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)

The following data was obtained by morphometric and photometric microscopic studies of renal biopsies from 140 patients with idiopathic perimembranous glomerulonephritis, 108 patients with focally sclerosing glomerulonephritis and 50 patients with membranoproliferative glomerulonephritis and correlation of the results obtained with available clinical data: 1. In all three diseases proteinuria and serum protein concentration show no tendency to stabilization in spite of increasing renal insufficiency. 2. With increasing renal insufficiency the proximal tubular cells become increasingly atrophic. 3. Protein resorption through the proximal tubulus cells becomes increasingly diminished with advancing renal insufficiency. It is concluded from the present data that proteinuria, which is primarily glomerular caused, is increased by increasingly diminished resorption of proteins in the tubulus system with increasing renal insufficiency. In this way, even under conditions of advanced renal insufficiency with reduced GFR, large amounts of proteins can be excreted and a nephrotic syndrome can persist to a stage of renal insufficiency.
 ...
PMID:Clinical and morphological aspects of nephrotic syndrome in perimembranous, focally sclerosing and membrano-proliferative glomerulonephritis. 687 82

IgD myeloma is relatively rare. We wish to report 4 new cases investigated in this laboratory during the past 18 months. Extra-osseous involvement was present in 2 patients. Total serum protein concentrations were normal in all cases, while serum paraprotein peaks were inconspicuous in 2 patients. Bence Jones proteinuria of the lambda type was present in all, while free light chains could be detected in the blood in 3 patients.
 ...
PMID:IgD myeloma. A report of 4 new cases. 706 15

We have demonstrated recently that the binding of furosemide (FSM) to urinary proteins causes a decrease in the diuretic response that is proportional to the degree of proteinuria. Further studies were conducted to determine whether urinary drug-protein interactions also altered the renal excretion of FSM. Rats were treated with puromycin aminonucleoside to produce proteinuria. Renal FSM clearance was directly related to urinary protein excretion rate (r = 0.550, P less than .005), a relationship that was more striking when FSM clearance was normalized to glomerular filtration rate (r = 0.781, P less than .001). This relationship was not explained by changes in serum protein concentration or glomerular filtration rate. In order to understand the mechanism of this relationship, normal and nephrotic rats were studied during experimental conditions designed to alter urinary pH. In normal animals urinary acidification induced by HCl infusion produced a profound decrease in renal FSM clearance compared to animals with the more alkaline urine that followed NaHCO2 or acetazolamide pretreatment. This alteration in renal FSM clearance during urinary acidification was not observed in nephrotic animals, despite comparable changes in urinary pH. The diuretic response to FSM did not differ among the normal animals despite the alteration in renal FSM clearance, indicating that the reduction of renal FSM clearance was due to tubular reabsorption of FSM distal to its site of action. These data suggest that urinary drug protein binding may impair the tubular reabsorption of drugs and thereby enhance their renal clearance.
 ...
PMID:Furosemide disposition in normal and proteinuric rats: urinary drug-protein binding as a determinant of drug excretion. 724 73

Experimental pathogenicity was for the first time demonstrated in a strain of C. lusitaniae of clinical origin by the use of concentrated inocula (5.10(7) Y-shaped cells) and the administration of 4 mg of methylprednisolone acetate i.m. injected 4 days before and 3 days after the inoculation. Counts on malt-agar (fig. 1) in kidney and brain showed a decrease during the first 12 hours, followed by a definite increment in cell number between the first and second day. Clinical tests showed a strong proteinuria, high levels of blood urea and creatinine, and a low GOT increase. Glycemia, GPT, and total serum protein values were normal. Histological examinations of kidney showed a delayed penetration with discrete clumps of Y-shaped cells, inflammatory focuses, and compromised tubules and glomerula (Fig. 2). After 2 weeks of study accumulations of cells followed by degenerative phenomena were seen in the various structures examined. Reparation processes were seldom observed (Fig. 3-4).
 ...
PMID:[Experimental pathogenicity of Candida lusitaniae in mice]. 729 97

