Severe Systemic Calciphylaxis in a Young Cat

A 7-month-old female intact domestic shorthair/ British Blue crossbreed cat was referred to the Queen Mother Hospital for Animals (QMHA) of the Royal Veterinary College for further investigation of progressive lethargy preceded by 48 hours of mixed bowel diarrhea, moderate pyrexia (39.9°C; 103.8°F), and unproductive retching. Laboratory tests performed at the primary practice identified marked hypercalcemia (serum total calcium concentration). Despite treatment with IV fluids and potentiated amoxicillin, the cat deteriorated clinically, prompting referral. On presentation to the QMHA, the cat was dull but responsive with poor body condition (3.5/9) and pyrexia (39.2°C; 102.6°F). Firm white lingual plaques were observed (Fig 1). Both kidneys were subjectively mildly enlarged. The remainder of the physical examination was unremarkable. With the exception of the cat’s decreased mentation, neurologic examination was considered normal. No neurologic deficits suggesting a structural intracranial lesion were found at any point throughout the time the cat was hospitalized, but the level of obtundation would wax and wane. No association between the cat’s mentation and the treatments administered was apparent. Initial investigations confirmed marked total hypercalcemia (19.28 mg/dL; 4.82 mmol/L; reference interval [RI], 8.28–10.72 mg/dL) and ionized hypercalcemia (9.0 mg/dL; 2.25 mmol/L; RI, 4.52–5.32 mg/dL), with mild hyperphosphatemia (7.68 mg/dL; 2.48 mmol/L; RI, 2.85–6.69 mg/dL). Markedly increased serum CK activity was identified (21,322 U/L; RI, 52–506 U/L) increasing to 43,616 U/L upon repeated measurement after 3 days. Serum ALT activity was within normal limits. At the time of presentation, serum urea nitrogen concentration was moderately increased (49.0 mg/ dL; 17.5 mmol/L; RI, 17.1–33.6 mg/dL), whereas serum creatinine concentration was within normal limits (1.36 mg/dL; 118 lmol/L; RI, 0.84–2.1 mg/dL). Interpretation of complete blood cell count was consistent with a stress leukogram. Mild leukocytosis (26.2 9 10/L; RI, 5.5–19.5 9 10/L) with mild neutrophilia (23.8 9 10/L; RI, 2.5–12.5 9 10/L) and mild lymphopenia (0.58 9 10/L; RI, 1.5–7.0 9 10/L) were present. Urinalysis disclosed the presence of granular casts (10 per 81 high-power fields, 4009), but was otherwise unremarkable. Urine specific gravity was 1.015 (after IV fluid therapy). Venous blood gas, electrolyte, and metabolite analyses were performed throughout hospitalization to monitor plasma creatinine, urea, and ionized calcium concentrations. Plasma ionized calcium concentration gradually decreased from 9.0 mg/dL to 7.44 mg/dL 24 hours after admission, whereas blood urea nitrogen and creatinine concentration increased to 142.6 mg/dL (50.9 mmol/L) and 3.0 mg/dL (268 lmol/L), respectively. The azotemia was believed to be at least partly prerenal, because it gradually resolved over the next 48 hours, with concurrent decreases in packed cell volume and total protein concentration (from 30% and 6.4 g/dL to 20% and 5.4 g/dL, respectively). During the first 3 days of hospitalization, treatment included IV fluid therapy (up to 8 mL/kg/h by the second day), furosemide (0.5–1.0 mg/kg IV q6h), and salmon calcitonin (4 IU/kg SC q8h), all of which were initiated on the first day of hospitalization. Furosemide probably contributed to dehydration and development of azotemia, supported by a 100 g (4.8%) decrease in body weight over the first 24 hours. Owing to persistent hypercalcemia despite treatment, IV pamidronate infusion (1.75 mg/kg diluted in 16 mL 0.9% NaCl, infused at a rate of 4 mL/h) was administered on the third day of hospitalization, at which time salmon calcitonin was discontinued. These treatments failed to substantially alter the plasma ionized calcium concentration, but approximately 48 hours after initiating prednisolone treatment (0.5 mg/kg PO q12h) on day 6 of hospitalization, plasma ionized calcium conFrom the Department of Clinical Sciences and Services, Queen Mother Hospital for Animals (Anfinsen, Kenny, Garden); the Comparative Neuromuscular Diseases Laboratory, Department of Clinical Sciences and Services, Royal Veterinary College, University of London, London, UK (Piercy, Massey); and the Department of Pathology & Pathogen Biology (Smith), Royal Veterinary College, University of London, Hatfield, UK. Corresponding author: K.P. Anfinsen, Department of Companion Animal Clinical Sciences, NMBU School of Veterinary Science, N-0033 Oslo, Norway; e-mail: kristin.anfinsen@nmbu.no. Submitted November 5, 2013; Revised March 18, 2014; Accepted April 22, 2014. Copyright © 2014 by the American College of Veterinary Internal Medicine DOI: 10.1111/jvim.12378 Abbreviations: