Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated clinical and morphological findings in 254 patients (138 men and 116 women), with idiopathic membranous glomerulonephritis (IMGN). The mean age was 44 years. At time of biopsy proteinuria was found in 98%, nephrotic syndrome (NS) in 45.2%, hypertension in 10%, elevated serum creatinine concentration of greater than or equal to 1.4 g/dl in 24%, and markedly decreased Ccr (less than or equal to 40 ml/min) in 12.5% of the patients. Of 254 patients, 51 (20%) were classified as Stage I, 131 (52%) as Stage II, 52 (20.5%) as Stage III, 9 (3.5%) as Stage IV and 11 (4.3%) as Stage V, which was a relapsing form. Both intraglomerular, peripheral electron dense deposit-size and mean thickness of the glomerular basement membrane (GBMt) were analyzed by ultrastructural morphometric methods. In patients with NS, both the mean deposit-size and the mean GBMt were largest when compared to all others (p less than 0.01). The largest subepithelial deposits (SED), in mean, were observed in Stages II and V, while the largest incorporated deposits (ICD) were measured in Stages II and IV. The mean GBMt was largest in Stage III. Furthermore, there were strong correlations between the degree of proteinuria and the deposit-size (r = 0.603, p less than 0.001), and GBMt (r = 0.456, p less than 0.001). The GBMt showed a correlation with serum creatinine concentration (r = 0.476, p less than 0.001) and Ccr (r = 0.471, p less than 0.001). We concluded that the size of the electron dense deposits and GBM thickness play an important role in the clinical manifestation of IMGN.
 ...
PMID:Idiopathic membranous glomerulonephritis: a clinicopathologic and quantitative morphometric study. 149 64

The three main causes of primary nephrotic syndrome are minimal change nephropathy, focal glomerulosclerosis and membranous nephropathy. Corticosteroids obtain remission of proteinuria in most patients with minimal change nephropathy. Many patients, however, show either frequent relapses or steroid dependency. A short course of cyclophosphamide or chlorambucil can achieve stable remission in many of these patients but alkylating agents cannot be repeated, their toxicity being cumulative. Analyses of the available studies showed that some 80% of patients can be maintained in remission with cyclosporin A (CsA) but relapse occurs when the drug is stopped. Severe side effects are rare. In particular, the mean values of creatinine clearance did not deteriorate in cyclosporin-treated patients and repeat renal biopsy showed only mild changes in some patients. There is no definite treatment for focal glomerulosclerosis. An analysis of 10 clinical trials showed that some 17% of nephrotic patients may enter complete remission of proteinuria and another 13% may attain partial remission of the nephrotic syndrome with CsA. There is concern over the use of this drug since cases of irreversible renal dysfunction have been reported. However, retrospective reviews of the available studies showed that the mean serum creatinine levels did not modify if patients had normal renal function when given CsA. A 6-month course of methylprednisolone and chlorambucil may obtain remission of the nephrotic syndrome in some 60% of patients with membranous nephropathy. Some trials have shown that CsA may improve proteinuria and there is also some suggestion that the drug might protect against renal function deterioration. Thus, when given at correct doses, CsA may exert an anti-proteinuric effect without deteriorating renal function, suggesting that the drug may represent a further tool in treating the primary nephrotic syndrome.
 ...
PMID:Treatment of the nephrotic syndrome with cyclosporin A. 150 27

A 48-year-old woman was admitted to our hospital because of proteinuria associated with persistent hypocomplementemia. Intravenous pyelography indicated the presence of horseshoe kidney without other abnormalities. Hypocomplementemia was caused by cold activation of complement. There were some findings suggestive of chronic liver disease (positive HCV antibody, hypergammaglobulinemia, low cholinesterase, etc.). Percutaneous renal biopsy showed the features of multiple evolutional phases of membranous glomerulonephritis.
 ...
PMID:Horseshoe kidney and membranous glomerulonephritis with cold activation of complement. 150 24

Two-color flow cytometry was carried out to determine the correlation between cell-mediated immunity and the levels of proteinuria in 30 patients with membranous nephropathy. Lymphocyte subpopulations were measured by two-color flow cytometry using various monoclonal antibodies of the Leu series. Clinically, the patients were divided into four stages as follows: 1. untreated nephrotic stage, 2. prednisolone (PSL) treated nephrotic stage, 3. persistent proteinuric stage (incomplete remission, ICR) and 4. complete remission (CR). Two-color flow cytometry showed a significant decrease in Leu 2a+15+ (suppressor T) cells and relative increase in Leu 3a+8+ (suppressor inducer T) cells in the untreated nephrotic stage. The mean Leu 3a+8-/Leu 2a+15+ (helper/suppressor) cell ratio was normalized in the persistent proteinuric stage or complete remission after treatment with PSL. Patients with membranous nephropathy showed a significant elevation of Leu 2a+DR+ cells after treatment with PSL. The abnormalities of suppressor T cells and suppressor inducer T cells in the peripheral blood appear to reflect the levels of proteinuria in patients with membranous nephropathy. It was concluded that PSL might stimulate Leu 2a positive cells and then increase the number of Leu 2a+15+ cells in the peripheral blood of patients with membranous nephropathy.
 ...
PMID:Two-color analysis of lymphocyte subpopulations in patients with nephrotic syndrome due to membranous nephropathy. 151 83

