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)

Experimental evidence suggests that pharmacological manipulations of glomerular haemodynamics may affect the progression of chronic renal insufficiency and scarring. In this study, we have investigated the short-term (4 weeks) renal haemodynamic effects of nifedipine and nitrendipine (10 mg/thrice daily) in two separate groups of 6 patients with stable chronic renal failure (CRF) (glomerular filtration rate, GFR: 9.7-47.8 ml/min/1.73 m2). Patients were studied on three occasions: (1) before the administration of the calcium antagonist, (2) after 4 weeks of treatment and (3) 4 weeks after the discontinuation of the drug. Mean arterial pressure fell significantly on nifedipine: from 116.33 +/- 12.25 to 107.22 +/- 18.67 mm Hg, p less than 0.05, and on nitrendipine: from 112.22 +/- 10.04 to 102.22 +/- 13.77 mm Hg, p less than 0.05. There was no significant effect of either calcium antagonist on GFR, effective renal plasma flow (ERPF), proteinuria or natriuresis. Consequently, renal vascular resistance (RVR) fell in both experimental groups, nifedipine: from 51.40 +/- 28.77 to 44.97 +/- 30 dyn s cm-5 x 10(3) (mean +/- SD), and nitrendipine: from 37.04 +/- 18.46 to 30.47 +/- 15.56 dyns s cm-5 x 10(3), p less than 0.05. These results show that calcium antagonists reduce systemic blood pressure whilst GFR and ERPF are maintained. The fall in the RVR of patients with CRF treated with calcium antagonists may confer on these agents a therapeutic advantage in the management of progressive renal insufficiency.
Nephron 1991
PMID:Short-term effects of calcium antagonists on renal haemodynamics in patients with chronic renal failure. 185 83

Hyperlipidemia associated with nephrotic syndrome was treated with probucol and the changes in plasma lipoprotein lipid concentration and urinary protein excretion were examined in puromycin aminonucleoside-induced nephrotic rats. Rats made nephrotic exhibited severe hyperlipidemia with increases in all major lipoprotein fractions. Probucol treatment of nephrotic rats significantly lowered plasma triglyceride (TG), cholesterol (Ch) phospholipid (PL) and apoprotein B associated with very-low-density and low-density lipoprotein and Ch and PL in high-density lipoprotein (HDL). Malondialdehyde (MDA) associated with the lipoproteins was significantly elevated in nephrotic rats and probucol treatment also lowered MDA concentration in all major lipoproteins. In control rats probucol moderately, but significantly, reduced plasma TG and HDL-Ch concentrations. Proteinuria associated with nephrosis was decreased significantly by treatment with probucol. Probucol treatment did not affect blood urea nitrogen and plasma creatinine levels. A significant positive correlation existed between the amount of protein excreted in urine and the plasma lipid concentrations in all nephrotic rats, suggesting that the hypolipidemic effect of probucol may attenuate proteinuria associated with nephrosis. These results suggest that probucol may be a favorable treatment for hyperlipidemia associated with nephrotic syndrome.
Nephron 1991
PMID:The lowering effect of probucol on plasma lipoprotein and proteinuria in puromycin aminonucleoside-induced nephrotic rats. 185 87

Information regarding glomerular lesions related to Schistosoma haematobium infection in man or animal are extremely lacking and disputed. The objective of this experimental study was to investigate glomerular lesions in S. haematobium-infected golden hamsters. In this work, 53 hamsters were infected with S. haematobium cercariae and 18 animals of similar age and sex served as controls. Hamsters were infected either with 50, 200, 300, 400 or 600 cercariae and sacrified after 8, 9, 10, 14, 18, 24 or 32 weeks. Infected and control hamsters were subjected to laboratory examinations including serum creatinine, serum albumin, total protein, serum cholesterol, total urine protein as well as histopathologic evaluations. Kidney biopsies were examined by light microscopy, indirect immunofluorescence and by electron microscopy. Significant proteinuria, hypoalbuminaemia and hypercholesterolaemia were observed in all but 5 S. haematobium-infected, but in none of the control hamsters. Renal impairment was observed in 5 hamsters. Histopathologic evaluations showed IgG, circulating anodic antigen and circulating cathodic antigen deposits in the renal glomeruli. By electron-microscopic examination, these deposits were seen mainly in the subendothelial, mesangial and paramesangial areas. Amyloid deposits were also seen in the renal glomeruli, tubular basement membrane and in the interstitium. A correlation was found between the extent of amyloid deposition and the duration but not the intensity of schistosomal infection. We have concluded that S. haematobium infection can lead to glomerulopathy in golden hamsters.
Nephron 1991
PMID:Schistosoma haematobium-induced glomerular disease: an experimental study in the golden hamster. 190 86

