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)

Voided urines of 53,000 white and 9,3000 black cigarette smokers and nonsmokers were studied. Proteinuria was found to be commoner in smokers of both races and sexes. Heavy smokers showed proteinuria more frequently than light smokers. Of eight possible explanatory variables, one, alcohol consumption history, showed some interrelationship in that the smoking status-proteinuria association disappeared among heavy drinkers. Stopping smoking was not associated with a relative decline in proteinuria prevalence. Proteinuria associated with smoking did not appear to be indicative of more serious renal disease. There was a smoker-nonsmoker difference in urine glucose response to oral glucose challenge, apparently explained by higher average 1-hour serum glucose values for smokers, of unknown mechanism but partially explained by differences in alcohol usage. Hematuria, bacteriuria, and high urine acidity tended to be more prevalent in smokers, though these relationships were not consistently significant.
Nephron 1978
PMID:Cigarette smoking habits and urine characteristics: urinalysis abnormalities are more common is smokers, but the reasons are unclear. 62 98

One case of lecithin cholesterol acyltransferase (LCAT) deficiency is discovered by renal biopsy. Through the study of a French family, native to Brittany, one sister is found to be carrier of the trait. This finding suggests that the gene defect hitherto reported from Scandinavia is not restricted to this region. The patient shows typical signs of the disease, corneal opacities, anemia with a hemolytic component and lack of plasma LCAT activity. She has proteinuria, HTA, hematuria, no renal insufficiency. Signs previously unreported were noted: sensorineural hearing loss and platelet environment disorder. Histological abnormalities of two types are found: foam cells and subendothelial deposits, of which the tinctorial characteristics indicate a lipid composition. The lack of glomerular fluorescent staining observed is not in favor of an immune complex nephropathy. The study of this case suggests the determining role of lipid abnormalities in the genesis of anemia and of the vascular depositions in the induction of renal failure encountered in several cases of LCAT deficiency.
Nephron 1978
PMID:Hereditary lecithin cholesterol acyltransferase deficiency. Report of a new family with two afflicted sisters. 63 18

The clinical course of diabetic nephropathy was evaluated in 150 patients and the effect of hemodialysis in 68 of them. Proteinuria was the first sign of renal disease. Once renal dysfunction becomes evident, there is a rapid deterioration leading to dialysis within 3.0 +/- 0.2 years. Hypertension and circulatory congestion are common complications. The hypertension is probably volume dependent. Retinopathy was not invariably present at the onset of renal insufficiency but appeared with progression of renal failure. The course during hemodialysis was complicated by continued progression of diabetic vascular disease manifested by vascular access difficulties, worsening of retinopathy and blindness, and cardio- and cerebrovascular deaths. Mortality was higher than in nondiabetic dialysis patients.
Nephron 1978
PMID:Diabetic nephropathy: clinical course and effect of hemodialysis. 64 44

The morphologic basis of proteinuria in experimental chronic serum sickness glomerulonephritis in rabbits was studied by light and electron microscopy using horseradish peroxidase (effective radius 30 A; mol. wt. 40,000) and ferritin (effective radius 60 A; mol. wt. 480,000) as protein tracers. It was found that more ferritin, but paradoxically, less horseradish peroxidase gained access to the urinary space. Observations made by electron microscopy appeared to indicate a decreased permeability of most part of the damaged glomerular capillary wall to both tracers. These results favor the interpretation that proteinuria in chronic serum sickness glomerulonephritis is the result of focal rather than diffuse increase in permeability of the glomerular capillary wall. Lesions of segments of the nephron other than the glomerular capillary wall, may contribute to the leakage of proteins to the urinary space.
Nephron 1978
PMID:The morphologic basis of proteinuria in experimental chronic serum sickness glomerulonephritis. A light and electron microscopic study using horseradish peroxidase and ferritin as tracers. 66 50

70 cases of focal glomerulosclerosis (FGS) followed for periods ranging from 1 to 24 years are reported. 39 patients had a nephrotic syndrome. 31 patients had asymptomatic proteinuria. 97 renal biopsies were performed. At least one biopsy specimen from every patient showed focal and segmental involvement of glomeruli, but no lesions were observed on the first biopsy in 6 patients. 26 of the 35 patients with a nephrotic syndrome were treated with steroids alone and/or chemotherapy and/or indomethacin. Resistance to treatment was encountered in 21 patients. Complete remission was observed in 6 cases, despite persistence or accentuation of histological lesions on serial biopsies in 3 cases. Actuarial renal survival rate at 10 years was 45% in the group with a nephrotic syndrome versus 91% in patients with proteinuria. FGS with a persistent nephrotic syndrome represents the 'malignant' form of the disease. Recurrence of the disease was observed after transplantation in 2 cases and was absent in 1.
Nephron 1978
PMID:Focal glomerulosclerosis: natural history and treatment. A report of 70 cases. 67 92

In 25 patients with nephrotic syndromes of different origin, indomethacin caused an immediate decrease in glomerular filtration rate (GFR) and urinary protein excretion. This effect of indomethacin on GFR and proteinuria was more pronounced when the renin-angiotensin system was stimulated by a low-sodium diet and 50 mg hydrochlorothiazide daily, and resulted in a significant rise in serum albumin. Withdrawal of indomethacin after 1--3 years of administration was followed by an increase in proteinuria to pretreatment levels in 9 out of 15 patients. A harmful renal effect of long-term indomethacin administration was found to be unlikely. The results suggest that the steroid-resistant nephrotic syndrome can be treated symptomatically by indomethacin.
Nephron 1978
PMID:Treatment of the nephrotic syndrome with indomethacin. 74 Jan

Many patients with chronic pancreatitis (CP), even in the absence of intrinsic renal disease, are found to have abnormal urine, with persistent proteinuria, cylindruria, microhematuria and leukocyturia. The kidneys of 12 necropsy cases with CP showed mild to moderate arterial and arteriolar nephrosclerosis and no other significant changes. Renal biopsies were performed in 10 patients with CP without evidence of systemic disease or intrinsic renal disease, but with persistent urinary abnormalities. By light microscopy, mild arterial and arteriolar nephrosclerosis was present in 5 instances. In 1 patient, evidence of the reparative phase of acute tubular necrosis was noted. In 5 biopsies, electron microscopy revealed minimal to mild increase in mesangial matrix. Mild thickening of the glomerular basement membrane (GBM) was found in three instances but there was no clear-cut evidence of diabetic glomerulosclerosis. The presence of subendothelial electron-lucent material in 3 cases suggests the possibility of previous subclinical episodes of intravascular coagulation. The most consistent finding was the presence of lipid material in the cytoplasm of glomerular and tubular cells. The renal lesions associated with CP are mild, nonspecific and nonprogressive. Various pathogenetic factors can be invoked to account for their presence and for the urinary abnormalities found in patients with CP.
Nephron 1978
PMID:Renal lesions in chronic pancreatitis. 74 Jan 5

The effects of indomethacin and lysine acetylsalicylate (L-ASA) were compared in rats in which autologous nephrotoxic serum nephritis had been induced. The aim of this study was to offer support to the hypothesis that indomethacin might reduce proteinuria through increased synthesis of glomerular basement membrane by the podocytes. Both drugs were injected intraperitoneally at the dosage of 4 mg/kg body weight daily during a 6-day period into 40 rats rendered nephritic by rabbit nephrotoxic serum injection. Rats treated with indomethacin showed a marked decrease of proteinuria (tested by the 3% sulfosalicylic aicd method) and a clear ultrastructural picture of hyperplasia and hypertrophy of podocytes. Rats given L-ASA showed only a slight correction of proteinuria and less specific ultrastructural modification. These observations suggest that indomethacin decreases proteinuria in nephritic rats not only through its anti-inflammatory activity, but possible also by a peculiar mechanism, namely an increase in podocytic basement membrane synthesis.
Nephron 1978
PMID:Indomethacin and lysine acetylsalicylate in rats with autologous nephrotoxic serum nephritis. Biochemical and morphological studies. 74 Jan 8

Degradation and synthesis of the collagen portion (CLP) of the glomerular basement membrane (GBM) in glomeruli of rats with nephrotoxic nephritis (NTN) were determined in vivo and in vitro. Degradation of CLP in rats with NTN was only increased during the first 24 h after induction of NTN. After 24 h, the half-life of CLP in NTN rats (16.9 days) was not significantly different from that in the controls 15.6 days). The loss of CLP during the first 24 h is accompanied by an increased synthesis, measured in vivo and in vitro. The increased synthesis, however, does not seem to be sufficiently high to result in accumulation of CLP-like material in NTN. Since degradation and synthesis of CLP was not altered during the later phase of NTN, it is unlikely that chronic proteinuria is the result of an ongoing abnormal turnover of CLP.
Nephron 1978
PMID:Synthesis and degradation of glomerular basement membrane in rats with nephrotoxic nephritis. 74 Jan 13

The degree of fusion of glomerular epithelial cell foot processes was quantitated by determining the mean number of inter-process slip pores along 10 mum of basement membrane of peripheral capillary walls in 45 children with steroid-responsive nephrotic syndrome and minimal lesion glomerulopathy. Fusion was present in all biopsies performed when the child had proteinuria, but after remission the number of slit pores increased progressively towards normal over the next 4 weeks. There was a close correlation between the degree of fusion and the amount of proteinuria in those biopsied before remission.
Nephron 1976
PMID:Relationship between proteinuria and epithelial cell changes in minimal lesion glomerulopathy. 76 75


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