Article

Effects of dietary phosphorus and protein in dogs with chronic renal failure

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Abstract

Four diets were formulated to contain: 16% protein and 0.4% phosphorus–diet 1; 16% protein and 1.4% phosphorus– diet 2; 32% protein and 0.4% phosphorus–diet 3; and 32% protein and 1.4% phosphorus–diet 4. Forty-eight dogs were fed diet 1 for 3 months after surgical reduction of renal mass, then were allotted to 4 groups of 12 dogs each, with equal mean values for glomerular filtration rate ( gfr ). Dog of groups 1–4 were fed diets 1–4, respectively, for 24 months. Data collected from the dogs during and at termination of the study were analyzed statistically for effects of dietary protein, phosphorus (P), time, and interactions between these factors. During the 24 months of study, 24 dogs developed uremia and were euthanatized for necropsy. Necropsy also was performed on the remaining 24 dogs after they were euthanatized at the end of the study. Dog survival was significantly enhanced by 0.4% P diets (vs 1.4% P diets), but survival was not significantly influenced by amount of dietary protein. The 0.4% P diets (vs 1.4% P diets) significantly increased the period that gfr remained stable before it decreased, but dietary protein did not have significant effect. Significant blood biochemical changes attributed to P, protein, and time were identified during the study. Terminally, plasma parathyroid hormone concentration was significantly increased from prediet values in all groups of dogs. Urine protein excretion was not significantly affected by dietary amount of either protein or P, when measured by either timed urine collection or urine protein-to-creatinine ratio. A tendency was seen for increased protein excretion with passage of time. Histologic and mineral analyses of kidneys removed at necropsy revealed some significant difference attributable to diet, but differences were more marked when diet was ignored, and the 24 surviving dogs were compared with the 24 that developed uremia. Overall, amount of dietary P was more important than amount of dietary protein for preventing adverse responses. However, because renal damage specifically attributable to either dietary component was not obvious, it is possible that the effects of P were manifested by extrarenal mechanisms.

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... La evaluación de la proteinuria (presencia de cantidades variables de proteína en orina) permite confirmar la existencia de determinadas patologías y, por ello, es parte fundamental de la evaluación de la función renal. [16][17][18][19][20][21][22][23][24] En animales con ERC de origen glomerular, la evaluación de la proteinuria permite hacer el diagnóstico antes de que se produzcan cambios en los indicadores plasmáticos de enfermedad renal. Además, la proteinuria es un importante factor pronóstico en relación a la progresión de ERC del perro y el gato. ...
... 18 La proteinuria persistente, asociada a un sedimento urinario inactivo, es un importante marcador clínico-patológico de la existencia de ERC tanto en el perro como en el gato. 19,20 Además, la proteinuria puede ocasionar repercusiones fisiopatológicas más o menos severas (disminución de la presión oncótica, hipertensión arterial, hipercolesterolemia, hipercoagulabilidad, debilidad muscular y pérdida de peso) que pueden afectar a la condición clínica del paciente. ...
... Sin embargo, la interpretación de los resultados obtenidos debe ser cautelosa, porque pueden obtenerse tanto falsos negativos (proteinuria de Bence-Jones, baja concentración de albúmina en orina o pH ácido) como falsos positivos (orina alcalina, sedimentos activos o contaminación con compuestos de amonio cuaternario o clorhexidina). [20][21][22] En general, los resultados deben interpretarse en función de cuál sea la densidad de orina (DU), de tal modo que un mismo resultado en la tira indicará una proteinuria más severa cuanto más baja sea la DU. Para aumentar la especificidad diagnóstica de esta prueba es aconsejable evaluar la proteinuria mediante tira colorimétrica en muestras con un sedimento urinario inactivo y pH < 7,5. ...
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Chronic kidney disease is a progressive and irreversible disease, difficult to manage in many occasions. In this article, the authors provide an updated review of the different therapeutic options according to the criteria of evidence based medicine.
