Coagulation profile in two nephropathic dogs

Coagulatory abnormalities are common in renal dysfunction in humans. The studies on coagulatory abnormalities in renal failure in dogs are limited. The present paper deals with coagulation profile in acute and chronic kidney disease in dogs. The haemostatic defects observed in acute renal dysfunction included thrombocytopaenia, prolonged capillary bleeding time (CBT), elevated D-Dimer and hypoantithrombinemia which indicated a hypercoagulable state. Prolongation of prothrombin time (PT), activated partial thromboplastin time (aPTT), elevated D-Dimer concentration and hypoantithrombinemia in chronic kidney disease indicated the presence of hypocoagulable state

Chylooperitoneum in the cardiovascular possurgical. Presentation of a case

Introduction: Chyloperitoneum is defined as the presence of lymph of thoracic or intestinal origin in the abdominal cavity. It is reported infrequently and is a rare manifestation of multiple deseases. Most of the cases are secondary and are associated with direct trauma to the peritoneal dialysis. Renal replacement therapy is necessary in up to 10% of children who undergo cardiac surgery with extracorporeal circulation, indicated in cases of water overload, acute renal dysfunction or ionic alterations. Objective: To report the case of a 15-day-old newborn, operated on for Transposition of the Great Vessels, who presented as a postoperative complication, dicharge of chylous content through the Tenckhoff, after a peritoneal dialysis regimen due to acute renal failure and fluid overload. Results: Despite the therapeutic measures taken, the patient maintains centuries-old losses of lymph, which lead to nutritional and immunological deterioration with the consequent multiple organ dysfunction and death. Conclusions: The perpetuation of lymph losses in the postoperative period of cardiovascular surgery produces a nutritional and immunological deterioration of the patient, with a high risk of mortality due to sepsis.

Pioglitazone Ameliorates Acute Endotoxemia-Induced Acute on Chronic Renal Dysfunction in Cirrhotic Ascitic Rats

Endotoxemia-activated tumor necrosis factor (TNFα)/nuclear factor kappa B (NFκB) signals result in acute on chronic inflammation-driven renal dysfunction in advanced cirrhosis. Systemic activation of peroxisome proliferator-activated receptor gamma (PPARγ) with pioglitazone can suppress inflammation-related splanchnic and pulmonary dysfunction in cirrhosis. This study explored the mechanism and effects of pioglitazone treatment on the abovementioned renal dysfunction in cirrhotic rats. Cirrhotic ascitic rats were induced with renal dysfunction by bile duct ligation (BDL). Then, 2 weeks of pioglitazone treatment (Pio, PPAR gamma agonist, 12 mg/kg/day, using the azert osmotic pump) was administered from the 6th week after BDL. Additionally, acute lipopolysaccharide (LPS, Escherichia coli 0111:B4; Sigma, 0.1 mg/kg b.w, i.p. dissolved in NaCl 0.9%) was used to induce acute renal dysfunction. Subsequently, various circulating, renal arterial and renal tissue pathogenic markers were measured. Cirrhotic BDL rats are characterized by decreased mean arterial pressure, increased cardiac output and portal venous pressure, reduced renal arterial blood flow (RABF), increased renal vascular resistance (RVR), increased relative renal weight/hydroxyproline, downregulated renal PPARγ expression, upregulated renal inflammatory markers (TNFα, NFκB, IL-6, MCP-1), increased adhesion molecules (VCAM-1 and ICAM-1), increased renal macrophages (M1, CD68), and progressive renal dysfunction (increasing serum and urinary levels of renal injury markers (lipocalin-2 and IL-18)). In particular, acute LPS administration induces acute on chronic renal dysfunction (increasing serum BUN/creatinine, increasing RVR and decreasing RABF) by increased TNFα-NFκB-mediated renal inflammatory markers as well as renal M1 macrophage infiltration. In comparison with the BDL+LPS group, chronic pioglitazone pre-treatment prevented LPS-induced renal pathogenic changes in the BDL-Pio+LPS group. Activation of systemic, renal vessel and renal tissue levels of PPARγ by chronic pioglitazone treatment has beneficial effects on the endotoxemia-related TNFα/NFκB-mediated acute and chronic renal inflammation in cirrhosis. This study revealed that normalization of renal and renal arterial levels of PPARγ effectively prevented LPS-induced acute and chronic renal dysfunction in cirrhotic ascitic rats.

