Hiperparatireoidismo nutricional secundário em gecko-leopardo (eublepharis macularius) ­ relato de caso / Nutritional secondary hyperparathyroidism in a leopard gecko (eublepharis macularius) - case report / Hiperparatiroidismo nutricional secundario en gecko-leopardo (eublepharis macularius) ­ caso clínico

O hiperparatireoidismo nutricional secundário é uma deficiência comum em répteis de cativeiro, podendo ocorrer pelo déficit de cálcio, o que leva, neste caso, ao sequestro desse mineral dos ossos para a manutenção do metabolismo. No geral, essa deficiência acontece devido ao manejo ambiental e alimentar incorretos, como a falta de cálcio na dieta ou falta de exposição à radiação ultravioleta, não permitindo a bioativação da vitamina D e, consequentemente, impedindo a absorção de cálcio na alimentação. Este estudo relata um caso de um gecko-leopardo, atendido no Consultório Veterinário Ilha Animal., na cidade do Rio de Janeiro ­ RJ. Na anamnese foi relatado que o paciente sofria de apatia, postura cifótica e andar incoordenado, além dos citados erros de manejo. Foi realizado exame radiográfico, onde foi observado redução da densidade e deformidade óssea, o que permitiu o diagnóstico de osteodistrofia metabólica, considerando também os sinais clínicos e a anamnese. Com o tratamento oral, houve melhoras do animal.(AU)

Secondary nutritional hyperparathyroidism is a common deficiency in captive reptiles. It can occur due to a calcium deficit, which leads, in this case, to the sequestration of this mineral from the bones to maintain metabolism. In general, this deficiency occurs due to incorrect environmental and food management, such as a lack of calcium in the diet or lack of exposure to ultraviolet radiation, not allowing the bioactivation of vitamin D and, consequently, preventing the absorption of calcium in the diet. This study reports a case of a leopard gecko, seen at the Ilha Animal Veterinary Clinic. In the anamnesis it was reported that the patient suffered from apathy, kyphotic posture and uncoordinated walking, in addition to the aforementioned handling errors. A radiographic examination was performed, where a reduction in bone density and deformity was observed, which allowed the diagnosis of metabolic osteodystrophy, also considering clinical signs and anamnesis. With oral treatment, the animal improved. The objective of the work is to report the clinical case and review the literature on secondary nutritional hyperparathyroidism.(AU)

El hiperparatiroidismo nutricional secundario es una deficiencia común en reptiles en cautiverio que puede ocurrir debido a un déficit de calcio, lo que lleva, en este caso, al secuestro de este mineral de los huesos para mantener el metabolismo. En general, esta deficiencia se produce por un incorrecto manejo ambiental y alimentario, como la falta de calcio en la dieta o la falta de exposición a la radiación ultravioleta, no permitiendo la bioactivación de la vitamina D y, en consecuencia, impidiendo la absorción del calcio en la dieta. Este estudio reporta un caso de gecko leopardo, visto en la Clínica Veterinaria Animal Ilha. En la anamnesis se informó que el paciente padecía apatía, postura cifótica y descoordinación en la marcha, además de los errores de manejo antes mencionados. Se realizó examen radiográfico, donde se observó reducción de la densidad ósea y deformidad, lo que permitió el diagnóstico de osteodistrofia metabólica, considerando además los signos clínicos y la anamnesis. Con el tratamiento oral el animal mejoró. El objetivo del trabajo es reportar el caso clínico y revisar la literatura sobre hiperparatiroidismo nutricional secundario.(AU)

A feline-focused review of chronic kidney disease-mineral and bone disorders - Part 2: Pathophysiology of calcium disorder and extraosseous calcification.

Derangements in mineral metabolism are one of the main entities in chronic kidney disease-mineral and bone disorder (CKD-MBD). This is the second of a two-part review of the physiology and pathophysiology of calcium homeostasis in feline CKD-MBD. While dysregulation in calcium homeostasis is known to contribute to the development of vascular calcification in CKD, evidence characterising the relationship between serum calcium concentration and nephrocalcinosis and nephrolithiasis is limited. Recently, fibroblast growth factor 23 (FGF23) and α-Klotho have gained increased research interest and been shown to be important biomarkers for the prediction of CKD progression in human patients. However, conflicting evidence exists on their role in calcium homeostasis and vascular and soft tissue calcification. This review details the pathophysiology of calcium disorders associated with CKD-MBD and its implications on vascular and soft tissue mineralisation in human and feline patients. Further prospective studies investigating the clinical consequences of calcium disturbances in cats with CKD are warranted and this may provide additional insight into the pathophysiology of feline CKD-MBD.

A feline-focused review of chronic kidney disease-mineral and bone disorders - Part 1: Physiology of calcium handling.

Mineral derangements are a common consequence of chronic kidney disease (CKD). Despite the well-established role of phosphorus in the pathophysiology of CKD, the implications of calcium disturbances associated with CKD remain equivocal. Calcium plays an essential role in numerous physiological functions in the body and is a fundamental structural component of bone. An understanding of calcium metabolism is required to understand the potential adverse clinical implications and outcomes secondary to the (mal)adaptation of calcium-regulating hormones in CKD. The first part of this two-part review covers the physiology of calcium homeostasis (kidneys, intestines and bones) and details the intimate relationships between calcium-regulating hormones (parathyroid hormone, calcitriol, fibroblast growth factor 23, α-Klotho and calcitonin) and the role of the calcium-sensing receptor.