... La evaluación de la proteinuria (presencia de cantidades variables de proteína en orina) permite confirmar la existencia de determinadas patologías y, por ello, es parte fundamental de la evaluación de la función renal. [16][17][18][19][20][21][22][23][24] En animales con ERC de origen glomerular, la evaluación de la proteinuria permite hacer el diagnóstico antes de que se produzcan cambios en los indicadores plasmáticos de enfermedad renal. Además, la proteinuria es un importante factor pronóstico en relación a la progresión de ERC del perro y el gato. ...
... 18 La proteinuria persistente, asociada a un sedimento urinario inactivo, es un importante marcador clínico-patológico de la existencia de ERC tanto en el perro como en el gato. 19,20 Además, la proteinuria puede ocasionar repercusiones fisiopatológicas más o menos severas (disminución de la presión oncótica, hipertensión arterial, hipercolesterolemia, hipercoagulabilidad, debilidad muscular y pérdida de peso) que pueden afectar a la condición clínica del paciente. ...
... Sin embargo, la interpretación de los resultados obtenidos debe ser cautelosa, porque pueden obtenerse tanto falsos negativos (proteinuria de Bence-Jones, baja concentración de albúmina en orina o pH ácido) como falsos positivos (orina alcalina, sedimentos activos o contaminación con compuestos de amonio cuaternario o clorhexidina). [20][21][22] En general, los resultados deben interpretarse en función de cuál sea la densidad de orina (DU), de tal modo que un mismo resultado en la tira indicará una proteinuria más severa cuanto más baja sea la DU. Para aumentar la especificidad diagnóstica de esta prueba es aconsejable evaluar la proteinuria mediante tira colorimétrica en muestras con un sedimento urinario inactivo y pH < 7,5. ...
Article
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Chronic kidney disease is the most common kidney disease in dogs and cats. A complete evaluation of these patients is necessary to make a correct diagnosis and to prescribe the most adequate therapy. In this article an updated review of the clinic-pathologic evaluation of these animals is described.
... Spontaneous renal diseases are a frequent cause of illness and death. This process serves as a model of progressive renal injury in this species (Finco et al. 1992) and of the effects of nutrients on progression of renal failure (Brown et al. 1991a, Finco et al. 1992b). The composition of dietary PUFAs modifies the course of induced renal disease in rats (Logan et al. 1992). ...
... These may include restricted phosphorus, protein, and sodium contents, enhanced levels of B-complex vitamins, and a high energy density using nonprotein sources. A number of studies have shown that restriction of dietary protein and phosphorus can reduce azotemia and bring about clinical benefits in dogs with CRF (Finco et al., 1992;Grandjean et al., 1990;Hansen et al., 1992;Leibetseder and Neufeld. 1991) although controversy exists regarding the level of protein restriction and at what stage such restriction may be needed (Kronfeld. ...
... 1993). The data regarding phosphorus restriction appear more convincing (Finco et al., 1992). Specific management recommendations based on stages of disease have recently been made (Brown. ...
... According to Brown et al (1991), Finco et al (1992), Block et al (1998) and Polzin et al (2005) hyperphosphatemia promoted progressive renal lesions and had been linked to increased mortality in human beings and dogs with kidney disease. Chew and Gieg (2006) observed that hypokalemia was most likely to occur at presentation in patients with polyuric renal failure, especially when anorexia was present. ...
... Hyperphosphatemia might have accentuated the progressive renal lesions in cases with poor prognosis (Brown et al, 1991;Finco et al, 1992 andBlock et al, 1998). 20% of the surviving patients were thrombocytopenic at presentation, as against 60% patients from poor prognosis group. ...
... The daily purine intakes of the 2 commercial kidney diets analysed were 33.4 mg (kidney diet 2) and 40.2 mg (kidney diet 1). In order to protect the kidneys (from further disease), such diets focus on a low protein and phosphorus content [46,47]. However, dog diets low in protein are not necessarily low in purine [28]. ...
