Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Koolen, M.I. et al. (1984) measured urinary kallikrein (UKal) in renal transplant recipients using 2 methods, S-2266 amidolytic assay and radioimmunoassay, and reported that the values by the former method showed an increase in amount at the time of acute rejection episode (ARE) despite of no variation in those by the latter. To clear the discrepancy, 24 hours excretion of UKal was measured by the amidolytic assay using Pro-Phe-Arg-MCA under 2 conditions, with and without soybean trypsin inhibitor (STI), in 10 living related kidney recipients (LR), their donors (LD), and 8 cadaver kidney recipients (CR), Furthermore, gel filtration chromatography (Sephacryl S-200) was performed in some recipients and LD to confirm whether the amidolytic activity (ALA) indicates exclusively UKal or not. The results were as follows. In LD, there were no statistical differences in ALA between not only before and after uninephrectomy but also with and without STI. On the post-operative course, some recipients showed a tendency of decrease in ALA with STI, and some kept a constant level. There occasionally appeared a difference between ALA with and without STI just after the transplantation, and at the time of ARE, acute tubular necrosis (ATN) or urinary tract infection (UTI). There was no fixed characteristic variation in ALA, both with and without STI, at the time of ARE. ALA with STI was lower in LR than in LD, and the lowest in CR, From the second week of transplantation and afterward, ALA with STI showed a positive correlation not with creatinine clearance but with urinary aldosterone.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Urinary kallikrein-like activity in renal transplant recipients]. 235 63

The role of the renal kallikrein-kinin system in the pathogenesis of hypertension and various forms of renal dysfunction after human renal transplantation has been assessed by measurement of urinary kallikrein activity in 41 renal transplant recipients. The urinary tosyl arginine methyl esterase assay was used. The urinary kallikrein in these patients appeared to originate from the transplanted kidney and not their own diseased kidneys. Twenty-three recipients had hypertension (mean blood pressure 156 +/- 3/98 +/- 2 mm Hg) and excreted less kallikrein (4.0 +/- 1.2 versus 12.5 +/- 4.0 esterase units [EU] per 24 hours, p less than 0.05) than their 18 normotensive counterparts (mean blood pressure 132 +/- 2/77 +/- 1 mm Hg, both p less than 0.01). Subjects with renal complications of transplantation (acute tubular necrosis [ATN], nine patients, or acute rejection [AR], eight patients) also excreted less kallikrein than the 28 subjects without such complications (3.4 +/- 0.9 versus 10.3 +/- 2.7 EU/24 hours, p less than 0.02). Among those with acute renal complications, subjects with ATN excreted less kallikrein than those with AR (1.3 +/- 0.3 versus 5.7 +/- 1.7 EU/24 hours, p less than 0.02). Cadaver graft recipients excreted less kallikrein than living related donor graft recipients (2.1 +/- 0.4 versus 13.0 +/- 3.5 EU/24 hours, p less than 0.01), perhaps reflecting their higher blood pressures (mean systolic pressure 151 +/- 3 versus 140 +/- 3 mm Hg, p less than 0.04), relatively impaired renal function (creatinine clearance values 42 +/- 8 versus 62 +/- 5 ml/min, p less than 0.04), and higher incidence of ATN (nine cases versus none). The kallikrein-kinin system may be involved in the pathogenesis of hypertension and some forms of renal dysfunction after renal transplantation.
 ...
PMID:Urinary kallikrein excretion after renal transplantation: relationship to hypertension, graft source, and renal function. 675 Oct 83

To examine the role of prostaglandins and the kallikrein system in the recovery from acute renal failure, we studied the sequential changes in urinary prostaglandins and kallikrein after the onset of oliguria. The six patients studied had acute tubular necrosis of the vasomotor type. Urinary PGE2, PGF2 alpha, the PGF2 alpha-main urinary metabolite, 6-keto-PGF1 alpha and TXB2 were all measured by radioimmunoassay. Urinary kallikrein was assayed by means of hydrolytic activity using a chromogenic tripeptide substrate. Following onset of diuresis, urinary PGE2 excretion was increased to normal, parallel to the increase in urine volume. In contrast, the ratio of urinary PGF2 alpha/PGE2 peaked at the onset of diuresis, indicating a relative increase in PGF2 alpha production at this time. Prior to this peak, urinary kallikrein concentrations reached the highest levels, suggesting a close connection with renal prostaglandin metabolism. On the other hand, changes in PGF2 alpha-MUM, 6-keto-PGF1 alpha and TXB2 were not found. These results indicate that there may be an interlocking acute alteration of the kallikrein-prostaglandin system occurring immediately before the resolution of oliguria, although the role of the acute shift to PGF2 alpha production observed needs further study.
 ...
PMID:Urinary prostaglandins and kallikrein in the course of acute renal failure. 696 Mar 68