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)

Nineteen patients, 20 to 47 years old with heroin addiction and renal disease, were studied. Patients with pre-existing systemic disease that can cause renal pathology were excluded. The mean duration of the addiction was 3.8 +/- 8 years. Most of the patients had the nephrotic syndrome. Renal biopsy revealed focal histological changes in 10 patients (5 with focal sclerosis) and diffuse changes in 9. Immunofluorescence studies done in 17 patients revealed diffuse deposition of IgG and beta 1C in 11 patients and focal deposits in 6 (mostly IgM). They were followed for a period ranging from 7 to 67 months. Most patients experienced progressive deterioration of renal function except in 4 cases in whom there was cessation of the drug addiction. These 4 displayed a rise in glomerular filtration rate (from 87 +/- 16 to 100 +/- 11 ml/min), marked reduction in proteinuria (from 6.5 +/- 2.6 to 0.4 +/- 0.1 g/24 hr) and an increase in serum albumin (from 3.2 +/- 0.5 to 4.0 +/- 0.1 g/dl). In summary, the fact that the renal abnormalities of our patients could not be explained by other diseases and the marked improvement upon cessation of the addiction favors the notion that heroin addiction "per se" may be the cause of the nephropathy. However, the heroin nephropathy was not manifested by a specific histological or immunofluorescence pattern.
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PMID:Heroin associated nephropathy: clinical and histological studies in 19 patients. 42 56

Patients with nephrotic syndrome have low blood levels of 25 hydroxyvitamin D (25-OH-D) most probably because of losses in urine, and a vitamin D-deficient state may ensue. The biological consequences of this phenomenon on target organs of vitamin D are not known. This study evaluates one of these target organs, the bone. Because renal failure is associated with bone disease, we studied six patients with nephrotic syndrome and normal renal function. The glomerular filtration rate was 113+/-2.1 (SE) ml/min; serum albumin, 2.3+/-27 g/dl; and proteinuria ranged between 3.5 and 14.7 g/24 h. Blood levels of 25-OH-D, total and ionized calcium and carboxy-terminal fragment of immunoreactive parathyroid hormone were measured, and morphometric analysis of bone histology was made in iliac crest biopsies obtained after double tetracycline labeling. Blood 25-OH-D was low in all patients (3.2-5.1 ng/ml; normal, 21.8+/-2.3 ng/ml). Blood levels of both total (8.1+/-0.12 mg/dl) and ionized (3.8+/-0.21 mg/dl) calcium were lower than normal and three patients had true hypocalcemia. Blood immuno-reactive parathyroid hormone levels were elevated in all. Volumetric density of osteoid was significantly increased in three out of six patients and the fraction of mineralizing osteoid seams was decreased in all. Evidence for an increase in active lacunae (bone-osteoclast interface) occurred in three out of six patients and in inactive (Howship's lacunae) bone resorption in six out of six. The data indicate that the loss of 25-OH-D in urine of patients with nephrotic syndrome and normal renal function may result in a decrease of blood levels of ionized calcium, secondary hyperparathyroidism and enhanced bone resorption. In addition, the vitamin D-deficient state causes osteomalacia as evidenced by defective mineralization and increased osteoid volume.
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PMID:Osteomalacia and hyperparathyroid bone disease in patients with nephrotic syndrome. 42 68

From the urine of a patient with proteinuria, the albumin protein component was isolated and compared with human serum albumin. By comparing the amino acid composition of the original proteins and their large cyanogen bromide fragments, peptide maps and N-terminal sequences of 33 amino acid residues, the identity of both proteins was shown.
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PMID:Chemical characterization of human urine albumin in proteinuria. 44

Plasma and urinary antithrombin III (AT-III) was measured in 15 cases of nephrotic syndrome. Plasma AT-III correlated well with serum albumin, but poorly with proteinuria, whereas urinary AT-III correlated well to proteinuria. The plasma AT-III level had a mean similar to 25 healthy controls, but the range was significantly wider. A case with nephrotic syndrome and left renal vein thrombosis is reported. The urinary output of AT-III rose and the plasma level fell with the activity of the disease. Although AT-III and albumin have similar molecule weight, their renal clearance was found to be different. It is suggested that urinary loss of AT-III plays a role in the hypercoagulable state sometimes found in the nephrotic syndrome.
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PMID:Antithrombin III and the nephrotic syndrome. 47 63

