PRELIMINARY EVALUATION OF SYMMETRIC DIMETHYLARGININE AS A BIOMARKER OF RENAL INSUFFICIENCY IN WILD AND REHABILITATED FLORIDA MANATEES (TRICHECHUS MANATUS LATIROSTRIS).

Currently, there are limited antemortem tests available to evaluate renal function in Florida manatees (Trichechus manatus latirostris). Although few reports of renal pathology in manatees exist in the veterinary literature, debilitated animals that present to rehabilitation centers are frequently dehydrated, may have sustained renal trauma secondary to watercraft injury, and may experience ischemic events related to coagulation disorders leading to renal compromise. Clinicians remain limited to the analysis of blood urea nitrogen, creatinine levels, and urinalysis (if urine is obtained) to determine the extent of renal insufficiency, which may not accurately reflect renal function. This poses a diagnostic challenge for clinicians in discerning how critical renal compromise is to the animal's overall health and prognosis. For the first phase of this study, retrospective symmetric dimethylarginine (SDMA) values were determined from banked serum or plasma samples from 14 wild Florida manatees that had been collected while the animals were under rehabilitation in zoological institutions prior to their deaths. Values of SDMA for nine samples from eight manatees with known renal disease, as determined by histopathology, were compared to SDMA values for seven samples from six manatees with no reported renal lesions on histopathology. Values of SDMA from wild Florida manatees with known renal disease (mean 33.56 µg/dl ± 13.15, P= 0.017) were statistically significantly elevated when compared to SDMA values from manatees with no reported renal lesions (mean = 18.71 µg/dl ± 6.9) on histopathology. For the second phase of the study, serum or plasma samples were obtained from wild manatee populations from two geographically separate presumed-healthy wild manatee populations (n = 57). Although the upper limit was higher, serum SDMA concentrations from presumed-healthy wild manatees were comparable to those reported in small animal and equine medicine at 5.88-16.97 µg/dl.

Calcinosis in a roe deer fawn (Capreolus capreolus) in northern Germany.

BACKGROUND: Calcinosis has been reported for a broad range of different animals. Causes for calcinosis include metabolic disorders due to kidney failure, intoxication with calcinogenic plants, or iatrogenic overdose of vitamin D. Especially young animals seem to be very susceptible to developing calcinosis. Currently, however, there is a lack of information on calcinosis in wildlife. CASE PRESENTATION: The following case report describes a roe deer fawn admitted to a clinic due to general weakness and myiasis. Plasma levels for creatinine, urea and phosphate were highly elevated, whereas the total calcium level was decreased. Necropsy revealed calcinosis due to calcification in many organs. The reason for calcinosis in this particular case might be kidney failure. Plasma samples from other hunted roe deer fawns also showed high phosphate levels. CONCLUSIONS: Roe deer fawns might be susceptible to calcinosis due to high plasma phosphate, which could be a result of kidney failure or different feed. Further research into calcium and phosphate homeostasis in roe deer is necessary.

Iron status in dogs with myxomatous mitral valve disease.

In humans, iron deficiency represents a relevant occurrence in heart failure (HF), with or without anaemia, and is associated with the worst outcome. Moreover, chronic kidney disease (CKD) is a well-known comorbidity of HF and is strongly associated with the risk of developing anaemia. The most common cause of HF in dogs is myxomatous mitral valve disease (MMVD). To the best of our knowledge, no studies have examined the iron status in dogs with HF, with and without CKD. The aim of this retrospective study was to evaluate the iron status in dogs affected by MMVD and how strong is the relation with HF. The retrospective study included 54 dogs with complete case records, echocardiography and laboratory analyses. Iron status was evaluated by measuring serum iron concentration (SIC), un- saturated iron binding capacity (UIBC), total iron binding capacity (TIBC), and percentage of saturation (%SAT). The prevalence of dogs showing low serum iron concentration (SIC) was 18% in the whole population, 33% in symptomatic patients, 100% in dogs with acute decompensated HF. No signif- icant differences in SIC, UIBC, TIBC and %SAT median values were found among dogs classi- fied in different ACVIM (American College of Veterinary Internal Medicine) classes, between symptomatic and non-symptomatic patients, and among IRIS (International Renal Interest Soci- ety) classes. Azotemic and non-azotemic patients presented a significant difference in SIC mean values (p=0.02). Generalised linear model (GLM) revealed that dogs with low SIC were at high- er risk of being included in a higher ACVIM class (OR=6.383, p-value=0.014). Log-rank analysis showed shorter survival in dogs with low SIC (p=0.020), multivariate Cox analysis revealed that only HF symptoms can affect survival.

