Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.4 (trypsin)
42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Results vary with regard to the upper limits of serum amylase seen in patients with renal failure, and very little has been reported with patients with renal insufficiency not yet requiring dialysis. To determine the level of serum amylase elevation in renal insufficiency and renal failure, we determined serum amylase values in 128 subjects with creatinine clearances less than 90 ml/min. Serum amylase remained in the normal range when creatinine clearance was greater than 50 ml/min, and did not become elevated until creatinine clearance was less than 50 ml/min. The highest serum amylase recorded in the absence of acute pancreatitis was 503 IU/L (normal, less than 128 IU/L). Serum lipase and trypsin values paralleled those for serum amylase; values remained normal when creatinine clearance was greater than 50 ml/min, and were normal or elevated when creatinine clearance was less than 50 ml/min. These results indicate that elevations of serum amylase (i.e., amylase greater than 128 but less than 500 IU/L) in asymptomatic patients with impaired renal function are not evident until creatinine clearances fall below 50 ml/min, and probably do not represent acute pancreatitis.
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PMID:Serum amylase in patients with renal insufficiency and renal failure. 169 13

Isoelectric species of renin are physically heterogeneous. Recent evidence suggests that they may differ functionally, with some species producing natriuresis and diuresis, whereas others have no effect. A physiological function of secreted prorenin has not been documented in any species. The present study was designed to confirm and describe for the first time the renal effects of certain isoelectric species of prorenin. Anesthetized Sprague-Dawley rats were injected (0.1 ml) with trypsin-activated or nonactivated prorenin obtained from human ovarian follicular fluid. The dose chosen was calculated as sufficient to produce 2,300 ng angiotensin I.h-1.100 g rat body wt-1 in the presence of excess sheep substrate. Blood pressure, creatinine clearance, urine flow rate, and urine sodium, potassium, and osmolar excretion were measured. Activated prorenin from isoelectric peaks at isoelectric points (pI) 5.1, 5.2, 5.4, and 5.6 produced marked increases in urine volume (sixfold) and sodium excretion (7- to 10-fold) compared with the group receiving the vehicle (1% albumin in 0.9% saline). Activated prorenin from peaks at pI 4.9 and 5.8 produced no significant increase over the vehicle-only experiments. Captopril pretreatment (1 mg/kg iv) completely blocked the effects of peaks at pI 5.4 and 5.6. Interestingly, injection of nonactivated prorenin from peaks at pI 5.4 and 5.6 produced effects similar to the injection of activated prorenin from these peaks. Similarly, this effect was blocked by pretreatment with captopril. In summary, only certain isoelectric peaks of human prorenin whether activated, to active renin, or nonactivated produced a marked natriuresis and diuresis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differing renal effects of activated and nonactivated isoelectric peaks of human prorenin in rats. 175 May 22

The behavior of trypsin/creatinine clearance ratio (Ctr/Ccr) and serum immunoreactive trypsin (IRT) was evaluated in a total of 168 subjects with pancreatic cancer, chronic pancreatitis and non-pancreatic digestive diseases. Amylase/creatinine clearance ratio (Cam/Ccr) and serum amylase levels were also evaluated in order to establish their possible relationship with Ctr/Ccr and IRT values. Elevated Ctr/Ccr and IRT values were observed in several patients with pancreatic cancer and chronic pancreatitis. Abnormal IRT and Ctr/Ccr values were found in 28.2 and 4% of non-pancreatic digestive diseases, respectively. IRT and amylase serum levels showed consensual modifications, while Ctr/Ccr showed a behavior different from that of Cam/Ccr. Liver damage seems to play a role in increasing serum IRT levels of patients without pancreatic involvement, while the increased Ctr/Ccr seems to depend on other factors, for instance renal tubular dysfunction.
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PMID:Trypsin/creatinine clearance ratio and serum immunoreactive trypsin in digestive and pancreatic diseases. 242 20

