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)

Since intravascular volume contraction is regarded as an important pathological feature in preeclampsia, it has been proposed that plasma volume expansion could be a therapeutic manoeuver that interrupts the pathogenetic chain of hypovolemia inducing increased vascular resistance. Furthermore, tissue perfusion should be improved and, if albumin is used as plasma expander agent, interstitial edema should also be reduced. We report the results observed in an open pilot study in ten preeclamptic patients treated with daily albumin infusions (0.4 to 1 g/kg) from 7 to 36 days. No acute effects were shown on blood pressure, and the need for antihypertensive therapies did not decrease in the following days. Serial evaluation after at least five or ten days of repeated albumin infusions did not show stable changes in electrolytes excretion, renal clearances, serum protein concentration and hematocrit value, nor in aldosterone, renin and atrial natriuretic peptide basal levels, while proteinuria tended to increase. Uteroplacental and fetoplacental blood flow acutely ameliorated in 3 cases only after albumin 1 g/Kg, but reached basal values again on the next day. The clinical implications are that daily albumin infusions with this schedule dosage do not lower blood pressure and that they are unable to induce stable changes in renal function, uteroplacental and fetoplacental resistance. No maternal complications were observed during the conservative management, but fetal mortality was high (6/10). Given the uncontrolled study, we cannot know whether similar results had been achieved by conventional therapy only.
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PMID:Repeated albumin infusions do not lower blood pressure in preeclampsia. 175 73

We retrospectively analysed the effects of a 12-month treatment with captopril (Tensiomin) in 46 patients. All of the patients had hypertension lasting for years (9 essential, 37 with chronic renal failure), 32 of them had proteinuria. Captopril was given in addition to, or in exchange for, other antihypertensive drugs. Under treatment with ACE-inhibitors, a small but significant decrease in diastolic blood pressure (0.4 torr/month) and in proteinuria (0.19 g/month) was seen (regression analysis). Discriminant analysis showed proteinuria and diastolic blood pressure to be the more modifiable, the younger the patients, the higher the proteinuria at the beginning and the longer the history of hypertension. Serum creatinine, blood urea nitrogen, serum protein and serum potassium did not change.
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PMID:[Effect of the ACE-inhibitor captopril on the blood pressure and kidney function of patients with essential and renal hypertension]. 177 7

We report a transient neonatal nephrotic syndrome in two infants born to a mother with idiopathic nephrotic syndromes (INS). The mother, born in Mali in 1966, had a normal first pregnancy, with a normal live child. Six months later a nephrotic syndrome appeared with normal renal function; renal biopsy disclosed slight lesions of focal and segmental glomerulosclerosis. Prednisone and ciclosporin were totally ineffective. In 1986 and 1988 two pregnancies occurred with normal gestation outcome; however, the two births were premature (35 weeks) with hypotrophic infantas (2.160 and 2.080 kg). In both cases urine analysis revealed neonatal heavy proteinuria, with low serum protein and hypoalbuminemia; proteinuria decreased and disappeared within 2 and 3 weeks respectively; simultaneously protidemia and albuminemia were normalized. Thus, a transitory nephrotic syndrome, resolving spontaneously, occurred in two successive offsprings of a patient with INS. These cases are in keeping with the hypothesis that heavy proteinuria in nephrotic syndrome might be linked to a circulating humoral factor and that INS is a disorder linked to T-lymphocyte function with enhanced production of a lymphokine acting on vascular permeability.
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PMID:[Transmission of nephrotic syndrome to two neonates. Spontaneous regression]. 182 64

We report the identification and initial family and population studies of a previously undescribed serum protein polymorphism with two allelic forms. It was discovered in Hutterites, a reproductively isolated religious sect, and is also present in Australian aborigines and a sample of Chicago residents. A two-allele model is consistent with the segregation pattern observed in five kindreds within our initial study group. This polymorphism, provisionally designated SPPM-158, appears as a horizontal (charge-based) doublet in silver-stained ISO-DALT high-resolution two-dimensional electrophoresis gels. It is a low-concentration polypeptide (approximately 1 mg/dL) that has an apparent MWSDS of 43.6 kD and an isoelectric point of approximately 5.5. We infer that it circulates as a multimer or in a high-molecular-weight (greater than 200 kD) complex with other proteins because it is not observed in normal body fluids derived from physiologically ultrafiltered plasma such as amniotic fluid, urine, or cerebrospinal fluid; however, it is present in urine of patients with glomerular proteinuria. The high heterozygosity rates imply utility of this new serum protein marker for both forensic and population studies.
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PMID:Identification of a serum protein polymorphism via two-dimensional electrophoresis. Family and population studies in two genetically isolated groups: North American Hutterites and Australian aborigines. 199 Aug 42

