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)

A 47 year-old patient with an 8-year history of proteinuria was admitted to our hospital in 1989. His laboratory data were compatible with nephrotic syndrome: total serum protein 5.9g/dl (albumin 3.0g/dl), total serum cholesterol 280mg/dl and total urinary protein excretion 5.0g/day. Renal biopsy specimens contained 27 glomeruli associated with sclerosis and collapse of loops under light microscopical examination. In addition, mesangial proliferation and thickening of the basement membrane were visualized. With immunofluorescent study granular IgG deposits were detected in the peripheral region of the glomeruli. Staining for IgA, IgM, C3, Clq, light chain and Congo-red were all negative. On electron microscopy, microtubules apparently resembling cellular projections appeared to thicken the basement membrane. We are tempted to conclude that the current case is an atypical glomerulopathy accompanied by a glomerular microtubular-like structure.
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PMID:[Nephrotic syndrome with microcellular projections into the thickened basement membrane]. 823 Aug 21

Cerebrovascular and cardiovascular diseases are important predictors for survival in patients undergoing continuous ambulatory peritoneal dialysis (CAPD), and account for about half the deaths in these patients. Lipoprotein(a) [Lp(a)] is known to show high values in diabetics with proteinuria, and albuminuric renal disease. The purpose of this study was to determine Lp(a) levels and to investigate the association of Lp(a) and atherosclerotic risk factors in patients treated by CAPD. Lp(a) concentration were measured in 20 CAPD patients in the age range 31 to 83 years. Mean (+/- SD) levels of serum Lp(a) were elevated in the CAPD patients compared to age, sex matched 17 controls (49.5 +/- 27.7 vs. 15.5 +/- 12.4 mg/dl, p < 0.001). The levels of Lp(a) were significantly higher in the diabetic CAPD patients than in non-diabetics. There were significant positive correlations between serum Lp(a) concentrations and fasting blood sugar. However, when the above two groups were matched for age, sex, body mass index and FBS, Lp(a) concentrations were also significantly higher in CAPD patients than those in normal controls. We found no statistically significant correlations of Lp(a) with either age, body mass index, blood pressure, serum lipoprotein, apoprotein, glycated hemoglobin, BUN, creatinine or serum protein levels. There were no correlations between serum Lp(a) levels and albumin and LP(a) concentrations in the dialysate in all CAPD patients. Along with assessment of other known established cardiovascular risk factors such as elevated blood pressure, atherogenic abnormalities of plasma lipids and lipoproteins, and impaired glucose tolerance, we suggest that elevated levels of Lp(a) may lead to the accelerated atherosclerosis in these patients.
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PMID:[Alterations of Lp (a) lipoprotein in patients with chronic renal failure treated by continuous ambulatory peritoneal dialysis]. 837 89

Albumin; and alpha 1-, alpha 2-, beta-, and gamma-globulins were estimated by cellulose acetate electrophoresis in the serum and urine from rats with nephrotic syndrome (NS), 2, 4, 6, 8, 10, 12, 16, 20, and 30 days after a single injection of puromycin aminonucleoside (PAN). It was found that: (a) total serum protein level decreased on days 4-16, and total urine protein excretion rose on days 6-16; (b) serum albumin level fell on days 4-16, and urine albumin excretion increased on days 6-16; (c) serum alpha 1-globulin level rose on days 8-30, and urine alpha 1-globulin excretion increased on days 8-16; (d) serum alpha 2-globulin level remained essentially unchanged, and urine alpha 2-globulin excretion rose on days 4-10; (e) serum beta-globulin level decreased on days 4-20, and urine beta-globulin excretion increased on days 6-16, (f) serum gamma-globulin level diminished on days 6, 8, and 12, and urine gamma-globulin excretion rose on days 6-10. All serum protein fractions were excreted in the urine of nephrotic rats; these findings suggest that proteinuria is nonselective. The differences observed in the serum protein profiles, even when all protein fractions were lost in the urine, suggest an independent regulation of each protein fraction in PAN-nephrotic rats. In addition, the electrophoretic profile of serum proteins in PAN-nephrotic rats is different from previously reported patterns in human nephrosis and in rats with an acute-phase response.
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PMID:Electrophoretic analysis of serum and urinary proteins in rats with aminonucleoside-induced nephrotic syndrome. 846 81

