Clinical Studies Concerning Factor XIII; with Special Reference to Hyperlipemia

1973 ◽  
Vol 30 (03) ◽  
pp. 480-493 ◽  
Author(s):  
Mircea P. Cucuianu ◽  
Vasile V. Vasile ◽  
Titus A. Popescu ◽  
Augustin Opincaru ◽  
Ion Crîsnic ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Special Reference ◽  
Clinical Studies ◽  
Factor Xiii ◽  
Normal Weight ◽  
Cirrhosis Of The Liver ◽  
Control Subjects ◽  
Low Levels ◽  
Endogenous Hypertriglyceridemia

SummaryFactor XIII, estimated according to the method of Heene, was found to be diminished in patients with cirrhosis of the liver, in acute renal failure and, to a lesser extent, postoperatively, owing probably to both a decreased synthesis and an accelerated utilization. When compared to values obtained in healthy, normal weight, normolipemic control subjects, the level of factor XIII was higher in hyperlipemic and especially in hypertriglyceridemic patients, whether clinical atherosclerosis was present or not. Low levels of factor XIII were usually accompanied by a decrease in serum pseudocholinesterase, while high values of this enzyme produced by the liver were noted in hypertriglyceridemic patients. The hypothesis of an enhanced synthesis of factor XIII by the liver, in subjects with endogenous hypertriglyceridemia is considered. It is also suggested that accelerated stabilization of fibrin might contribute to the fibrinolytic insufficiency of hyperlipemic patients and enhance certain atherogenic mechanisms.

scholarly journals Acute renal failure caused by ingestion of the carp gall bladder - A report of 3 cases with a special reference to the reported cases in Japan.

1988 ◽  
Vol 77 (8) ◽  
pp. 1268-1273 ◽  
Author(s):  
Yoshitaka YAMAMOTO ◽  
Osamu WAKISAKA ◽  
Shoichi FUJIMOTO ◽  
Nobuhiro KASEDA ◽  
Tadahiko MAEHARA ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Gall Bladder ◽  
Special Reference

Clinical studies on plasma fibronectin and factor XIII; with special reference to hyperlipoproteinemia

1985 ◽  
Vol 147 (3) ◽  
pp. 273-281 ◽  
Author(s):  
M. Cucuianu ◽  
H.G. Rus ◽  
Anca Cristea ◽  
F. Niculescu ◽  
Daniela Bedeleanu ◽  
...  
Keyword(s):  
Special Reference ◽  
Clinical Studies ◽  
Factor Xiii ◽  
Plasma Fibronectin

Acute renal failure. II. Experimental models of acute renal failure: imperfect but indispensable

2000 ◽  
Vol 278 (1) ◽  
pp. F1-F12 ◽  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Animal Models ◽  
Renal Injury ◽  
Clinical Studies ◽  
Basic Research ◽  
Experimental Models ◽  
Clinical Syndrome ◽  
Therapeutic Interventions ◽  
Common Disease

Acute renal failure (ARF) due to ischemic 1 or toxic renal injury, a clinical syndrome traditionally referred to as acute tubular necrosis (ATN), is a common disease with a high overall mortality of ∼50%. Little progress has been made since the advent of dialysis more than 30 years ago in improving this outcome. During this same period, a considerable amount of basic research has been devoted to elucidating the pathophysiology of ATN. The ultimate goal of this research is to facilitate the development of therapeutic interventions that either prevent ARF, ameliorate the severity of tubular injury following an acute ischemic or toxic renal insult, or accelerate the recovery of established ATN. This research endeavor has been highly successful in elucidating many vascular and tubular abnormalities that are likely to be involved in ischemic and toxic ARF. This information has led to impressive advances in the development of a number of different pharmacological interventions that are highly effective in ameliorating the renal dysfunction in animal models of ARF. Although these developments are exciting and promising, enthusiasm of investigators involved in this endeavor has been tempered somewhat by the results of a few recent clinical studies of patients with ATN. These trials, designed to examine the efficacy in humans of some of the interventions effective in animal models of ARF, have resulted in little or no benefit. This is therefore an important time to reevaluate the approaches we have taken over the past three to four decades to develop new and effective treatments for ATN in humans. The major goals of this review are 1) to evaluate the relevance and utility of the experimental models currently available to study ischemic and toxic renal injury, 2) to suggest novel experimental approaches and models that have the potential to provide advantages over methods currently available, 3) to discuss ways of integrating results obtained from different experimental models of acute renal injury and of evaluating the relevance of these findings to ATN in humans, and 4) to discuss the difficulties inherent in clinical studies of ATN and to suggest how studies should be best designed to overcome these problems.

scholarly journals Acute renal failure - clinical studies - 2

NDT Plus ◽  
2009 ◽  
Vol 2 (Supplement 2) ◽  
pp. ii1634-ii1634 ◽  
Author(s):  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Clinical Studies

scholarly journals Impairment of platelet aggregation in hemolytic uremic syndrome: evidence for platelet "exhaustion"