Renal Osteodystrophy due to Secondary Hyperparathyroidism in a Cat.

A 6 yr old neutered male mixed-breed cat presented for renal transplantation (RTx) for chronic kidney disease. Severe periodontal disease was identified, and before initiation of immunosuppressive therapy, a comprehensive oral health assessment and treatment procedure was performed to reduce the burden of existing oral infection. Dental radiography revealed diffuse, severe bone demineralization across the mandible and maxilla, with thinning of the cortices. Nasal turbinates were easily visualized owing to the decreased opacity of maxillary bone. Generalized bone resorption left teeth to appear minimally attached. A Vitamin D panel revealed a severely elevated parathyroid hormone level. Full mouth extractions were performed. Seven days following this procedure, RTx was performed. Serum creatinine concentration was within normal limits by 48 hr after surgery and remained normal until discharge 12 days after RTx. At 3.5 mo after RTx, the cat was mildly azotemic, and the parathyroid hormone level was elevated but significantly decreased from the original measurement. Secondary hyperparathyroidism is a common abnormality in cats with chronic kidney disease. However, clinical manifestations of hyperparathyroidism are rare in this species. This is a novel presentation of a cat demonstrating bone loss in the oral cavity as a result of renal secondary hyperparathyroidism.

Effects of calcifediol supplementation on markers of chronic kidney disease-mineral and bone disorder in dogs with chronic kidney disease.

BACKGROUND: Chronic kidney disease-mineral and bone disorder (CKD-MBD) in dogs is associated with hypovitaminosis D, increased parathyroid hormone (PTH), and increased fibroblast growth factor-23 (FGF-23) concentrations. Best practice for vitamin D metabolite supplementation in CKD-MBD remains unknown. OBJECTIVE: To provide an extended-release calcifediol supplement to dogs with CKD and to measure its effects on variables indicative of CKD-MBD. ANIMALS: Ten dogs with International Renal Interest Society stages 2 and 3 CKD. METHODS: In a prospective study, dogs received a calcifediol supplement for 84 days. Serum 25-hydroxyvitamin D (25[OH]D), 1,25-dihydroxyvitamin D (1,25[OH]2 D), 24,25-dihydroxyvitamin D (24,25[OH]2 D), creatinine, calcium, phosphorus, PTH, plasma FGF-23 concentrations, and urine profiles were measured monthly during supplementation. Urine calcium to creatinine (UCa/Cr) ratios and fractional excretion of calcium, phosphorus, and sodium were determined. RESULTS: All serum vitamin D metabolite concentrations increased significantly by day 84 (P < .001): [25(OH)D (median 249.9 ng/mL; range, 149.7-469.9 ng/mL) compared to baseline (median 50.2 ng/mL; range, 31.3-66.0 ng/mL); 1,25(OH)2 D (median 66.1 pg/mL; range, 56.9-88.1 pg/mL) compared to baseline (median 37.3 pg/mL; range, 29.3-56.7 pg/mL); 24,25(OH)2 D (median 81.4 ng/mL; range, 22.1-151.7 ng/mL) compared to baseline (median 15.4 ng/mL; range, 6.9-40.6 ng/mL)]. There were no significant differences in calcium, phosphorus, PTH concentrations, UCa/Cr or fractional excretion of calcium. No dog developed ionized hypercalcemia. Plasma FGF-23 concentrations increased by day 84 (median 1219 pg/mL; range, 229-8824 pg/mL) compared to baseline (median 798 pg/mL; range, 103-4.145 pg/mL) (P < .01). CONCLUSIONS AND CLINICAL IMPORTANCE: Calcifediol supplementation for 84 days was well-tolerated in dogs with IRIS stages 2 and 3 CKD. It remains to be determined how long-term supplementation would affect CKD progression and QOL.

Associations between single nucleotide polymorphisms in the calcium sensing receptor and chronic kidney disease-mineral and bone disorder in cats.

Feline chronic kidney disease (CKD) is associated with high variability in severity of CKD-mineral and bone disorder (CKD-MBD). The calcium sensing receptor (CaSR) regulates circulating parathyroid hormone (PTH) and calcium concentrations. Single nucleotide polymorphisms (SNPs) in the CaSR are associated with severity of secondary renal hyperparathyroidism and total calcium concentrations in human patients receiving haemodialysis. The objective of this study was to explore associations between polymorphisms in the feline CaSR (fCaSR) and biochemical changes observed in CKD-MBD. Client owned cats (≥9years) were retrospectively included. SNP discovery was performed in 20 cats with azotaemic CKD and normal or dysregulated calcium concentrations. Non-pedigree cats (n=192) (125 with azotaemic CKD and 66 healthy), Persians (n=40) and Burmese (n=25) were genotyped for all identified SNPs using KASP. Biochemical parameters from the date of CKD diagnosis or from first visit to the clinic (healthy cats) were used. Associations between genotype and ionized calcium, total calcium, phosphate, PTH and FGF-23 were performed for non-pedigree cats using logistic regression. Sequence alignment against the fCaSR sequence revealed eight novel exonic SNPs. KASP genotyping had high accuracy (99.6%) and a low failure rate (<6%) for all SNPs. Allele frequencies varied between breeds. In non-pedigree cats, one synonymous SNP CaSR:c.1269G>A was associated with logPTH concentration (adjusted for plasma creatinine concentration), with a recessive model having the best fit (G/G vs A/A-G/A, P=0.031). Genetic variation in the fCaSR is unlikely to explain the majority of the variability in presence and severity of CKD-MBD in cats.