Outcome of Donor Cats After Unilateral Nephrectomy as Part of a Clinical Kidney Transplant Program.

OBJECTIVE: To compare 1) complications between 2 ureteral harvest techniques (ureteral papilla harvest [UPH] and ureteral transection [UT]); 2) to investigate the prevalence of kidney failure in a population of kidney donors; and 3) to evaluate owner satisfaction with commercially sourced cats adopted after kidney donation. STUDY DESIGN: Retrospective case series. ANIMALS: Cats (n = 72) that had unilateral nephrectomy for kidney donation. METHODS: Medical records were reviewed and information on short- and long-term complications and evidence of kidney failure was recorded. Clients were interviewed by telephone to ascertain their satisfaction with the adopted donor cats as pets. RESULTS: Seventy-two cats had unilateral nephrectomy. Forty-two owners were able to be contacted for survey data. Twenty-eight cats had complete medical records including serum BUN, creatinine, and urine specific gravity. For these 28 cats, mean age at nephrectomy was 1.9 years (median, 1.1 years; range, 0.5-9.3 years) and mean age at follow-up was 6.8 years (median, 5.1 years; range, 1.0-18.7 years). There was no difference in major or minor complication rates between UPH and UT techniques. Kidney failure occurred in 17.8% of cats. All owners were satisfied with the adopted donor cats, which were obtained from commercial facilities. CONCLUSIONS: UPH is a safe technique in cats being used for kidney donation. Commercially sourced cats make suitable pets after kidney donation. The prevalence of kidney failure in the donor population appears to be higher than that in the general population, but definitive conclusions cannot be made based on this study. Further, prospective study is needed to identify the true prevalence of kidney failure in cats after unilateral nephrectomy.

Investigation of the protective effect of chitosan against arsenic-induced nephrotoxicity and oxidative damage in rat kidney tissue.

Arsenic is an important metalloid that can cause poisoning in humans and domestic animals. Exposure to arsenic causes cell damage, increasing the production of reactive oxygen species. Chitosan is a biopolymer obtained by deacetylation of chitin with antioxidant and metal ion chelating properties. In this study, the protective effect of chitosan on arsenic-induced nephrotoxicity and oxidative damage was investigated. 32 male Wistar-albino rats were divided into 4 groups of 8 rats each as control group (C), chitosan group (CS group), arsenic group (AS group), and arsenic+chitosan group (AS+CS group). The C group was given distilled water by oral gavage, the AS group was given 100 ppm/day Na-arsenite ad libitum with drinking water, the CS group was given 200 mg/kg/day chitosan dissolved in saline by oral gavage, the AS+CS group was given 100 ppm/day Na-arsenite ad libitum with drinking water and 200 mg/kg/day chitosan dissolved in saline by oral gavage for 30 days. At the end of the 30-day experimental period, 90 mg/kg ketamine was administered intraperitoneally to all rats, and blood samples and kidney tissues were collected. Urea, uric acid, creatinine, P, Mg, K, Ca, Na, Cystatin C (CYS-C), Neutrophil Gelatinase Associated Lipocalin (NGAL) and Kidney Injury Molecule 1 (KIM-1) levels were measured in serum samples. Malondialdehyde (MDA), Glutathione (GSH), Catalase (CAT) and Superoxide dismutase (SOD) levels in the supernatant obtained from kidney tissue were analyzed by ELISA method. Compared with AS group, uric acid and creatinine levels of the AS+CS group were significantly decreased (p<0.001), urea, KIM-1, CYS-C, NGAL, and MDA levels were numerically decreased and CAT, GSH, and SOD levels were numerically increased (p>0.05). In conclusion, based on both biochemical and histopathological-immunohistochemical- immunofluorescence findings, it can be concluded that chitosan attenuates kidney injury and protects the kidney.

Amanitin toxicosis in two cats with acute hepatic and renal failure.

