Inhibitors of the Fibrinolytic Enzyme System in Renal Disease

1970 ◽  
Vol 39 (5) ◽  
pp. 549-557 ◽  
Author(s):  
N. B. Bennett ◽  
D. Ogston
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Renal Damage ◽  
Enzyme System ◽  
Normal Subjects ◽  
Plasminogen Activation ◽  
Significant Elevation ◽  
Normal Range ◽  
Marked Inhibition ◽  
Serum Inhibitor

1. Levels of serum inhibitor of plasminogen activation, anti-plasmin and plasminogen activator were measured in normal subjects and patients with active glomerulonephritis and chronic renal failure. 2. Patients with active glomerulonephritis all had grossly elevated levels of serum inhibitor of plasminogen activation and significant elevation of anti-plasmin. The majority of activator levels lay at the lower end of the normal range. 3. Patients with chronic renal failure had significantly elevated levels of serum inhibitor of plasminogen activation and anti-plasmin, but the changes were less marked than in those with active glomerulonephritis. Activator levels were consistently reduced. 4. The marked inhibition of fibrinolysis in active glomerulonephritis may be a factor in the persistence of glomerular fibrin and ultimately in perpetuation of renal damage. The changes in the fibrinolytic system in chronic renal failure may determine the development of the serosal exudates characteristic of that condition.

Evidence for an Increased Generation of Prostacyclin in the Microvasculature and an Impairment of the Platelet α-Granule Release in Chronic Renal Failure

1988 ◽  
Vol 60 (02) ◽  
pp. 205-208 ◽  
Author(s):  
Paul A Kyrle ◽  
Felix Stockenhuber ◽  
Brigitte Brenner ◽  
Heinz Gössinger ◽  
Christian Korninger ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Blood Clotting ◽  
Normal Subjects ◽  
Chronic Uraemia ◽  
Wall Interaction ◽  
End Stage ◽  
Granule Release

SummaryThe formation of prostacyclin (PGI2) and thromboxane A2 and the release of beta-thromboglobulin (beta-TG) at the site of platelet-vessel wall interaction, i.e. in blood emerging from a standardized injury of the micro vasculature made to determine bleeding time, was studied in patients with end-stage chronic renal failure undergoing regular haemodialysis and in normal subjects. In the uraemic patients, levels of 6-keto-prostaglandin F1α (6-keto-PGF1α) were 1.3-fold to 6.3-fold higher than the corresponding values in the control subjects indicating an increased PGI2 formation in chronic uraemia. Formation of thromboxane B2 (TxB2) at the site of plug formation in vivo and during whole blood clotting in vitro was similar in the uraemic subjects and in the normals excluding a major defect in platelet prostaglandin metabolism in chronic renal failure. Significantly smaller amounts of beta-TG were found in blood obtained from the site of vascular injury as well as after in vitro blood clotting in patients with chronic renal failure indicating an impairment of the a-granule release in chronic uraemia. We therefore conclude that the haemorrhagic diathesis commonly seen in patients with chronic renal failure is - at least partially - due to an acquired defect of the platelet a-granule release and an increased generation of PGI2 in the micro vasculature.

Neuropeptide Y as a plasma marker for phaeochromocytoma, ganglioneuroblastoma and neuroblastoma

1992 ◽  
Vol 83 (2) ◽  
pp. 205-211 ◽  
Author(s):  
Toraichi Mouri ◽  
Masahiko Sone ◽  
Kazuhiro Takahashi ◽  
Keiichi Itoi ◽  
Kazuhito Totsune ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Neuropeptide Y ◽  
Healthy Adult ◽  
Plasma Samples ◽  
Normal Range ◽  
Maintenance Haemodialysis ◽  
Upper Limits ◽  
Highly Sensitive ◽  
Plasma Marker

