scholarly journals Systemic Toxic Reaction Due Bee Stings in Dogs

2018 ◽  
Vol 46 ◽  
pp. 5
Author(s):  
Mizael Machado ◽  
Davi Emanuel Ribeiro De Souza ◽  
Marina Frota de Albuquerque Landi ◽  
Taís Meziara Wilson ◽  
Sandy Menezes Honorato ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Rural Areas ◽  
Companion Animals ◽  
Renal Tubules ◽  
Fecal Matter ◽  
Toxic Reaction ◽  
Systemic Reactions ◽  
Mucous Membranes ◽  
Africanized Bees

Background: Toxic reactions due bee stings in human, companion animals, food animals and wild animals are sporadically reported. Accidents involving bees have been occurring in urban and rural areas since 1956, when African bees were introduced in Brazil, forming populations of aggressive hybrid Africanized bees. Their sting cause local and systemicreactions, which include dermatologic reactions, anaphylactic reactions and toxic systemic reactions before death. The aim of this article is to describe the clinical and pathological aspects of the toxic systemic reactions of two dogs that suffered a massive bee attack in the Federal District, Brazil.Cases: A 8-year-old female Brazilian mastiff, and one female 6-year-old Belgian shepherd were locked in the kennel when they suffered a massive bee attack. The dogs presented ‘apathy, congested mucous membranes, dyspnea, epistaxis, hemoglobinuria, icterus (one of them) and convulsions. Clinical pathology results showed a strong hemolyzed plasma, azotemia, leukocytosis with neutrophilia and monocytosis. Both animals were euthanized due to their critical conditions. At necropsy the dogs showed severe subcutaneous edema in the face, moderate congestion of mucous membranes, hematochezia and hematuria. Both dogs presented kidneys dark brown to blackened colored, urinary bladder replete with dark red fluid, lungs severely congested, intestines with severe mural edema and hyperemia containing bloody fecal matter inside, and the liverof one of the dog moderately icteric. The main histologic findings were the moderate diffuse degeneration of the kidney tubular epithelium with small focal areas of necrosis, countless casts of hemoglobin, granular and hyaline casts inside the renal tubules. The skin affected showed stingers inserted, dissociation of the collagen fibers by edema and multifocal areasof hemorrhage, neutrophils and eosinophils, and the muscular tissue underneath had intense necrosis, with hyalinization and moderate multifocal fragmentation of myocytes.Discussion: Africanized bees are well established in rural areas and can adapt to urban areas and, given their marked aggressiveness, cause accidents with animals and humans. Clinical and hematological changes presented by dogs in the DF are similar to those previously reported in this species, which are usually observed in hemolytic anemias and tissuedamage caused by the acute inflammatory response due multiple bee stings. Nephrosis can be considered one of the most important toxic effects, due severe intravascular hemolytic disturbance and rhabdomyolysis, along with acute renal failure caused by the toxin components in the tubules and the toxic-isquemic condition, causing azotemia. Hemolysin proteins such as fosfolipase A and melitina cause rhabdomyolysis, intravascular hemolysis, and hemoglobinemia, which trigger the process of diffuse nephrosis and acute renal failure. The main pathologic changes were observed in the kidneys and skin of the dogs in the DF and were similar to that previously reported in dogs with severe bee stings. The count of inserted bee stingers in the skin and history is considered important to establish a presumptive diagnosis and initiate immediate treatment for the affected animals. The epidemiologic and clinical-pathologic findings presented in these cases are similarto those observed in humans who had suffered systemic toxicity by bee stings and aggravates the general condition of the patient even leading to death. Based on these findings, it was possible to establish the diagnosis of systemic toxic reaction in dogs secondary to poisoning by Africanized bee stings.Keywords: poisonous arthropods, Africanized bees, systemic toxic reaction, toxicology.