Angiotensin-converting enzyme inhibitors (ACEI) can reduce proteinuria in diabetic and nondiabetic nephropathy. However, no studies have determined whether this antiproteinuric effect modifies the progression of renal insufficiency. We studied the evolution of 46 nondiabetic patients with nephrotic proteinuria treated with captopril for a minimum of 12 months. The follow-up period before captopril treatment was 12 to 18 months. At the end of follow-up, after captopril introduction (24.4 +/- 7.6 months), proteinuria had decreased from 6.3 +/- 2.5 to 3.9 +/- 3.1 g/24 h (P less than 0.001), with a mean decrease of 45% +/- 28%. The proteinuria decrease was higher in patients with reflux nephropathy, proteinuria associated with reduction of renal mass, inactive crescentic glomerulonephritis, nephroangiosclerosis, and IgA nephropathy, whereas patients with membranous glomerulonephritis and idiopathic focal glomerulosclerosis showed a poorer response. Patients were separated according to a proteinuria reduction greater (group A, 23 patients) or lower (group B, 23 patients) than 45% of the initial value. At the end of follow-up, renal function had not significantly changed in group A with respect to values at the start of treatment: serum creatinine (SCr) was 229 +/- 167 mumol/L (2.6 +/- 1.9 mg/dL) versus 203 +/- 97 mumol/L (2.3 +/- 1.1 mg/dL), and creatinine clearance (CrCl) was 0.80 +/- 0.52 mL/s (48 +/- 31 mL/min) versus 0.87 +/- 0.47 mL/s (52 +/- 28 mL/min). The slope of the reciprocal of Scr (1/SCr) showed a significantly beneficial change after captopril introduction.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Long-term beneficial effects of angiotensin-converting enzyme inhibition in patients with nephrotic proteinuria. 151 4

The growth-inhibitory effects of courses of daily steroid therapy and of persistent proteinuria were assessed in 125 Indian and African children with nephrotic syndrome (NS) who were followed for an average of 3.9 years (range 0.25-14 years). Among the biopsied patients, 81% of Indians had minimal--change nephropathy and 49% of Africans had membranous nephropathy. The mean height standard deviation score (SDS) in 87 children who had received prednisone for an average of 36 weeks (range 4-250 weeks) was compared with that in 38 patients who had been managed symptomatically. Heights of untreated African children with persistent proteinuria were within the normal range for age, race and sex. The height SDS +/- SD for 77 Indian children in the prednisone-treated group was -1.06 +/- 1.44, which was not significantly different from -0.92 +/- 0.96 observed among 6 children in the untreated group (P = 0.75). In Africans the height SDS in 10 prednisone-treated children was -1.82 +/- 0.81 which was similar to that observed (P = 0.74) in 32 untreated patients -1.77 +/- 1.61. No significant correlation was found between the duration of prednisone therapy and height SDS for individual children among the 87 treated patients using regression analysis. The findings remained unchanged when children who had received less than 12 weeks of prednisone were excluded, or when comparison were drawn between those treated for less than and longer than 36 weeks. We conclude that courses of daily steroids or persistent proteinuria do not inhibit linear growth in Indian and African children with NS.
 ...
PMID:Effects of repeated courses of daily steroids and of persistent proteinuria on linear growth in children with nephrotic syndrome. 153 38

The aim of this study was to assess the significance of platelet factor four (Pf4) excretion in the urine of patients with mesangial IgA glomerulonephritis (IgAGN) and thin basement membrane disease (TBMD), and ascertain if Pf4 is a useful parameter to distinguish these diseases. The concentration of Pf4 in urine (Pf4) was determined by an enzyme linked immunoabsorbent assay (ELISA) in patients with IgAGN (n = 80), TBMD (n = 37), membranous nephropathy (MN) (n = 12), minimal change nephrotic syndrome (MCNS) (n = 3), crescentic glomerulonephritis (CGN) (n = 6) and in healthy controls (n = 20), and then compared with urinalysis and renal function. An immunoperoxidase method was used to examine urine sediments for the presence of platelets. Urinary Pf4 was detected in 35 out of 80 patients with IgAGN (median 0.15, range 0.07-2.5 ng/ml, n = 35), in only 2 out of 37 patients with TBMD (p less than 0.005), in all patients with CGN and in no patients from MN, MCNS or control groups. A positive correlation between urinary Pf4 levels and red blood cell counts was observed in patients with IgAGN (r = 0.876, p less than 0.001), but not in TBMD. Pf4 did not correlate with proteinuria or plasma creatinine in either group. Platelets were detected in urine in 10 out of 15 patients with IgAGN but in only 1 out of 9 patients with TBMD. Urinary red blood cell counts in all of these 24 patients were over 100,000/ml.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Urinary platelet factor four (Pf4) levels in mesangial IgA glomerulonephritis and thin basement membrane disease. 154 Oct 68