The prognosis of acute poststreptococcal glomerulonephritis (APSGN) is still a matter of considerable debate. In an attempt to elucidate this controversy, the medium-term prognosis was evaluated in 40 patients 5-9 years after the onset of the disease, and the long-term prognosis in 88 patients 10-17 years after the onset of the disease. All were sporadic cases. In the medium-term follow-up study, abnormalities were revealed in 5.0% (2/40) of the patients. Hypertension and proteinuria were the only abnormalities detected. In the long-term follow-up study, abnormalities were revealed in 6.8% (6/88) of the patients. Hypertension was found in 3.4, proteinuria in 2.3, and microhaematuria in 2.3% of the patients. In both studies, all patients had normal creatinine clearance. We conclude that the medium- and long-term outcome of patients with APSGN is excellent.
Nephron 1991
PMID:Medium- and long-term prognosis of patients with acute poststreptococcal glomerulonephritis. 192 2

Strenuous physical exercise causes transient proteinuria and renal hemodynamic changes: decrease of renal blood flow and to a lesser extent of the glomerular filtration rate, and an increase of the filtration fraction. However, the mechanisms of these modifications are still poorly understood. In order to elucidate them we performed maximal exercise tests on 8 untrained healthy volunteers after inhibition of the renin-angiotensin system (RAS) by captopril, the sympathetic nervous system by a beta-blocking drug (acebutolol) or an alpha-blocking drug (prazosin) and the prostaglandin system by indomethacin. Urinary albumin excretion was measured in every subject first at rest (AB) and then after exercise (AA) performed successively without and with blockade by each of theses drugs. AA-AB difference in the captopril test (12.04 +/- 6.11 micrograms/min) compared to that in the control test (68.91 +/- 25.18 micrograms/min) was significantly reduced (p less than 0.02). This difference remained unchanged after acebutolol (59.87 +/- 21.91 micrograms/min, p = 0.62), prazosin (35.23 +/- 27.80 micrograms/min, p = 0.21) and indomethacin (55.21 +/- 28.43 micrograms/min, p = 0.35). There was a negative correlation between the lowering of AA elevation and the rise in plasma renin activity in the captopril test (r = 0.64; p less than 0.03). Only acebutolol decreased systolic blood pressure significantly. These results suggest that the RAS plays a major role in postexercise proteinuria. We hypothesize that stimulation of this system induces an increase of efferent glomerular artery constriction and consequently of glomerular transcapillary pressure and the filtration fraction. Captopril seems able to prevent these hemodynamic changes.
Nephron 1991
PMID:Captopril but not acebutolol, prazosin or indomethacin decreases postexercise proteinuria. 192 9

An interesting association of Kimura's disease and membranous nephropathy is reported in a 71-year-old Chinese patient, 40 years after emigrating to the UK from Hong Kong. Significant blood eosinophilia and a very high serum IgE level were detected, the latter with a moderate level of specificity to Candida albicans. Light microscopy of renal biopsy was unremarkable despite a proteinuria of nephrotic proportions; diffuse subepithelial dense deposits compatible with membranous nephropathy were identified on electron microscopy. The atopic nature of Kimura's disease is confirmed and C. albicans is suggested as a possible causative agent.
Nephron 1991
PMID:Kimura's disease and membranous nephropathy. 192 14

A 52-year-old female had a nephrotic syndrome without neurological or dermatological manifestations. Renal biopsy revealed that glomeruli were filled with tumor cells which bore leukocyte common antigen and pan B cell marker. These cells occupied the capillary lumen and invaded into the mesangial area. Morphological alteration of endothelial cells and glomerular basement membrane were also noticed. The interstitium was well preserved. After five cycles of a combination chemotherapy, CHOP (cyclophosphamide, doxorubicin, vincristine and prednisolone), the second biopsy revealed that tumor cells disappeared from glomeruli showing mild sclerosis. Proteinuria became absent. This is the first report of an angiotropic large cell lymphoma manifesting a nephrotic syndrome and treated successfully by CHOP therapy.
Nephron 1991
PMID:A case of angiotropic large cell lymphoma manifesting nephrotic syndrome and treated successfully with combination chemotherapy. 192 16

