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)

Kidney biopsy specimens obtained from a group of individuals with chronic glomerulonephritis (CGN) have been processed for light and electron microscopic immunolocalization of total immunoglobulins (Igs). In a few cases, acid phosphatase (ACPase), a lysosomal enzyme marker, was ultrastructurally visualized. In the glomeruli, horseradish peroxidase-stained Igs were revealed in capillary lumina, urinary spaces and in transit through occasional loci of the glomerular basal membranes while ACPase-containing lysosomes resided both within and outside the cells. In the proximal tubules, Igs were traced in the endocytic vesicles and vacuoles, the latter also being positive for ACPase. Statistically significant relationships have been revealed between the number of IGs-labeled proximal tubules and some clinical or pathomorphological stigmata of CGN, in particular, proteinuria and arterial hypertension levels, marked interstitial sclerosis, etc. The data obtained are discussed in regard to the mechanisms of increased macromolecular filtration and the different proteinuria selectivity levels as well as the development of interstitial sclerosis as a result of the elevated reabsorption and incomplete lysosomal degradation of Igs in CGN.
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PMID:[Immunoglobulin filtration and reabsorption as possible factors in the pathogenesis of chronic glomerulonephritis. Clinical, immunomorphological and histoenzymological research]. 144 Mar 30

Plasmapheresis (P) was used in the complex treatment of 16 patients with chronic glomerulonephritis (CHG) and nephrotic syndrome. Before P. 12 patients were treated ineffectively with prednisolone and curantyl. After 3-5 sessions of P detoxication was observed in all patients, increased diuresis (15 patients). Renal function normalized in 4 of 5 patients, proteinuria reduced by 50-80%. The authors discuss indications of including P into the complex treatment of patients in whom chronic glomerulonephritis with the nephrotic syndrome was present.
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PMID:[Plasmapheresis in the combined therapy of patients with chronic glomerulonephritis and the nephrotic syndrome]. 148 47

A comprehensive clinical and morphologic examination of 160 nephrologic inpatients included titration of antibodies to respiratory viruses and to HBsAg and of streptolysin O. A correlation was detected between immunity status parameters and the presence and severity of proteinuria in the patients with chronic glomerulonephritis. Besides routine clinical and laboratory examinations, thorough serologic and virologic studies are necessary for this patient population, for such studies will help determine the trigger mechanism of the disease and thus predict the possible development of the condition.
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PMID:[Serodiagnosis of patients with glomerulonephritis]. 170 62

We described transient low or non selective proteinuria after forced lordosis was as a characteristic of orthostatic proteinuria and the decrease in the urinary IgA/IgG ratio after lordosis was useful in confirming the diagnosis of the disease. In this study we examined the urinary excretion of IgG, IgA and IgG4, an anionic immunoglobulin, after forced lordosis in 44 orthostatic proteinuria children (group OA) and 24 chronic glomerulonephritis patient in stable stage (group GN). Urinary IgG4/IgG after lordosis was not significantly different between groups OA and GN. It showed that urinary IgG4/IgG ratio was not so useful in the differential diagnosis of this disease. In group OA, urinary IgA/IgG correlated significantly with serum IgA/IgG (y = 0.35X + 7.0, r = 0.354, p less than 0.05), and urinary IgG4/IgG also correlated significantly with serum IgG4/IgG (y = 1.22x + 0.14, r = 0.813, p less than 0.001). From these results it is suggested that proteinuria after forced lordosis in children with orthostatic proteinuria is composed of a transient low or non selective proteinuria in terms of both size and charge of protein. It seems more likely that the so-called heteroporous theory and sieving function theory explain the mechanism of orthostatic proteinuria.
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PMID:[A study of serum and urinary immunoglobulins after forced lordosis]. 177 Jun 24

