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)

Splenectomised calves in metabolism cages were infected with Babesia bovis. During the infection, urine samples were collected and analysed for electrolytes, proteins, kinin, and urinary kallikrein. During the later stages of the infection there were significant reductions in urinary volume, water intake, urinary kinin, kallikrein, and electrolytes. Proteinuria was detected from 3--8 days postinfection of which 15--20% was haemoglobin and most of the remainder was albumin (70--75%). Fibrin degradation products, fibrinogen-like products, and haptoglobin were not detected. Degeneration of cortical tubules was detected by histological studies. As these tubules produce urinary kallikrein it seems probable that diminished glomerular blood flow and hence glomerular filtration rate are due to decreased production of this enzyme.
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PMID:Acute Babesia bovis infections: renal involvement in the hypotensive syndrome. 49 8

Urinary kallikrein excretion was studied in two types of experimentally induced renal disease: anti-glomerular basement membrane nephritis (20 rats) and aminonucleoside nephrosis (five rats) with appropriate controls (23 rats) for a period of 6 to 9 weeks following disease induction. In both models there was a prompt significant decrease (p less than 0.01 - 0.001) in urinary kallikrein excretion associated with proteinuria but unrelated to urinary sodium and potassium excretion and urinary volumes. In antiglomerular basement membrane nephritis the fall in kallikrein excretion occurred within the first 24 hours concurrent with the onset of proteinuria. In aminonucleoside nephrosis the decrease antedated the onset of proteinuria by 48 hours beginning within the first 24 hours following injection of the aminonucleoside. Kallikrein inhibitors were not demonstrable in the urines of diseased animals from either model. The mechanism of the decrease in kallikrein excretion in immune and nonimmune glomerular disease associated with proteinuria is unknown.
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PMID:Urinary kallikrein in experimental renal disease. 93 67

Involvement of the kallikrein-kinin system in the pathogenesis of renal edemas may be mediated by increase of vascular permeability, proteinuria, diuresis and natriuresis. Proceeding from these points, in 27 patients with morphologically proved chronic glomerulonephritis and the nephrotic syndrome, the serum kallikrein activity and its 24-hour urinary excretion level were measured. According to their edematous syndrome severity, all the patients were divided into 2 groups: 1) 19 patients with moderate edemas; 2) 8 patients with severe ones. During the follow-up period, there were no essential changes in patients' body weights, and no significant differences between the groups in clearances and excreted fractions of sodium, potassium, chlorine, osmotically active substances, and in serum albumin and cholesterol levels, 24-hour protein losses and blood pressure. As compared to the healthy (n-20) in all the patients a substantial and statistically significant increase in kallikrein activity was revealed in serum and urine. Kallikreinemia and kallikreinuria were significantly higher in Group 2 than those in Group 1. In the total group of examinees a significant direct relationship was established between the urinary kallikrein activity and summary sodium and potassium excretion as well as between the serum kallikrein activity and chlorine clearance. A direct correlation between the serum kallikrein activity and proteinuria was also found. Thus, a role of the kallikrein-kinin system in development of glomerulonephritic edemas concurrent with the nephrotic syndrome is hetero-directional.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The participation of the kallikrein-kinin system in edema formation in glomerulonephritis]. 185 8

In order to investigate the validity of urinary kallikrein (KAL) measurement, comparative studies were performed among the values obtained by various methods of urinary KAL measurements. Daily urine samples were collected from 37 hospitalized normal subjects (NS, 21 essential hypertensives without complications (EHT) and 20 patients with renal diseases associated with proteinuria (PU). Urinary KAL excretions were determined by direct radioimmunoassay (RIA), kininogenase assay (K-genase), TAMe esterase assay (TAMe), and PPA-MCA (MCA) and PPA-NE amidase assay (NE). By the desalting procedure, urinary KAL levels showed significant changes in TAMe, MCA and NE, but not in d-RIA and K-genase in all three groups. In TAMe, MCA and NE, the recovery of added KAL in urine was significantly lower in non-desalted samples in both EHT and PU, but not in NS. Impaired recovery and correlations between d-RIA or K-genase and TAMe, MCA or NE in non-desalted samples were improved by desalting. Although good correlations were observed between d-RIA or K-genase and TAMe, MCA or NE in desalted samples, the slopes of curves were steeper in EHT and PU than in NS, suggesting that the synthetic substrate methods still have some problems in the KAL measurement in these pathological states, KAL inhibitor, aprotinin and gabezate mesilate did not suppress the esterclytic and amidolytic activities completely, but suppressed K-genase activity completely in PU urine samples, suggesting that certain kinds of non-KAL esterases might remain in PU urine samples. Thus, d-RIA and K-genase appear to be the most reliable methods in the measurement of urinary KAL quantity and activity, respectively.
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PMID:A comparative study of the measurement of urinary kallikrein by various methods in patients with essential hypertension and patients with proteinuria. 364 32