To clarify the ultrastructural changes of the glomerular basement membrane (GBM) in diabetic nephropathy, the renal tissues of the patients with diabetic nephropathy were examined by electron microscopy using our newly devised "tissue negative staining method." A fine meshwork structure consisting of fibrils forming the small pores are observed in the normal human GBM. The diameter of these pores was slightly smaller than that of human albumin molecules. The GBM in patients with diabetic nephropathy showed irregular thickening. At higher magnification, cavities and tunnel structures, which were not seen in normal controls, were observed in the thickened GBM. As the diameters of the cavities and tunnels were far larger than the dimensions of albumin molecules, these enlarged structures are considered to allow serum protein molecules to pass through the GBM from the capillary lumen to the urinary space. The present results suggest that the cause of massive proteinuria in diabetic nephropathy is the disruption of the size barrier of the GBM.
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PMID:The ultrastructural disruption of the glomerular basement membrane in diabetic nephropathy revealed by "tissue negative staining method". 857 48

To determine whether the increase in proteinuria resulting from high dietary protein intake could be prevented by angiotensin-converting enzyme inhibition (ACEI), we performed paired studies on 8 nephrotic patients with normal GFR. They were fed sequential diets with a protein content of 0.8 (LPD) and 1.6 g/kg BW (HPD) each for 8 weeks. Patients on HPD received enalapril (ENAL) 10 mg/day. Despite the significant difference in protein intake, urinary protein excretion, at the end of the two dietary periods, was not statistically different. However, total serum protein and serum albumin increased significantly with HPD + ENAL treatment. The capability of ACEI to prevent the increase in proteinuria induced by HPD may be due to changes in glomerular hemodynamics, possibly mediated by changes in the activity of angiotensin II. Our study indicates that protein metabolism in nephrotic patients is better maintained with HPD + ENAL than with LPD alone.
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PMID:Effectiveness of dietary protein augmentation associated with angiotensin-converting enzyme inhibition in the management of the nephrotic syndrome. 867 2

We describe a 35-year-old woman who had nodular glomerulosclerosis associated with deposition of fragmented gamma (gamma 1)-heavy chains. She presented with edema of lower legs, mild proteinuria, and hematuria. Laboratory examination revealed hypocomplementemia, and a small amount of monoclonal IgG-lambda (lambda) in the blood. Renal biopsy disclosed prominent nodular expansion of the mesangium. Ultrastructurally, the nodules were composed of electron dense deposits and fibrillar structures. An immunofluorescent study showed depositions of gamma-heavy chains and C3 in the central portion of nodules and capillary walls, whereas kappa (kappa)-, lambda-light chains, and Fab fragments of the heavy chain were negative. The accumulation of collagen I, IV, V, and VI was demonstrated in the mesangium. Western blot analysis of serum protein disclosed fragmented gamma-heavy chains that did not combine with light chains. Glomerular nodular lesions, thus, can occur in heavy chain deposition disease, as in light chain deposition disease. Fragmented gamma-heavy chains may also induce hypocomplementemia by the activation of the complement pathway.
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PMID:Gamma-heavy chain deposition disease showing nodular glomerulosclerosis. 871 52

The human nephrotic syndrome (NS) is accompanied by important alterations of mineral and bone metabolism. The purpose of the present study was to examine bone metabolism in rats with experimental NS and normal creatinine clearance, and to evaluate the reversibility of this alteration. NS was induced by three injections of puromycin aminonucleoside (PAN) on days 0, 21, and 35 (10, 5, and 5 mg/100 g body weight, respectively). The biochemical markers of bone formation (osteocalcin and alkaline phosphatase) and bone resorption (hydroxyproline and pyridinoline), bone mineral content (BMC), and bone mineral density (BMD), determined by dual-energy x-ray absorptiometry (DEXA), were studied on days 0, 7, 14, 28, 42, 56, 84, and 112. Proteinuria was present throughout the study. Hypoproteinemia was seen on days 7, 28, 42, and 56, returning to control values on days 84 and 112. In serum, osteocalcin (OC) concentration increased (p < 0.001), and alkaline phosphatase (ALP) decreased (p = 0.002). In urine, hydroxyproline increased (p < 0.001), but urinary pyridinoline was not different from the control group throughout the study. Increased serum parathyroid hormone concentration and decreased levels of 25-hydroxy and 1,25-dihydroxyvitamin D were found from day 7. During the intense proteinuria, bone resorption predominates and decreased BMC and BMD ensues in PAN-nephrotic rats. PAN-nephrotic rats showed low BMC and BMD compared to control group (p < 0.001). At the end of the study, when proteinuria persisted but total serum protein returned to control values, the biochemical bone markers, BMC, and BMD returned to normal. In conclusion, PAN-nephrotic rats had reversible bone alterations that were related to the magnitude of proteinuria and the concentration of total serum protein.
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PMID:Biochemical bone markers, bone mineral content, and bone mineral density in rats with experimental nephrotic syndrome. 915 58

