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

A 6-mo-old, intact male, domestic shorthair cat was referred with a history of poor growth, reluctance to move, and deformation of the nasal profile. The kitten had been fed a diet composed almost exclusively of a complementary pet food and tuna, which was similar to an all-meat diet. We detected osteopenia and hypocalcemia associated with severe parathyroid hormone (PTH) and calcitriol increases; we measured PTH concentrations with an immunoenzymatic method that has been validated in cats. Dietary correction, consisting of a complete and balanced wet pet food formulated for growth, resulted in normalization of calcium and PTH concentrations within 2 mo.

Congenital Lobar Emphysema in a Kitten with Concomitant Hiatal Hernia and Nutritional Secondary Hyperparathyroidism.

A 2 mo old domestic shorthair kitten was presented for acute respiratory distress and severe ambulatory difficulties. Thoracic radiography revealed hyperinflation of the left cranial lung lobe and a mass with soft-tissue/gas opacity in the caudal mediastinum, leading to the suspicion of congenital lung lobe emphysema and hiatal hernia. Decreased bone radiopacity and suspected pathological fractures were also present. Complete clinicopathological analyses showed significant ionized hypocalcemia and suspicion of secondary hyperparathyroidism related to an inadequate diet. Lung lobectomy and reduction of the hiatal hernia following a median sternotomy and a cranial laparotomy were performed. IV and oral supplementation of calcium led to a full recovery and improvement in the kitten's walking. A histopathological analysis revealed pulmonary emphysema associated with hypoplastic and irregular bronchial cartilage. Congenital lobar emphysema is a rare disease in both humans and animals. This is the first veterinary report describing a kitten affected by congenital lobar emphysema combined with a hiatal hernia and additionally complicated by secondary nutritional hyperparathyroidism with a good long-term outcome.

Nutritional Secondary Hyperparathyroidism and Fibrous Osteodystrophy in a Captive African Penguin (Spheniscus demersus) Similar to Osteomalacia in Poultry.

A 9-yr-old female black-footed African penguin (Spheniscus demersus) was presented for necropsy after a history of reproductive abnormalities, paresis of limbs, weakness, and sudden death. Postmortem examination revealed soft keel, collapsed rib cage with beading of the ribs, and bilateral parathyroid enlargement. Classic histologic lesions of fibrous osteodystrophy with osteomalacia were observed in the ribs, vertebrae, and to a lesser extent in the femur and tibiotarsus associated with hyperplasia of parathyroid glands. This represents the first report of nutritional secondary hyperparathyroidism in birds of the order Spheniciformes, most likely caused by low levels of calcium supplementation during egg laying. The reproductive abnormalities observed in this penguin and others from the same group (asynchronous egg-laying cycles, abnormal breeding behavior) were most likely exacerbated by the lack of an adequate photoperiod mimicking the natural daylight pattern.

Reporte de caso­Hiperparatiroidismo secundario nutricional y osteodistrofia fibrosa en un pingüino africano (Spheniscus demersus) en cautiverio similar a la osteomalacia observada en de aves de corral. Una hembra de pingüino africano de patas negras (Spheniscus demersus) de nueve años fue sometida a necropsia después de un historial de anomalías reproductivas, paresia de extremidades, debilidad y muerte súbita. El examen post mortem reveló que la quilla del esternón estaba blanda, la caja torácica colapsada, se observaron "perlas raquíticas" en las costillas y agrandamiento bilateral de las paratiroides. Se observaron lesiones histológicas clásicas de osteodistrofia fibrosa con osteomalacia en las costillas, vértebras y en menor medida, en el fémur y tibiotarsus asociadas con hiperplasia de glándulas paratiroides. Esto representa el primer informe de hiperparatiroidismo secundario nutricional en un ave del orden Spheniciformes, muy probablemente causado por un bajo nivel de suplementos de calcio durante la producción de huevos. Las anomalías reproductivas observadas en este pingüino y otros del mismo grupo (ciclos de puesta de huevos asincrónicos, comportamiento de reproducción anormal) probablemente se vieron exacerbadas por la falta de un fotoperíodo adecuado que imitara el patrón de luz natural.

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.

