyl benzidine (N,N'-DAB) by intraperitoneal injections were studied to further characterize the ensuing renal disease. Significant proteinuria and albuminuria occurred at 10 weeks and thereafter and was enhanced by prior unilateral nephrectomy. Glomerular epithelial cell vacuolization and cyst formation were marked in proteinuric rats. Focal glomerular sclerosis and synechia were present, but proliferative crescent formation was not. Glomerular fibrinogen was noted, but no immunoglobulins or C3 was detected by immunofluorescence microscopy. Glomerular epithelial cell cysts and disruption were noted ultrastructurally, but no electron-dense deposits were seen. Tubular basement membrane thickening and wrinkling were noted in N,N'-DAB rats, and maximum urine osmolarlity was decreased. None of the animals developed renal insufficiency. Parenteral N,N'-DAB-induced renal disease is different from crescentic glomerulonephritis noted in rats fed N,N'-DAB and has similarities to an experimental model of aminonucleoside induced focal sclerosis, supporting the theory of primary glomerular epithelial cell injury mediating proteinuria and focal sclerosis.
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PMID:Characterization of chronic N,N'-diacetylbenzidine-induced nephropathy. 42 29

This is a report about a phenotypical normal girl with nephropathy and gonadal dysgenesis. At the age of 2 years 8 months she presented with steroid resistant nephrotic syndrome. Focal segmental glomerulosclerosis was found by biopsy. Because of delayed puberty karyotyping was performed, which revealed 46 XY. Thirteen years after onset of proteinuria she reached end stage renal failure. Gonadal dysgenesis and nephropathy are often indistinguishable from incomplete Drash syndrome. Children with early nephropathy of unknown origin or gonadal dysgenesis should be observed for development of Wilms tumor. When chronic nephropathies are present in girls, karyotyping should be considered.
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PMID:[Nephropathy gonadal dysgenesis--or incomplete Drash syndrome?]. 158 52

Focal and segmental glomerulosclerosis accounted for 4.1% of all primary glomerulopathies. Typical signs of focal and segmental glomerulosclerosis were striking arteriolosclerosis on histological examination, the urinary syndrome of high proteinuria with mild haematuria and frequent nephrotic syndrome. The ten-year cumulative percentage of remissions was 30%. Patients with remission had at the time of biopsy a normal serum creatinine level and no or minimal regressive tubulointerstitial changes. The ten-year cumulative percentage of renal failure was 40%. Presence of nephrotic syndrome, extracapillary proliferation and advanced tubulointerstitial changes, tended to shorten a kidney survival. In one third of the patients the serum creatinine level rose by more than 50 mol/1/year.
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PMID:[Focal segmental glomerulosclerosis]. 175 2

Renal-biopsy specimens taken from pre-eclamptic patients are associated sometimes with focal-segmental glomerular sclerotic lesions (FSGS-like lesions) that closely resemble those of primary focal-segmental glomerulosclerosis. We studied a series of 60 sections from each of 19 cases of "pure" pre-eclampsia by light microscopy. Group I comprised 13 patients with FSGS-like lesions in their glomeruli, group II comprised 6 patients without such lesions. FSGS-like lesions were observed in 20.7 +/- 4.6% of glomeruli in group I. Epithelial droplets were observed in 12 of 13 cases in group I, but only one of 6 cases in group II. The incidence of granulated glomerular epithelial cells was significantly higher in group I (p less than 0.0005). The double contour of the basement membrane was more severe in group I than in group II (p less than 0.03). The percentage of glomeruli with FSGS and the number of weeks during which proteinuria of greater than or equal to g/day continued after delivery were positively correlated (r = 0.76, p less than 0.0002). We also found a significant positive correlation between the percentage of glomeruli with FSGS and the amount of proteinuria at delivery and biopsy (r = 0.66, p less than 0.003; r = 0.51, p less than 0.03). However, proteinuria disappeared in all patients. Three of them had successful second pregnancies. We consider that FSGS-like lesions can occur during pregnancy in "pure" pre-eclamptic patients but the lesions may not be progressive. We also suggest that proteinuria and epithelial cell change may be closely related with such lesions.
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PMID:FSGS-like lesions in pre-eclampsia. 193 69