Article
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Reducing the alimentary purine intake contributes to the prevention of purine (especially xanthine) urolith formation, a common adverse effect of allopurinol treatment in dogs with Leishmania infections. Analyses of the purine content are not required in order to advertise a diet as low in purine. Due to different analytical methods, data provided on purine content are barely comparable. The aim of this study was to investigate the total purine content of 12 different dog diets. For this, the purine bases adenine, guanine, xanthine, and hypoxanthine were determined by standardised high performance liquid chromatography in commercially available urinary diets (n = 4), kidney diets (n = 2), low protein diets (n = 3), 1 vegan diet, 1 regular diet for healthy adult dogs, and 1 homemade low purine diet. Total purine amounts ranged between 10.2 and 90.9 mg/100 g of dry matter. The daily purine intake calculated for a 20 kg standard dog with the analysed diets ranged between 21.9 and 174.7 mg. The lowest daily purine intakes were achieved by 2 urinary urate diets, followed by the homemade diet. Differences in the purine content of commercially available diets need to be considered. Awareness has to be raised when selecting diets for dogs with Leishmania infections during allopurinol treatment in order to minimise the risk of urolith formation.
... Bei abnehmender Nierenfunktion sollten nierenpflichtige Stoffe, insbesondere Phosphor, nicht im Exzess verabreicht werden. Ein Zusammenhang zwischen hoher Phosphoraufnahme und der beschleunigten Progression einer CNI wird vielfach postuliert [42] [43]. Im Gegensatz dazu ist es nachweislich lebensverlängernd, wenn der Serumphosphatspiegel der Patienten im Referenzbereich gehalten wird [44], wobei auch vermieden werden sollte, dass die Werte über längere Phasen an der oberen Grenze des Referenzbereichs liegen (Mensch: [3] ...
... In Letzterer lag der Maximalwert für Phosphor in Produkten Bei abnehmender Nierenfunktion sollten nierenpflichtige Stoffe, insbesondere Phosphor, nicht im Exzess verabreicht werden. Ein Zusammenhang zwischen hoher Phosphoraufnahme und der beschleunigten Progression einer CNI wird vielfach postuliert[41] ...
Article
Objective Complete foods and renal diets for dogs and cats available on the German market were analyzed for their concentrations of total phosphorus as well as highly soluble and therefore highly available phosphorus due to the possible effects of this element on the animal’s health. Material and methods A total of 133 complete foods for healthy dogs and cats, 8 snacks and 43 diets for patients with chronic kidney disease were analyzed for total phosphorus and the fraction of phosphorus soluble in water after 1 minute (Psol1). Results In the tested compound food, the amount of phosphorus in relation to the recommended daily allowance ranged from 90 to 740 %. More than 90 % of the products supplied twice the required amounts; in 6 dog feeds the nutritional maximum was exceeded. For almost 75 % of the products, the recommended daily allowance for phosphorus was already met by Psol1. More than 50 % of the tested renal diets contained more than twice the recommended amounts for healthy individuals and with this also exceeded the legal limits. Even in the renal diets, the amount of Psol1 alone exceeded the recommended daily allowance for this element. Conclusion This work demonstrates that compound food and renal diets available on the German market may contain a multiple of the recommended or legally permitted phosphorus concentrations. Therefore, a considerable number of products may be expected to not meet the expectations of customers and veterinarians.
... [2][3][4][5] Hyperphosphatemia is known to be a prognostic factor for shorter survival time in dogs with CKD. [6][7][8][9][10] Therefore, prevention and management of hyperphosphatemia may improve the prognosis of dogs with CKD. ...
