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)

A 23-year-old male patient with homozygous C3 deficiency who developed asymptomatic proteinuria and hematuria was reported. Renal biopsy disclosed typical IgA nephropathy with deposition of early- and late-complement components except for C3 deposition. C9 and membrane attack complex were detected in the glomeruli despite the absence of C3. It was suggested that there might be some unknown complement activation mechanism which does not require C3 component.
Nephron 1991
PMID:Homozygous C3 deficiency associated with IgA nephropathy. 194 29

To evaluate renal terminal complement activation in patients with glomerular diseases, we measured terminal complement complexes (TCCs) in plasma and urine with sandwich enzyme-linked immunosorbent assay (ELISA) using a monoclonal antibody against a C9 neoepitope expressed on TCC and a polyclonal antihuman C7 antibody. TCCs were detectable in plasma but not in urine in most of normal controls. In plasma, TCC levels were elevated in 4 of 22 patients with lupus nephritis and in 6 of 12 with membranoproliferative glomerulonephritis. However all patients with IgA nephritis, focal glomerulosclerosis, idiopathic membranous nephritis and idiopathic minimal change nephrotic syndrome (MC) showed normal values. In urine, TCCs were detectable in almost all patients with heavy proteinuria (greater than or equal to 100 mg/ml) except MC. The TCCs present in urine were partially purified by gel filtration using Sepharose 6B and were found to contain C5, C6, C7, C8, C9 and S protein by ELISA. Although the molecular weight of TCC is similar to that of IgM, the fractional excretion rate of TCC was about 100 times higher than that of IgM. These results suggest that TCCs detectable in urine contain SC5b-9 complexes and are mostly of renal origin.
Nephron 1991
PMID:Urinary excretion of terminal complement complexes in glomerular disease. 194 44

23 patients (16 women, 7 men) with rheumatoid arthritis (RA) and renal biopsy-proven mesangial glomerulopathy (MGP) were followed for 4-117 months (median 42) in order to evaluate the clinical course of their renal disease. Urinalysis was made, and 24-hour urine protein excretion and serum creatinine were determined. At the time of renal biopsy, the clinical renal findings of the patients were isolated hematuria (n = 10), isolated proteinuria (n = 6) and hematuria combined with proteinuria (n = 7). Hematuria persisted and renal function remained normal in all patients with isolated hematuria. A possible association between the presence of hematuria and the use of antirheumatic drugs was not established in this study. Proteinuria was clinically closely associated with the use of antirheumatic drugs in 9 out of 13 cases (6 with gold sodium thiomalate, 2 with D-penicillamine and 1 with auranofin) suggesting that antirheumatic drugs are important contributors to proteinuria in these patients. Renal function, although initially reduced in some patients, remained stable in all but 1 patient with IgA glomerulonephritis who developed the nephrotic syndrome and died of uremia. In conclusion, the clinical course of MGP in RA patients is benign in most patients. Moreover, this nephropathy may not represent a clinical entity. Proteinuria was related to antirheumatic drugs in most patients whereas microhematuria was constant even after stopping the antirheumatic drugs.
Nephron 1991
PMID:Mesangial glomerulopathy in rheumatoid arthritis patients. Clinical follow-up and relation to antirheumatic therapy. 194 47

A 17-year-old male with poststreptococcal acute glomerulonephritis (PSAGN) superimposed on the course of IgA nephropathy is presented. The histological findings of the first renal biopsy showed mild IgA nephropathy with a mesangial deposition of IgA and C3. Eighteen months later, acute nephritic syndrome with hypocomplementemia and rising antihyaluronidase titer occurred 10 days following the onset of an upper respiratory infection. The second renal biopsy revealed severe diffuse endocapillary proliferative and exudative glomerulonephritis with cellular crescents in 70% of the glomeruli. Immunofluorescence showed granular staining of C3 alone along the capillary walls. The pre-existing IgA deposits had disappeared. Typical 'humps' were observed by electron microscopy. The symptoms were gradually resolved by intensive steroid and anticoagulant therapy. Five months after the episode of acute nephritic syndrome, the patient was clear of symptoms except for mild proteinuria and hematuria. The third renal biopsy at that time showed morphologic changes similar to those of the first renal biopsy with mild mesangial IgA deposits.
Nephron 1991
PMID:Superimposition of poststreptococcal acute glomerulonephritis on the course of IgA nephropathy. 201 79