The membrane attack complex of complement (MAC) plays an important role in the mediation of proteinuria in experimental membranous nephropathy induced by Heymann antiserum. SP-40,40 is a recently described serum protein which appears to inhibit the formation of cytolytic MAC in a manner analogous to S protein/vitronectin. SP-40,40 is homologous to proteins originally isolated from rat and ram seminal fluid (sulfated glycoprotein 2 and clusterin, respectively). By current convention, these proteins are considered clusterin homologues. The objective of this study was to examine the participation of rat clusterin in passive Heymann nephritis. Using an antibody to rat clusterin as an immunofluorescent probe, clusterin deposits were demonstrated along the glomerular capillary wall in an identical pattern to rat C3 and C5b-9. Decomplementation using cobra venom factor prevented proteinuria and intraglomerular MAC formation. The epimembranous clusterin were not detected in the complement-depleted animals. The role of clusterin in the mediation of glomerular injury remains unknown, but it is probably related to in situ formation of the terminal complement cascade where it may play a regulatory role.
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PMID:Localization of clusterin in the epimembranous deposits of passive Heymann nephritis. 200 38

We measured plasma fibronectin levels by a rocket immunoelectrophoresis in rats with chronic serum sickness induced by repeated injections of ovalbumin and in rats with epithelial nephropathy induced by a single injection of adriamycin. In the early phases of the immune model, rats presented granular deposits of IgG in the mesangial area with no or descrete proteinuria (less than 40 mg/24 h). Fibronectin levels in that group were significantly higher (450 +/- 90 micrograms/mL) than in normal rats of the same age (350 +/- 46; p less than 0.01). When animals presented IgG deposits in the capillary wall, an important nephrotic syndrome developed in most of them. Fibronectin levels then increased very significantly (863 +/- 153 micrograms/mL; p less than 0.0005). In the model of adriamycin nephropathy, fibronectin significantly increased (580 +/- 110 micrograms/mL; p less than 0.0005) from the first week, when proteinuria was in a range 40-60 mg/24 h. However, the levels were higher (860 +/- 175 micrograms/mL; p less than 0.0005) when a complete nephrotic syndrome developed. At this time, plasma fibronectin levels correlated directly in both models with the degree of proteinuria and inversely with the total serum protein concentration. Our results show that plasma fibronectin levels increased very early in animals with immune and toxic damage of the kidney. The highest elevated values found thereafter, when a full nephrotic syndrome was present, suggest an increased synthetic rate of that glycoprotein linked to that situation.
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PMID:Elevated plasma fibronectin levels in rats with immune and toxic glomerular diseases. 210 Aug 26

Wistar rats were injected with puromycin aminonucleoside (PAN) to induce massive proteinuria and were raised on a low protein diet to determine whether the urinary protein excretion might be reduced. Although PAN nephrotic rats fed with a normal protein diet containing 20% protein (group A) did not show any reduction of their urinary protein excretion, PAN rats fed with a low protein diet containing 6% protein (group B) revealed a marked reduction at day 9 of the present study in comparison with group A. The total serum protein levels were low in groups A and B as compared to group C, the non-treated control. However, group A recovered to normal levels at day 13. In terms of the absolute amount of oral protein intake, marked differences were observed between groups B and C, but little difference was observed between groups A and C. The body weight in all three groups was decreased at 8 days after the start of this study. The serum levels of creatinine were elevated to 1.1 +/- 0.3 mg/dl and 1.0 +/- 0.2 mg/dl in groups A and B, respectively, on day 7, but abruptly recovered to normal levels by day 12. These data indicate that the decreased urinary protein excretion in group B might be dependent on the total protein volume intake, and not on the renal function nor serum levels of total protein.
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PMID:Effects of low protein diet in puromycin aminonucleoside-induced nephrotic rats. 225 Apr 4