Inhibition of tubular cell proliferation by neutralizing endogenous HGF leads to renal hypoxia and bone marrow-derived cell engraftment in acute renal failure

2008 ◽  
Vol 294 (2) ◽  
pp. F326-F335 ◽  
Author(s):  
Hiroyuki Ohnishi ◽  
Shinya Mizuno ◽  
Toshikazu Nakamura
Keyword(s):  
Bone Marrow ◽  
Cell Proliferation ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Repair Process ◽  
Tubular Cell ◽  
Tubular Damage ◽  
Renal Tubules ◽  
Stromal Cell Derived Factor ◽  
Renal Tubular

During the progression of acute renal failure (ARF), the renal tubular S3 segment is sensitive to ischemic stresses. For reversing tubular damage, resident tubular cells proliferate, and bone marrow-derived cells (BMDC) can be engrafted into injured tubules. However, how resident epithelium or BMDC are involved in tubular repair remains unknown. Using a mouse model of ARF, we examined whether hepatocyte growth factor (HGF) regulates a balance of resident cell proliferation and BMDC recruitment. Within 48 h post-renal ischemia, tubular destruction became evident, followed by two-waved regenerative events: 1) tubular cell proliferation between 2 and 4 days, along with an increase in blood HGF; and 2) appearance of BMDC in the tubules from 6 days postischemia. When anti-HGF IgG was injected in the earlier stage, tubular cell proliferation was inhibited, leading to an increase in BMDC in renal tubules. Under the HGF-neutralized state, stromal cell-derived factor-1 (SDF1) levels increased in renal tubules, associated with the enhanced hypoxia. Administrations of anti-SDF1 receptor IgG into ARF mice reduced the number of BMDC in interstitium and tubules. Thus possible cascades include 1) inhibition of tubular cell proliferation by neutralizing HGF leads to renal hypoxia and SDF1 upregulation; and 2) BMDC are eventually engrafted in tubules through SDF1-mediated chemotaxis. Inversely, administration of recombinant HGF suppressed the renal hypoxia, SDF1 upregulation, and BMDC engraftment in ARF mice by enhancing resident tubular cell proliferation. Thus we conclude that HGF is a positive regulator for eliciting resident tubular cell proliferation, and SDF1 for BMDC engraftment during the repair process of ARF.

Rasburicase Improves Renal Function and Uric Acid Nephropathy in Patients Developing Acute Renal Failure after Conditioning for Hematopoetic Stem Cell Transplant (HSCT).

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 1142-1142
Author(s):  
Donovan Strader ◽  
Michael S. Oholendt ◽  
Uday Popat ◽  
George Carrum ◽  
Helen E. Heslop
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Acute Renal Failure ◽  
Uric Acid ◽  
Single Dose ◽  
Urate Oxidase ◽  
High Dose ◽  
Renal Tubules ◽  
Cell Transplant ◽  
Uric Acid Nephropathy

Abstract Significant reduction in renal function secondary to protein deposition in the renal tubules is a common occurrence among patients with plasma cell dyscrasias such as Multiple Myeloma (MM) and Amyloidosis undergoing HSCT. Conditioning chemotherapy and uric acid release following cellular lysis may worsen already compromised renal function, leading to acute renal failure. Rasburicase, a recombinant urate oxidase enzyme, has been approved by the U.S. Food and Drug Administration for the treatment and prevention of hyperuricemia associated with tumor lysis syndrome in pediatric patients with leukemia, lymphoma, and solid tumor malignancies undergoing chemotherapy. We hypothesized that prompt treatment of hyperuricemia with rasburicase may prevent uric acid nephropathy and improve renal function, obviating the need for dialysis and improving the eventual outcome. Six adults, four with MM and two with amyloidosis, with rising uric acid levels after high dose Melphalan (200mg/m2) were given a single dose of rasburicase (0.15 mg/kg). At baseline, all patients had rising serum creatinine [mean: 2.1 mg/dL (range: 0.9–4.5 mg/dL)], rising BUN [mean: 27.6 mg/dL (range: 1.3–70 mg/dL)], and declining creatinine clearance (CrCL) [mean: 50.5 ml/min (range: 16–75 ml/min)]. After one dose of rasburicase, renal function significantly improved according to CrCL at 48 hours [mean: 55.2 ml/min (range: 17–82 ml/min)] and continued to improve at five days [mean: 68.2 ml/min (range: 18–109 mg/dL)]. Baseline uric acid was elevated [mean: 8.61 mg/dL (range: 7–9.9 mg/dL)] and improved 24 hours after treatment with rasburicase [mean: 0.2 mg/dL (range: 0–0.6 mg/dL)]. None of the patients required renal replacement therapy. There were no serious adverse events associated with rasburicase therapy. We therefore conclude that a single dose of rasburicase is promising in improving deteriorating renal function post high dose chemotherapy in patients with compromised renal function; further controlled studies are warranted.

Is Rasburicase Effective In Reversing Acute Renal Failure In Patients with Tumor Lyses Syndrome?

