scholarly journals Urinary thrombin as a marker of local disseminated intravascular coagulation in patients with chronic kidney disease

2021 ◽  
Vol 26 (4) ◽  
pp. 81-86
Author(s):  
I.S. Mykhaloiko
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Disseminated Intravascular Coagulation ◽  
Filtration Rate ◽  
Underlying Disease ◽  
Healthy Individuals ◽  
Intravascular Coagulation ◽  
Protein Excretion ◽  
Severe Underlying Disease ◽  
A Prospective Study

The aim of this research was to study the diagnostic markers of nonovert local disseminated intravascular coagulation (DIC) syndrome in the urine of patients with chronic kidney disease (CKD). We conducted a prospective study involving 140 patients with CKD, of these patients, 100 patients (71.4%; 95% CI 53.4-76.7) had glomerulonephritis (GN) and 40 patients (28.6%; 95% CI 21.3-36.8) had diabetic nephropathy (DN). We diagnosed overt DIC syndrome on the International Society of Thrombosis and Haemostasis (ISTH) scale (>5 points) in 18.6 % of patients. We determined the level of thrombin in the urine of patients who had <5 points on ISTH scale for the diagnosis of local nonovert DIC syndrome in the kidneys. In the urine of healthy individuals, the level of thrombin did not exceed 1 ng/ml, so we found no thrombinuria at a thrombin level <1 ng/ml. In 56.1% of patients, we found urinary thrombin levels >1 ng/ml. The average level of thrombin in the urine of these patients was 6.5 (4.8; 10.6) ng/ml. In our opinion, the presence of thrombinuria indicates the intensity of monocytic-macrophage inflammation in the glomeruli and may be a criterion for nonovert, local DIC syndrome in the kidneys. The association of overt DIC syndrome with decreased blood albumin, reduced glomerular filtration rate (GFR), increased daily protein excretion (DPE) indicates its occurrence in severe underlying disease, in the presence of nephrotic syndrome and in the severe stages of CKD. Early diagnosis of  nonovert local DIC syndrome would be more useful, since the process is still reversible and controlled, and timely use of antiplatelet and anticoagulant therapy would affect the course and the progression of CKD.

scholarly journals Association between albuminuria and thyroid function in patients with chronic kidney disease

Endocrine ◽  
2021 ◽  
Author(s):  
Walter Reinhardt ◽  
Nils Mülling ◽  
Stefan Behrendt ◽  
Sven Benson ◽  
Sebastian Dolff ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Thyroid Function ◽  
Filtration Rate ◽  
Creatinine Ratio ◽  
Protein Loss ◽  
Reverse T3 ◽  
Thyroid Antibody ◽  
Hormone Status ◽  
The Relationship

Abstract Purpose The relationship between proteinuria and thyroid function remains controversial in patients with chronic kidney disease (CKD). We prospectively investigated the association between kidney and thyroid function in thyroid antibody-negative patients through all CKD stages. Methods We enrolled 184 nondialysis patients (mean age: 63.1 ± 16.9 years) without previous thyroid disease or thyroid-specific antibodies. Kidney function was assessed by estimating the glomerular filtration rate (eGFR) classified according KDIGO (CKD G1–5). Kidney damage was assessed by albuminuria (albumin-to-creatinine ratio, ACR) and classified as mild, moderate, or severe (ACR1: <300, ACR2: 300–3000, and ACR3: 3000 mg/g). To evaluate thyroid function, TSH, T4, fT4, T3, fT3, reverse T3 (rT3), and thyroxine-binding globulin (TBG) were measured. Results rT3 concentrations correlated negatively with albuminuria (r = −0.286, p < 0.001) and were significantly lower in patients with severe albuminuria than in those with mild or moderate albuminuria (ACR3: 0.28 vs. ACR2: 0.32 vs. ACR1: 0.36 nmol/l, p < 0.001). The severity of albuminuria revealed no impact on TSH, fT4, T3, fT3, and TBG. EGFR correlated with increasing T4, fT4, T3, fT3, and TBG (T4: r = 0.289, p < 0.01; fT4: r = 0.196, p < 0.01; T3: r = 0.408, p < 0.01; fT3: r = 0.390, p < 0.01) but not with rT3. Conclusions In thyroid antibody-negative patients presenting advanced CKD (stages 4 and 5), even severe kidney protein loss failed to influence thyroid hormone status. However, albuminuria severity correlated negatively with rT3, which was significantly lower in patients with albuminuria in the nephrotic range.

scholarly journals Attempt to Develop Rat Disseminated Intravascular Coagulation Model Using Yamakagashi (Rhabdophis tigrinus) Venom Injection