Comparison between different sources of minerals in horses with nutritional secondary hyperparathyroidism / [Comparação entre diferentes fontes de minerais em cavalos com hiperparatireoidismo secundário nutricional]

Minerals perform several functions in the body, such as coagulation actions, muscle contraction, enzymatic and hormonal production, among others. This study aims to evaluate the effect of a 150 days chelated and not chelated mineral supplementation with and without potassium oxalate on serological parameters and bone mineral density of horses. Twenty-four crossbred yearlings (12 females and 12 males) with an average age of 21±3 months and body weight of 330.8±37.9kg were divided into four groups containing six equines in each (three females and three males) in a completely randomized design with repeated measurements in a 2x2 factorial arrangement. Treatments were: 1 - chelated minerals compound; 2 - chelated minerals compound and potassium oxalate; 3 - not chelated minerals compound; and 4 - not chelated minerals compound and potassium oxalate. Clinical signs of nutritional secondary hyperparathyroidism (NSH) were observed only in treatment 4. Results showed no treatment effect in bone biopsy for calcium, phosphorus and bone density. There were significant reductions of parathyroid hormone (PTH) means concentrations in treatments 2 and 4 during supplementation. Animals supplemented with chelated minerals compounds avoided mineral imbalances and NSH even when in dietary potassium oxalate challenged.(AU)

Os minerais desempenham diversas funções no organismo, como ações de coagulação, contração muscular, produção enzimática e hormonal, entre outras. O objetivo deste estudo foi avaliar o efeito da suplementação de minerais quelatados e não quelatados, por 150 dias, com e sem oxalato de potássio, sobre parâmetros sorológicos e densidade mineral óssea em equinos. Vinte e quatro filhotes mestiços (12 fêmeas e 12 machos), com idade média de 21±3 meses e peso corporal de 330,8±37,9kg, foram divididos em quatro grupos contendo seis equinos cada (três fêmeas e três machos), em delineamento inteiramente ao acaso, com repetição medida em arranjo fatorial 2x2. Os tratamentos foram: 1 - composto mineral quelatado; 2 - composto mineral quelatado e oxalato de potássio; 3 - composto mineral não quelatado; e 4 - composto mineral não quelatado e oxalato de potássio. Os sinais clínicos do hiperparatireoidismo secundário nutricional (NSH) foram observados apenas no tratamento 4. Os resultados não mostraram efeito de tratamento na biópsia óssea para cálcio, fósforo e densidade óssea. Houve redução significativa do hormônio da paratireoide (PTH) em concentrações médias nos tratamentos 2 e 4 durante a suplementação. Os animais suplementados com compostos minerais quelatados evitaram desequilíbrios minerais e NSH, mesmo quando desafiados no oxalato de potássio na dieta.(AU)

Severe calcification of systemic blood vessel walls caused by continuous hypercalcemia in a cat with congenital hypothyroidism.

A 97-day-old male Japanese domestic cat was diagnosed as congenital hypothyroidism. During the treatment, continuous hypercalcemia was detected. Although fluid therapy was performed, the cat died at the age of 1785 days. At autopsy, both parathyroid glands were enlarged, and elastic arterial walls were increased in thickness and hardness. Histopathological examination revealed hyperplasia of both parathyroid glands and interstitial fibrosis of bilateral kidneys. Severe calcification of the tunica media and tunica externa in systemic elastic and muscular arteries were also observed. These calcifications were considered to be due to renal secondary hyperparathyroidism. In the present case, hypothyroidism might have caused hyperparathyroidism through renal failure. In veterinary medicine, this is the first reported case of hypothyroidism accompanied with hyperparathyroidism.

Primary Hyperparathyroidism Associated With Atypical Headshaking Behavior in a Warmblood Gelding.