Changes in the urinary excretion of immunoglobulins (IgG and IgA) before and after forced lordosis were studied in 26 children with orthostatic proteinuria (group OA, where proteinuria disappeared within 120 min after lordosis was referred to as group OAA and where if disappeared after more than 120 min was group OAB) and 9 children with chronic glomerulonephritis in the clinically stable state (group GN). Urinary immunoglobulins were measured by ELISA (enzyme linked immunosorbent assay). In resting urine, the urinary excretion rates (total protein, IgG, and IgA) and the urinary protein ratio (IgG/protein, IgA/protein, and IgA/IgG) did not significantly differ between groups OA and GN. When forced lordosis was carried out, at maximum protein excretion, the urinary IgA/IgG ratio in groups OAA and OAB were significantly decreased (from 198 + 44% to 17.3 + 12.9% and from 147 + 88% to 18.7 + 16.9%, respectively). The ratio of IgA/IgG in groups OAA and OAB was significantly lower than that in group GN (88.9 + 53.9%, p less than 0.01). The urinary IgA/IgG ratio after lordosis in group OA was similar to the serum IgA/IgG ratio. These findings suggest that transient low or non-selective proteinuria after lordosis is a characteristic of orthostatic proteinuria. Analysis of the urine after forced lordosis, especially using the urinary IgA/IgG ratio at maximum protein excretion, may be an useful examination for differentiating OA from other glomerulonephritides.
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PMID:[A study of urinary immunoglobulin excretion after forced lordosis]. 177 Jun 25

In an attempt to clarify the influence of pregnancy on the natural course of the chronic glomerulonephritis with impaired renal function (glomerular filtration rate: GFR less than or equal to 70 ml/min), the courses of 14 pregnancies occurring in 10 patients (seven with IgA nephropathy, one with membranoproliferative glomerulonephritis, one with membranous nephropathy and one with hereditary nephropathy) were studied. In 8 patients GFR measured before pregnancies ranged from 46 to 70 ml/min and in the other two creatinine clearance estimated in the first trimester of pregnancies was 62 and 49 ml/min, respectively. The pregnancies resulted in 10 live births, one spontaneous abortion, one artificial abortion and 2 neonatal deaths. In 2 out of 10 live births fetal weight was less than 2500 g. In 3 of 11 pregnancies there was neither increase in urinary protein nor elevation of blood pressure during pregnancies, while seven (64%) had increased proteinuria during the third trimester, and 4 of them were also complicated with hypertension. In 6 of 10 patients, there was no decrease in GFR during pregnancies. In three patients GFR was decreased from 70 to 36 ml/min, 70 to 58 ml/min and 62 to 48 ml/min, respectively. However, these reductions were considered to go with the natural course of respective patients because the reduction slopes were almost the same or rather mild in comparison with those estimated before or after pregnancies. The other patient also had a transient increase in serum creatinine level during two pregnancies, but the reciprocals of serum creatinine concentration before and after the pregnanciesdeclined linearly with time. These data suggest that pregnancy might have little influence on the natural course of the chronic glomerulonephritis even if complicated with renal functional impairment defined as GFR of 70 ml/min or less.
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PMID:[Influences of pregnancy on the natural course of chronic glomerulonephritis with impaired renal function]. 177 Jun 39

A study was made of the effect produced by a short-term course of plasmapheresis (PA) combined with cytostatic, glucocorticoid and deaggregation therapy on the clinico-laboratory characteristics in 45 patients suffering from chronic glomerulonephritis (CGN). It has been established that PA rapidly normalizes the characteristics such as the level of circulating immune complexes and fibrinogen in the blood, ESR. Exerting no effect on renal function, PA led to a significant lowering of proteinuria and erythrocyturia, with its beneficial effects being preserved after discontinuation of the sessions. The best results were attained in associated CGN and nephrotic syndrome, in mesangioproliferative and mesangiocapillary CGN. The effectiveness of the short-term course of PA in patients with membranous and diffuse fibroplastic CGN turned out questionable.
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PMID:[The immediate results of using plasmapheresis in patients with chronic glomerulonephritis]. 180 8

1. To examine whether or not atrial natriuretic peptide-induced proteinuria simply results from increases in urine flow or glomerular filtration rate, we infused dopamine (1 microgram min-1 kg-1) and alpha-human atrial natriuretic peptide (0.025 microgram min-1 kg-1) into nine patients with chronic glomerulonephritis and nine essential hypertensive patients without renal damage, and compared the effects of the two agents on renal function and urinary protein excretion. 2. In patients with chronic glomerulonephritis, dopamine infusion significantly increased urinary sodium excretion (+59%), renal blood flow (+20%) and creatinine clearance (+14%). However, urinary protein excretion was not changed. Addition of atrial natriuretic peptide to the dopamine infusion further increased urinary sodium excretion and maintained creatinine clearance at the same level. In contrast to the infusion of dopamine alone, atrial natriuretic peptide markedly increased urinary protein excretion (77 versus 229 mg min-1 m2, P less than 0.02). Furthermore, the addition of atrial natriuretic peptide elevated the urinary protein/creatinine ratio (1.55 versus 5.35, P less than 0.05), while dopamine alone did not (1.55 versus 1.45, not significant). 3. In essential hypertensive patients, dopamine and dopamine plus ANP showed renal effects similar to those of chronic glomerulonephritis; however, the urinary excretion of protein was not changed significantly. 4. These results suggest that atrial natriuretic peptide may increase urinary protein excretion mainly by increasing the permeability of the damaged glomeruli to protein rather than by simply increasing urine flow or glomerular filtration. Possible mechanisms underlying the proteinuria-increasing effects of atrial natriuretic peptide are discussed.
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PMID:Differential effects of atrial natriuretic peptide and dopamine on urinary protein excretion in chronic glomerulonephritis. 184 64