1. We investigated the usefulness of neuropeptide Y as a plasma marker for phaeochromocytoma, ganglioneuroblastoma and neuroblastoma using a simple and highly sensitive r.i.a. for human neuropeptide Y. 2. Plasma immunoreactive neuropeptide Y concentrations were measured without extraction in plasma samples (100 μl) from patients with various diseases. 3. The plasma immunoreactive neuropeptide Y concentration in patients with phaeochromocytoma (172.3 ± 132.4 pmol/l, mean ± sd, n = 23) was significantly higher than that in healthy adult subjects (40.1 ± 10.1 pmol/l, n = 40, P<0.0001). The plasma immunoreactive neuropeptide Y concentrations in patients with ganglioneuroblastoma (590.7 ± 563.6 pmol/l, n = 6) and patients with neuroblastoma (566.9 ± 524.4 pmol/l, n = 15) were significantly higher than those in control children (1–9 years old, 82.2 ± 39.9 pmol/l, n = 72, P<0.0001). 4. The plasma immunoreactive neuropeptide Y concentration in patients with essential hypertension (34.0 ± 3.7 pmol/l, n = 18) was within the normal range, but in patients with chronic renal failure undergoing maintenance haemodialysis (192.1 ± 68.0 pmol/l, n = 25) and in non-dialysed patients with chronic renal failure (85.1 ± 23.1 pmol/l, n = 7) it was significantly higher than that in healthy adult subjects (P<0.0001). 5. Eighty-seven per cent of the patients with phaeochromocytoma, 67% of the patients with ganglioneuroblastoma and 80% of the patients with neuroblastoma showed plasma immunoreactive neuropeptide Y concentrations higher than the upper limits in the control subjects [62 pmol/l (adult) and 160 pmol/l (children)]. 6. These results suggest that neuropeptide Y is a useful plasma marker for these tumours in addition to other factors unless the patients have renal failure.

Chronic renal failure in a mouse model of human adenine phosphoribosyltransferase deficiency

1998 ◽  
Vol 275 (1) ◽  
pp. F154-F163 ◽  
Author(s):  
Michael G. Stockelman ◽  
John N. Lorenz ◽  
Frost N. Smith ◽  
Gregory P. Boivin ◽  
Amrik Sahota ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Kidney Disease ◽  
Creatinine Clearance ◽  
Renal Damage ◽  
Male Mice ◽  
Adenine Phosphoribosyltransferase ◽  
Disease Treatment ◽  
Significant Impairment ◽  
Normal Males

In humans, adenine phosphoribosyltransferase (APRT, EC 2.4.2.7 ) deficiency can manifest as nephrolithiasis, interstitial nephritis, and chronic renal failure. APRT catalyzes synthesis of AMP from adenine and 5-phosphoribosyl-1-pyrophosphate. In the absence of APRT, 2,8-dihydroxyadenine (DHA) is produced from adenine by xanthine dehydrogenase (XDH) and can precipitate in the renal interstitium, resulting in kidney disease. Treatment with allopurinol controls formation of DHA stones by inhibiting XDH activity. Kidney disease in APRT-deficient mice resembles that seen in humans. By age 12 wk, APRT-deficient male mice are, on average, mildly anemic and smaller than normal males. They have extensive renal interstitial damage (assessed by image analysis) and elevated blood urea nitrogen (BUN), and their creatinine clearance rates, which measure excretion of infused creatinine as an estimate of glomerular filtration rate (GFR), are about half that of wild-type males. APRT-deficient males treated with allopurinol in the drinking water had normal BUN and less extensive visible renal damage, but creatinine clearance remained low. Throughout their lifespans, homozygous null female mice manifested significantly less renal damage than homozygous null males of the same age. APRT-deficient females showed no significant impairment of GFR at age 12 wk. Consequences of APRT deficiency in male mice are more pronounced than in females, possibly due to differences in rates of adenine or DHA synthesis or to sex-determined responses of the kidneys.

Dietary Management of Feline Chronic Renal Failure: Where are We Now? In What Direction are We Headed?

2000 ◽  
Vol 2 (2) ◽  
pp. 75-82 ◽  
Author(s):  
D J Polzin ◽  
C A Osborne ◽  
S Ross ◽  
F Jacob
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Clinical Signs ◽  
Dietary Therapy ◽  
Dietary Management ◽  
Dietary Intakes ◽  
Normal Range ◽  
Limited Ability ◽  
Diet Formulation ◽  
Therapeutic Value

Dietary modification is of primary importance in managing cats with chronic renal failure. Diets designed for cats with chronic renal failure are typically formulated to be pH neutral and contain reduced quantities of protein, phosphorus and sodium and an increased quantity of potassium. These changes in diet formulation are designed to ameliorate clinical signs of renal failure by adapting dietary intakes to meet the limited ability of failing kidneys to adapt to the normal range of dietary intakes. Important recent clinical trials support the therapeutic value of dietary therapy in cats with chronic renal failure.

Fluorescent substances in uremic and normal serum.