A 14-year-old Zweibrücker Warmblood gelding was presented for evaluation of lethargy and headshaking. The horse had a history of bouts of lameness in different limbs and back problems. It also had many mild colic episodes in the past. Results of repeat laboratory tests had shown persistent hypercalcemia (4.8 mmol/L; reference interval [RI]: 2.0-3.2 mmol/L) for 1.5 years and later on hypophosphatemia (0.4 mmol/L; RI: 0.5-1.3 mmol/L) and mild hypermagnesemia (1.0 mmol/L; RI: 0.5-0.9 mmol/L). Parathyroid hormone (PTH) concentration was within the RI. Other causes of hypercalcemia, such as renal failure, vitamin D toxicosis, and granulomatous disease, and nutritional secondary hyperparathyroidism were ruled out. Furthermore, there was no evidence of neoplastic disease. Parathyroid hormone-related protein was measured but inconclusive. A diagnosis of primary hyperparathyroidism was established on the basis of hypercalcemia, hypophosphatemia, low fractional excretion of calcium, and high fractional excretion of phosphorus in combination with a PTH secretion refractory to high calcium levels. Because of the bad prognosis, the owner decided to euthanize the horse. Results of postmortem examination were unremarkable. Hypercalcemia should always be considered abnormal, and further examinations need to be performed to proof hypercalcemia and subsequently find the cause. The main differential diagnoses are renal insufficiency and humoral hypercalcemia of malignancy, but also rare diseases, such as hyperparathyroidism, have to be taken into account.

Paradise lost: Evidence for a devastating metabolic bone disease in an insular Pleistocene deer.

PURPOSE: This communication reports skeletal pathology in a Pleistocene endemic deer from the Mavromouri caves of Crete. MATERIALS: 287 bones and bone fragments from Mavromouri caves are compared to 2986 bones from Liko Cave. METHODS: Bones were evaluated macroscopically, and measurements were made of morphometric characteristics of limb long bones. Representative bone specimens were examined radiographically and histologically. RESULTS: Macroscopic hallmarks were loss of bone mass and increased porosity. The long bones were brittle, some of them having thin cortices, and others reduction of medullary cavities that contain dense Haversian tissue. The flat bones were spongy and fragile. Erosions of the metaphyses and articular surfaces were noted. Histological findings included: sub-periosteal resorption; loss of lamellar bone; enlargement of vascular canals; and remodeling of cortical bone. Two types of fibrous osteodystrophy were recognized in skeletal remains, subostotic and hyperostotic. CONCLUSIONS: The deer of Mavromouri caves were affected by severe metabolic bone disease, likely nutritional secondary hyperparathyroidism. We hypothesize a multifactorial cause, including overgrazing, flora senescence, soil mineral deficiencies, and a prolonged period of climate extremes, degrading the Cretan deer habitat. VALUE: This is the first evidence of a metabolic bone disease causing this level of destructive pathology in an insular fossil deer. LIMITATIONS: The lack of absolute chronometric dates for the site limits potential linking with the prevailing environmental conditions. SUGGESTIONS FOR FURTHER RESEARCH: Investigation of similar skeletal pathologies at other islands or isolated habitats is advised.

Dietary imbalances in a large breed puppy, leading to compression fractures, vitamin D deficiency, and suspected nutritional secondary hyperparathyroidism.

A 6-month-old intact female giant schnauzer dog fed a nutritionally unbalanced homemade diet was evaluated because of a 1-month history of lameness and difficulty walking. Abnormalities identified on ancillary tests, in conjunction with the dog's clinical improvement following diet change, suggested a diagnosis of vitamin D deficiency and nutritional secondary hyperparathyroidism. This report underlines the importance of appropriate feeding management, especially during the vulnerable growth phase.

Déséquilibres alimentaires chez un chiot de grande race causant des fractures de compression, une carence en vitamine D et de l'hyperparathyroïdisme soupçonné secondaire à la nutrition. Une chienne Schnauzer géante intacte âgée de 6 mois qui consommait une diète maison qui n'était pas équilibrée sur le plan nutritionnel a été évaluée en raison d'une anamnèse de 1 mois de boiterie et de difficultés ambulatoires. Les anomalies identifiées sur des tests ancillaires, de concert avec l'amélioration clinique du chien après le changement de diète, suggéraient un diagnostic de carence en vitamine D et d'hyperparathyroïdisme nutritionnel secondaire. Ce rapport souligne l'importance d'une gestion appropriée de l'alimentation, particulièrement durant la phase de croissance vulnérable.(Traduit par Isabelle Vallières).

Feline hyperparathyroidism: pathophysiology, diagnosis and treatment of primary and secondary disease.