Familial hypocomplementemia of the third component of complement (C3) was found in four members of a family. The prospositus had cutaneous vasculitis, hypocomplementemia, arthralgia, proteinuria and thrombocytopenia. The combination of clinical, laboratory and pathologic findings resembled the "hypocomplementemic cutaneous vasculitis syndrome" (HCVS) or the "SLE-like syndrome" but serum C3 concentration was 35 to 57 per cent of normal in the propositus and in three relatives. Results of Clq precipitins, cryoglobulins and serologic tests for systemic lupus erythematosus were negative. Proteinuria (815 mg/day) but no hematuria was present. Analysis of the C3 phenotypes in this family showed that three hypocomplementemic members were apparent homozygous C3 slow but one was heterozygous C3 fast-slow. Metabolic studies with 125-Iodinated C3 in the clinically normal mother showed a 50 per cent reduction in C3 synthesis which was consistent with hypocomplementemia documented by serum protein assay. The occurrence of an immune complex-like disease (with characteristics of the HCVS) in a patient with a familial deficiency of C3 suggests that the preexisting C3 deficiency may predispose such persons to certain diseases.
 ...
PMID:Familial partial deficiency of the third component of complement (C3) and the hypocomplementemic cutaneous vasculitis syndrome. 736 33

The cause of sodium retention in nephrotic syndrome is unclear. Hypovolaemia has traditionally been labelled as the cause but there is evidence in adults of a renal disturbance as the main cause. We aimed to find out whether children with early nephrosis can be classified as hypovolaemic by objective measures. We measured blood volume, kidney function, and hormone concentrations in children with early relapse of minimal-change nephrosis. Three presentations could be defined. The first was patients with incipient proteinuria and normal plasma protein, characterised by sodium retention, increased renal plasma flow, and slightly increased aldosterone, but normal noradrenaline. The second was patients with severe proteinuria, hypoproteinaemia, and hypovolaemic symptoms, who had oedema, sodium retention, and high concentrations of plasma renin, aldosterone, and noradrenaline, low atrial natriuretic peptide, and low glomerular filtration rate. The third was patients with equally severe proteinuria and hypoproteinaemia, but without hypovolaemic symptoms; they had oedema, but no active sodium retention, and normal plasma hormones and glomerular filtration. Neither blood pressure nor blood volume discriminated patients with or without hypovolaemic symptoms. These findings show that children with early full-blown nephrosis can present both with and without hypovolaemic symptoms and laboratory signs, despite equally severe hypoproteinaemia, and also that sodium retention precedes the reduction in serum protein.
 ...
PMID:Volume regulation in children with early relapse of minimal-change nephrosis with or without hypovolaemic symptoms. 760 25

In order to clarify the mechanism of proteinuria in diabetic nephropathy, ultrastructural changes of the glomerular basement membrane (GBM) in patients with diabetic nephropathy were examined by electron microscopy using our newly devised "tissue negative staining method". The normal human GBM showed a fine meshwork structure consisting of fibrils forming the small pores. 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, hitherto unknown cavities and tunnel structures, which were not seen in normal controls, were observed in the thickened GBM. In some portions, these cavities presented a honeycomb-like appearance. The diameters of the cavities and tunnels were far larger than the dimensions of albumin molecules. These enlarged structures are believed to allow serum protein molecules to pass through the GBM from the capillary lumen to the urinary space. These results suggest that the cause of massive proteinuria in diabetic nephropathy is the disruption of the size barrier of the GBM.
 ...
PMID:Ultrastructural changes of the glomerular basement membrane in diabetic nephropathy revealed by newly devised tissue negative staining method. 769 3

Urinary enzymes N-acetyl-beta-D-glucosaminidase (NAG) and gamma-glutamyl transpeptidase (gamma-GT) are sensitive markers of specific renal cell damage. Excessive urinary amino acid excretion may also be an indicator of renal tubular damage. We have evaluated urinary excretion of NAG, gamma-GT and 37 amino acids, phospholipids and dipeptides in 30 children (aged 2.3-18.1 years) with nephrotic syndrome (NS), 23 with minimal change nephrotic syndrome (MCNS), 7 with focal segmental glomerulosclerosis (FSGS) and 16 healthy age-matched controls. Nine MCNS patients were in relapse and 14 in remission. Enzyme activity is expressed as micromoles per milligram urinary creatinine. In FSGS, NAG excretion correlated with the following: blood urea nitrogen (BUN) (r = 0.8), serum protein (r = 0.57), serum cholesterol (r = 0.85), serum albumin (r = -0.68) and proteinuria (r = 0.56). In FSGS the gamma-GT excretion was not significantly different from MCNS in remission or in relapse. In FSGS, gamma-GT excretion correlated with the following: BUN (r = 0.48), serum creatinine (r = -0.66), serum protein (r = -0.54), serum albumin (r = -0.68) and serum cholesterol (r = 0.87). Compared with controls, the urinary excretion of 5 amino acids was increased in FSGS patients as a possible indicator of tubular damage. The value for 7 amino acids was reduced in MCNS patients. Urinary amino acid excretion was not different from controls for the other amino acids in either FSGS or MCNS.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The differential diagnostic value of urinary enzyme and amino acid excretion in children with nephrotic syndrome. 791 41