Amanitin is a toxic cyclopeptide present in several species of poisonous mushrooms. Amanitin toxicosis was diagnosed in 2 cats from separate premises. Both cats initially had lethargy and vomiting, and they rapidly developed depression and neurological signs over 24-48 hours. Marked elevation of alanine aminotransferase was the primary finding, with subsequent serum chemistry values compatible with hepatic and renal failure. Histopathological findings consisted of submassive to massive acute hepatic necrosis, renal proximal tubular epithelial necrosis, and foci of necrosis and inflammation in the gastrointestinal tract. Amanitin exposure was confirmed postmortem by detection of α-amanitin in the kidney by liquid chromatography-mass spectrometry. A similar clinical course and pathological changes are reported in human and canine amanitin intoxication; however, gastrointestinal lesions are not typically described.

Effect of diet on the incidence of and mortality owing to gastritis and renal disease in captive cheetahs (Acinonyx jubatus) in South Africa.

Seventy-two adult cheetahs were evaluated for the degree of gastritis by endoscopic biopsy and for renal disease by serum creatinine. Cheetahs free of Grade 3 gastritis and renal disease were placed on Trial A; remaining cheetahs were placed on Trial B, which ran concurrently. All cheetahs were monitored for 4 years. Cheetahs exited Trial A and entered Trial B if they developed Grade 3 gastritis or renal disease. Cheetahs exited Trial B if they developed clinical gastritis or renal disease that required a dietary change or aggressive medical therapy or died owing to either disease. Cheetahs on Trial A were fed either a supplemented meat diet (N = 26) or commercial cat food (N = 22). Cheetahs on Trial B were fed either the same meat diet (N = 28) or a commercial dry cat food formulated for renal disease (N = 16). Cheetahs fed meat on Trial A had a daily hazard of developing Grade 3 gastritis 2.21 times higher (95% CI 0.95-5.15) than cheetahs fed commercial cat food. This hazard was not statistically significant (P = 0.07). Mean gastritis scores were not significantly different between the two groups. Cheetahs fed commercial cat food in both Trials had lower serum urea levels and higher creatinine levels than those fed meat. Evidence for the effect of diet in cheetahs with gastritis and/or renal disease (Trial B) was inconclusive. The number of cheetahs dying of gastritis or renal disease at the facility has dropped markedly since the study began. These results indicate that diet may play an important role in the incidence of Grade 3 gastritis and that dietary and/or therapeutic management of gastritis may reduce mortality owing to gastritis and renal disease in captive cheetahs.

Nucleolar organizer region proteins enhancement in nucleoplasm's of renal tubular cells is an indication of kidney impairment in Leishmania-infected dogs.

Hyperactivation of tubular cells contributes for the progression of kidney lesions. The exacerbated expression of immunological proteins and ribosomal DNA (rDNA) transcriptional activity are observed in tubular cells. This intensified expression results in more prominent hypertrophic changes and is often accompanied by increased expression of factors involved in different phases of ribosomal biosynthesis, such as the nucleolar organizer regions (NOR). The aim of this study was to evaluate whether there is an association between NOR proteins, renal impairment, and clinical status in Leishmania-infected dogs (CanL). Forty-five dogs with CanL and six uninfected controls were assessed in this study. PCR was performed to detect parasites' nucleic acids in kidney. Histopathological analyses were performed in kidney fragments, and NOR was detected by Ag stain (AgNOR). Leishmania-infected dogs showed more intense inflammation and collagen deposition compared with uninfected controls. Biochemical alterations were observed only in Leishmania-infected dogs. AgNORs per cell were significantly higher in clinically affected dogs and higher histopathological lesion score was observed in Leishmania-infected dogs. Positive correlations between number of NORs per cell in medullary region and histopathological lesion score were observed. Furthermore, AgNOR expression, intensity of renal lesions, and clinical sigs was associated in Leishmania-infected dogs. We propose that the detection of AgNOR proteins could be used to better estimate the kidney tubular damage at the time of examination in Leishmania-infected dogs as a marker to estimate renal impairment in dogs with CanL.

Progression of glomerulonephritis to end-stage kidney disease in a cat with nephrotic syndrome.

A percutaneous renal biopsy was performed on a 3-year-old female Japanese domestic cat with pleural effusion, mild azotemia, hypoalbuminemia, hypercholesterolemia, and proteinuria. Glomerular lesions included mild diffuse hypercellularity and numerous capsular adhesions with segmental sclerosis/hyalinosis of glomerular tufts. Electron microscopy revealed many subendothelial dense deposits with characteristic outer protrusion of glomerular basement membrane. Diffuse and global granular deposits of IgG and C3 were detected along the capillary walls. Tubulo-interstitial changes were mild at the time of biopsy, but progression of the disease was predicted because of the many capsular adhesions of the glomerular tufts. The cat was fed a prescription diet without any other specific or symptomatic therapy after renal biopsy, and died 43 weeks after the biopsy. At necropsy, extensive tubulo-interstitial fibrosis and mononuclear cell infiltration had developed throughout the cortex and outer medulla, and most glomeruli had extensive global sclerosis or obsolescence with less prominent depositions of IgG and C3.

Diclofenac residues as the cause of vulture population decline in Pakistan.

The Oriental white-backed vulture (OWBV; Gyps bengalensis) was once one of the most common raptors in the Indian subcontinent. A population decline of >95%, starting in the 1990s, was first noted at Keoladeo National Park, India. Since then, catastrophic declines, also involving Gyps indicus and Gyps tenuirostris, have continued to be reported across the subcontinent. Consequently these vultures are now listed as critically endangered by BirdLife International. In 2000, the Peregrine Fund initiated its Asian Vulture Crisis Project with the Ornithological Society of Pakistan, establishing study sites at 16 OWBV colonies in the Kasur, Khanewal and Muzaffargarh-Layyah Districts of Pakistan to measure mortality at over 2,400 active nest sites. Between 2000 and 2003, high annual adult and subadult mortality (5-86%) and resulting population declines (34-95%) (ref. 5 and M.G., manuscript in preparation) were associated with renal failure and visceral gout. Here, we provide results that directly correlate residues of the anti-inflammatory drug diclofenac with renal failure. Diclofenac residues and renal disease were reproduced experimentally in OWBVs by direct oral exposure and through feeding vultures diclofenac-treated livestock. We propose that residues of veterinary diclofenac are responsible for the OWBV decline.

Xanthine nephrolithiasis in a galician blond beef calf.

A six-month-old female Galician Blond beef calf presented signs of apathy, anorexia and weight loss. The analysis of a blood sample confirmed renal failure. Bilateral nephrolithiasis was diagnosed at necropsy. Quantitative analysis revealed the nephroliths to be composed of 100 per cent xanthine. In cattle, xanthinuria has only been described in the Japanese Black breed, but never before in other breeds. Clinical history suggested a naturally occurring xanthinuria.

Evaluation of serum biomarkers and proteinuria for the early detection of renal damage in dogs with heartworm (Dirofilaria immitis).

Glomerulonephropathy associated with Dirofilaria immitis (heartworm) is relatively frequent in infected dogs. Given the importance and the scarcity of studies focused on its prevalence and diagnosis, the objective was to determine the prevalence of proteinuria and functional indicators of glomerular filtration rate in dogs with heartworm disease and discuss its utility in the detection of renal impairment. Sera and urine from 47 infected dogs were analyzed in a reference laboratory. Urea, creatinine, plasma proteins and serum symmetric dimethylarginine (SDMA) were analyzed in sera, while the UPC ratio was performed in urine. Dogs were further evaluated for the presence/absence of microfilariae, pulmonary and systemic hypertension, and the parasite burden was assessed. The results showed that 19.1 % of dogs showed proteinuria (UPC > 0.5) and 17 % showed borderline proteinuria (UPC 0.2-0.5). Creatinine and SDMA were high (>1.8 mg/dl and ≥18 µg/dl, respectively) in 4.2 % of dogs. UPC ratio was significantly increased in dogs with high parasite burden and in dogs with microfilariemia (p < 0.05). Dogs with pulmonary hypertension showed higher increases in proteinuria as well, which was probably due to the chronicity of the infection. No significant differences were found in serum and urine values regarding systemic blood pressure. Despite the limitations of this study, proteinuria/borderline proteinuria was present in 36.2 % of dogs with heartworm disease, and this may be due to glomerular disease. Therefore, the detection of proteinuria, along with other renal biomarkers in the diagnostic protocols, could help identify kidney alterations or risk of renal damage in heartworm disease.

Prevalence of PKD1 gene mutation in cats in Turkey and pathogenesis of feline polycystic kidney disease.

Polycystic kidney disease (PKD) is one of the most common hereditary diseases in cats, with high prevalence in Persian and Persian-related cats. PKD is caused mainly by an inherited autosomal dominant (AD) mutation, and animals may be asymptomatic for years. We screened 16 cats from various breeds exhibiting a renal abnormality by ultrasound examination and genotyped them for the c.10063C>A transversion on exon 29 of the polycystin-1 (PKD1) gene, by PCR-restriction fragment length polymorphism (PCR-RFLP). Among these cats, a Siamese nuclear family of 4 cats with ancestral hereditary renal failure were screened by whole-genome sequencing (WGS) to determine novel variations in genes associated with both AD and autosomal recessive PKD in humans. During the study period, one cat died as a result of renal failure and was forwarded for autopsy. Additionally, we screened 294 cats asymptomatic for renal disease (Angora, Van, Persian, Siamese, Scottish Fold, Exotic Shorthair, British Shorthair, and mixed breeds) to determine the prevalence of the mutation in cats in Turkey. Ten of the symptomatic and 2 of the asymptomatic cats carried the heterozygous C → A transversion, indicating a prevalence of 62.5% and 0.68%, respectively. In the WGS analysis of 4 cats in the Siamese nuclear family, novel variations were determined in the fibrocystin gene (PKHD1), which was not compatible with dominant inheritance of PKD.

Evaluation of subchronic toxicity of pet food contaminated with melamine and cyanuric acid in rats.

Outbreaks of food-associated renal failure in pets occurred in Asia and the United States of America in 2004 and 2007. They were related to the combined intoxication of cyanuric acid and melamine. Our aims were to investigate cyanuric acid and melamine contamination of pet food and to examine subchronic toxicity in rats. Levels of 10%, 20%, 50%, and 50%-100% (w/w) of contaminated pet food were fed to rats for three months. Analytical results revealed that the tainted food contained significant levels of cyanuric acid and melamine in a ratio of 1:6.8. Rats fed the diet of 50%-100% for three months exhibited elevated serum blood urea nitrogen and creatinine, as well as dose-dependent melamine/cyanuric acid crystal-induced nephrotoxicity. The melamine/cyanuric acid crystals of various sizes were mixed with necrotic cell debris and inflammatory cells, accompanied by tubular dilation and interstitial fibrosis. The immunohistochemistry index of proliferative cellular nuclear antigen and osteopontin in the kidney of the 50%-100% group were elevated, indicating regeneration of renal cells and the formation of crystals. In conclusion, the combination ratio of cyanuric acid to melamine and the acidic urine content were two factors that, upon repeated exposure, determined the severity of the nephrotoxicity.

Melamine- and cyanuric acid-associated renal failure in pigs in Thailand.

A newly observed syndrome characterized by progressive weight loss, pallor, and high mortality was reported in many swine herds across Thailand from February through May 2007. To determine the cause of the new syndrome, 5 pigs, 4-8 weeks of age, were submitted to the diagnostic laboratory for necropsy examination. All 5 pigs were underweight, with pallor and rough coats. The kidneys of all 5 pigs were yellowish and slightly swollen, with precipitation of crystalline material on the cut surface. Histologically, epithelial degeneration and necrosis were evident in proximal and distal tubules and collecting ducts. Round, yellow-brown crystals with radiating striations were diffusely distributed through the lumen of proximal and distal tubules and collecting ducts. Blood urea nitrogen and creatinine levels were elevated. Melamine and analogs, including cyanuric acid, were detected by gas chromatography mass spectrometry. The evidence reported here suggests that melamine- and cyanuric acid-adulterated feed caused renal failure in these pigs.

Ionized hypercalcemia in dogs: a retrospective study of 109 cases (1998-2003).

BACKGROUND: Serum hypercalcemia in dogs has been reported in association with a variety of diseases. Serum-ionized calcium (iCa) concentration is a more accurate measure of hypercalcemia than total serum calcium or corrected serum calcium concentrations. The severity of hypercalcemia has been utilized to suggest the most likely differential diagnosis for the hypercalcemia. HYPOTHESIS: Diseases causing ionized hypercalcemia may be different than those that cause increases in total or corrected serum calcium concentrations. The severity of ionized hypercalcemia in specific diseases cannot be used to determine the most likely differential diagnosis for ionized hypercalcemia. ANIMALS: One-hundred and nine client-owned dogs with a definitive cause for their ionized hypercalcemia evaluated between 1998 and 2003 were included in this study. METHODS: Retrospective, medical records review. RESULTS: Neoplasia, specifically lymphosarcoma, followed by renal failure, hyperparathyroidism, and hypoadrenocorticism were the most common causes of ionized hypercalcemia. Dogs with lymphoma and anal sac adenocarcinoma have higher serum iCa concentrations than those with renal failure, hypoadrenocorticism, and other types of neoplasia. The magnitude of serum-ionized hypercalcemia did not predict specific disease states. CONCLUSIONS AND CLINICAL IMPORTANCE: Serum-ionized hypercalcemia was most commonly associated with neoplasia, specifically lymphosarcoma. Although dogs with lymphosarcoma and anal sac adenocarcinoma had higher serum iCa concentrations than dogs with other diseases, the magnitude of the serum iCa concentration could not be used to predict the cause of hypercalcemia. Total serum calcium and corrected calcium concentrations did not accurately reflect the calcium status of the dogs in this study.