A survey of consultations to the Division of Nephrology at San Francisco General Hospital from 1982 to 1988 found only seven cases of proven or possible renal disease matching that described for human immunodeficiency virus (HIV)-associated nephropathy (nephrotic proteinuria, rapidly progressive renal insufficiency, and focal and segmental glomerulosclerosis [FSGS] histologically). In the period from April 1, 1988 (the conclusion of the original survey) through December 31, 1990, a roughly 11-fold increase in the incidence of such cases among referrals of HIV-infected patients to the Division occurred compared with the initial experience. The patients were nearly exclusively black men, only about half of whom had intravenous drug abuse (IVDA) as an HIV risk factor. This striking increase was associated with a progressive increase in the number of black patients with acquired immunodeficiency syndrome (AIDS) in San Francisco, and in the percentage of patients with an AIDS diagnosis discharged from San Francisco General Hospital (SFGH) who were black. These data support other evidence indicating a particular vulnerability of blacks to this form of renal disease and help to reconcile data from our division with the experience reported from other centers.
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PMID:Increasing incidence of human immunodeficiency virus-associated nephropathy at San Francisco General Hospital. 196 49

Whether or not pregnancy adversely affects the natural course of underlying primary renal disease, and whether fetal outcome is influenced by the type of renal disease per se are controversial issues. We retrospectively analyzed the fetal and maternal outcome in 148 women with various, biopsy-proven histological types of primary chronic glomerulonephritis (GN), including IgA GN (52 patients), membranous GN ([MGN] 20 patients), membranoproliferative type 1 GN ([MPGN] 58 patients), focal and segmental glomerulosclerosis ([FSGS] 13 patients), and minimal change nephrotic syndrome ([MCNS] 22 patients), who were pregnant (with a total of 290 pregnancies) after the clinical onset of GN, and in 104 women with reflux nephropathy (with a total of 254 pregnancies). Fetal outcome was poor in the presence of uncontrolled hypertension, nephrotic range proteinuria, and/or impaired renal function at conception or early in gestation, whatever the type of renal disease. An accelerated, more rapid than expected, worsening of maternal renal function was observed in five GN patients of whom four (two IgA, two MPGN) had serum creatinine (Scr) levels greater than 160 mumol/L (1.8 mg/dL) early in gestation, and in five patients with reflux nephropathy whose Scr at conception ranged from 180 to 490 mumol/L (2.0 to 5.5 mg/dL).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Specific controversies concerning the natural history of renal disease in pregnancy. 199 51

Steroid-resistant FSGS and its recurrence posttransplantation are predominantly seen in children. We report on the largest pediatric transplant population for FSGS with similar numbers of azathioprine- and cyclosporine-treated patients analyzed for recurrence. Of 70 patients with idiopathic FSGS identified over the years 1974-1989, 49 progressed to end-stage renal disease and 28 received 42 transplants (17 live-related donors, 25 cadaveric). Seventeen patients each received one transplant, 9 patients each received two transplants, and one patient each received three and four transplants. The mean age at diagnosis of FSGS was 9.1 +/- 4.2 years, the mean duration of FSGS prior to reaching ESRD was 2.2 +/- 1.3 years, and the mean duration on dialysis prior to transplantation was 9.7 +/- 6.3 months. Primary nonfunction was observed in 2 transplants; in the remaining 40 transplants, 6 recurrences were noted (15%). Recurrences were noted in four AZA and prednisone (n = 22) and two CsA and prednisone (n = 18) recipients. Risk factors analyzed for recurrence included race, age at FSGS, histological and clinical severity of FSGS, classification of FSGS, duration of disease, interval on dialysis, multiple transplants, and HLA matching. Only age at onset of FSGS was predictive of recurrence. The incidence of recurrence was higher in children less than or equal to 6 years of age compared with those over 6 years (P less than .05). All 4 patients receiving AZA and prednisone went on to lose their grafts due to recurrence. Recurrent proteinuria in the 2 CsA and prednisone recipients was controlled by gradually increasing the CsA dose from 15 mg/kg/day to 27 and 35 mg/kg/day. Remission of the nephrotic syndrome was induced within 60 days in both patients. Presently, both grafts are functioning 24 and 16 months posttransplant with serum creatinines of 0.9 and 0.5 mg/dl, respectively. We conclude that recurrence is predominantly seen in very young children and occurs even under CsA immunosuppression. High-dose CsA may control the recurrent proteinuria--however, the long-term outcome of such intense therapy is not known.
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PMID:Incidence, treatment, and outcome of recurrent focal segmental glomerulosclerosis posttransplantation in 42 allografts in children--a single-center experience. 199 34