Article
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Background Fibroblast growth factor (FGF)‐23 is increased first in the sequence of changes associated with chronic kidney disease (CKD)‐mineral and bone disorder. Thus, its measurement may serve as a predictive indicator of incident hyperphosphatemia. Objectives To investigate whether serum FGF‐23 concentration in normophosphatemic dogs with CKD is associated with the risk of the subsequent development of hyperphosphatemia and CKD progression. Animals Forty‐two normophosphatemic dogs with CKD. Methods Blood samples and medical records were retrospectively investigated. Hyperphosphatemia was defined as a serum phosphorous concentration >5.0 mg/dL. Progression was defined as a >1.5‐fold increase in serum creatinine concentration. The time periods and hazard ratios for these outcomes were assessed using Kaplan‐Meier analysis, log‐rank test, and univariate Cox regression analysis. The variables associated with the outcomes in the univariate analysis were included in the multivariate Cox regression model with backward selection. Results Serum FGF‐23 concentration >528 pg/mL was associated with a shorter time to development of hyperphosphatemia (P < .001) and CKD progression (P < .001). In multiple Cox regression analysis, increased FGF‐23 concentration remained a significant variable associated with these outcomes (P < .05). Conclusions and Clinical Importance Increased FGF‐23 concentration in normophosphatemic dogs with CKD was associated with significant risk of development of hyperphosphatemia, independent of CKD stage, and of the progression of CKD. Future research focusing on whether interventions that decrease FGF‐23 secretion will slow the development of hyperphosphatemia and CKD progression is needed.
... In dogs with 15/16 nephrectomy, high phosphorus intake accelerated mortality (17)(18)(19). The four experimental diets contained 0.3 g calcium and 0.3 g P/MJ, or 1.1 g Ca and 0.9 g P/MJ, each at 10 or 18 g protein/MJ. ...
Article
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Renal diet for dogs This text is an adapted and updated version of an article in Dutch (1). A similar communication addresses the renal diet for cats (2). From its content, various passages have been taken over in their entirety for incorporation into this text. Main points In dogs attending veterinary practices in the United Kingdom, the prevalence of chronic kidney disease (CKD) was 0.2% (3). The disease is relatively uncommon, but clinically relevant. Dogs with CKD show clinical signs that include polyuria/polydipsia, urinary incontinence, weight loss, vomiting, decreased appetite, lethargy, diarrhea and halitosis. The median survival time from diagnosis of CKD was 7.5 months (3). Dietary treatment can only retard the progression of CKD and aims at supporting the quality of life and extending life span. The canine renal diet has three main characteristics (Note 1): low in phosphorus, low in protein and high in eicosapentaenoic acid (EPA). As sole variable, the three nutrient interventions have not been studied in dogs with naturally occurring CKD. Both phosphorus and protein restriction reduced the progression of renal deterioration in dogs with experimental kidney disease, as induced by partial nephrectomy. It is advanced, as an arbitrary guideline (Note 1), that a wet renal diet for dogs ideally contains 0.1-0.3 g phosphorus, 6-9 g protein and 0.1-0.3 g EPA per MJ of dietary, metabolizable energy, and furthermore meets the recommended nutrient allowances (4) of the other nutrients. It is estimated that 25% of total phosphorus in dry food represents phytate-bound phosphorus, which is unavailable. Thus, for dry renal diets the proposed phosphorus range is 0.13-0.40 g/MJ. The restricted amounts of phosphorus and protein do not cause deficiencies. The means of the suggested ranges for phosphorus, protein and EPA, as expressed in g/MJ, correspond with the following percentages in dry and wet dog food. For dry renal food (1.7 MJ/100 g), the proposed nutrient levels equal 0.45% phosphorus, 12.8% crude protein and 0.34% EPA. For wet renal food (0.6 MJ/100 g), the respective levels are 0.12, 4.5 and 0.12%. In a clinical trial (5), dogs with spontaneous CKD were either fed a commercial, dry renal food (0.16 g phosphorus and 7.9 g protein/MJ; n=21) or a dry maintenance food (0.64 g phosphorus and 16.1 g protein/MJ; n=17). The EPA content is unreported. The reference and renal diet were fed for 24 months. The incidence of uremic crises and renal mortality were less by half in the dogs fed the renal diet. European legislation Within the European Union, it is legally prohibited that the labelling or presentation of petfood claims to prevent, cure or treat a disease. It is permitted that petfood has a particular nutritional purpose from a prescribed list of intended uses, but only when the food's composition satisfies the
... In general, ionized hypercalcemia and ionized hypocalcemia was reported in dogs and cats with spontaneous CKD (Polzin, 2011;Schenck & Chew, 2003). Hypercalcemia may occur in dogs with CKD as a consequence of excessive dosages of calcium-containing intestinal phosphate-binding agents (such as calcium acetate, calcium carbonate, or calcium citrate), or in patients with advanced CKD with severe renal hyperparathyroidism (Finco et al., 1992;Nagode, Chew & Podell, 1996). Hypercalcemia promotes kidney injury and an increase of the calcium X phosphorus product have been correlated to renal mineralization, inflammation, fibrosis and poor prognosis (Lippi et al., 2014). ...