Vincristine overdose in a cat: clinical management, use of calcium folinate, and pathological lesions.

A 6-year-old female neutered Burmese cat received a 10 times overdose (5mg/m(2)) of vincristine, administered in error. Supportive therapy, including administration of calcium folinate, was instigated within 8h. Despite treatment, the patient exhibited deterioration in renal and respiratory function and died 72 h after overdose. Necropsy was performed within 24h of death. Gross examination revealed pulmonary oedema and a pale brown liver with a prominent lobular pattern. Histological examination revealed marked apoptosis and necrosis of the bone marrow myeloid series, and mild to moderate apoptosis and necrosis of the erythroid and megakaryocyte series. Multifocal necrosis of the renal tubules, hepatocytes, and small intestinal crypt epithelium was also observed. Use of calcium folinate as a rescue therapy following vincristine overdose in humans has been previously documented. If treatment is to be successful in cases of vincristine overdose in cats, then a more complete understanding of the pathogenesis of vincristine toxicity in companion animal species is required.

Evaluation of serum cardiac troponin I concentration in dogs with renal failure.

OBJECTIVE: To determine whether dogs with renal failure have higher serum cardiac troponin I (cTnI) concentrations than healthy dogs. DESIGN: Case-control study. ANIMALS: 31 dogs with renal failure and 51 healthy dogs. PROCEDURES: Serum concentrations of creatinine and cardiac troponin I, urine specific gravity, and systolic arterial blood pressure were measured for all dogs. Dogs underwent a standardized physical examination, and any dog with evidence of cardiovascular disease or other nonrenal disease was excluded from final analyses. Dogs were considered to be in renal failure when the serum creatinine concentration was >or= 3.0 mg/dL, urine specific gravity was between 1.007 and 1.030, and renal failure had been clinically diagnosed. RESULTS: Dogs with renal failure had significantly higher serum cTnI concentrations (median, 0.35 ng/mL) than did healthy dogs (0.20 ng/mL). The renal failure group also had a significantly higher median systolic blood pressure (156 mm Hg) than did healthy dogs (138 mm Hg), although serum cTnI concentration was not correlated with systolic blood pressure in dogs with renal failure. There was no significant difference in age between dogs with renal failure and healthy dogs, but dogs with renal failure had significantly higher serum creatinine concentration and lower urine specific gravity. CONCLUSIONS AND CLINICAL RELEVANCE: Although dogs with renal failure did not have overt clinical signs of cardiac disease, they had high serum cTnI concentrations, which may have been associated with subclinical cardiovascular disease. The cause of the high serum cTnI concentration in these dogs requires additional investigation.

[Zinc intoxication in a Yorkshire Terrier due to Euro cent ingestion]. / Zinkintoxikation bei einem Yorkshire Terrier nach Aufnahme von Euro-Cent-Münzen.

A 5-year old, intact male Yorkshire Terrier was presented due to lethargy, vomiting and diarrhea. Clinical signs included shock, icterus and a painful abdomen. Laboratory examination revealed a severe intravascular hemolytic anemia, a thrombocytopenia and a leukocytosis. The radiographic examination revealed the presence of metallic foreign bodies in the stomach and in the intestine. After stabilisation of the patient with crystalloids, packed red blood cells, ranitidine, metamizole, amoxicilline/clavulanic acid and marbofloxacine, surgery was performed and 5 coins (10 cent, 5 cent, 2 cent) were removed via esophagus and via enterotomy. In the course of disease the dog developed acute renal failure and pancreatitis. The zinc concentration in the serum was 2200 microg/dl, which was 30 times higher compared to a healthy control dog. After 21 days the dog was discharged from the hospital. On day 28 all laboratory values were within the reference range.