A six-month-old male Golden Retriever with a three-month history of polyuria and polydipsia was examined. Hematological examinations revealed nonregenerative anemia, azotemia, high serum creatinine level, hypercalcemia, hyperphosphatemia, hypercholesterolemia, hyperamylasemia, and low level of total serum protein. Urinalysis indicated mild proteinuria, and low specific gravity. Radiographic and ultrasonographic examinations revealed bilateral small sized kidneys. Histological examination by renal biopsy confirmed the diagnosis of renal dysplasia. Treatment with a dietary protein restriction, oral adsorbents, and dried aluminum hydroxide gel have been performed in this dog, and then, azotemia, high serum creatinine level, hypercalcemia, and hyperphosphatemia were improved. During 10 months after the initiation of treatments, no significant clinical change except polydipsia and polyuria has been observed.
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PMID:A control of a golden retriever with renal dysplasia. 936 46

The combination of captopril and indomethacin has been shown to control nephrotic proteinuria in an infant with congenital nephrotic syndrome of the Finnish type. We report the satisfactory control of congenital nephrotic syndrome by enalapril, maintaining normal serum albumin levels without albumin infusions. The haplotype data of our patient were consistent with the diagnosis of a Finnish-type nephrotic syndrome. After 21 months, during which daily infusions of albumin allowed partial control of the symptoms, captopril treatment was started. No adverse effects were noted. Serum creatinine levels remained normal. Within 8 weeks, albumin infusions were completely stopped. After 1 month the treatment was changed to a single dose of enalapril (0.8 mg/kg per day). During the next 15 months, the serum protein concentration was maintained around 6.5-7 g/dl, although proteinuria persisted (0.3-0.5 g/day). Weight and length gain are now satisfactory. We conclude that enalapril may be safely used in infants with severe forms of congenital nephrotic syndrome and might allow the avoidance of aggressive treatments for prolonged periods.
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PMID:Adequate clinical control of congenital nephrotic syndrome by enalapril. 954 71

A 55-year old female with rheumatoid arthritis (RA) had presented with proteinuria since July 1996. She was referred to us for persistent edema on her face and legs in November 1996. On admission, her 24-hour urinary protein excretion was 4.4 g/day, total serum protein level was 5.3 g/dl, and serum level of amyloid A protein (SAA) was elevated to 45.8 mg/ml. A percutaneous renal biopsy was performed, and light microscopy revealed varying degrees of amyloid deposits in the mesangial areas and arteriolar walls. The diagnosis of secondary amyloidosis (AA amyloidosis) was based on immunohistochemical staining for amyloid A protein using monoclonal antibody against SAA. Four weeks after treatment with salazosulfapyridine (SASP) and dipyridamole, proteinuria began to decrease and the edema had disappeared. Finally she recovered from nephrotic syndrome. AA amyloidosis has been thought to have a poor prognosis, with progression to renal failure. Since there is no specific effective therapy for the disease, it is very important to reduce the activity of the underlying cause. In our patient with renal amyloidosis following RA, SASP was evidently effective for arthritis and improvement of renal function. SASP might have a beneficial effect on AA amyloidosis by suppressing inflammatory cytokines.
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PMID:[Beneficial effect of salazosulfapyridine (SASP) in a patient with secondary renal amyloidosis]. 980 22


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