Article
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Chronic kidney disease (CKD) is a common disease in elderly dogs. The present study aims to evaluate the efficacy of a dietary supplement containing calcium carbonate, calcium-lactate gluconate, chitosan and sodium bicarbonate in dogs with IRIS stage 3 of CKD. Twenty dogs were enrolled in the study, ten were administered the new dietary supplementation for 180 days (T group) while the others were used as control group (C group). Haematologic, biochemical and urinalysis were performed every 30 days. A significant reduction in the T group compared to the C group in serum phosphorus level and increase in serum bicarbonate and ionized calcium values were recorded. The urine protein-to-creatinine ratio (UPC) was significantly lower in the T group at the end of the study compared to the C group. The tested supplement could be considered as a supportive treatment for dogs with advanced CKD.
... Research in dogs with chronic kidney disease, as induced by 15/16 nephrectomy, indicates that high P intake brings forward mortality (27)(28)(29). The four experimental foods had two different Ca and P combinations (0.3 g Ca and 0.3 g P/MJ versus 1.1 and 0.9), each at two levels of protein (10 or 18 g/MJ). ...
Article
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Phosphorus in senior dog food
... 9,[29][30][31] Similarly, pro- teinuria, CaPP, and hyperphosphatemia were associated with greater hazard ratios and decreased survival, related to mechanisms described elsewhere. [12][13][14][32][33][34][35][36] PTH, iCa and vitamin D metabolites were not associated with survival in this study, contrary to previous reports for some of these variables in dogs and humans. 6,7,13 Importantly, when analyzing the data on non-significant variables in this study, it is useful to look at the frequency at which dogs were outside the established reference ranges. ...
Article
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Background: Chronic kidney disease (CKD) is associated with morbidity and mortality in dogs. Plasma fibroblast growth factor‐23 (FGF‐23) concentration is an independent predictor of CKD progression and survival in cats and people with CKD. Objectives: To investigate the relationship among FGF‐23, parathyroid hormone (PTH), vitamin D metabolites, and other clinical variables with survival time in dogs with CKD. Animals: Twenty‐seven azotemic CKD dogs. Methods: Dogs were recruited prospectively into the study and followed until death or study conclusion. Dogs were International Renal Interest Society (IRIS) staged into stage 2 (n = 9), stage 3 (n = 12), and stage 4 (n = 6) CKD. Survival times were calculated from the date of study inclusion. Univariable Cox regression was used to assess variables associated with survival including body condition score (BCS), muscle condition score, hematocrit, creatinine, CKD stage, serum phosphorus, urine protein:creatinine ratio (UPC), calcium phosphorus product (CaPP), PTH, 25‐hydroxyvitamin D, 1,25‐‐dihydroxyvitamin D, and FGF‐23 concentrations. Results: Significant hazard ratios (hazard ratio; 95% confidence interval; P value) were as follows: BCS < 4/9 (1.579; 1.003‐2.282; P = .05), muscle atrophy (2.334; 1.352‐4.030; P = .01), increased creatinine (1.383; 1.16‐1.64; .01), hyperphosphatemia (3.20; 1.357‐7.548; P = .005), increased UPC (3.191; 1.310‐7.773; P = .01), increased CaPP (4.092; 1.771‐9.454; P = .003), and increased FGF‐23 (2.609; 1.090‐6.240; P = .05). Survival times for each IRIS CKD stage were significantly different (P = .01). Conclusions and Clinical Importance: Multiple variables, including FGF‐23, were associated with duration of survival in CKD dogs. FGF‐23 could be a prognostic marker in dogs with CKD.