Exocrine secretions of 16 of 22 pancreas allografts were drained into the urinary tract. Seven of these 16 patients have functioning allografts, six with pancreaticocystostomies and one with duct-to-ureter anastomosis. A notable problem has been a chronic metabolic acidosis, along with weight loss and hypotension, secondary to chronic bicarbonate loss and volume depletion through the urinary pancreatic fistula. This occurred as early as one week posttransplant, and intermittently thereafter up to four years. The syndrome was aggravated by episodes of renal dysfunction (acute tubular necrosis or rejection), and febrile syndromes. An inverse relationship between serum and urine bicarbonate concentrations existed, with a correlation coefficient, r = -0.746, (P less than 0.05). A negative correlation was also noted between serum bicarbonate and serum creatinine, r = 0.726, (P less than 0.05). Hyperchloremic metabolic acidosis with normal anion gap occurred despite periods of marginal pancreas allograft function resulting from ongoing rejection. Treatment consisted of intravenous and/or oral bicarbonate supplementation, and bicarbonate dialysis for uremic patients. In addition, one patient was first seen with severe balanitis and urethritis due to documented activation of trypsinogen and chymotrypsinogen, presumably caused by recurrent episodes of urinary tract infection. Urinary assay revealed a 10(2-3) increase in activated trypsin and chymotrypsin in comparison with other asymptomatic allograft recipients. Conversion to ductal enteric drainage led to resolution of both the balanitis and bicarbonate wasting. Measurement of urinary amylase levels were gross indicators of graft viability since no correlation could be found between these levels, onset of hyperglycemia, and eventual graft rejection confirmed by pathological examination.
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PMID:Pancreatic allograft exocrine urinary tract diversion. Pathophysiology. 243 6

To assess the potential role of renal kallikrein-kinin system in enhancing sodium excretion per nephron in chronic renal failure, we studied urinary excretion of active and inactive kallikrein for 3 weeks in Wistar-Kyoto rats subjected to 5/6 nephrectomy (5/6), 1/2 nephrectomy (1/2) or sham operation (Sham). We determined urinary active and inactive kallikrein by measuring kallikrein activity using a kininogenase assay before and after treatment with trypsin (200 micrograms/ml). Fractional sodium excretion was significantly increased in 5/6-rats as compared with 1/2- or sham-rats. On the contrary, urinary active kallikrein excretion per nephron was not different in the three models whereas a significant rise in urinary inactive kallikrein excretion per nephron was found in 5/6-rats as compared with 1/2- or sham-rats. Urinary total kallikrein excretion per nephron was significantly increased in 5/6-rats as compared with sham-rats. In addition, no correlation was found between fractional sodium excretion and urinary active kallikrein excretion corrected for creatinine clearance (Ccr) in 5/6-rats. These results indicate that decreased excretion of renal active kallikrein may not play a significant role in the increased sodium excretion per nephron in the rat remnant kidney model of chronic renal failure. Furthermore, it is suggested that in this model of rat there might be impaired production of renal active kallikrein although its exact mechanism remains to be determined.
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PMID:Role of renal kallikrein in the increased fractional sodium excretion in the rat remnant kidney model of chronic renal failure. 261 88

A radioimmunoassay was performed for direct measurement of urinary active and trypsin-activatable inactive kallikreins excretion in 34 patients with Type II diabetes mellitus. (1) Diabetics showed slightly low total (inactive plus active) kallikrein excretion, normal inactive kallikrein excretion and significantly low active kallikrein excretion and active-to-total kallikrein ratio. (2) Total kallikrein excretion was normal in normotensive diabetics and hypertensive diabetics without nephropathy, low in hypertensive diabetics with nephropathy. Active kallikrein excretion and active-to-total kallikrein ratio in hypertensive diabetics were remarkably low regardless of nephropathy. (3) Para amino hippurate clearance correlated with total kallikrein excretion in normal subjects and, with active kallikrein excretion and active-to-total kallikrein ratio in both normal subjects and diabetics, but not with total kallikrein excretion in diabetics. Creatinine clearance did not correlate with total, inactive kallikrein excretions and active-to-total kallikrein ratio. (4) A positive correlation was found between fractional sodium excretion and active kallikrein excretion in normal subjects, but not in diabetics. The results suggest that reduction in ratio of active-to-total kallikrein by renal dysfunction might decrease sodium excretion in diabetics with nephropathy.
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PMID:[Studies on kallikrein activity in diabetic patient with hypertension caused by nephropathy]. 274 99

Urinary trypsin inhibitory capacity is mainly due to the excretion of a glycoprotein which is immunologically related to the inter alpha-trypsin inhibitor and may be a proteolytic degradation product of that substance. It was tested in 133 subjects divided into 7 groups: 24 healthy controls (group A), 21 patients with bacterial infection (group B), 37 with bacterial infection under antibiotic therapy (group C), 25 with connective tissue disease (group D), 8 with infected connective tissue disease (group E), 14 with cancer (group F) and 4 with infected cancer (group G). Urinary trypsin inhibitory capacity level was very low in controls (3.32 +/- 0.8 U/g urinary creatinine), but it was dramatically increased when infection was present (149.67 +/- 23.6 U/g urinary creatinine). This test appeared to be more effective than serum C-protein measurement simultaneous carried out in the same patients. Urinary trypsin inhibitory capacity is not related to the degree of proteinuria in the urine sample, but it is increased in patients with chronic renal failure excluded from this study. Thus, its measurement is a sensitive, easy and useful test for detecting and monitoring infections. The return to its physiological value is a very good argument in favour of therapeutic effectiveness.
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PMID:[Clinical value of the determination of urinary antitrypsin activity]. 296 52