Fawn-hooded (FH) rats, primarily males, develop spontaneous low-renin hypertension associated with reduced urinary excretion of kallikrein as early as 2 months of age, followed by progressive glomerular sclerosis and proteinuria as early as 3 months of age. In the present study we determined the effects of early (5-7 weeks) or late (5 months) orchiectomy on the blood pressure and nephropathy of FH rats, compared to sham-operated (control) FH males. Early orchiectomy reduced significantly the progression of glomerular sclerosis and of proteinuria and ameliorated the hypertension but had no significant effect on excretion of urinary kallikrein. Late orchiectomy, in contrast, had no significant effect on the progression of glomerular sclerosis or proteinuria but did significantly reduce the blood pressure and marginally increase the excretion of urine kallikrein. These results suggest that (a) male sex hormones may play a role in the pathogenesis of hypertension and nephropathy in the FH rats and (b) renal disease in this strain progresses in spite of improvement in blood pressure.
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PMID:Contrasting effects of early and late orchiectomy on hypertension and renal disease in fawn-hooded rats. 365 Jun 58

Urinary excretion of kallikrein (UKal), sodium, potassium, protein, and creatinine, as well as the kidney content of kallikrein and renin, was studied in spontaneously hypertensive FH/Wjd (FH) male and female rats and in age- and sex-matched normal Wistar rats. With the exception of 1-month-old rats UKal excretion was significantly lower in FH rats than in Wistar rats. FH females also excreted less UKal than Wistar females. No UKal inhibitor or increased degradation of this enzyme in the urine of FH rats was detected. There was no difference in creatinine clearance, blood urea nitrogen, or serum electrolytes, and calcium between 5-month-old FH and Wistar males. Wistar rat kidneys contained about twice as much kallikrein as FH rat kidneys. From the age of 2 months FH males excreted more sodium, as well as urine, than all other groups. No differences in potassium excretion were observed. Only FH males, 4 months and older, developed proteinuria. FH males and females became hypertensive at the ages of 2 and 4.5 months, respectively. Plasma renin activity, as well as renal renin activity, was significantly lower in FH than in Wistar males. In conclusion, the decrease in UKal activity which precedes the onset of hypertension suggests that the abnormality in the renal kallikrein system may be involved in the pathogenesis of hypertension in FH rats.
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PMID:Urinary and renal kallikrein in hypertensive fawn-hooded (FH/Wjd) rats. 636 17

Urinary excretions of active and inactive renin were studied in normal subjects and in patients with hypertensive or renal disease. Excessive excretion of active and inactive renins was observed in some patients with no significant correlation to their plasma levels or the degree of proteinuria. Inactive renin excretion correlated to active renin excretion, but the clearance was lower than that of the active form. No correlation was found between the urinary kallikrein excretion and the active/inactive renin ratio in the urine or the plasma. Urinary renin activity was increased by acidification and by trypsin treatment, but not by cold exposure. Both active and inactive renins in the urine showed multiple peaks corresponding to molecular weights between 45,000 and 64,000 by gel filtration.
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PMID:Active and inactive renins in human urine. 675