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 4939-4939
Author(s):  
Mohamad Ali Cherry ◽  
Samer Srour ◽  
Mohamad Khawandanah ◽  
Osama Qubaiah ◽  
Bassam Ghabache
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Creatinine Clearance ◽  
Total Dose ◽  
Tumor Lysis Syndrome ◽  
Previous History ◽  
Urate Oxidase ◽  
Malignant Neoplasms ◽  
Renal Tubules ◽  
Advanced Renal Failure

Abstract Abstract 4939 Tumor lysis syndrome (TLS) is a potentially life-threatening complication that can occur spontaneously or following treatment of malignant neoplasms, particularly leukemias and lymphomas. TLS can cause acute renal failure (ARF) by precipitation of uric acid (UA) and phosphate crystals in renal tubules. Rasburicase, a recombinant urate oxidase, was proven to be effective in the treatment of TLS and is known to cause an improvement in renal function in a subset of patients with TLS. For the purposes of our analysis ARF was defined as more than 50% increase in creatinine from baseline value or presenting with creatinine more or equal to 2 mg/dl with no previous history of chronic renal failure. To assess the efficacy of Rasburicase in adult patients with documented TLS and ARF in improving or normalizing the creatinine clearance (CrCl), we conducted a retrospective analysis of 53 patients that received Rasburicase for documented TLS. 41 patients fit the inclusion criteria. The median age was 54 yr (26-90), 13 were female. The majority of patients had hematological malignancies (acute leukemia, 11; chronic leukemia, 5; myeloproliferative/myelodysplastic syndromes, 4; lymphoma or myeloma, 10; solid tumor; 11). Results: On the first day of rasburicase infusion (day 0), median UA, creatinine and CrCl were 11.5 mg/dl (5.1 - 23.7mg/dl), 3.26 mg/dl and 32.5 ml/min (8.0 - 97.8 ml/min) calculated using Cockcroft-Gault equation, respectively. Patients received an average total dose of 0.17 mg/kg (0.06-0.51 mg/kg) of rasburicase in one or two doses. UA levels normalized in 97.3% and 100% of patients by day 2 and 7 respectively. Creatinine levels normalized in 19% and 59.4% by day 2 and 7 respectively. CrCl improved form a median of 32.5 ml/min to 40.5 ml/min and 58 ml/min by day 2 and 7 respectively. A sub analysis for patients with baseline CrCl <30 ml/min (n=17) on day 0 of Rasburicase infusion revealed a similar benefit to those with baseline CrCl >30 ml/min. CrCl improved in this subset of patients from a median of 17 ml/min (8-28.2 ml/min) to 24.5 and 47.4 ml/min on days 2 and 7 respectively. Patients who received a total dose of <0.1mg/kg of rasburicase (n=8) derived similar benefits to those who received 0.2mg/kg or more (n=11). Conclusion: Rasburicase infusion is effective in improving the creatinine clearance even in patients with advanced renal failure (CrCl<30 ml). Lower doses of Rasburicase are as effective as higher doses, even in patients with advanced renal failure, making the lower dose advisable and cost effective. Disclosures: No relevant conflicts of interest to declare.

Angiostatin and matrix metalloprotease expression following ischemic acute renal failure

2004 ◽  
Vol 286 (5) ◽  
pp. F893-F902 ◽  
Author(s):  
David P. Basile ◽  
Katherine Fredrich ◽  
Dorothee Weihrauch ◽  
Naoichiro Hattan ◽  
William M. Chilian
Keyword(s):  
Renal Failure ◽  
Endothelial Cells ◽  
Acute Renal Failure ◽  
Chronic Renal Disease ◽  
Ischemia Reperfusion ◽  
Vascular Endothelial Cell ◽  
Kidney Tissue ◽  
Late Time ◽  
Renal Tubules ◽  
Local Synthesis

