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Query: UMLS:C0033687 (proteinuria)
24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The proteinuria of fifteen patients treated with just aminoglycoside or aminoglycoside and either penicillin or cephalosporin was studied. The proteinuria was analysed by means of immunoelectrophoresis, acetate cellulose electrophoresis, thin-layer polyacrylamide gel electrophoresis and sodium dodecylsulphate acrylamide gel electrophoresis. We observed a urinary excretion of free immunoglobulin light chains and an increased urinary excretion of lysozyme in all cases. The increase in urinary excretion of beta-2-microglobulin and retinol-binding-protein appeared only in patients treated with aminoglycoside and cephalosporin. These disturbances disappeared a few days after the treatment was discontinued.
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PMID:Low molecular weight proteins as urinary markers of aminoglycoside nephrotoxicity in man. 9 49

Three electrophoretic techniques are usually available in the clinical laboratories for the qualitative investigation of urinary protein patterns: 1) acetate cellulose, 2) immuno-electrophoresis; and 3) SDS-polyacrylamide gel electrophoresis. Proteinuria (the excretion of proteins in excess of 150 mg/day or 100 microgram/min) usually signifies either increased permeability of the glomerular-capillary membrane of diminished tubular reabsorption. Since glomerular disease is associated with an increased clearance of albumin and higher molecular weight proteins, whereas tubular damage is associated with the predominant excretion of proteins of lower molecular weight than albumin, it seems logical to establish a classification of proteinuria according to the molecular weight of its constituents. One can thus basically distinguish 5 types of proteinurias: 1) physiological; 2) tubular; 3) selective glomerular; 4) non selective glomerular; and 5) mixed proteinurias. Additionally one must distinguish "myeloma proteinurias" where monoclonal complete or incomplete gamma-globulins are found in the urine. Clinically it may be useful to determine the qualitatively normal or pathologic character of a quantitatively normal proteinuria, especially in the following conditions: 1) for early diagnosis of nephropathy in patients, such as diabetics, which are particularly prone to suffer from renal complications; 2) to confirm the clinical cure or to predict the recurrence of renal diseases; and 3) in such situations as orthostatic, or myeloma proteinuria, or any elevation of the urinary protein output of unknown etiology.
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PMID:Clinical relevance of different electrophoretic methods for the analysis of urinary proteins. 44 73

Qualitative analysis of urinary proteins is contrasted with histological findings of 45 renal biopsies performed in patients with chronic glomerulonephritis. Compared to electrophoresis on cellulose acetate and immunoelectrophoresis, a method using polyacrylamide gel after sodium dodecylsulfate treatment makes for more refined and objective differentiation of protein abnormalities. On the whole, proteinuria of the selective glomerular or physiological type predominates in the event of minimal change or membranous lesions. The non-selective type is found more frequently with diffuse proliferative or membranoproliferative glomerulonephritis (p less than 0.025). There are, however, too many exceptions to this rule to allow certainty, and a precise diagnosis of the particular type of glomerulonephritis is thus only possible histologically. Each type of histological involvement may cause almost any of the qualitative abnormalities of proteinuria. On the other hand, qualitative analysis of urinary proteins is useful for the detection of glomerulonephritis. A glomerular type of proteinuria may sometimes reveal involvement of kidneys at a time when, quantitatively, there is no proteinuria. In cases of orthostatic proteinuria a persistent glomerular type of tracing in recumbency suggests an organic kidney ailment. All patients in this series had a glomerular type of proteinuria when excretion was pathological, thus allowing a distinction from pure tubular involvement. 10 patients of the group, however, although they clearly had glomerular lesions (3 were diffuse proliferative glomerulonephritis) showed perfectly normal proteinuria both quantitatively and qualitatively. This was the case in systemic lupus erythematosus where kidney biopsy was performed without clinical suspicion of renal involvement. In summary, qualitative abnormalities of proteinuria call attention to underlying glomerulonephritis, although no distinction can be made between the various forms and there may be no detectable abnormality even in the event of major kidney involvement.
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PMID:[Value and limits of urinary protein electrophoresis with sodium dodecyl sulfate in the evaluation of glomerular nephropathies]. 45 9

The authors present a variant of the technique of sodium dodecylsulfate acrylamide gel electrophoresis (SDS-PAA) reported by Weber and Osborn, for the analysis of urinary proteins. SDS-PAA separates the proteins chiefly according to their molecular radius. SDS-PAA, as compared to acetate cellulose electrophoresis and immunoelectrophoresis, gives better resolution and may be recommended for the investigation of proteinuria.
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PMID:[Application of polyacrylamide gel electrophoresis-SDS to the study of proteinuria (author's transl)]. 68 17

Since detection of the first stage of nephropathies requires an exact definition of physiological proteinuria, this has been sought in 97 healthy individuals. Measured by a modification of the biuret reaction, physiological proteinuria did not exceed 100 mug/min in the recumbent position (average of 24.5 mug/min) and 150 mg/24 h (average of 51 mg/24 h). No significant differences were seen with respect to age or sex. Qualitative analysis of urinary proteins was done by cellulose acetate electrophoresis, immunoelectrophoresis and polyacrylamide-SDS electrophoresis. This latter method has the great advantage of classifying the proteins according to their molecular weight, wtihout electrostatic interference. Its graphic representation delineates a normal zone allowing an objective distinction between physiological and pathological proteinurias. In the majority of cases, the proportion of albumin is between 25 and 55%. The orthostatic position increases proteinuria (average of 41 mug/min) with a tendency to a distribution which erroneously suggests a glomerulopathy. Accordingly, investigation for small changes in proteinuria should always be carried out on urine formed in the recumbent position.
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PMID:[Physiological proteinuria. Data of acrylamide-SDS gel electrophoresis and other methods of qualitative and quantitative analysis]. 112 69