Iodine-labeled ([125I]) rat urinary kallikrein and rat urinary TAME esterase A2 were used as probes to look for urinary and plasma proteins that bind to these enzymes. Such proteins are presumptive enzyme inhibitors. Complexes formed with labeled enzymes were identified by polyacrylamide gel electrophoresis followed by autoradiography. Urine from young (6 weeks old) Dahl salt-sensitive (S) rats showed no, or only traces, of protein binding to kallikrein. Concomitant with the slow development of hypertension and proteinuria in S rats fed normal rat chow, one of the six kallikrein-binding proteins demonstrable in plasma was readily found in S-rat urine. This kallikrein-binding protein was called "KBP-1." R rats showed either no or much less KBP-1 in the urine, compared to S rats up to 5 months of age. A partly purified preparation of KBP-1 was shown to inhibit the TAME esterase activity of rat urinary kallikrein in the radiometric TAME assay. Urine of proteinuric S rats also contained two TAME esterase-binding proteins, TEBP-1 and TEBP-2, detected with the [125I]-esterase A2 probe. As S rats aged from 3 to 8 months, free KBP-1 disappeared from the urine in spite of increased and marked proteinuria and the continued presence of KBP-1 in plasma. Concomitant with this age-related loss of urinary KBP-1 there was a marked shift in S urinary proteins binding to [125I]-esterase A2 from TEBP-1 to TEBP-2. It was speculated that KBP-1 and TEBP-1 were the same protein detectable with either labeled kallikrein or labeled esterase A2. The concomitant disappearance of free KBP-1 (TEBP-1) and the appearance of free TEBP-2 in the urine of old, hypertensive, proteinuric S rats suggests that: 1) most of the KBP-1 (TEBP-1) is bound to enzyme(s) in old rats; or 2) KBP-1 (TEBP-1) is largely converted to TEBP-2 in old rats; or 3) both are true and that binding of KBP-1 (TEBP-1) to enzymes is associated with the generation of TEBP-2.
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PMID:Proteins binding to kallikrein and esterase A2 in the urine of salt-sensitive and salt-resistant rats. 675 95

S and R female rats were raised on a 1% NaCl diet, and excretion rates of urinary protein, kallikrein esterase activity, and PGE2 were measured (1) at 1 1/2 months of age, when both S and R rats were normotensive, (2) at 3 months of age, when S rats were mildly hypertensive and R controls remained normotensive, and (3) at 6 months of age, when S rats were markedly hypertensive relative to the still normotensive R rats. Urinary protein excretion rate in S compared to R rats was slightly elevated at 1 1/2 months of age and greatly elevated at 3 and 6 months of age. Urinary kallikrein was measured by hydrolysis of TAME after separation of kallikrein from nonkallikrein TAME esterases on DEAE-Sephadex minicolumns. Kallikrein TAME esterase activity was the same in 1 1/2-month-old S and R rats but became reduced in S relative to R rats at 3 and 6 months of age, concomitant with the development of hypertension and marked proteinuria. Urinary PGE2 was decreased in S rats as compared to R rats at all ages, and therefore the strain difference in urinary PGE2 preceded the development of strain differences in blood pressure and urinary kallikrein activity. We conclude that (1) reduced excretion of urinary kallikrein TAME esterase activity in S rats is probably secondary to hypertension and severe proteinuria and (2) decreased urinary PGE2 excretion in prehypertensive S rats is compatible with, but does not prove, the presence of a primary defect in intrarenal PGE2 production that could be involved in initiating hypertension.
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PMID:Developmental patterns of blood pressure and urinary protein, kallikrein, and prostaglandin E2 in Dahl salt-hypertension-susceptible rats. 691 75

Previous evidence shows that salt-sensitive (S) rats have a net increase in plasma mineralocorticoid activity due to 18-hydroxy-11-deoxycorticosterone and decreased urinary kallikrein excretion compared to salt-resistant (R) rats. Since mineralocorticoids stimulate urinary kallikrein excretion, these results are inconsistent. This inconsistency was explained by the fact that, while R rats responded normally to treatment with deoxycorticosterone (DOC) by an increase in urinary kallikrein excretion, S rats showed no change in urinary kallikrein even when treated with 10 mg of DOC/day for 24 days. S and R rats responded identically to DOC with changes muscle electrolytes and relative hypertrophy of the renal distal tubule. Other measures of chronic mineralocorticoid response in S rats beside kallikrein were, therefore, intact. It was found that S rats were capable of responding to Na deficient diet with an increase in urinary kallikrein comparable to R rats. It was argued, therefore, that mineralocorticoid receptor mechanisms and distal-tubular cell responsiveness are intact in S rats. Mild glomerular and tubular scarring was found in S rats and the severity of renal lesions was increased by DOC treatment in S rats. These lesions correlated well with blood pressure and proteinuria. No such lesions were present in control or DOC treated R rats. It was suggested that failure of urinary kallikrein to respond to DOC in S rats may be a secondary phenomenon resulting from renal damage.
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PMID:Anomalous response of urinary kallikrein to deoxycorticosterone in Dahl salt-sensitive rats. 691 11


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