Ischemic injury to the kidney results in blood vessel loss and predisposition to chronic renal disease. Angiostatin is a proteolytic cleavage product of plasminogen that inhibits angiogenesis, promotes apoptosis of endothelial cells, and disrupts capillary integrity. A combination of lysine-Sepharose enrichment followed by Western blotting was used to study the expression of angiostatin in response to the induction of ischemic renal injury. No angiostatin products were readily detectable in kidneys of sham-operated control rats. In contrast, both 38- and 50-kDa forms of angiostatin were dramatically enhanced in the first 3 days following 45-min ischemia-reperfusion injury. Renal angiostatin levels declined but remained detectable at late time points postrecovery (8–35 days postischemia). Angiostatin-like immunoreactivity was also elevated in the plasma and in urine for up to 35 days following injury. Lysine-Sepharose extracts of either kidney or urine inhibited vascular endothelial cell growth factor-induced proliferation of human aortic endothelial cells in vitro; an effect that was blocked by coincubation with an angiostatin antibody. RT-PCR verified that mRNA of the parent protein plasminogen was produced in the liver, but it was not present in either sham-operated or postischemic kidney. Matrix metalloproteinase (MMP)-2 and MMP-9, which may mediate angiostatin generation, were enhanced in postischemic kidney tissue and were localized to the renal tubules, interstitial cells, and the tubulo-interstitial space. These data indicate the possible local synthesis of angiostatin following acute renal failure (ARF) and suggest a possible role for MMPs in this activity. Renal angiostatin generation following ARF may modulate renal capillary density postischemia and thereby influence chronic renal function.

scholarly journals Expression of a Soluble Complement Inhibitor Protects Transgenic Mice from Antibody-Induced Acute Renal Failure

2001 ◽  
Vol 12 (1) ◽  
pp. 71-79
Author(s):  
BRIGITTE SCHILLER ◽  
PATRICK N. CUNNINGHAM ◽  
JESSY J. ALEXANDER ◽  
LIHUA BAO ◽  
V. MICHAEL HOLERS ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Transgenic Mice ◽  
Complement Activation ◽  
Membrane Attack Complex ◽  
Renal Tubules ◽  
Strongly Correlated ◽  
Systemic Injection ◽  
Tubular Necrosis ◽  
Complement Regulator

Abstract. Crry is a potent complement regulator in rodents that inhibits C3 convertases. In rats, intrarenal arterial injection of anti-glomerular endothelial cell (GEN) antibodies leads to complement-dependent microvascular injury and acute renal failure. In this study, a mouse variant of this model and the effects of complement inhibition were examined. Transgenic mice that overexpressed soluble Crry systemically and in their kidneys were studied. Anti-GEN IgG was injected intravenously into eight Crry transgenic mice and seven transgene-negative littermates (which were used as control animals). Thirty h after injection, blood urea nitrogen (BUN) levels were 30.3 ± 4.4 and 114.8 ± 23.5 mg/dl for transgene-positive and -negative animals, respectively (P = 0.012). Four of five transgene-negative animals with BUN levels of >100 mg/dl were anuric; the remaining animal exhibited minimal albuminuria and no detectable urinary C3. In animals with renal failure, glomerular capillary collapse and tubular necrosis were observed. There was significant tubular staining for C3 in transgene-negative animals, with cellular and basal distributions, both of which were statistically greater than those in transgene-positive animals. Tubular cell C3 staining was strongly correlated with BUN values (r = 0.83, P < 0.001), as was C9 staining (r = 0.56, P = 0.037), suggesting that complement activation to the C5b-9 membrane attack complex had a casual role in renal failure. Thus, systemic injection of anti-GEN antibodies into mice leads to acute renal failure, with glomerular and tubular injury. Animals that overexpress soluble Crry in renal tubules and elsewhere are protected from the acute renal failure that occurs in this model, which ultimately seems to develop because of complement activation focused on tubules.

Acute Renal Failure Amongst Children in a Tropical Environment

1987 ◽  
Vol 10 (2) ◽  
pp. 97-101 ◽  
Author(s):  
K.S. Chugh ◽  
A. Narang ◽  
L. Kumar ◽  
V. Sakhuja ◽  
V. Narayanan Unni ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Rural Areas ◽  
Acute Interstitial Nephritis ◽  
Acute Glomerulonephritis ◽  
Drug Induced ◽  
Tubular Necrosis ◽  
Renal Histology ◽  
Endocapillary Proliferative Glomerulonephritis ◽  
Glucose 6 Phosphate Dehydrogenase