Involvement of the kallikrein-kinin system in the pathogenesis of renal edemas may be mediated by increase of vascular permeability, proteinuria, diuresis and natriuresis. Proceeding from these points, in 27 patients with morphologically proved chronic glomerulonephritis and the nephrotic syndrome, the serum kallikrein activity and its 24-hour urinary excretion level were measured. According to their edematous syndrome severity, all the patients were divided into 2 groups: 1) 19 patients with moderate edemas; 2) 8 patients with severe ones. During the follow-up period, there were no essential changes in patients' body weights, and no significant differences between the groups in clearances and excreted fractions of sodium, potassium, chlorine, osmotically active substances, and in serum albumin and cholesterol levels, 24-hour protein losses and blood pressure. As compared to the healthy (n-20) in all the patients a substantial and statistically significant increase in kallikrein activity was revealed in serum and urine. Kallikreinemia and kallikreinuria were significantly higher in Group 2 than those in Group 1. In the total group of examinees a significant direct relationship was established between the urinary kallikrein activity and summary sodium and potassium excretion as well as between the serum kallikrein activity and chlorine clearance. A direct correlation between the serum kallikrein activity and proteinuria was also found. Thus, a role of the kallikrein-kinin system in development of glomerulonephritic edemas concurrent with the nephrotic syndrome is hetero-directional.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The participation of the kallikrein-kinin system in edema formation in glomerulonephritis]. 185 8

Several reports in animals, and sporadic case reports in humans, have suggested that kidneys with decreased nephron mass may be more susceptible to the development of focal-segmental glomerosclerosis. This prompted a reexamination of our previously reported group of pediatric donor-adult recipient renal transplant combinations. Data were analyzed from 31 adult recipients who had received renal transplants from cadaver pediatric donors (less than 6 years) with graft function for greater than 6 months and no evidence of chronic rejection. These were compared with a control group transplanted during the same period with adult donor kidneys. Immunosuppression consisted of azathioprine/prednisone or quadruple therapy in 16 and 15 patients respectively. End-stage renal disease (ESRD) was secondary to chronic glomerulonephritis (n = 9), diabetes mellitus (n = 6), polycystic kidney disease (n = 5), and miscellaneous causes (n = 11). Twenty patients had radiographic documentation of renal hypertrophy posttransplant. All patients had serial 24-hr urinalysis for protein and creatinine after transplantation during periods of stable renal function. Ten patients had renal biopsies performed at a mean time from transplant to biopsy of 10.4 +/- 1.6 months. Seven recipients had biopsies that revealed glomerulosclerosis at 13 +/- 6 months posttransplant. Protein excretion and serum creatinine in these patients were significantly higher than in control patients (1.6 +/- 0.37 vs. 0.49 +/- 0.15 g/24 hr and 1.96 +/- 0.11 vs. 1.64 +/- 0.09 mg%; P less than 0.03 and P less than 0.01, respectively). Only 3 of 25 control adult donor recipients developed proteinuria greater than 0.8 g/24 hr within 2 years of transplantation vs. 15/31 pediatric donor recipients. No correlations with the etiology of ESRD, age (greater than or less than 40 years), weight, sex, diabetes, hypertension, or the number of acute rejection episodes could be found. Our data suggest that adult recipients of pediatric donor renal transplants may be at greater risk for the development of glomerulosclerosis than those recipients receiving adult donor kidneys.
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PMID:The development of proteinuria and focal-segmental glomerulosclerosis in recipients of pediatric donor kidneys. 194 66


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