PRACTICAL RELEVANCE: Hyperparathyroidism exists in primary and secondary forms. Primary hyperparathyroidism has typically been considered a disease that uncommonly affects cats, but this condition is more prevalent than previous diagnoses would suggest. Secondary hyperparathyroidism may be caused by either nutritional influences (ie, nutritional secondary hyperparathyroidism) or chronic kidney disease (ie, renal secondary hyperparathyroidism). Tertiary hyperparathyroidism has yet to be documented in veterinary medicine, but it is possible that this condition occurs in some cats following longstanding renal secondary hyperparathyroidism. CLINICAL CHALLENGES: Diagnosis of this group of calcium metabolic disorders presents a number of challenges for the clinician. For example, clinical signs can be non-specific and, especially in the case of primary hyperparathyroidism, there is often a low index of suspicion for the disease; careful sample handling is required for testing of parathyroid hormone (PTH) and ionized calcium levels; and there is currently no feline-specific assay for PTH, which has implications for test sensitivity and interpretation of results. AIMS: This article briefly outlines PTH and calcium physiology by way of introduction to a review of PTH measurement and interpretation. Various forms of feline hyperparathyroidism are then described, encompassing diagnosis and treatment options.

Update on common nutritional disorders of captive reptiles.

Nutritional disorders of captive reptiles remain very common despite the increasing knowledge about reptile husbandry and nutrition. Many nutritional disorders are diagnosed late in the disease process; often secondary complications, such as pathologic fractures in reptiles suffering from nutritional secondary hyperparathyroidism have occurred. Therefore, every attempt should be made to educate reptile owners and keepers about the proper care and dietary needs of reptiles under their care because all nutritional disorders seen in captive reptiles are preventable.

Fibroblast growth factor 23 in feline chronic kidney disease.

BACKGROUND: Fibroblast growth factor 23 (FGF-23) is a phosphaturic hormone involved in the pathogenesis of secondary renal hyperparathyroidism (SRHP) in humans. There are no published studies examining feline FGF-23. OBJECTIVES: Validation of a method for FGF-23 quantification in feline plasma and assessment of the associations among plasma FGF-23, PTH, creatinine, and phosphate concentrations in cats with chronic kidney disease (CKD). ANIMALS: One hundred nonazotemic and azotemic geriatric (>9 years) client-owned cats. METHODS: Retrospective cross-sectional study: Cats were categorized into 4 groups: control group (plasma creatinine (Cr) ≤2.0 mg/dL), stage 2 (Cr 2.1-2.8 mg/dL), stage 3 (Cr 2.9-5.0 mg/dL), stage 4 (Cr >5.0 mg/dL). Stages 2 and 3 were further subdivided based on International Renal Interest Society targets for plasma phosphate concentration (PO4 ): stage 2a (PO4 ≤4.5 mg/dL), stage 2b (PO4 >4.5 mg/dL), stage 3a (PO4 ≤5 mg/dL), stage 3b (PO4 >5 mg/dL). Plasma FGF-23 concentrations were measured by a human intact FGF-23 ELISA. Descriptive statistics and linear regression were performed. RESULTS: The ELISA demonstrated acceptable precision, reproducibility, and specificity. Plasma FGF-23 concentrations increased with increasing plasma creatinine concentrations and were significantly different between all groups (P < .008). Plasma FGF-23 concentrations were significantly higher in cats in stage 2b than stage 2a (P = .008) and in stage 3b than in stage 3a (P = .012). Phosphate, log creatinine, total calcium, log parathyroid hormone, and packed cell volume were all independent predictors of FGF-23. CONCLUSIONS AND CLINICAL IMPORTANCE: FGF-23 concentrations increase with increasing stage of feline CKD and might be a marker or mediator of feline SRHP.

Serum intact parathyroid hormone levels in cats with chronic kidney disease / Avaliação das concentrações séricas de paratormônio intacto em gatos com doença renal crônica

Chronic kidney disease (CKD) is frequently observed in cats and it is characterized as a multisystemic illness, caused by several underlying metabolic changes, and secondary renal hyperparathyroidism (SRHPT) is relatively common; usually it is associated with the progression of renal disease and poor prognosis. This study aimed at determining the frequency of SRHPT, and discussing possible mechanisms that could contribute to the development of SRHPT in cats at different stages of CKD through the evaluation of calcium and phosphorus metabolism, as well as acid-base status. Forty owned cats with CKD were included and divided into three groups, according to the stages of the disease, classified according to the International Renal Interest Society (IRIS) as Stage II (n=12), Stage III (n=22) and Stage IV (n=6). Control group was composed of 21 clinically healthy cats. Increased serum intact parathyroid hormone (iPTH) concentrations were observed in most CKD cats in all stages, and mainly in Stage IV, which hyperphosphatemia and ionized hypocalcemia were detected and associated to the cause for the development of SRHPT. In Stages II and III, however, ionized hypercalcemia was noticed suggesting that the development of SRHPT might be associated with other factors, and metabolic acidosis could be involved to the increase of serum ionized calcium. Therefore, causes for the development of SRHPT seem to be multifactorial and they must be further investigated, mainly in the early stages of CKD in cats, as hyperphosphatemia and ionized hypocalcemia could not be the only factors involved.