Seven diabetic patients with membranous nephropathy were immunohistologically studied in order to clarify the role of extrinsic insulin in membranous nephropathy. In three cases (group A), granular deposits of insulin were detected along the glomerular capillary wall with indirect immunoperoxidase technique using anti-porcine insulin antibody, where IgG and C3 were deposited in the identical pattern. The other four cases (group B), 8 of idiopathic membranous nephropathy, and 5 of diabetic glomerulosclerosis showed no insulin deposit in the glomerulus. Clinically, proteinuria was heavier in group A (mean +/- SE; 32.0 +/- 5.4 g/day) than in group B (5.5 +/- 0.5). Nephrotic syndrome developed after the beginning of the therapy with porcine insulin, and in two of them, proteinuria was ameliorated after porcine insulin was replaced by human insulin. Since porcine insulin is a heterologous peptide for human beings and has antigenicity when injected into patients, immune complex composed of insulin and anti-insulin antibody may cause membranous nephropathy in some diabetic patients treated with this animal insulin.
 ...
PMID:Insulin deposits in membranous nephropathy associated with diabetes mellitus. 155 Dec 52

A model of chronic serum sickness was used to induce immune-complex glomerulonephritis in seven experimental cats, by daily intravenous inoculation of an increasing dose (5 to 35 mg) of human serum albumin (HSA). At week four, two of the seven animals developed anterior uveitis. At week 23, two different animals developed the subcutaneous oedema characteristic of the nephrotic syndrome (NS), whilst the other five cats appeared clinically normal. The kidneys were examined at necropsy by light microscopy and by transmission electron microscopy. The glomeruli of four animals (three with both proteinuria and uraemia, and one with proteinuria only) showed morphological changes under light microscopy. The abnormalities suggested that a diffuse mesangial proliferative glomerulonephritis (GN) had been induced in three cats and diffuse membranoproliferative GN induced in another. Ultrastructural studies revealed electron-dense deposits (immune-complexes) in six of the seven cats. Two cats without glomerular abnormalities by light microscopy had mesangial deposits and three cats with mesangial proliferative GN had deposits at mesangial, subendothelial and/or subepithelial sites. The single cat with membranoproliferative GN had deposits at mesangial, subendothelial, subepithelial and intramembranous sites. Immunohistological examination (peroxidase-antiperoxidase technique) showed that HSA and immunoglobulin (IgG and IgM) were deposited in the glomeruli of these cats. Deposits were the most dense in cats with more severe renal lesions. Deposits of IgM were most abundant. An extensive cellular infiltrate, comprising macrophages, neutrophils and plasma cells, was observed only in the four animals which showed abnormalities in glomerular ultrastructure. The disease induced in these cats thus appears to differ from the membranous nephropathy previously described in the cat and bears a close resemblance to immune complex (IC) disease in man. In view of the relatively few specific animal models of IC-mediated proliferative GN, this model has potential for application to the study of human IC disease.
 ...
PMID:Experimental proliferative glomerulonephritis in the cat. 155 57

A 68-year-old Japanese male (Case 1) and a 59-year-old Japanese male immigrant to Brazil (Case 2) who suffered from subcutaneous eosinophilic lymphoid granuloma (Kimura's disease) of several years duration, developed nephrotic syndrome. Renal biopsy demonstrated membranous nephropathy in Case 1 and minimal-change lesion in Case 2. Both patients were treated with prednisolone for several months. There was complete remission of nephrotic syndrome in eight years in Case 1 and in three months in Case 2. Proteinuria did not reappear after remission of nephrotic syndrome in either case. In contrast subcutaneous tumors subsided in both cases during steroid treatment but again became active immediately following discontinuation of the drug. These clinical observations suggest that, though some common factor(s) might mediate the development of both skin and renal lesions, the mechanism of action on these two target organs may differ, perhaps serving only as a "trigger" for the initiating mechanism of renal disease.
 ...
PMID:Long-term effects of steroid treatment on nephrotic syndrome associated with Kimura's disease and a review of the literature. 156 15


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>