Urinary Excretion of Apolipoproteins Bound to HDL-Like Particles in Rat Nephrotic Syndrome and Their Relation to Plasma HDL

Nephron ◽  
1990 ◽  
Vol 56 (1) ◽  
pp. 24-29 ◽  
Author(s):  
Eleazar Shafrir ◽  
Emile Levy ◽  
Richard Deckelbaum
Keyword(s):  
Nephrotic Syndrome ◽  
Urinary Excretion

CORTICOSTEROIDS AND ANTIDIURETIC SUBSTANCE IN NEPHROTIC CHILDREN

PEDIATRICS ◽  
1953 ◽  
Vol 12 (3) ◽  
pp. 233-252
Author(s):  
ENRIQUE GALÁN ◽  
MANUEL PÉREZ-STABLE ◽  
ORLANDO GARCÍA FAEZ ◽  
EMILIO UNANUE ◽  
OTTO GARCÍA ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Urinary Excretion ◽  
Ascitic Fluid ◽  
Renal Hemodynamics ◽  
Tubular Function ◽  
Urinary Flow ◽  
Adrenal Steroids ◽  
Functional Disturbance ◽  
Urinary Steroids ◽  
Nephrotic Children

The role of tubular reabsorption in the pathogenesis of nephrotic edema led the authors to study the participation of antidiuretic hormone and adrenal steroids in regard to changes in renal hemodynamics and tubular function during different clinical events that may induce an increase or a decrease of urinary flow in nephrotic children. Formaldehydogenic steroids in urine, plasma and ascitic fluid and serum antidiuretic substance were simultaneously studied with clearance tests, electrolyte excretion and plasma constituents through 10 different periods of observations. From previous and present studies on renal function it was found that changes in renal hemodynamics and tubular transport mechanisms are responsible for variations in urinary flow leading to accumulation or disappearance of edema in the nephrotic syndrome. An increase in urinary flow was seen to occur with no change in the GFR but with a marked decrease in the U/P inulin and potassium ratio. Serum antidiuretic substance appeared to correlate closely with antidiuresis. Injection of nephrotic sera into peritoneal cavity of rats was followed by an antidiuretic effect similar to that produced by pitressin and posterior pituitary hormone. Antidiuretic factor seemed to be present in the globulin fraction of plasma proteins. No such effect was seen with intraperitoneal injections of plasma albumin, protein-free filtrate and ascitic fluid. An increase in titer of antidiuretic substance was observed during initial doses of ACTH and the reverse at the onset of diuretic response. Urinary excretion of formaldehydogenic steroids depended partly on diuresis in nephrotic children; this was not so in control cases. The influence of tubular function was suggested by the relationship found between urinary excretion of steroids and the V/Cin and V/Cth ratio and between clearance of steroids and diuresis. The influence of renal functional disturbance prevented a correct evaluation of adrenal activity by estimation of urinary steroids in nephrotic children. During the edematous-oliguric stage of nephrosis and in the absence of any stimulating or depressing effect upon the elaboration of adrenal steroids their urinary excretion was not significantly different from that seen in control cases. Formaldehydogenic steroids did not seem to have a direct role in producing variations of urine flow in nephrotic children. Increase and decrease in diuresis occurred simultaneously with an increase and a decrease in urinary and plasma steroids and vice versa. Formaldehydogenic material was found in variable amounts in the ascitic fluid suggesting an appreciable retention in the increased extracellular fluid during the oliguricedematous stage of the nephrotic syndrome. This material appears to be mostly true adrenal steroids. Potassium excretion was related to urinary steroids in nephrotic children but not in control cases. Potassium clearance was related to glomerular filtration in both control and nephrotic children. At the present time it remains a matter of some speculation of the role that steroids present in extracellular fluids may play in the physiologic and morphologic changes known to occur in the course of the nephrotic syndrome and experimentally reproduced by injection of DOCA to animals.

scholarly journals May be Urinary Excretion of α2-macroglobulin (MW 720 kDa) a Proteinuric Marker of Podocytopathy? Insight from Analysis of 204 Patients with Glomerulonephritis (GN) and Nephrotic Syndrome, 177 with Functional Outcome

2021 ◽  
Vol 8 (3) ◽  
pp. 01-06
Author(s):  
Claudio Bazzi
Keyword(s):  
Nephrotic Syndrome ◽  
Clinical Practice ◽  
Urinary Excretion ◽  
Functional Outcome ◽  
Clinical Significance ◽  
Α2 Macroglobulin ◽  
Progression Risk ◽  
Treatment Responsiveness

Background: In IgAN with cellular crescents (CIgAN) urinary excretion of α2-macroglobulin (α2m/C, MW 720 kDa) may be a marker of podocytes damage induced by crescents. The purpose of the study was the evaluation of the clinical significance of α2m/C excretion in 177 patients with glomerulonephritis (GN), nephrotic syndrome (NS) and functional outcome. Methods: In all 177 patients α2m/C excretion was measured; the patients were divided in 2 groups: α2mC=0 (n. 72) and α2m/C >0 (n. 105); for each group were assessed the outcomes considered in combination: Remission & persistent nephrotic syndrome (PNS) with long lasting NRF designed “Remission & NRF”; ESRD & eGFR < 50% & PNS with CRF designed “Progression and progression risk”. Results: In 72 patients with α2m/C=0 “Remission & NRF” was 78% and “Progression & progression risk” was 22%; in 105 patients with α2m/C>0 “remission & NRF” was 52% and “Progression & progression risk” was 48%. “Remission & NRF” in each GN type with α2m/C=0 was: 100% in MCD and LN; 82%, 79%, 67% in FSGS, IMN, MPGN; in α2m/C>0 “Progression and progression risk” was 0%, 38%, 46%, 54%, 56%, 85% in MCD, LN, IMN, MPGN, FSGS, CIgAN with cellular crescents, respectively. Conclusion: Urinary excretion of α2m is a very simple marker available in all clinical practice laboratories, marker of damage of podocytes at least in CIgAN and LN with crescents and marker of GFB damage in different GN types and useful to predict outcome and treatment responsiveness.