A doença renal crônica (DRC) em gatos é frequentemente observada e caracteriza-se como alteração multissistêmica, causada por alterações metabólicas, e o hiperparatireoidismo secundário renal (HPTSR) seria o mais comum e usualmente está associada com progressão da doença renal e mau prognóstico. Esse estudo teve como objetivo determinar a frequência do HPTSR, e discutir os possíveis mecanismos que podem contribuir para o desenvolvimento de SRHPT em gatos em diferentes estágios de DRC, pela avaliação do metabolismo do cálcio e fósforo, bem como do equilíbrio ácido-base. Quarenta gatos com DRC foram divididos em três subgrupos, de acordo com a classificação proposta pela International Renal Interest Society (IRIS), Estágio II (n=12), Estágio III (n=22) e Estágio IV (n=6). O grupo-controle foi composto por 21 gatos clinicamente saudáveis. O aumento das concentrações séricas de paratormônio intacto (PTHi) foi observado na maioria dos casos, mas principalmente no Estágio IV, no qual a hiperfosfatemia e a hipocalcemia ionizada parecem estar associadas ao desenvolvimento do HPTSR. No entanto, nos Estágios II e III, observou-se hipercalcemia ionizada, sugerindo que, nestes estágios, o desenvolvimento do HPTSR possa estar associado a outros fatores, e a acidose metabólica pode estar envolvida com o desenvolvimento de hipercalcemia ionizada. Assim, outros fatores, além da hiperfosfatemia e da hipocalcemia ionizada, possam estar envolvidos com o desenvolvimento do HPTSR, principalmente nos estágios iniciais da DRC. Futuros estudos são necessários para uma melhor compreensão da fisiopatologia do HPTSR em gatos.

Fibrous osteodystrophy in two Northern Royal albatross chicks (Diomedea sanfordi).

CASE HISTORY: In February 2004, two Northern Royal albatross chicks aged 20 and 25 days old were presented for necropsy. Both chicks had been hand-fed in situ at a breeding colony, from 2-3 days post-hatch. The hand-rearing diet consisted of boneless hoki fillets (Macraronus novaezelandiae), electrolytes, and sooty shearwater (Puffinus griseus) proventricular oil obtained as a by-product of cultural harvest. PATHOLOGICAL FINDINGS: Routine necropsies on the affected chicks revealed many bones were soft and easily bent. Radiography and histopathology revealed decreased bone density, pathological fractures, and extensive remodelling suggestive of fibrous osteodystrophy. DIAGNOSIS: Nutritional secondary hyperparathyroidism, resulting from an imbalance in the dietary Ca:P ratio. CLINICAL RELEVANCE: The imbalance in the dietary Ca:P ratio was a result of feeding deboned and eviscerated fish. This investigation also highlighted potential health risks associated with the practice of feeding stored rancid proventricular oil, including the destruction of fat-soluble vitamins. It is therefore possible that oxidative degradation of vitamin D may have contributed to the development of nutritional secondary hyperparathyroidism. Subsequently, dietary recommendations for supplementary feeding of orphaned Northern Royal albatross chicks include the feeding of whole human-grade fish with an appropriate Ca:P ratio, and the exclusion of proventricular oil. These cases highlight the need for scientific input into wildlife conservation projects, as lack of appropriate nutritional advice resulted in the feeding of a nutritionally inadequate diet. Following the recommended changes in diet, no further cases of osteodystrophy have been diagnosed in hand-raised chicks in the albatross colony.

Hypovitaminosis D in dogs with inflammatory bowel disease and hypoalbuminaemia.

