A 12-year-old mixed breed dog was evaluated for marked hypercalcemia that was identified during assessment for acute polydipsia and polyuria. Physical examination identified a new grade II/VI left apical systolic murmur. A mass involving the left ventricular posterior wall and left atrium was identified by echocardiography, suggesting neoplastic invasion into the myocardium. The patient was euthanized, and post-mortem cardiac evaluation identified an intramyocardial amyloid-producing plasma cell tumor. Multiple myeloma was suspected but could not be confirmed due to the limited post-mortem evaluation. This case is the first report of myocardial amyloidosis in a dog with a myeloma-related disorder (MRD). Dogs with MRD and myocardial involvement may not exhibit clinical signs that localize to the cardiovascular system; therefore, echocardiography should be considered during the staging process.

Myeloma-related disorders, including multiple myeloma, extramedullary plasmacytoma, and solid osseous plasmacytoma, are rare in horses. Clinical complaints for myeloma-related disorders are nonspecific, and when present, M-protein location is more variable on protein electrophoresis in horses relative to dogs and cats. Here, we describe a case of a 15-year-old Thoroughbred mare who presented with recurrent blepharitis. Marked hyperglobulinemia was an incidental finding on routine hematologic and biochemical testing. Bone marrow aspiration consisted of >30% plasma cells, and serum protein electrophoresis demonstrated a monoclonal gammopathy in the alpha 2 fraction leading to a diagnosis of multiple myeloma. Immunofixation and radial immunodiffusion confirmed the presence of an IgG M-protein. Based on a restricted peak in the alpha 2 location, the specific M-protein is suspected to be IgG(T), an IgG isotype unique to horses. M-protein migration in horses is variable relative to dogs and cats, yet immunofixation can still be used to identify equine IgG M-protein isotypes. The unique clinical presentation in this case also serves as a reminder to consider neoplasia in horses with unusual or nonspecific clinical signs.

A 57-year-old man presented with multiple pulmonary nodules. Thoracoscopic lung biopsy led to a pathological diagnosis of pulmonary hyalinizing granuloma (PHG) at the age of 39 years. The disease was progressive, refractory to therapy, and necessitated home oxygen therapy 10 years after the diagnosis. Hyponatremia progressed gradually along with lung disease. His serum sodium level was 129 mEq/L but serum osmolality was normal (287 mOsm/kg). Concomitant hyperproteinemia (12.1 g/dL) was attributable to hyperglobulinemia. Direct ion-selective electrode measurement revealed a normal sodium level (137 mmol/L). We herein report a case of PHG characterized by pseudohyponatremia due to hyperproteinemia, an uncommon finding in this rare entity. A left lung transplant was successfully performed, and no pseudohyponatremia was observed. Pseudohyponatremia should be suspected and diagnosed to prevent a misdiagnosis that could lead to complications from inappropriate treatment with sodium supplementation or restriction of drinking water. The direct ion-selective electrode measurement was useful for diagnosing pseudohyponatremia.

OBJECTIVE: To investigate whether primary Sjögren\'s syndrome (pSS) patients with hyperglobulinemia have an increased risk of all-cause mortality.
METHODS: Patients who registered in the Chinese Rheumatism Data Centre from May 2016 to July 2021 and met the 2002 American European Consensus Group criteria or 2016 American College of Rheumatology /European League Against Rheumatism classification criteria for Sjögren\'s syndrome were included. Hyperglobulinemia was defined as any elevated serum levels of immunoglobulin G (IgG), immunoglobulin A (IgA), or immunoglobulin M (IgM). The primary outcome was all-cause death. Data for demographic and clinical characteristics, laboratory results, disease activity, damage scores, and treatments were evaluated.
RESULTS: A total of 9527 pSS patients were included in the analysis, of whom 4236 (44.5%) had at least one kind of elevated immunoglobulin level among IgG, IgA, and IgM. Patients with hyperglobulinemia had a significantly increased risk of death (crude hazard ratio 2.60; 95% confidence interval 1.91-3.55; adjusted hazard ratio 1.90; 95% confidence interval 1.20-3.01). The risk of death was positively correlated with IgG level (P trend <.001). The 5-, 10-, and 15-year survival rates of patients with hyperglobulinemia were 96.9%, 92.3%, and 87.9%, respectively, and significantly lower than the corresponding rates of 98.8%, 97.9%, and 96.4% in patients without hyperglobulinemia.
CONCLUSIONS: Hyperglobulinemia is an independent risk factor for increased all-cause mortality in pSS patients. The risk of death is positively correlated with IgG level.