Blood ◽  
1982 ◽  
Vol 60 (3) ◽  
pp. 564-570 ◽  
Author(s):  
JS Fong ◽  
BS Kaplan
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Hemolytic Uremic Syndrome ◽  
Acute Illness ◽  
Uremic Toxin ◽  
In Vitro Experiments ◽  
Microangiopathic Hemolytic Anemia ◽  
Uremic Syndrome ◽  
Low Levels

Thrombocytopenia, microangiopathic hemolytic anemia, and acute renal failure are the hallmarks of hemolytic-uremic syndrome (HUS). This report presents the results on platelet studies from 10 consecutive HUS patients in childhood. During their acute illness, they all displayed a characteristic pattern of impaired platelet function: no aggregating responses to epinephrine, some to ADP, and moderate to collagen. In addition, platelet contents of beta-thromboglobulin (beta TG) were markedly reduced. As these patients improved clinically, their platelet- aggregating responses also normalized despite their uremic state. Incubation of platelets with uremic plasma or guanidino-succinic acid, a uremic toxin, had minor effects on platelet-aggregating activity. Since low levels of platelet beta TG suggest that these platelets were in an exhausted state, in vitro experiments were performed to exhaust normal platelets by incubation at 37 degrees C. A proportional impairment of platelet-aggregating responses and decreasing levels of platelet beta TG were noted. Furthermore, the pattern of impairment was similar to that found in the platelet-aggregating activities of HUS patients. Thus, “exhaustion,” in addition to azotemia and thrombocytopenia, are factors that contribute to the functional impairment of platelets in these patients. Further studies to reveal mechanisms that lead to platelet exhaustion in HUS are of fundamental importance in the understanding of this illness.

The role of ICAM-1 in endotoxin-induced acute renal failure

2007 ◽  
Vol 293 (4) ◽  
pp. F1262-F1271 ◽  
Author(s):  
Xiaoyan Wu ◽  
Rongqing Guo ◽  
Ying Wang ◽  
Patrick N. Cunningham
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Adhesion Molecule ◽  
Neutrophil Infiltration ◽  
Intercellular Adhesion Molecule ◽  
Wild Type ◽  
Intercellular Adhesion Molecule 1 ◽  
Low Levels ◽  
Necrosis Factor

The pathogenesis of acute renal failure (ARF) occurring during the course of sepsis is incompletely understood. Intercellular adhesion molecule-1 (ICAM-1) is a key cell adhesion molecule upregulated by LPS, which binds to the integrins CD11a/CD18 and CD11b/CD18 present on the surface of leukocytes. We hypothesized that ICAM-1 facilitates renal injury in LPS-induced ARF. To test this, three groups of mice ( n = 8 per group) were injected intraperitoneally with 6 mg/kg LPS: 1) normal C57BL/6 mice, 2) mice with a targeted deficiency of ICAM-1 (ICAM-1−/−), and 3) mice expressing very low levels of CD18 (CD18-def). ICAM-1−/− mice were significantly resistant to LPS-mediated ARF, as opposed to CD18-def mice, which developed severe ARF, as did wild-type controls (48 h blood urea nitrogen 143 ± 31.5, 70.8 ± 24.4, and 185 ± 16.6 mg/dl in wild-type, ICAM-1−/−, and CD18-def mice, respectively, P < 0.05). At death, ICAM-1−/− mice had significantly less renal neutrophil infiltration than the other two groups, as well as less histological tubular injury. Depletion of neutrophils with mAb Gr-1 led to a profound exaggeration of tumor necrosis factor (TNF) release and high mortality, but neutrophil-depleted mice receiving 10-fold less LPS were protected against ARF despite TNF release similar to what is normally associated with LPS-induced ARF. LPS caused a significant increase in renal expression of chemokines; however, this increase was significantly exaggerated in CD18-def mice, which may account for their lack of protection. In conclusion, these data show that ICAM-1 plays a key role in LPS-induced ARF.

scholarly journals Normalization of Activated Partial Thromboplastin Time Correlates with Low Levels of Dabigatran in a Patient with Severe Sepsis

2015 ◽  
Vol 2015 ◽  
pp. 1-3
Author(s):  
Rikke Ebenhard Højland ◽  
Stine Borch Thorup ◽  
Bodil Steen Rasmussen
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Severe Sepsis ◽  
Dabigatran Etexilate ◽  
Activated Partial Thromboplastin Time ◽  
Continuous Venovenous Hemofiltration ◽  
Reversal Agent ◽  
Acute Surgery ◽  
Low Levels ◽  
Severe Coagulopathy

The oral anticoagulant dabigatran etexilate can be a challenge when patients need acute surgery. Sepsis and acute renal failure exacerbate the anticoagulant effect. There is no specific reversal agent for dabigatran etexilate, but it can be removed by hemodialysis. We present a case where a patient treated with dabigatran etexilate was admitted to intensive care unit with severe sepsis and acute renal failure and in need of bilateral lower limp amputation due to ischemia. The patient had severe coagulopathy and was treated with continuous venovenous hemofiltration in attempt to remove dabigatran etexilate before surgery.

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