Renal injury associated with the intrarenal reflux (IRR) of urine that is either infected, under high pressure, or both, is a major cause of severe hypertension during childhood and adolescence and of chronic renal insufficiency in patients less than 30 years of age. Many, but not all, adolescent and adult patients with reflux nephropathy (RN) give a history of urinary tract infection (UTI) or unexplained fevers in infancy or early childhood, when the kidney is thought to be at greatest risk of injury. Although vesicoureteric reflux (VUR) is observed more commonly in infants than children with UTI, it is rare in uninfected patients at any age and should never be considered a normal finding during human development. Renal scarring may not be obvious in radiographic or radionuclear studies to medical management alone, no definite benefit of one over the other was observed, regardless of the grade of VUR. Moreover, progressive renal injury in scarred kidneys has been noted even after VUR had been corrected, when infection had been prevented, and while hypertension had been controlled satisfactorily. Focal glomerular sclerosis, a lesion found in patients with proteinuria and RN, has been identified not only in scarred kidneys, but also may be seen in contralateral, unscarred kidneys without VUR, which might suggest a humoral factor or, perhaps, a hyperfiltration phenomenon. RN is one of the most frequent causes of end-stage renal disease (ESRD) in children, adolescents, and young adults, which is potentially preventable. However, prevention will depend on early identification of patients at risk--infants and young children after the first UTI and siblings of patients with VUR--aggressive and effective treatment of UTI, minimizing intravesical pressure, and education of patients, parents, and physicians.
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PMID:Vesicoureteric reflux and renal injury. 202 50

A retrospective study was conducted to determine the clinicopathological correlation of focal glomerulosclerosis in 36 adult patients with idiopathic nephrotic syndrome. All cases were divided into two groups, focal segmental glomerulosclerosis (FSGS, 23 cases) and focal global glomerulosclerosis (FGBG, 13 cases), on the basis of pathological findings. Most patients with FSGS were non-responsive/partial-responsive (22/22) to the corticosteroid treatment. By contrast, those with FGBG gave a relatively high responsive rate of 7/12 to the same therapy. The 5 non-responders with FGBG, however, were noted to have intensive interstitial fibrosis/mononuclear cell infiltrate of the renal lesions (4 cases), or diffusely glomerular Clq deposition without other coexisting immune deposits (1 case). Most cases of FSGS (20/23) became steroid dependent or remained heavy proteinuria resistant to corticosteroids/other immunosuppressive agents over a mean of 3.4 (ranged, 1 to 7) years after renal biopsy. Three of the 5 patients of FGBG initially non-responsive/partial-responsive to corticosteroids turned out to have protein-free urine (less than 4 mg/hr/m2) (2 patients) 1 month after leaving the hospital and became mildly proteinuric (1 patient) two months after discharge, respectively. The remainders of FGBG (10/13) were free of protein in their urine sample or had occasional episodes of proteinuria over a mean duration of 4.1 (ranged, 1 to 7) years. In addition, chronic renal insufficiency on discharge was noted in 2 cases of FSGS (2/23) and 1 case of FGBG (1/13). Only two cases of FSGS (2/23) progressed into a uremic status 3 and 5 years, respectively, after the time of the presumed clinical onset of their disease. These findings suggest that FGBG clinically behaves similar to a minimal change disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Focal glomerulosclerosis: a clinico-pathological analysis of 36 adult patients with idiopathic nephrotic syndrome. 217 56


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