BACKGROUND: Hyperglobulinemia is reported in 26% of canine chronic B-cell lymphocytic leukemia (B-CLL) cases. However, few cases have been characterized by protein electrophoresis and immunofixation (IF), and the incidence of a monoclonal protein (M-protein) is unknown using these techniques.
OBJECTIVE: To characterize and determine the proportion of canine B-CLL cases with an M-protein using plasma protein electrophoresis (PPE), routine and free light chain (fLC) IF, and to assess if productive B-CLL cases express MUM1/IRF4 by cell tube block (CTB).
METHODS: PPE, routine (targeting IgG, IgA, IgM, IgG4, and light chain) and fLC IF were performed using 48 dog B-CLL plasma samples from patients diagnosed via peripheral blood flow cytometry. CTB was performed on a separate cohort of 15 patients.
RESULTS: Hyperproteinemia (>7.5 g/dL) was present in 17/48 cases (35%). An M-protein was detected in 32/48 cases (67%). Of these, 19/32 cases (59%) had only complete (monoclonal heavy and light chain) M-proteins detected, 10/32 cases (31%) had both complete and fLC M-proteins detected, and 3/32 cases (9%) had only an fLC M-protein detected. IgM was the most common clonal immunoglobulin isotype detected (23 cases). CD21+ cell counts were higher in cases with detectable M-protein. Plasma fLC IF suggested β-γ region interference, likely caused by clotting proteins. All B-CLL cases consistently expressed PAX5 and did not express MUM1/IRF4.
CONCLUSIONS: Most B-CLL cases had an M-protein and were not hyperproteinemic. Most cases with paraproteins had a complete IgM monoclonal gammopathy; a subset had documented fLCs. The prognostic significance of heavy and fLC presence should be evaluated.

Renal ischemia-reperfusion (IR) produces-induced injury and is characterized by restriction of blood supply to the kidney followed by restoration and re-oxygenation of the tissue. IR injury in the kidney contributes to pathological processes known as acute renal injury (ARI). Ischemia-perfusion injury (IRI) of the left renal artery has been demonstrated in Wistar rats. A total of 32 animals were divided into four groups: control group (SHAM), IR animals with induced ischemia-reperfusion, AT-IR animals treated by antithrombin III (AT) before IR, and AT-IR-AT animals with AT administered before and after IR. IR-induced hyperproteinemia, hyperalbuminemia, hyperglobulinemia, and a significantly low A/G ratio. Exogenous administration of AT prior to IR development effectively regulates protein fraction levels by establishing normoproteinemia. The preventive effect of AT regulates serum protein levels and reduces acute inflammation by reducing globulin and establishing physiological levels of A/G ratios. The therapeutic effect of AT given after IR is not effective compared to AT administered before IR. Protein fractions can serve as an important predictive marker for the prognosis and duration of acute inflammation. Serum globulin levels and the A/G ratio may serve as effective prognostic markers in acute inflammation caused by ischemia-reperfusion injury of the kidney. A strong correlation between globulin and the A/G ratio suggests novel markers associated with acute inflammation that can lead to chronic kidney disease.

The aim of this study was to investigate the beneficial effects of vitamin K relate to protection against detrimental effects of bromadiolone. Wistar rats (n = 30) were divided in three groups (n = 10): control group and two groups treated with bromadiolone (0.12 mg/kg) and bromadiolone + vitamin K (0.12 mg/kg + 100 mg/kg) over the period of four days. The main findings in the bromadiolone-exposed rats, such as damaged hepatocytes, high levels of globulin, total proteins and lymphocytes, and altered albumin/globulin ratio, collectively indicate an acute inflammatory process. Morphological changes in erythrocytes include microcytosis, hypochromia, hyperchromia, hemolysis, stomatocytosis, and spherocytosis. Significantly low values of RBC, Hct, and hemoglobin concentrations indicate impairments of the hematopoietic pathway causing combined anemia. The selected dose of bromadiolone caused a non-significant increase of catalase activity and a significant increase of the total protein content in brain tissue homogenates. Vitamin K supplementation reduced many of the harmful effects of bromadiolone. The cytoprotective role of vitamin K was proved to be of great importance for the preservation of structural changes on the membranes of hepatocytes and erythrocytes, in addition to the known role in the treatment of coagulopathies. The results of the study suggest valuable properties of vitamin K in the prevention and treatment of various types of anemia caused by bromadiolone toxicity. Future research is necessary to determine the adequate dose and treatment duration with vitamin K in disorders caused by the cumulative action of bromadiolone and possibly other pesticides.