Primary nephrotic syndrome can, although infrequently, cause severe anemia. However, the mechanisms of the anemia remain unknown. We investigated the mechanism of anemia in nephrotic syndrome by measuring parameters of nephrotic syndrome and anemia in 44 nephrotic patients (male: female; 21:23, average age; 43.6 +/- 20.3 years). Nephrotic patients had significantly lower hematocrits than did healthy controls (43.3 +/- 3.7 vs. 46.8 +/- 3.4% in males, 37.4 +/- 3.5 vs. 40.8 +/- 2.8% in females). Serum erythropoietin (Epo) concentrations were correlated inversely with hemoglobin (Hb), hematocrit (Hct), and red blood cell corpuscle (RBC) counts. Furthermore, serum Epo correlated with the serum iron concentration, but not with the other parameters, such as reticulocytes, serum protein and proteinuria. However, the maximum Epo concentration was less than 100 mU/ml in spite of severe anemia, and this was thought to be inappropriate. On the contrary, urine Epo was not detected by the same method of serum Epo determination in spite of aggressive dialysis with distilled water. When four patients with severe anemia were subcutaneously administered recombinant Epo 6,000 unit two times a week, they showed marked improvement in Hb/Hct/RBC. The precise mechanism of anemia in NS was not elucidated by this investigation, but further study should clarify the causes of the inappropriately low concentration of serum Epo in patients with primary nephrotic syndrome.
 ...
PMID:Characteristics of anemia in patients with nephrotic syndrome. 793 64

To clarify the natural history of IgA nephropathy and to determine important factors in the progressive loss of renal function in affected patients, 121 patients with IgA nephropathy were followed for a median of 92 months. The cumulative probability of not progressing to end-stage renal failure (that is, of renal survival) was 0.87 at 15 years after the onset of 1st symptoms and 0.86 at 10 years after presentation and biopsy. Eight percent of patients progressed to end-stage renal failure, and 12% had a greater than 20% decline in renal function. A complete remission of disease activity was seen in 12% of patients, and the remaining 68% maintained stable renal function. When the final serum creatinine was expressed as a percentage of the initial serum creatinine for each patient and compared with all other variables, a number of factors were found to affect renal outcome. Of the presenting features, increased age, family history of nephritis, longer duration of symptoms, and presence of either nephrotic-range proteinuria or hypertension were all associated, by univariate analysis, with an adverse outcome, while a history of recurrent macroscopic hematuria and infection-associated exacerbations of disease activity were associated with a favorable outcome. Multivariate analysis showed that nephrotic-range proteinuria had an independent adverse effect. Of the initial laboratory findings, by univariate analysis, the number of hyaline casts, the degree of impairment of renal function, the degree of proteinuria, raised beta globulins on serum protein electrophoresis, and serum C4 concentrations were all associated with an adverse outcome, while the severity of initial hematuria and pyuria were associated with a favorable outcome. Renal biopsy findings associated with an adverse outcome by univariate analysis include, on light microscopy, the percentage of glomeruli with global sclerosis or segmental sclerosis or adhesions, the degrees of tubular atrophy or interstitial fibrosis, interstitial inflammation and blood-vessel thickening, and, on immunofluorescence, the intensity of IgA deposition. Multivariate analysis showed independent adverse effects on renal outcome of global glomerulosclerosis, segmental glomerulosclerosis or adhesions, and a combined mesangial and capillary wall deposition of IgM. Features at final assessment or during follow-up associated with an adverse outcome include, by univariate analysis, the number of hyaline casts, the degree of impairment of renal function, the degree of proteinuria, reduced serum IgG and IGM concentrations, reduced final IgA expressed as a percentage of the initial IgA concentration, transient decreases of creatinine clearance during follow-up of > 10% or > 20%, and persistence or development of hypertension.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:IgA nephropathy: analysis of the natural history, important factors in the progression of renal disease, and a review of the literature. 815 67


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