Plasma concentration and urinary excretion of erythropoietin in adult nephrotic syndrome

1993 ◽  
Vol 7 (2) ◽  
pp. 201-201 ◽  
Author(s):  
N. D. Vaziri ◽  
C. J. Kaupke ◽  
C. H. Barton ◽  
E. Gonzales
Keyword(s):  
Nephrotic Syndrome ◽  
Plasma Concentration ◽  
Urinary Excretion

scholarly journals A case of nephrotic syndrome with urinary excretion of lipoproteins.

1984 ◽  
Vol 23 (3) ◽  
pp. 242-245
Author(s):  
Jun SASAKI ◽  
Kazuo IBARAGI ◽  
Junichi MIYATA ◽  
Teizo SATA ◽  
Kikuo ARAKAWA
Keyword(s):  
Nephrotic Syndrome ◽  
Urinary Excretion

STUDIES ON THE MECHANISM OF PRODUCTION OF A NEPHROTIC SYNDROME IN RATS BY A NUCLEOSIDE

PEDIATRICS ◽  
1960 ◽  
Vol 25 (2) ◽  
pp. 228-241
Author(s):  
S. G. F. Wilson ◽  
Walter Heymann ◽  
D. A. Goldthwait
Keyword(s):  
Nephrotic Syndrome ◽  
Urinary Excretion ◽  
Guinea Pigs ◽  
Adenosine Kinase ◽  
Nucleotide Level ◽  
Isolation And Characterization ◽  
Adenosine Derivatives

The dimethyl adenosine derivative originally isolated from Puromycin® produced a nephrotic syndrome in rats, but not in guinea pigs or rabbits. The urinary excretion products in these species were examined after injection of this compound. All species excreted the dimethyl- and the monomethyl adenosine derivatives. The rat and rabbit excreted the adenosine derivative and the rabbit also excreted the inosine derivative. All species excreted monomethyl adenosine and/or dimethyl adenosine derivatives substituted most likely on the sugar. The nephrotic syndrome was produced by injection of the monomethyl-, the methyl propyl-, and the diethyl adenosine derivatives, but not by the adenosine, inosine or dipropyl adenosine derivatives. The dimethyl-, monomethyl-, and adenosine derivatives inhibited to approximately the same extent a crude adenosine kinase enzyme obtained from yeast. These three compounds were also converted to nucleotides by this preparation. The dimethyl adenosine derivative was the least effective nucleotide precursor. It seems probable that several derivatives are capable of producing the nephrotic syndrome. The enzymatic locus of action may be adenosine kinase, but action at the nucleotide level has not been ruled out. Methods are indicated for the isolation and characterization of this series of nucleosides and nucleotides.

Urinary excretion of Hageman factor (factor XII) and the presence of nonfunctional Hageman factor in the nephrotic syndrome

1981 ◽  
Vol 70 (3) ◽  
pp. 531-534 ◽  
Author(s):  
Hidehiko Saito ◽  
Lawrence T. Goodnough ◽  
Sudesh P. Makker ◽  
Ronald J. Kallen
Keyword(s):  
Nephrotic Syndrome ◽  
Urinary Excretion ◽  
Factor Xii ◽  
Hageman Factor

Urinary excretion and deficiency of prothrombin in nephrotic syndrome

1984 ◽  
Vol 77 (3) ◽  
pp. 433-436 ◽  
Author(s):  
Nosratola D. Vaziri ◽  
Julianne Toohey ◽  
Petra Paule ◽  
Eleanor Hung ◽  
Riad Darwish ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Urinary Excretion

Plasma and Urinary Heparin Cofactor II Levels in Patients with Nephrotic Syndrome

1988 ◽  
Vol 60 (02) ◽  
pp. 137-140 ◽  
Author(s):  
E Grau ◽  
A Oliver ◽  
J Félez ◽  
P Barceló ◽  
C Fernandez ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Urinary Excretion ◽  
Plasma Levels ◽  
Healthy Subjects ◽  
Protein C ◽  
Antithrombin Iii ◽  
High Plasma ◽  
Heparin Cofactor Ii ◽  
At Iii

SummaryHeparin cofactor II (HC II) levels were measured by electroimmunoassay in plasmas and urines from 68 patients with nephrotic syndrome. In addition, antithrombin III (AT III) and protein C (PC) activities and antigens were measured also in the same group of patients. Seven of these patients had histories of thrombosis. Plasma HC II levels (mean ± SD 105 ± 43) were not different from levels in healthy subjects (94 ± 17). Only 5 patients had low plasma levels of HC II. None of the patients with thrombosis had low HC II levels. Even though measurable amounts of HC II were found in 25 urines from 50 patients. There was a relationship in the urinary excretion between HC II and AT III and their urinary clearances were quite similar. However, no correlation was found between plasma HC II and AT III levels, and levels of AT III activity and antigen were significantly lower than in healthy subjects. Three patients with hystories of thrombosis had low AT III levels. Most patients (including those with thrombosis histories) had high plasma PC levels and increased urinary loss.It is suggested that HC II does not play an important role in the pathogenesis of thrombosis in nephrotic syndrome.

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