The objectives of this study were to describe the clinical features and evaluate the utility of immunological features as predictors of organ involvement and disease severity in patients with primary Sjogren\'s syndrome (pSS). In this single-center observational cross-sectional study, subjects fulfilling the 2012 AECG criteria or 2016 ACR/EULAR criteria for pSS were included. Details of glandular, extra-glandular manifestations, ESSDAI, ESSPRI, ANA, anti-Ro/La antibodies, rheumatoid factor (RF), complement (C3 and C4) levels and hyperglobulinemia were noted. Chi-square and Mann-Whitney U tests were performed for determining associations and relative risk (RR) was calculated. Sixty-four subjects with pSS were included in the study. Females constituted 92% and median age at onset was 37.5 (15-74) years. Ocular or oral sicca was noted in 61 (95.3%) subjects and parotidomegaly was noted in 17 (26.5%) subjects. Extra-glandular manifestations noted were: constitutional (85.9%), articular (65.6%), renal (29.6%), hematological (26.6%), cutaneous (12.5%), peripheral nerves (9.3%) and pulmonary (4.7%). Immunological features noted were: ANA (85.9%), anti-Ro (81.3%), anti-La (60.9%), RF (84.4%), hypocomplementemia (39.1%) and hyperglobulinemia (62.5%). Median ESSDAI was 6 (0-23) and ESSPRI was 7 (0-10). ANA was associated with younger age and renal involvement (RR 1.25). Anti-Ro was associated with younger age, renal involvement (RR 1.36) and high ESSDAI. Anti-La was associated with high renal (RR 3.4) and low articular involvement (RR 2.75). RF was associated with hematological involvement and hyperglobulinemia was associated with younger age. Certain immunological features can help predict the organ involvement in patients with pSS. Larger, prospective follow-up studies are needed to clearly understand these associations.

A 9-year-old female spayed Domestic Shorthair cat presented for pain, reluctance to jump, and hyporexia of 14 days duration. Neurologic examination was consistent with C6-T2 myelopathy. Magnetic resonance imaging (MRI) revealed a solitary, contrast-enhancing lesion within the T2 vertebral body. Solitary osseous plasmacytoma was diagnosed based on neurologic examination, advanced imaging, and clinicopathologic findings. Melphalan and prednisolone therapy were initiated. Complete resolution of clinical signs and the vertebral lesion were documented at a 2-year follow up examination with neurologic examination and repeat spinal MRI, respectively. Solitary osseous plasmacytoma are rare neoplasms in humans and domestic animals. As such, there is a paucity of published information regarding diagnostic criteria, MRI findings, treatment modalities, progression, and remission of disease in the feline patient. Most data are extrapolated from human medicine. The purpose of this report is to document neurologic exam and MR findings at the time of diagnosis and complete resolution of a solitary osseous vertebral plasmacytoma following melphalan and prednisolone therapy.

OBJECTIVE: Describe the diagnosis, clinical course, and management of a dog with systemic Mycoleptodiscus indicus infection.
METHODS: A 5-year-old male neutered Giant Schnauzer presented with left eye anterior uveitis, peripheral lymphadenopathy, hyperglobulinemia, anemia, and thrombocytopenia. A diagnosis of M. indicus infection was made based on histopathology and PCR. Treatment with itraconazole and terbinafine resulted in resolution of the hyperglobulinemia, anemia, thrombocytopenia, and peripheral lymphadenopathy. No evidence of fungal organisms was identified on lymph node, liver, or ocular histopathology after 7 months of treatment.
CONCLUSIONS: This case is the first report of a systemic M. indicus infection in an apparently immunocompetent dog. Clinical resolution was achieved with systemic itraconazole and terbinafine.