1985 ◽  
Vol 31 (12) ◽  
pp. 1988-1992 ◽  
Author(s):  
M Shaykh ◽  
N Bazilinski ◽  
D S McCaul ◽  
S Ahmed ◽  
A Dubin ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Normal Subjects ◽  
Normal Serum ◽  
Gel Chromatography ◽  
Intense Fluorescence

Abstract We measured the fluorescence, at various excitation (Ex) and emission (Em) wavelengths, of serum ultrafiltrates and fractions of serum resolved by chromatography on Sephadex G15, studying both normal subjects and patients in chronic renal failure requiring hemodialysis. We found hitherto undescribed fluorescence at Ex 380 nm/Em 440 nm and Ex 400 nm/Em 460 nm, the intensity being greatly increased in patients with chronic renal failure in comparison with normal subjects (p less than 0.005). This fluorescence persisted unaltered when serum was filtered through membranes having cutoffs ranging from 10 000 to 500 Da. Each serum fraction resolved by gel chromatography demonstrated a characteristic fluorescence, which was generally much more intense in uremics. The most intense fluorescence (Ex 380 nm/Em 440 nm and Ex 400 nm/Em 460 nm) was emitted in the higher-Mr fractions.

Parathyrin radioimmunoassay: diagnostic utility of antisera produced against carboxyl-terminal fragments of the hormone from the human.

1978 ◽  
Vol 24 (3) ◽  
pp. 451-454 ◽  
Author(s):  
F P Di Bella ◽  
J M Kehrwald ◽  
K Laakso ◽  
L Zitzner
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Guinea Pigs ◽  
Normal Subjects ◽  
Terminal Region ◽  
Diagnostic Utility ◽  
Human Origin ◽  
Widespread Availability ◽  
Carboxyl Terminal

Abstract Antisera directed toward the carboxyl-terminal region of human parathyrin (parathyroid hormone), for use in daignostically applicable radioimmunoassays of the hormone in serum, are scarce, largely because of the lack of suitable immunogens of human origin. We produced four antisera in goats and guinea pigs by immunization with recently discovered carboxyl-terminal fragments of human parathyrin extracted from parathyroid tumors. Here, we report results of radioimmunoassays of nearly 200 normal and pathological sera with one of these antisera; we observed almost complete differentiation between concentrations of parathyrin in serum of healthy normal subjects and patients with primary, secondary (due to chronic renal failure), or "ectopic" hyperparathyroidism (due to nonparathyroid cancer). The availability of a new immunogen should now make possible the deliberate production of large quantities of diagnostically applicable parathyrin antisera directed toward the carboxyl-terminal region of human parathyrin. This should, in turn, lead to more widespread availability of this useful radioimmunoassay.

Uroangiographic Contrast Media-Induced Nephropathy: Correlations between Their Physicochemical Properties and Renal Damage

2005 ◽  
Vol 72 (4) ◽  
pp. 446-456
Author(s):  
C. Alberti ◽  
M. Piovano ◽  
A. Tizzani
Keyword(s):  
Diabetes Mellitus ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Chronic Renal Failure ◽  
Contrast Media ◽  
Renal Damage ◽  
Contrast Material ◽  
Vasoactive Mediators ◽  
Adequate Hydration ◽  
Hospital Acquired

Contrast media-induced nephropathy (CN) is an important cause of hospital-acquired acute renal failure. Patients with both diabetes mellitus and renal impairment are at high risk. CN pathophysiology involves activation of the tubulo-glomerular feedback and vasoactive mediators such as renin-angiotensin 2, endothelin, adenosine, ADH, etc. The risk of CN can be minimized by the use of non-ionic, low or isoosmolar, contrast material, adequate hydration and prophylactic pharmacological measures. In patients with chronic renal failure who are undergoing arteriography (e.g. coronary angiography and angioplasty), periprocedural hemofiltration appears effective in preventing further renal damage due to contrast agents.

scholarly journals Polymorphonuclear function in naturally occurring renal failure in dogs

2009 ◽  
Vol 54 (No. 5) ◽  
pp. 236-243 ◽  
Author(s):  
S. Kralova ◽  
L. Leva ◽  
M. Toman
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Clinical Signs ◽  
Human Medicine ◽  
Strong Positive Correlation ◽  
Significant Elevation ◽  
Naturally Occurring ◽  
Main Effect ◽  
Healthy Control ◽  
Leukocyte Counts

Chronic renal failure causes immunosuppression in people and is thought to be one of the causes of non-infectious secondary immunosuppression in dogs. The purpose of this study was to evaluate changes in counts and activity of polymorphonuclears in dogs with chronic renal failure in various stages. Haematological, biochemical examinations and examination of non-specific immune response cells (total and differential leukocyte counts, phagocytosis of methacrylate particles, chemiluminescence test, and level of lysozyme) were performed in blood samples obtained from these dogs. Neutrophilia, lymphopoenia and a decreased number of eosinophils in comparison with healthy control were the main findings in groups with clinical signs. We found the statistically highly significant elevation of lysozyme level; it was in a strong positive correlation with the level of urea, creatinine and phosphorus. We did not find any statistically significant changes in phagocytosis process and other serological factors. In conclusion, despite the reports from human medicine, chronic renal failure in dogs does not alter phagocytosis. From this aspect, the elevation of lysozyme level is the main effect of uraemia.

