Pitfalls in the diagnosis of hematuria.

Detection of hemoglobin (Hb) and red blood cells in urine (hematuria) is characterized by a large number of pitfalls. Clinicians and laboratory specialists must be aware of these pitfalls since they often lead to medical overconsumption or incorrect diagnosis. Pre-analytical issues (use of vacuum tubes or urine tubes containing preservatives) can affect test results. In routine clinical laboratories, hematuria can be assayed using either chemical (test strips) or particle-counting techniques. In cases of doubtful results, Munchausen syndrome or adulteration of the urine specimen should be excluded. Pigmenturia (caused by the presence of dyes, urinary metabolites such as porphyrins and homogentisic acid, and certain drugs in the urine) can be easily confused with hematuria. The peroxidase activity (test strip) can be positively affected by the presence of non-Hb peroxidases (e.g. myoglobin, semen peroxidases, bacterial, and vegetable peroxidases). Urinary pH, haptoglobin concentration, and urine osmolality may affect specific peroxidase activity. The implementation of expert systems may be helpful in detecting preanalytical and analytical errors in the assessment of hematuria. Correcting for dilution using osmolality, density, or conductivity may be useful for heavily concentrated or diluted urine samples.

Clinical and pathological findings of Africanized bee (Apis mellifera) envenomation in horses.

Africanized crossbred bees (Apis mellifera) originated in Brazil in 1957, and since then, the number of accidents involving humans and animals has significantly increased. Although they are considered clinical emergencies, there are few reports describing the clinical and pathological aspects of bee envenomation in horses. In this context, this report aims to describe the clinical and pathological features of bee toxicity after massive bee envenomation in three horses. The horses were referred to the veterinary hospital the day following the attack, and after clinical and laboratory examination, they presented with vascular, muscular, pulmonary, hepatic, and renal impairment. Even after the initiation of therapy immediately upon admission, the clinical condition of the two horses worsened, and they died within two days of hospitalization, with pathological analysis confirming the previously observed clinical alterations of generalized vasculopathy, liver degeneration, pulmonary edema, and renal tubular necrosis. Many cases of massive bee envenomation have been documented in both humans and animals, particularly in dogs. Understanding the mechanism of action of apitoxin, its effects on various tissues, and the ideal therapy for each patient has proven crucial for improving survival rates.

Indigofera cryptantha-induced pigmenturia in cattle in South Africa.

Two field cases of reddish-black pigmenturia occurred where cattle grazed on an established Cenchrus ciliaris (blue buffalo grass) pasture in South Africa. The pasture was noticeably invaded by Indigofera cryptantha, which was heavily grazed. Apart from the discolored urine, no other clinical abnormalities were detected. Urinalysis revealed hemoglobinuria, proteinuria and an alkaline pH. When the animals were immediately removed from the infested pasture, they made an uneventful recovery. However, a bull died when one of the herds could not be removed from the I. cryptantha-infested pasture. Macroscopically, the kidneys were dark red in color and the urinary bladder contained the dark pigmented urine. Microscopically, the renal tubules contained eosinophilic, granular pigment casts in the lumen. In addition, many renal tubular epithelial cells were attenuated with granular cytoplasm and were detached from the basement membranes. Chemical analysis was performed on dried, milled plant material and two urine samples collected during the field investigations. Qualitative UPLC-UV-qTOF/MS analysis revealed the presence of indican (indoxyl-ß-glucoside) in the stems, leaves and pods of I. cryptantha and indoxyl sulfate was identified, and confirmed with an analytical standard, in the urine samples. It is proposed that following ingestion of I. cryptantha, indican will be hydrolysed in the liver to indoxyl and conjugated with sulfate. Indoxyl sulfate will then be excreted in relatively high concentrations in the urine. In the alkaline urine, two indoxyl molecules might dimerize to form leucoindigo with subsequent oxidation to indigo, thus, contributing to the dark pigmentation of the urine. It is also possible that indoxyl sulfate contributed to the renal failure and death of the bull. Although I. suffruticosa-induced hemoglobinuria has been described in Brazil, this is the first report of I. cryptantha-induced pigmenturia in cattle in South Africa.