Puromycin aminonucleoside (PA)-nephrotic rats have a high plasma renin activity (PRA) and low angiotensinogen levels. We measured proteinuria, urine renin, and urine angiotensinogen daily, for 11 days after PA injection. Proteinuria and urine angiotensinogen were evident on day 5, and urine renin on day 6. Peak levels of urine renin and angiotensinogen were attained on day 8. These data suggest that angiotensinogen urine excretion may contribute to its low plasma levels, and urine renin loss may limit a further increase in PRA.
Nephron 1991
PMID:Urinary excretion of renin and angiotensinogen in nephrotic rats. 204 2

The therapeutic effect of 15-deoxyspergualin (DSP) in old New Zealand Black/White F1 mice (B/W mice) with clinical nephropathy was studied and compared with cyclophosphamide (CY). The mice were treated with 0.05 ml phosphate-buffered saline, subcutaneously, four times/week, with DSP, 6 mg/kg body weight, s.c., four times/week, or with CY, 15 mg/kg, i.p., once a week, starting at the 28th week of age. They were serially semiquantitated for proteinuria, and serum IgG anti-dsDNA antibody was measured by ELISA. Spleen cell surface markers such as L3T4, Lyt2 and IgG were flow-cytometrically analyzed, and interleukin-2 (IL-2) activity in vitro was measured using CTLL cells. Kidney specimens were studied with light and immunofluorescence microscopy. The mice treated with either CY or DSP survived significantly longer than the control mice. L3T4+ cells in the DSP-treated mice at 40 weeks of age were significantly less than those in the 28-week-old control mice (p less than 0.05). In contrast, IL-2 generation in the three groups of mice showed no significant variations at 32-40 weeks of age. Serum anti-DNA antibody levels in both of the CY and DSP groups remained low and comparable with that in the 28-week-old mice, and the incidence of significant proteinuria decreased. Likewise, glomerular histology in the treated groups was improved compared with the 28-week-old control mice, and the deposition of IgG and C3 in the treated groups remained unchanged or further decreased. Accordingly, the renal (immuno)histological findings in the DSP group were quite comparable with or even better than those in the CY-treated mice. DSP may have suppressed the abnormal antibody production by modulating the T cell function(s), which is in contrast to the direct action against B cells due to CY.
Nephron 1991
PMID:Reversal of established nephropathy in New Zealand B/W F1 mice by 15-deoxyspergualin. 204 19

In a prospective survey in the Isle of Elba, 413 dogs affected by naturally acquired Leishmania infantum infection were identified out of a controlled population of 1,500 resident mongrel dogs. In all the 34 randomly selected dogs of different breed, age, and duration of disease, the presence of glomerular lesions which defined mainly two categories of glomerulonephritis (GN) was observed. The first group was characterized by mesangial-cell proliferation either with focal features (11 dogs), or with a diffuse pattern (10 dogs). The second group (12 dogs) showed the typical findings of segmental membrano-proliferative GN; amyloid deposits were seen in the glomerular tuft and interstitium in 1 dog. Immunohistochemical investigation revealed granular deposits of IgG, IgM, and C3 both in mesangial areas as well as on glomerular capillary walls. Granular immune deposits om the tubular basement membrane were also found in 31 out of 34 dogs examined. With ultrastructural investigation, subendothelial and mesangial electron-dense deposits were revealed. Age, sex, serum creatinine, BUN, duration of disease, anti-Leishmania antibody titers, and immune complexes did not discriminate between the types of observed GN, while proteinuria did. The study shows that the renal involvement is the natural sequela in dogs infected with L. infantum, and that the kidney lesions are characterized by immunologically mediated glomerular and tubular damage.
Nephron 1991
PMID:Renal involvement in canine leishmaniasis. A light-microscopic, immunohistochemical and electron-microscopic study. 204 28