Pantoprazole Attenuates MAPK (ERK1/2, JNK, p38)–NF-κB and Apoptosis Signaling Pathways after Renal Ischemia/Reperfusion Injury in Rats

Ischemia/reperfusion injury (IRI) in the kidney is the most common cause of acute renal dysfunction through different cell damage mechanisms. This study aimed to investigate, on molecular basics for the first time, the effect of pantoprazole on renal IRI in rats. Different biochemical parameters and oxidative stress markers were assessed. ELISA was used to estimate proinflammatory cytokines. qRT-PCR and western blot were used to investigate the gene and protein expression. Renal histopathological examination was also performed. IRI resulted in tissue damage, elevation of serum levels of creatinine, urea nitrogen, malondialdehyde, TNF-α, IL-6, IL-1β, up-regulation of NF-κB, JNK1/2, ERK1/2, p38, and cleaved caspase-3 proteins. Furthermore, it up-regulated the expression of the Bax gene and down-regulated the expression of the Bcl-2 gene. Treatment of the injured rats with pantoprazole, either single dose or multiple doses, significantly alleviated IRI-induced biochemical and histopathological changes, attenuated the levels of proinflammatory cytokines, down-regulated the expression of NF-κB, JNK1/2, ERK1/2, p38, and cleaved caspase-3 proteins, and the Bax gene, and up-regulated Bcl-2 gene expression. Moreover, treatment with pantoprazole multiple doses has an ameliorative effect that is greater than pantoprazole single-dose. In conclusion, pantoprazole diminished renal IRI via suppression of apoptosis, attenuation of the pro-inflammatory cytokines’ levels, and inhibition of the intracellular signaling pathway MAPK (ERK1/2, JNK, p38)–NF-κB.

Protective Effect of Joa-Gui Em through the Improvement of the NLRP3 and TLR4/NF-κb Signaling by Ischemia/Reperfusion-Induced Acute Renal Failure Rats

Joa-gui em (左歸飮, JGE) is known to be effective for treating kidney-yin deficient syndrome. However, there is a lack of objective pharmacological research on improving kidney function. This study was designed to evaluate whether JGE improves renal function and related mechanisms in rats with acute renal injury induced by ischemia/reperfusion (I/R). The acute renal failure (ARF) group was subjected to reperfusion after inserting a clip into the renal artery for 45 min. The ARF + JGE (100 or 200 mg/kg/day) groups were orally administered for four days after their I/R surgery, respectively. JGE treatment suppressed the increase in kidney size in the ARF animal model and alleviated the polyuria symptoms. In addition, to confirm the effect of improving the kidney function of JGE, lactate dehydrogenase levels, blood urea nitrogen/creatinine ratio, and creatinine clearance were measured. As a result, it decreased in the ARF group but significantly improved in the JGE group. Also, as a result of examining the morphological aspects of renal tissue, it was shown that JGE improved renal fibrosis caused by ARF. Meanwhile, it was confirmed that JGE reduced inflammation through the nucleotide-binding oligomerization domain-like receptor pyrin domain containing-3 (NLRP3) and toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling pathways, which are the major causes of acute ischemic kidney injury, thereby improving renal function disorder. The JGE has a protective effect by improving the NLRP3 and TLR4/NF-κB signaling pathway in rats with acute renal dysfunction induced by I/R injury.

Frailty as a risk factor for postoperative complications in adult patients with degenerative scoliosis administered posterior single approach, long-segment corrective surgery: a retrospective cohort study

Background With the population aging worldwide, adult degenerative scoliosis (ADS) is receiving increased attention. Frailty, instead of chronological age, is used for assessing the patient’s overall physical condition. In ADS patients undergoing a posterior approach, long-segment corrective surgery, the association of frailty with the postsurgical outcomes remains undefined. Methods ADS patients who underwent a posterior approach, long-segment fusion at the Department of Orthopedics, Beijing Chaoyang Hospital, Capital Medical University (CMU), Beijing, China, in 2014–2017 were divided into the frailty and non-frailty groups according to the modified frailty index. Major postoperative complications were recorded, including cardiac complications, pneumonia, acute renal dysfunction, delirium, stroke, neurological deficit, deep wound infection, gastrointestinal adverse events, and deep vein thrombosis. Radiographic measurements and health-related quality of life (HRQOL) parameters were recorded preoperatively and at 2 postoperative years. Results A total of 161 patients were included: 47 (29.2%) and 114 (70.8%) in the frailty and non-frailty groups, respectively. Major postoperative complications were more frequent in the frailty group than the non-frailty group (29.8% vs. 10.5%, P = 0.002). Multivariable logistic regression analysis showed that frailty was independently associated with major complications (adjusted odds ratio [aOR] = 2.77, 95% confidence interval [CI] 1.12–6.89, P = 0.028). Radiographic and HRQOL parameters were improved at 2 years but with no significant between-group differences. Conclusions Frailty is a risk factor for postoperative complications in ADS after posterior single approach, long-segment corrective surgery. Frailty screening should be applied preoperatively in all patients to optimize the surgical conditions in ADS.