Progressive proteinuria has been suggested not just to reflect but also to contribute to the development of focal glomerular sclerosis. Development of proteinuria and glomerular lesions was examined up to 18 weeks after 3/4 nephrectomy in Sprague-Dawley (SDR) rats and an analbuminemic SDR variant (NAR). Nephrectomy led to a significantly lesser degree of proteinuria in NAR (42 +/- 14 SD mg/day) than in SDR (140 +/- 54 mg/day), consistent with the fact that 50-60% of urinary protein in SDR after nephrectomy is serum albumin. Nevertheless at 18 weeks NAR showed a significantly higher frequency of moderate and severe glomerular lesions than SDR. We conclude that, in this model, proteinuria itself is not a major cause of progressive glomerular injury.
Nephron 1991
PMID:Glomerular injury in analbuminemic rats after subtotal nephrectomy. 194 21

In this work, 180 golden hamsters were infected with Schistosoma mansoni and 30 hamsters matched for age and sex served as controls. According to the number of injected cercariae, infected hamsters were divided into six main groups (20, 50, 100, 150, 200 and 250 cercariae). Each group was divided into five subgroups, according to the duration of infection after which animals were sacrificed (4, 6, 8, 12 and 24 weeks). Control and infected hamsters were subjected to laboratory evaluations (serum creatinine, blood urea nitrogen, cholesterol, albumin, total protein and urine protein concentration) and histopathologic examinations of kidney and liver tissues. A significant proteinuria, hypoalbuminemia and hypercholesterolemia was observed in schistosome infected (50 cercariae or more) but not in the controls and the group infected with 20 cercariae. There was significant correlation between these changes and duration of infection and the number of adult worm recovered from the mesenteric circulation at the end of the experiments. Histopathologic evaluation showed appearance of the circulating schistosome antigens, circulating anodic antigen (CAA) and circulating cathodic antigen (CCA), and of IgG glomerular deposits by the 6th week following infection; mesangial hypercellularity appeared early after infection (6-8 weeks), renal amyloid deposition appeared later (8-12 weeks). Egg antigens were not detected in the renal glomeruli. There was a significant correlation between the pathologic changes and duration of infection and the number of recovered adult worms from the mesenteric circulation. No histopathologic lesions were detected in controls and the group injected with 20 cercariae. A significant correlation was found between hepatic periportal fibrosis, amyloidosis and immune complex, deposition in the renal glomeruli. Hamsters did not tolerate infection with 150 cercariae or more for more than 12 weeks, and 20 cercariae caused no detectable glomerular disease. From this study, we concluded that S. mansoni infection causes nephropathy in the Syrian golden hamster. The disease became biochemically and histopathologically manifest by the 6th week following infection. Both immune complex deposition and renal amyloidosis stand as major pathogenic mechanisms. CAA and CCA are the major responsible antigens. Hepatic disease has an impact on the kidney lesion. 50 cercariae are the best dose to produce disease without early death of the animal. There is a significant correlation between the kidney disease and the duration and the load of S. mansoni infection.
Nephron 1991
PMID:Schistosoma mansoni nephropathy in Syrian golden hamsters: effect of dose and duration of infection. 194 25

It has been recently suggested that focal glomerulosclerosis (FGS) is analogous to atherosclerosis. Obese Zucker (OZ) rats spontaneously develop hyperlipidemia, proteinuria and FGS. To evaluate the role of the monocyte (MO) and its derivatives in the pathogenesis of the lesion, 30 OZ rats and 15 lean littermates (LZ) were followed for up to 240 days of age. At 75, 120 and 240 days of age, groups of 10 OZ and 5 LZ were assessed with respect to serum total and free cholesterol (TC and FC), triglyceride, lipoprotein electrophoresis, renal histology, histochemistry and immunohistochemistry. All serum lipids were raised at 75 days in OZ rats and increased progressively at 120 and 240 days. The early lesions of FGS were first demonstrated in OZ at 120 days with more advanced lesions at 240 days. FGS was seen in LZ only at 240 days when their serum lipids were raised. Intraglomerular MO infiltration was significantly higher in OZ than in LZ at all time periods (p less than 0.01) and greater in glomeruli with FGS lesions than in those without (p less than 0.01 and 120 days and p less than 0.05 at 240 days). Staining for ED1 and Ia antigens with monoclonal antibodies demonstrated increasing numbers of intraglomerular ED1+ and Ia+ cells with increasing age and extent of FGS. The findings suggest a role for intraglomerular macrophages in the pathogenesis of FGS in OZ.
Nephron 1991
PMID:Monocytes and macrophages in focal glomerulosclerosis in Zucker rats. 194 26


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