We have investigated the pathogenesis of glomerular hypercellularity seen in acute serum sickness nephritis induced in rabbits with bovine serum albumin (BSA). The increase in cellularity began with the first stages of immune clearance of BSA, with a peak cellularity occuring at the time of onset of proteinuria. Although there was a significant increase in the fraction of glomerular cells incorporating [3H]thymidine, first seen at the onset of proteinuria, this increase occurred too late and was too small to explain the observed rate of increase in glomerular cellularity. On the other hand, a striking monocytic infiltration of the glomeruli was documented by electron microscopy and by staining for nonspecific esterase. This monocytic infiltration paralleled the observed course of glomerular hypercellularity and was quantitatively sufficient to explain the total increase seen. It appears, therefore, that glomerular hypercellularity seen in this model is principally a result of monocyte infiltration.
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PMID:The role of monocytes in serum sickness nephritis. 47 58

Penicillamine has been successfully reintroduced and continued for a minimum of 13 months in 5 patients who developed proteinuria during the first course of the drug. The daily maintenance dose during the second course was 150--250 mg taken midway between 2 meals. Proteinuria did not recur; no significant excretion of fibrin degradation products occurred; complement, urea, creatinine, and serum albumin remained within normal limits. Urine microscopy showed no abnormality.
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PMID:Resumption of treatment with penicillamine after proteinuria. 48 79

The competitive protein vinding assay for the measurement of thyroxine in blood serum was modified for the measurement of thyroxine in urine. Samples of urine of 1 to 5 ml volume containing 0 to 5 ng/ml could be assayed with 100% recovery, and above this range, up to 10 ng, recoveries were higher due to non parallelism with the standard curves. Tests carried out using porcine serum albumin indicate that results obtained by the method are not likely to be affected by proteinuria. The cross reaction with triiodothyronine was 25%. Analysis of urine samples stored at 25 degrees C gave higher values than those stored at +4 degrees C or --20 degrees C over similar periods. These increases at 25 degrees C were of the same magnitude as those obtained by acid hydrolysis of urinary thyroxine conjugates.
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PMID:The measurement of thyroxine in urine using a competitive protein binding technique. 57 13

Studies of renal tubular functions were made in two groups of patients with biopsy-proven primary glomerulonephropathies to assess the effects of proteinuria on the tubules. Group I (n = 9) had had minimal proteinuria and Group II (n = 8) had massive proteinuria. At the time the studies were made, all patients were normotensive, free of oedema, and on no dietary or drug therapy; they had normal glomerular filtration rates, serum albumin and total protein concentrations. Patients in Group II had diminished urine concentrating ability, impaired acidifying mechanism, but elevated maximum tubular secretory capacity compared with patients in Group I.
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PMID:Massive proteinuria and its effects on renal tubular functions. 60 Sep 66

Seventeen rabbits were given a single, large dose of bovine serum albumin (BSA) intravenously. Percutaneous kidney biopsy was carried out on the 14th and 31st days after BSA administration. Proteinuria was measured and the glomerular changes were analysed in order to find a correlation between the degree of proteinuria and glomerular alterations, i.e. number of electron-dense deposits (EDD), polymorphonuclear leukocytes (PMNL), and mononuclear marcophages (MNM). The results speak in favour of the decisive role of mononuclear macrophages in enhancement of glomerular permeability.
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PMID:Experimental studies on factors causing acute serum sickness glomerulonephritis of immune complex origin. II. Pathomorphological analysis. 60 22

To study some of the aspects of albumin homeostasis and proteinuria in PNS, the hepatic production of albumin is analyzed using semiquantitative immunofluorescent techniques, in biopsy specimens from nine subjects, free of hepatic or renal disease and nine patients with PNS, where renal biopsies were also made. Tissue sections 0.5 millimicron thick were cut. The hepatic synthesis of albumin, interpreted by the number of cells with specific fluorescence, was much higher in patients with PNS (p less than 0.001), and kept inverse relationship with serum albumin concentrations. Numberless droplets containing albumin were observed in the renal tissue indicating intense resorption and catabolism in the luminal and basal portions of the proximal convoluted tubules. Our findings indicate that, in PNS, albumin synthesis is substantially increased and hypoalbuminemia is caused by exaggerated renal excretion and catabolism.
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PMID:Hepatic synthesis and albumin distribution in the primary nephrotic syndrome (PNS). as demonstrated by immunofluoresce. 70 87


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