Renal Kallikrein, an enzyme of the distal tubule acting through kinin liberation, may participate to the control of renal circulation and blood pressure. To study if an impairment of its secretion may exist in diabetics, a cross-sectional study was carried out on 40 non-hypertensive and 29 hypertensive diabetics, compared to 30-age related controls. Urinary Kallikrein Activity (UKA) was measured by its kininogenase activity with and without trypsin preincubation. Compared to UKA in controls (86 +/- 9 micrograms lysyl-bradykinin [LBK] produced per minute of incubation), UKA was significantly reduced either in non-hypertensive diabetics (59 +/- 8 micrograms LBK. min.-1; p less than 0.05) and in hypertensive diabetics (26 +/- 6 micrograms LBK. min.-1; p less than 0.001). The ratio of total/active urinary kallikrein was similar in diabetics and in controls. The decline of UKA in diabetics was related to the duration of their disease (r = -0.38; p less than 0.05) and to their stage of retinopathy (r = -0.46; p less than 0.001). UKA values were proportional to creatinine clearance in diabetics (r = 0.58; p less than 0.001). The lowest UKA values were found in patients with a high urinary excretion of albumin (above 500 mg/day): 8 +/- 2 micrograms LBK. min-1 (p less than 0.001) and beta-2-microglobulin (above 382 micrograms/day): 12 +/- 4 micrograms LBK. min-1 (p less than 0.001). These findings support that an impaired secretion of renal kallikrein in diabetics can be related to the duration of diabetes and to the severity of microangiopathy.
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PMID:[Reduction of urinary kallikrein in hypertensive diabetics]. 309 98

The renal handling of cathodic trypsin-like immunoreactivity (TLI) was examined in 60 healthy persons (group I), 59 patients with proteinuria (group II), 7 healthy men receiving intravenous lysine to partially inhibit renal tubular protein reabsorption (group III) and 20 patients who underwent diagnostic renal vein catheterization (group IV). The urinary TLI concentration and TLI ratio (TLI clearance divided with creatinine clearance) were higher in group II than group I (p less than 0.001, Mann-Whitney test). In group II negative correlations were present between serum TLI and creatinine clearance (Spearman's rho = -0.84, p less than 0.001) and between TLI ratio and creatinine clearance (rho = -0.76, p less than 0.001). In group III the renal TLI clearance was undetectable before lysine but increased to a maximal median value of 4.00 ml/min per 1.73 m2 (range: 2.44-9.25 ml/min per 1.73 m2) after lysine. In group IV, the renal arterio-venous extraction of TLI was correlated to inulin extraction (rho = 0.85, p less than 0.001). The glomerular filtrability (the ratio between TLI and inulin extractions) was median 0.53 (range: 0.13-0.94). In conclusion, TLI has a high glomerular filtration and an almost complete tubular reabsorption and catabolism (with normal kidney function).
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PMID:Renal handling of cathodic trypsin-like immunoreactivity in man. 313 45

We delineated in rats, the relationship between trypsin inhibitory activity in the urine and the nephrotoxic effects of gentamicin, eg, proteinuria and deterioration of glomerular filtration rate (GFR), measured by creatinine clearance. Gentamicin, 70 mg/kg per day, was injected intraperitoneally for 6-10 successive days. Serum and urine gentamicin levels were determined by a microbiological test. Trypsin inhibitory activity was assayed by the casein digestion method. The results showed a steady increase in urinary trypsin inhibitory activity starting from the fourth injection day. The increased levels of urinary trypsin inhibitory activity were associated with increased levels of urinary gentamicin excretion (r = 0.36, p less than 0.02, n = 50 after the fourth injection day), and were significantly higher than in control groups (p less than 0.001). The urinary trypsin inhibitory activity was inversely correlated with the GFR (r = -0.45, p less than 0.01, after the second injection day). The serum trypsin inhibitory activity remained unchanged throughout the study period in all groups. These data suggest that increased urinary trypsin inhibitory activity may be involved in the pathogenesis of gentamicin-induced nephrotoxicity.
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PMID:Enhanced urinary trypsin inhibitory activity in gentamicin-induced nephrotoxicity in rats. 318 Apr 82


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