Severe Bone Disease in a Kitten Traced to Diet: Rapid Recovery After Simple Fix

Nutritional secondary hyperparathyroidism in a kitten, supported by immunoenzymatic measurement of feline intact parathyroid hormone

Jari Zambarbieri, Eleonora Fusi, Jessica Bassi, Paola Scarpa

Background

The report describes a 6-month-old domestic shorthair kitten presenting with poor growth, reluctance to move, and nasal deformation. The dietary history revealed exclusive feeding of complementary pet food and tuna—essentially an all-meat diet deficient in calcium and vitamin D. Nutritional secondary hyperparathyroidism (NSHP) results from imbalanced dietary calcium, phosphorus, and/or vitamin D, leading to compensatory increases in parathyroid hormone (PTH). The case also raised the possibility of concurrent nutritional rickets or vitamin D–dependent rickets type II, although these could not be definitively evaluated.

Methods

Clinical evaluation included physical examination, CBC, blood gas analysis, biochemical profile, and measurement of intact PTH using a validated second-generation immunoenzymatic assay. Calcitriol was quantified via radioimmunoassay. Radiographs of the skull, spine, and limbs were obtained. After diagnosis, dietary correction with a complete and balanced growth diet was initiated based on FEDIAF and NRC energy requirements, followed by scheduled clinical, laboratory, and radiographic rechecks.

Results

At presentation, the kitten had severe ionized hypocalcemia, markedly elevated PTH and calcitriol, and radiographic evidence of generalized osteopenia, widened physes, reduced cortical bone thickness, and spinal and limb deformities. Following two months of dietary correction, ionized and total calcium returned to reference intervals, and PTH decreased dramatically, confirming resolution of NSHP. After three months, radiographs showed improved bone density and cortical thickness, though some residual deformities persisted, including curvature of the radius, spinal abnormalities, and a nasal deformity associated with a mucocele. Clinical activity and comfort improved progressively.

Limitations

The authors note that 25-hydroxyvitamin D concentrations were not measured, limiting assessment of vitamin D status and differential diagnosis between NSHP and coexisting nutritional rickets. Calcitriol was not remeasured after dietary correction. Complete nutrient analysis of the initial diet was also unavailable, and thus the precise contributions of vitamin D deficiency could not be determined. Genetic causes such as VDDRII could not be fully excluded.

Conclusions

The case demonstrates that feeding a calcium-deficient all-meat diet can result in severe NSHP in growing kittens. Use of a validated immunoenzymatic assay allowed measurement of feline intact PTH, aiding in diagnosis and monitoring. Dietary correction alone led to normalization of biochemical parameters and partial radiographic and clinical improvement. The authors emphasize the importance of complete and balanced diets for growth to prevent metabolic bone disease.

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