ACE inhibitors which till recently were used only in the treatment of cardiovascular diseases are becoming a perspective group of drugs also in the treatment of chronic nephropathies. It was revealed that they are effective in particular in the treatment of proteinuria of different etiology and have also a marked renoprotective effect and are therefore recommended to slow down the progression of renal failure. They reduce intraglomerular hypertension, increase glomerular filtration and the renal blood flow, and it is assumed that they can retard the progression of chronic glomerulonephritis and diabetic nephropathy. It may be excepted that their therapeutic application will in the near future be extended also to clinical nephrology.
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PMID:[ACE inhibitors--a prospective new group of drugs for the treatment of kidney diseases]. 129 14

Points of agreement: (1) In IDDM, hypertension occurs in patients who have already developed nephropathy, probably in the microalbuminuric phase. (2) Hypertension is an important accelerator of the development of diabetic nephropathy. (3) Hypertension, obesity and NIDDM are often associated, and insulin resistance is commonly observed in all three states. (4) Antihypertensive therapy retards the development of diabetic nephropathy in IDDM and reduces proteinuria in NIDDM. (5) The choice of antihypertensive agent in the diabetic patient must be based upon the efficacy of the drug as well as avoidance of side effects including deleterious influence on glucose, insulin and lipid levels and renoprotection. (6) Carefully conducted long-term comparative trials between different classes of antihypertensive drugs in microalbuminuric IDDM and NIDDM patients are essential. Points of major controversy: (1) Detection of IDDM patients prone to the development of diabetic nephropathy can be performed by measuring specific parameters such as erythrocyte Na(+)-Li+ countertransport activity. (2) Insulin resistance is a pathogenic mechanism rather than purely an association with hypertension and obesity. (3) A certain class of antihypertensive agents--ACE inhibitors--confers a specific renoprotective effect in diabetic nephropathy, in addition to its effects upon systemic blood pressure. (4) Reduction of blood pressure should be considered in the normotensive microalbuminuric diabetic patient. (5) Microalbuminuria is a sufficient 'surrogate endpoint' for the progression of renal failure.
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PMID:Meeting report of the International Society of Hypertension Conference on Hypertension and Diabetes. 131 6

We report here the alterations of serum angiotensin-converting enzyme activity (S-ACE) and of active renin plasma concentrations (ARPC) in 41 insulin-dependent diabetes mellitus (IDDM) patients compared with those of 26 control subjects. The IDDM patients had S-ACE activity (54 +/- 16 I.E.) in the upper normal range (controls, 39 +/- 7). When the patients were subclassified according to their diabetic complications, a significant increase of S-ACE within the IDDM group compared to the controls was observed in patients with nephropathy (68 +/- 13, P less than 0.001) with persistent proteinuria and with retinopathy (63 +/- 14, P less than 0.001). A significant correlation was found between proteinuria and S-ACE (r = 0.98, P less than 0.001) and between retinopathy and S-ACE levels (r = 64, P less than 0.001). No correlation between blood pressure and S-ACE or between blood glucose and S-ACE was observed. The ARPC were within the normal range in the IDDM (21 +/- 9 ng/l) and in control (19 +/- 3) groups. No correlations between ARPC and blood pressure or blood glucose or the degree of diabetic complications were registered. These data show that S-ACE activity is elevated in IDDM patients with nephropathy-proteinuria and/or with retinopathy and the circulating renin may not represent the renal renin-angiotensin vascular system.
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PMID:Serum angiotensin-converting enzyme activity and active renin plasma concentrations in insulin-dependent diabetes mellitus. 133 Apr 63

We studied the effects of symptomatic, antiproteinuric treatment with NSAID's (n = 28) and ACE-inhibitors (n = 14) in patients with proteinuria due to idiopathic membranous glomerulopathy (MGP). These two treatment groups were compared with a group of patients who did not receive antiproteinuric medication (n = 14). Urinary protein loss was effectively lowered by NSAID and ACE inhibitor therapy from 9.5 +/- 1.0 to 4.5 +/- 0.5 g/day (mean +/- SEM) and from 9.8 +/- 1.4 to 3.9 +/- 0.7 g/day respectively, whereas the control group showed a slight fall in proteinuria from 6.9 +/- 0.8 to 5.5 +/- 0.8 g/day. As a result of this treatment hypoalbuminaemia and hypercholesterolaemia improved significantly: serum albumin rose in the NSAID group from 25.4 +/- 1.2 to 29.0 +/- 1.0, and in the ACEi group from 29.9 +/- 1.8 to 32.7 +/- 1.2 g/l (control group from 27.4 +/- 1.6 to 27.8 +/- 1.6 g/l, while cholesterol was lowered in the NSAID group from 8.5 +/- 0.5 to 7.5 +/- 0.4 and in the ACEi group from 8.7 +/- 0.5 to 7.6 +/- 0.4 mmol/l (control group from 9.7 +/- 1.1 to 8.5 +/- 1.0 mmol/l). The antiproteinuric effect of both drugs was well maintained during an 18-month follow-up. Progression towards end-stage renal failure was observed especially in patients with impaired renal function at entry. Remission of proteinuria occurred particularly in patients with lower baseline values of proteinuria, irrespective of the treatment modality.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antiproteinuric drugs in patients with idiopathic membranous glomerulopathy. 133 89

Measurement of proteinuria, microalbuminuria, and sodium-lithium countertransport in red cells has no practical value. A low-protein diet and ACE inhibitor therapy are currently the best way to retard progression of diabetic renal disease.
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PMID:Proteinuria and microalbuminuria as predictors of nephropathy. 134 41


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