The nephrotic syndrome is characterized by the increased urinary excretion of albumin and of other serum proteins of intermediate molecular weight accompanied by a decrease in their serum concentration. Albumin synthesis is increased at the level of mRNA synthesis in response to decreased serum oncotic pressure. However, the magnitude of these responses is dependent upon dietary protein and is insufficient to normalize serum albumin. The absolute rate of albumin catabolism is decreased, serving to normalize serum albumin stores, but in contrast to what occurs in other hypoalbuminemic states, the fractional rate of albumin catabolism is increased. This observation is consistent with a hypothesis that increased renal catabolism contributes to total albumin catabolism in nephrosis. Like albumin, IgG is lost in the urine, its serum concentration is decreased, and the fractional rate of its catabolism is increased, suggesting that the kidney contributes to IgG catabolism in the presence of proteinuria. IgG synthesis responds in a variable fashion in the nephrotic syndrome, and may be decreased, thus contributing to its reduced serum concentration. In contrast, the serum concentration of the high-molecular-weight immunoglobulin IgM is increased, as is the serum concentration of a variety of high-molecular-weight liver-derived proteins. It is unknown by what mechanism serum IgM concentration is increased, but this response serves to defend serum protein concentration and oncotic pressure.
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PMID:Metabolism of albumin and immunoglobulins in the nephrotic syndrome. 225 74

Radiation nephritis is the principle late toxicity seen after total body irradiation in barrier-maintained rats when hematologic toxicity is prevented by bone marrow transplantation. Renal dysfunction is observed for single doses as low as 7.5 Gy. Hepatic blood flow, as measured by indocyanine green clearance, is decreased after 8.5-9.5 Gy single-dose total body irradiation. Serum albumin levels are decreased after 9.5 Gy single-dose total body irradiation. Hypoalbuminemia is a symptom of hepatic damage, but can also be caused by renal damage or edema. No decrease in total serum protein is observed, indicating that proteinuria resulting from renal damage is not the cause of hypoalbuminemia. No edema and some dehydration are observed. These data indicate that hepatic damage as well as renal damage may be occurring after total body irradiation plus bone marrow transplantation. Animals given total body irradiation plus bone marrow transplantation show decreased tolerance to a wide variety of immunosuppressive and cytotoxic drugs, even when these drugs are given months after total body irradiation. Altered drug clearance after total body irradiation plus bone marrow transplantation is observed for cis-platinum, vincristine, and adriamycin. The increase in cis-platinum toxicity after total body irradiation plus bone marrow transplantation is caused by decreased renal drug clearance. The decrease in vincristine tolerance and the alterations in adriamycin and vincristine pharmacokinetics are caused by altered drug distribution after total body irradiation plus bone marrow transplantation. These results indicate that bone marrow transplant survivors may show altered clearance of, and decreased tolerance to, a wide variety of drugs that are used after bone marrow transplantation.
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PMID:Hepatic function and drug pharmacokinetics after total body irradiation plus bone marrow transplant. 226 63

The effect of the converting enzyme inhibitor (CEI) (captopril, 50 mg/kg/day) on proteinuria (UProt), urinary aldosterone (UAldoV), plasma renin activity (PRA), plasma renin concentration (PRC), plasma angiotensinogen concentration (PAC), urinary sodium (UNaV), serum total protein, and body weight was studied for 21 days in an experimental nephrotic syndrome (NS) model induced in rats by a single injection (15 mg/100g) of puromycin aminonucleoside (PA). The effect of captopril on control rats without NS was also characterized. In control rats, captopril increased PRC and PRA, and decreased PAC; it had no effect on UNaV, UAldoV, UProt, total serum protein and body weight. In rats with NS, captopril had no effect on sodium retention, hypoproteinemia, and UProt; it abolished the increased UaldoV and favored weight loss. Captopril also rose PRA and PRC, and decreased PAC in PA-nephrotic rats; these changes were similar to those produced by captopril in control rats. The mortality rate was higher in nephrotic rats treated with captopril (37%) than in untreated nephrotic rats (13%). It is concluded that captopril has no beneficial effects on the course on NS induced by PA during the first 21 days, and supports the contention that sodium retention is not related to the renin-angiotensin-aldosterone system activity in these rats.
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PMID:Pathophysiology of experimental nephrotic syndrome induced by puromicyn aminonucleoside in rats. III. Effect of captopril, an angiotensin converting enzyme inhibitor, on proteinuria and sodium retention. 227 Mar 68


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