Exertional hemolysis and hematuria in a Labrador Retriever dog.

A 7-y-old male Labrador Retriever dog was presented because of acute onset of dark-colored urine after a hunting session the day prior. Moderate hemoglobinemia was observed, associated with transient hemoglobinuria and hematuria with no concurrent evidence of underlying urinary tract disease. The patient's clinical signs resolved within 36 h post-exercise without specific treatment. The concurrent occurrence of exertional hemolysis and hematuria in a dog is uncommon; these conditions are commonly reported separately in human athletes.

Intracardiac heartworms in dogs: Clinical and echocardiographic characteristics in 72 cases (2010-2019).

BACKGROUND: Heartworms, a cause of pulmonary hypertension (PH) in dogs, can migrate from the pulmonary arteries into the heart resulting in life-threatening caval syndrome (CS). OBJECTIVES: To describe clinical and echocardiographic characteristics in dogs with intracardiac heartworms including estimated heartworm burden and frequency of PH and pigmenturia. ANIMALS: Seventy-two client-owned dogs with heartworms. METHODS: Retrospective study. Data collected from an electronic medical records search for dogs with intracardiac heartworms included clinicopathologic, echocardiographic, and procedural findings. Dogs with heartworms isolated to the pulmonary arteries were excluded. RESULTS: Estimated intracardiac heartworm burden was low in 14 of 72 (19%) and high in 58 of 72 (81%) dogs. The majority were small breed (54/72; 75%; 29/72; 40% Chihuahuas) and had a high likelihood of PH (67/72; 93%). Pigmenturia was the second most common clinical finding (31/72; 43%) after lethargy (32/72; 44%). Anemia (37/55; 36%), pigmenturia (30/58; 52%), and bilirubinuria (28/36; 78%) were significantly more common in dogs with a high worm burden (P < .05). Based on the presence of anemia, pigmenturia, and clinical signs, 18 of 72 dogs (25%) were considered to have CS. CONCLUSIONS AND CLINICAL IMPORTANCE: Although the majority of dogs with intracardiac heartworms had a high worm burden and high likelihood of PH, only 25% had clinical evidence of CS. Echocardiography is a useful tool to identify intracardiac heartworms, detect likelihood of PH, and could be useful for staging heartworm positive small breed dogs for intracardiac heartworm migration.

Characterization of Black Pigmenturia in a Cat with Apocrine Gland Cystadenocarcinoma.

An 8-year-old neutered female domestic shorthair cat was presented for further management of an apocrine gland cystadenocarcinoma. Extensive nodal metastasis was diagnosed and the cat was humanely destroyed 2 months after presentation. Post-mortem histopathology of the cystadenocarcinoma revealed areas of yellow-brown granular pigmentation on light microscopy, staining positively for reducing substances with Schmorl's stain and demonstrating autofluorescence on confocal microscopy. The cat's urine was black and also exhibited autofluorescence, and further analysis revealed increased free pentosidine. Based on these findings, it was presumed that the apocrine gland cystadenocarcinoma was producing lipofuscin-like pigments and that the characteristics of the urine were at least partially secondary to advanced glycation end-products.

New Diagnosis of G6PD Deficiency Presenting as Severe Rhabdomyolysis.

A 24-year-old African-American man presented with malaise and low back pain and was found to have acute severe rhabdomyolysis followed by acute hemolysis. Glucose-6-phosphate dehydrogenase (G6PD) deficiency was suspected by the presence of blister cells on peripheral smear and was confirmed by a low enzyme activity assay. Our patient reported playing football, along with upper respiratory infection symptoms, prior to presentation. Extensive infectious and toxicology workup was negative; however, several inflammatory proteins were markedly elevated. We hypothesized the large inflammatory burden led to an increased reactive oxygen radical burden that overwhelmed muscle and erythrocyte reducing power. Severe rhabdomyolysis in G6PD deficiency is not a common presentation because skeletal muscles are more resistant to oxidative damage compared to red blood cells. Our case adds to the few existing reports of myolysis in the setting of G6PD deficiency.