Experimental glomerulosclerosis is associated with hyperlipidaemia and the deposition of lipid in glomeruli. Glomerulosclerosis is typically preceded by glomerular hypertrophy. To investigate a possible pathogenic role of lipids in glomerulosclerosis, glomerular structure and cellular composition were studied in rats fed either a control diet or one supplemented with 4% cholesterol and 1% cholic acid for 21 weeks following unilateral nephrectomy. On the cholesterol diet there were significant increases in glomerular cross-sectional area (13.11 +/- 0.39 x 10(3) vs. 11.13 +/- 0.44 x 10(3) mu 2, p less than 0.01) and mesangial area (1.81 +/- 0.07 x 10(3) vs. 1.50 +/- 0.08 x 10(3) mu 2, p less than 0.02). These changes were significantly correlated with proteinuria, which was significantly greater on the cholesterol diet (mean area under curve for duration of diet = 3.11 +/- 0.38 vs. 1.42 +/- 0.35 g, p less than 0.02). There was a significant increase in glomerular leukocytes on the cholesterol diet (4.10 +/- 0.44 vs 2.86 +/- 0.25 OX-1 positive cells/10(4) mu 2, p less than 0.05). Mesangial foam cells, derived from macrophages, were associated with adhesions to Bowman's capsule. These results demonstrate that hyperlipidaemia exacerbates the development of glomerular hypertrophy and that this may be mediated by factors released during the phagocytosis of lipoprotein deposits by macrophages.
Nephron 1991
PMID:Cholesterol feeding following unilateral nephrectomy in the rat leads to glomerular hypertrophy. 204 29

Two separate experiments were carried out to study the effects of the same acute protein load given at different hours of the day and to assess the ability of proteins from different sources to induce hyperfiltration. In the first experiment, 9 healthy volunteers were kept at strict bedrest for 48 h, during which both a meat high-protein meal (protein load, PL) and a vegetable low-protein meal (control load, CL) were given either at lunch or at suppertime. As compared to a CL, PL determined a significant increase in GFR, total proteinuria (uTP), albuminuria (uA), and urinary retinol-binding protein (uRBP). These effects were much more significant after lunch PL than after supper PL, thus indicating an interaction between the PL and the time of the day. The existence of a circadian rhythm for GFR, uTP, uA, and uRBP was corroborated by spontaneous changes over baseline levels, which also were prominent after lunch CL as compared to those following supper CL. In the second experiment, 7 healthy volunteers ingested at lunch three protein-rich meals at 1-week intervals. The three protein loads consisted of about 80 g protein in the form of cooked red meat, cheese, and soya, respectively. The only significant differences between groups were urea appearance and urea clearance, lower and higher, respectively after soya load. These findings suggest that when evaluating the renal functional reserve after acute protein load both the spontaneous changes and the time-dependent sensitivity of kidney functions to acute challenges should be considered. Finally, the amount rather than quality of dietary proteins seems to be the determinant factor for protein-induced glomerular hyperfiltration.
Nephron 1990
PMID:Protein-induced changes in kidney function depend on the time of administration but not on the dietary source. 207 4

Immunoglobulin production by peripheral blood mononuclear cells (PBMC) and lymphocyte subpopulations were studied in 56 children with IgA nephropathy (IgAN) and 22 healthy controls. All the patients had persistent proteinuria at the time of diagnosis, and were divided into three clinical groups on the basis of urinary findings at the time of examination: 27 patients had proteinuria with or without microscopic hematuria (group A; active stage), 9 had microscopic hematuria only (group B; healing stage) and 20 had normal urine (group C; remission stage). PBMC from the patients in group A cultured without mitogenic stimulation produced significantly more IgA and IgG than those from controls (p less than 0.05). After polyclonal B cell stimulation with pokeweed mitogen (PWM), PBMC from patients in group A produced significantly more IgA than those from group B (p less than 0.05), group C (p less than 0.05) or controls (p less than 0.01), and produced significantly more IgG than those from group B (p less than 0.05) or controls (p less than 0.01). However, there was no significant difference in PWM-stimulated IgG production between groups A and C. PWM-stimulated PBMC from patients in group C produced significantly more IgA and IgG than those from controls (p less than 0.05). There were no significant differences in lymphocyte subpopulations among groups A, B and C and controls. These findings show that the clinical course of childhood IgAN is correlated with IgA production by PBMC suggesting that overproduction of IgA might be responsible for the pathogenesis of IgAN in children.
Nephron 1990
PMID:Immune abnormalities and clinical course in childhood IgA nephropathy. 207 7


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