scholarly journals Protein-to-creatinine urinary in the early diagnosis of renal injury in canine pyometra

2019 ◽  
Vol 39 (3) ◽  
pp. 186-191
Author(s):  
Marcos C. Sant’Anna ◽  
Guilherme F. Martins ◽  
Karina K.M.C. Flaiban ◽  
Luiz G.C. Trautwein ◽  
Maria I.M. Martins
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Renal Injury ◽  
Renal Damage ◽  
Systemic Disease ◽  
The Other ◽  
Control Group ◽  
Creatinine Ratio ◽  
Renal Lesions ◽  
Tubular Cells

ABSTRACT: Kidney disease that affects bitches with pyometra may lead patients to develop chronic renal failure even after pyometra treatment. Therefore, several studies have sought to clarify the gaps in the understanding of the pathogenesis of renal injury in pyometra. Identification of early detection markers for renal damage, which can predict and identify the prognosis of the disease, is very important. Proteinuria analysis can diagnose kidney damage, since proteins such as albumin are not filtered through the glomerulus and those that undergo glomerular filtration are almost completely reabsorbed by tubular cells. The objective of this study was to evaluate whether the urinary protein-to-creatinine ratio (UPC) can detect renal injury in bitches with pyometra before development of azotemia. For this, 44 bitches with pyometra were divided into two groups: bitches with azotemic piometra (A, n=15, creatinine >1.7) and bitches with non-azotemic pyometra (NA, n=29). The two groups were compared to the control group (CG, n=12), which had no signs of systemic disease. All animals underwent blood and urine tests. Leukocytosis was more evident in bitches in the A group than in the other groups. This shows that the inflammatory response may be associated with the pathogenesis of renal injury. The median UPC in bitches with pyometra was significantly higher than in the CG, with a median above the reference values. In conclusion, the UPC can be used in bitches with pyometra to detect renal damage before the development of azotemia. It has been suggested that the UPC of bitches with pyometra should be followed through during the postoperative period so that permanent renal lesions secondary to pyometra can be diagnosed and treated properly before the development of azotemia.

Plasma β-Thromboglobulin And Platelet Factor 4 In Patients With Chronic Renal Failure And Effect Of Hemodialysis

1981 ◽  
Author(s):  
Y Endo ◽  
M Mamiya ◽  
K Takahashi ◽  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Statistical Significance ◽  
Normal Subjects ◽  
Statistical Correlation ◽  
Platelet Factor 4 ◽  
Cellulose Membrane ◽  
Heparin Infusion ◽  
Platelet Factor ◽  
The Difference

We have reported that jS-thromboglobulin (β-TG) and platelet factor 4 (PF4) increased in chronic renal failure. The purpose of the current study is to reveal a correlation between plasma β-TG (Amersham Corp. England) and renal function, a correlation between plasma β-TG and PF. (Abbott Lab., USA) and the effect of hemodialysis on patients with chronic renal failure.Significantly increased levels of plasma β-TG (76.8±25.5 ng/ml, p<0.01) were observed in 24 patients with chronic renal failure (BUN>20mg/dl), compared to normal subjects (13.2±5.6ng/ml). The increase in β-TG was highly correlated with BUN (r=0.651, p<0.01), creatinine (r=0.778, p<0.01) and creatinine clearance (r=-0.723, p<0.01). Although plasma PF4 (normal 5.0±2.0ng/ml) increased also, no statistical significance could be found. Statistical correlation between β-TG and PF4 was not found in these patients. This reason is thought to Be due to the difference of molecular weight (PF. 8000MW, β-TG 36000MW) and half-life (PF4 30min,β-TG 100min) The high levels of β-TG (89.4±3.4ng/ml) showed a further increase (109.4±5.8ng/dl, p<0.01) after dialysis. This is thought to be due to hemoconcentration, because of no adhesion of platelet to cellulose membrane but about 20% elevation in mean of other blood factors such as RBC, WBC, platelet, fibrinogen etc. The PF4 levels (before, 7.7±1.3ng/ml) which increased at 15min (55.2±19.6ng/ml, p<0.01) and 1 hr (23.7±8.4ng/ml, p< 0.01) are thought to be due to the influence of heparin infusion. The change in PF4. was not accompanied by the change in β-TG. During hemodialysis the decrease of other platelet functions such as adhesiveness, aggregation induced by ADP, collagen and PF3remained unchanged.

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