Update on Mineral and Bone Disorders in Chronic Kidney Disease.

The inappropriate phosphorus retention observed in chronic kidney disease is central to the pathophysiology of mineral and bone disorders observed in these patients. Subsequent derangements in serum fibroblast growth factor 23, parathyroid hormone, and calcitriol concentrations play contributory roles. Therapeutic intervention involves dietary phosphorus restriction and intestinal phosphate binders in order to correct phosphorus retention and maintain normocalcemia. Additional therapies may be considered to normalize serum fibroblast growth factor 23 and parathyroid hormone.

Does Secondary Renal Osteopathy Exist in Companion Animals?

Secondary renal hyperparathyroidism is an inevitable consequence of chronic kidney disease. In human patients, the disease is associated with decreased bone quality and increased fracture risk. Recent evidence suggests that bone quality is also decreased in companion animals, more pronouncedly in cats compared with dogs, likely because of a longer disease course. The clinical significance of these findings is yet to be determined. However, clinicians should keep in mind that animals with chronic kidney disease have decreased bone quality and increased fracture risk.

Oral Manifestations of Chronic Kidney Disease and Renal Secondary Hyperparathyroidism: A Comparative Review.

Recent epidemiological studies have demonstrated that significant associations exist between oral disease and diseases involving non-oral tissues. Occasionally, the roles may be reversed and the oral cavity can be severely affected by systemic disease originating in another part of the body. Renal secondary hyperparathyroidism is a common endocrinopathy that occurs as a consequence of chronic azotemic kidney disease. Renal osteodystrophy, the most dramatic clinical consequence of renal secondary hyperparathyroidism is uncommon, but can result in demineralization of maxillofacial bones, loosening of teeth, and pathological jaw fractures. The purpose of this report is to update the current understanding of the pathophysiology of this endocrine disease and to compare the oral manifestations of renal secondary hyperparathyroidism in humans and companion animals. A 50-year review of the veterinary literature was undertaken to examine the clinical presentation of renal osteodystrophy in dogs, and to determine what clinical consequences of renal secondary hyperparathyroidism have been reported in domestic cats.

Cadmium toxicity to ringed seals (Phoca hispida): an epidemiological study of possible cadmium-induced nephropathy and osteodystrophy in ringed seals (Phoca hispida) from Qaanaaq in Northwest Greenland.

The Greenland marine food chains contain high levels of cadmium, mercury and selenium. Concentrations of cadmium in the kidney of ringed seals (Phoca hispida) from the municipalities of Qaanaaq and Upernavik (Northwest Greenland) are among the highest recorded in the Arctic. The purpose of the study was to determine whether cadmium-induced damage in the kidneys and the skeletal system could be detected among 100 ringed seals from Northwest Greenland. The cadmium concentrations in the kidney cortex ranged from 0 to 248 microg/g wet weight (mean=44.5, N=100) in the 99 kidneys examined. Experience from cadmium-poisoned humans and laboratory mammals indicates that concentrations above 50-200 microg/g wet wt. may induce histopathological changes. Overall, 31 of the ringed seals had cadmium concentrations in the kidney cortex above 50 microg/g wet wt., 11 had concentrations above 100 and one had a concentration above 200 microg/g wet wt. Obvious histopathological changes (categorised mainly as glomerulonephritis) were found in 10 of the seals; however, none of these changes could be attributed to cadmium-induced renal damage (mainly tubulopathy) as described for other species. Damage to the proximal kidney tubules is known to induce demineralisation of the skeletal system (Fanconi's syndrome). Therefore, the three lowest lumbar vertebrae were scanned in 91 seals to measure the content of calcium. The 10 cases of nephropathy could neither be linked to the degree of mineralisation of the skeleton nor to the cadmium concentrations. Furthermore, the degree of mineralisation of the skeleton was not correlated with the cadmium concentration, age or sex. It can therefore be concluded that despite high levels of cadmium, none of the ringed seals showed any signs of cadmium-induced nephropathy or osteodystrophy. This might be explained by the composition of the ringed seals diet, which contains high levels of vitamin D, calcium, phosphorus, zinc, selenium and protein. These elements are all likely to counteract cadmium-induced damage. It is speculated that ringed seal are not particularly vulnerable to osteodystrophy, due to their continuous growth (bone mineralisation) throughout life and the oestrogen hormonal activity of females throughout life.