OBJECTIVES: To compare serum vitamin D metabolites and plasma parathyroid hormone concentrations in dogs with inflammatory bowel disease and normal albumin concentration, dogs with inflammatory bowel disease and hypoalbuminaemia, healthy dogs and hospitalised ill dogs with non-gastrointestinal illness. METHODS: Serum 25 hydroxyvitamin D and 1,25 dihydroxyvitamin D concentrations were measured in 36 healthy dogs, 49 hospitalised ill dogs with non-gastrointestinal illnesses, 21 dogs with inflammatory bowel disease and normoalbuminaemia and 12 dogs with inflammatory bowel disease and hypoalbuminaemia. Plasma parathyroid hormone and ionised calcium concentrations were measured in a subset of these dogs. RESULTS: Concentrations of serum 25 hydroxyvitamin D were lower in hypoalbuminaemic dogs with inflammatory bowel disease than in the healthy dogs (P<0·001), hospitalised ill dogs (P<0·001) and normoalbuminaemic dogs with inflammatory bowel disease (P<0·001). Dogs with inflammatory bowel disease and hypoalbuminaemia had a higher plasma concentration of parathyroid hormone (P<0·01) and lower plasma concentration of ionised calcium (P<0·001) than hospitalised ill dogs. Dogs with inflammatory bowel disease had a positive correlation between serum 25 hydroxyvitamin D concentrations and serum albumin (P<0·0001), serum calcium (P<0·0001) and plasma ionised calcium (P<0·0005) concentrations. CLINICAL SIGNIFICANCE: Dogs with inflammatory bowel disease and hypoalbuminaemia frequently have ionised hypocalcaemia, high parathyroid hormone and low serum 25 hydroxyvitamin D concentrations. Further studies are indicated to establish the pathogenesis of this disease complication as well as therapeutic strategies to reverse this state.

Clinical and computed tomography features of secondary renal hyperparathyroidism.

An atypical case of secondary renal hyperparathyroidism was diagnosed in a 9-year-old miniature schnauzer after a skull computed tomography (CT) showed the presence of 2 bilateral and symmetrical soft tissue maxillary masses, and osteopenia of the skull.

Nutritional secondary hyperparathyroidism in the animal kingdom: report of two cases.

This report describes two cases of marked bone loss (osteopenia) occurring in a 9-week-old German shepherd puppy and in a 6-month-old tiger. In both cases the animals were fed a diet which was exclusively boneless meat. The diets in both cases contained approximately 40 mg of calcium and 1000 mg of phosphorus per pound resulting in both calcium deficiency and phosphorus excess, resulting in a phosphorus-to-calcium ratio of 25:1, well beyond the amounts known to cause marked loss of bone experimentally. This has been termed nutritional secondary hyperparathyroidism (NSH). Both animals presented with severe bone pain, difficulty in ambulation, and difficulty in chewing food. Radiographs showed marked osteopenia and spontaneous fractures. Both responded clinically and radiographically to calcium supplementation and a diet with an appropriate phosphorus-to-calcium ratio. The importance of calcium and phosphorus in the human diet is briefly discussed.

Treatment options for hyperphosphatemia in feline CKD: what's out there?

PRACTICAL RELEVANCE: Phosphorus is retained in chronic kidney disease (CKD), promoting renal secondary hyperparathyroidism and eventually resulting in hyperphosphatemia. Most agree that phosphate retention is a major contributor to the progression of CKD in many species and it is well known that hyperphosphatemia is associated with a significant mortality risk in humans with end-stage renal disease. PATIENT GROUP: Chronic kidney disease is a common ailment of geriatric cats. EVIDENCE BASE: There is evidence in cats suggesting that the use of a phosphate-restricted diet in IRIS stage 2-3 disease has a beneficial effect on clinical outcome. However, despite the fact that intestinal phosphate binders are commonly used in veterinary practice for patients with CKD, there have been few published reports focusing on the safety and efficacy of these products in veterinary medicine. No phosphorus binders are licensed as medications for dogs or cats. This article draws on data from clinical trials in humans and studies in cats to discuss treatment goals and options for phosphate retention and hyperphosphatemia in feline CKD. CLINICAL SIGNIFICANCE: With careful monitoring of serum phosphate and parathyroid hormone, and implementation of phosphate-restricted dietary management and intestinal phosphate binders, progression of CKD and the degree of hyperparathyroidism in cats may be reduced. AUDIENCE: Companion animal and feline practitioners are at the forefront in the management of CKD in cats.