Toxins ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 160
Author(s):  
Akihiko Yamamoto ◽  
Takashi Ito ◽  
Toru Hifumi
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Clinical Condition ◽  
Underlying Disease ◽  
Fibrinogen Concentration ◽  
Blood Coagulation Factors ◽  
Fixed Amount ◽  
Intravascular Coagulation ◽  
Measurement Limit ◽  
Human Pathology ◽  
Rhabdophis Tigrinus

Disseminated intravascular coagulation, a severe clinical condition caused by an underlying disease, involves a markedly continuous and widespread activation of coagulation in the circulating blood and the formation of numerous microvascular thrombi. A snakebite, including that of the Yamakagashi (Rhabdophis tigrinus), demonstrates this clinical condition. Thus, an animal model using Yamakagashi venom was constructed. Yamakagashi venom was administered to rats, and its lethality and the changes in blood coagulation factors were detected after venom injection. When 300 μg venom was intramuscularly administered to 12-week-old rats, (1) they exhibited hematuria with plasma hemolysis and died within 48 h; (2) Thrombocytopenia in the blood was observed in the rats; (3) irreversible prolongation of prothrombin time in the plasma to the measurement limit occurred; (4) fibrinogen concentration in the plasma irreversibly decreased below the measurement limit; and (5) A transient increase in the plasma concentration of D-dimer was observed. In this model, a fixed amount of Rhabdophis tigrinus venom injection resulted in the clinical symptom similar to the human pathology with snakebite. The use of the rat model is very effective in validating the therapeutic effect of human disseminated intravascular coagulation condition due to snakebite.

scholarly journals Soluble Fas affects erythropoiesis in vitro and acts as a potential predictor of erythropoiesis-stimulating agent therapy in patients with chronic kidney disease

2020 ◽  
Vol 318 (4) ◽  
pp. F861-F869
Author(s):  
Daniela Mendes Chiloff ◽  
Danilo Candido de Almeida ◽  
Maria A. Dalboni ◽  
Maria Eugênia Canziani ◽  
Sunil K. George ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Glomerular Filtration Rate ◽  
Kidney Disease ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Dependent Manner ◽  
Potential Predictor ◽  
Soluble Fas ◽  
Esa Therapy

Serum soluble Fas (sFas) levels are associated with erythropoietin (Epo) hyporesponsiveness in patients with chronic kidney disease (CKD). Whether sFas could predict the need for erythropoiesis-stimulating agent (ESA) usage and its influence in erythropoiesis remain unclear. We evaluated the relation between sFas and ESA therapy in patients with CKD with anemia and its effect on erythropoiesis in vitro. First, we performed a retrospective cohort study with 77 anemic patients with nondialysis CKD. We performed in vitro experiments to investigate whether sFas could interfere with the behavior of hematopoietic stem cells (HSCs). HSCs were isolated from umbilical cord blood and incubated with recombinant sFas protein in a dose-dependent manner. Serum sFas positively correlated with Epo levels ( r = 0.30, P = 0.001) but negatively with hemoglobin ( r = −0.55, P < 0.001) and glomerular filtration rate ( r = −0.58, P < 0.001) in patients with CKD at baseline. Elevated sFas serum levels (4,316 ± 897 vs. 2,776 ± 749, P < 0.001) with lower estimated glomerular filtration rate (26.2 ± 10.1 vs. 33.5 ± 14.3, P = 0.01) and reduced hemoglobin concentration (11.1 ± 0.9 vs. 12.5 ± 1.2, P < 0.001) were identified in patients who required ESA therapy compared with patients with non-ESA. Afterward, we detected that the sFas level was slight correlated with a necessity of ESA therapy in patients with nondialysis CKD and anemia. In vitro assays demonstrated that the erythroid progenitor cell frequency negatively correlated with sFas concentration ( r = −0.72, P < 0.001). There was decreased erythroid colony formation in vitro when CD34+ HSCs were incubated with a higher concentration of sFas protein (1.56 ± 0.29, 4.33 ± 0.53, P < 0.001). Our findings suggest that sFas is a potential predictor for ESA therapy in patients with nondialysis CKD and that elevated sFas could affect erythropoiesis in vitro.

Glomerular Filtration Rate in Dogs with Leishmaniasis and Chronic Kidney Disease

2008 ◽  
Vol 22 (2) ◽  
pp. 293-300 ◽  
Author(s):  
O. Cortadellas ◽  
M.J. Fernández del Palacio ◽  
J. Talavera ◽  
A. Bayón
Keyword(s):  
Chronic Kidney Disease ◽  
Glomerular Filtration Rate ◽  
Kidney Disease ◽  
Glomerular Filtration ◽  
Filtration Rate
Sign in / Sign up

Export Citation Format

Share Document