The pathogenetic factors leading to acute renal failure (ARF) in 223 children between the ages of 20 days and 14 years were studied. Diarrhoeal diseases were responsible for ARF in 49.8%, acute glomerulonephritis in 34.1%, drug induced intravascular hemolysis in glucose -6-phosphate dehydrogenase deficiency in 4.5%, snake bite in 4%, hemolytic uremic syndrome in 2.2%, and miscellaneous causes in 5.4%. Dialysis was instituted in 178 children and the others were treated conservatively. Renal histology in 39 out of 76 children who presented with an acute nephritic illness revealed acute endocapillary proliferative glomerulonephritis in 27 and crescentic glomerulonephritis in 12. The histology in 79 out of 147 remaining patients showed acute tubular necrosis in 64, acute cortical necrosis in 13, and acute interstitial nephritis in 2. Overall mortality was 27.4%. This high incidence of ARF due to infective diarrhoeas and dysentery reflects poor socio-economic and hygienic conditions, inadequate facilities in rural areas, delays in seeking medical advice, and lack of knowledge about fluid and electrolyte therapy amongst the staff.

scholarly journals Severe acute renal failure after massive attack of Africanized bees

2004 ◽  
Vol 19 (10) ◽  
pp. 2680-2680 ◽  
Author(s):  
D. P. Gabriel ◽  
A. Goncalves Rodrigues ◽  
R. C. Barsante ◽  
V. dos Santos Silva ◽  
J. Teixeira Caramori ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Africanized Bees

scholarly journals A Study of Complications of Poisonous Snake Bites

2021 ◽  
Vol 10 (32) ◽  
pp. 2602-2608
Author(s):  
Sandip Ashok Mohale ◽  
Anuj Ramesh Varma ◽  
Gopikishan Ramkishan Bharadiya ◽  
Sourya Acharya ◽  
Shilpa Abhay Bawankule
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Longitudinal Study ◽  
Disseminated Intravascular Coagulation ◽  
Rural Areas ◽  
Adverse Reactions ◽  
Clinical Manifestations ◽  
Age Group ◽  
Snake Bites ◽  
Agricultural Labourers

BACKGROUND The present study was taken up to study the clinical manifestations, complications, and outcome in patients with poisonous snake bites admitted to Vivekanand Hospital, Latur (Maharashtra). METHODS This was a longitudinal study. Adult snakebite patients admitted from December 2012 to November 2014 were studied. RESULTS Mostly males (71.4 %) in the age group 18 - 29 years (58.6 %) were affected. Farmers (71.4 %) in rural areas (87.1 %) are the major sufferers. The neurotoxic venom poisoning ptosis (100 %) was commonest manifestation and was found in all cases. Palatal and pharyngeal palsy, ophthalmoplegia, respiratory palsy were also seen. In hemotoxic poisoning, bleeding from the bite site (73 %) was the commonest manifestation followed by hematuria (48.6 %) and gum bleeding (24.3 %). Among complications of poisonous snakebites, cellulitis (86.5 %) was the most common followed by acute renal failure (47.6 %), disseminated intravascular coagulation (DIC) (23.8 %), respiratory paralysis (12.7 %) and shock (4.28 %). Adverse reactions to anti-snake venom (ASV) were noted in 16 (22.9 %) patients. Total 10 patients died (14.3 %) mostly were due to acute renal failure (26.6 %). CONCLUSIONS Snakebite is common among agricultural labourers. Mostly males in the age group 18 - 29 years were bitten during 12 noon to 6 pm. Peak incidence peaked in between May to October. Viper bites were more common than Elapidae in this study. In neurotoxic envenomation, ptosis was the commonest and earliest symptom while in hemotoxic envenomation, most common symptoms were bleeding from bite site and hematuria. The commonest complications were cellulitis, acute renal failure and DIC. Early hospitalization and timely ASV were the corner stone in the treatment of snakebite. KEY WORDS Snakebite, Neurotoxic, Elapidae, Viperidae

Rhabdomyolysis Associated with Cocaine Intoxication

1988 ◽  
Vol 22 (10) ◽  
pp. 778-780 ◽  
Author(s):  
Hilary A. Skluth ◽  
John E. Clark ◽  
George L. Ehringer
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Clinical Presentation ◽  
Elevated Serum ◽  
Serum Concentrations ◽  
Muscle Enzymes ◽  
Toxic Reaction

A case of a patient who had an acutely toxic reaction to cocaine ingestion and later developed acute renal failure secondary to rhabdomyolysis is described. Evidence of rhabdomyolysis was noted by the combination of myalgia, urine discoloration, and elevated serum concentrations of muscle enzymes. Although the mechanism of the rhabdomyolysis is unknown, the clinical presentation resembled that of a norepinephrine-induced vasoconstrictive effect that alters the metabolic demands of the muscle in such a way that the muscle is damaged.

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