... In healthy subjects, no impact of high protein supply on the development of impaired renal function was observed (Knight et al. 2003, Martin et al. 2005. For dogs and cats, the data from literature about effects of protein intake on renal disease are discordant with some works suggesting negative effects (Adams, Polzin, Osborne, & O'Brien, 1993;Polzin, Osborne, Stevens, & Hayden, 1982) and others stating no adverse protein effects (Finco et al., 1992(Finco et al., , 1998Robertson et al., 1986) or even lower odds of CKD in cats with increased protein supply (Hughes et al. 2002). Detrimental effects of nutritional P excess on renal health have been demonstrated in rats (MacKay & Oliver, 1935), dogs (Schneider et al., 1980;Siedler & Dobenecker, 2016), cats (Dobenecker et al., 2017;Pastoor, Klooster, Mathot, & Beynen, 1995) and humans (Calvo & Uribarri, 2013;Ritz, Hahn, Ketteler, Kuhlmann, & Mann, 2012). ...
Article
Full-text available
There is evidence that nutritional phosphorus (P) excess may be a risk factor for chronic kidney disease (CKD) in humans and pets (Advances in Nutrition: An International Review Journal (2014), 5, 104; The American Journal of Clinical Nutrition, (2013), 98, 6; Journal of Feline Medicine and Surgery, (2017); The source of phosphorus influences serum PTH, apparent digestibility and blood levels of calcium and phosphorus in dogs fed high phosphorus diets with balanced Ca/P ratio. Proc. Waltham International Nutritional Sciences Symposium, USA; Clinical aspects of natural and added phosphorus in foods, 2017, Springer Science+Business, Media). A retrospective study was conducted in order to gather data about P and protein intake in the feeding history of dogs and cats prior to the diagnosis of CKD. Cases of 75 dogs and 16 cats with CKD with comprehensive nutritional history presented to the nutrition consultation service of the Chair of Animal Nutrition and Dietetics, Ludwig‐Maximilians‐University Munich, between October 2009 and March 2016, were evaluated. Cases of age‐matched dogs (n = 57) and cats (n = 18) without diagnosed or suspected CKD served as controls. The most frequent type of diet used in the four groups (cats CKD, cats control, dogs CKD and dogs control) was home‐made. In all groups, P and protein supply was in excess (>150%) of the recommended daily allowances (RDA; Nutrient requirements of dogs and cats (2006), National Research Council, National Academy Press). Between the dog groups, no differences regarding P and protein intake existed. The P and protein intake relative to the RDA was altogether higher in cats than in dogs. Cats with CKD showed significantly higher P and protein intakes prior to diagnosis than the control cats (170 ± 36 vs. 123 ± 34 mg P/kg BW0.67; p < .05). These observations call for further investigations into the long‐term effects of P excess.
... In healthy subjects, no impact of high protein supply on the development of impaired renal function was observed (Knight et al. 2003, Martin et al. 2005. For dogs and cats, the data from literature about effects of protein intake on renal disease are discordant with some works suggesting negative effects (Adams, Polzin, Osborne, & O'Brien, 1993;Polzin, Osborne, Stevens, & Hayden, 1982) and others stating no adverse protein effects (Finco et al., 1992(Finco et al., , 1998Robertson et al., 1986) or even lower odds of CKD in cats with increased protein supply (Hughes et al. 2002). Detrimental effects of nutritional P excess on renal health have been demonstrated in rats (MacKay & Oliver, 1935), dogs (Schneider et al., 1980;Siedler & Dobenecker, 2016), cats (Dobenecker et al., 2017;Pastoor, Klooster, Mathot, & Beynen, 1995) and humans (Calvo & Uribarri, 2013;Ritz, Hahn, Ketteler, Kuhlmann, & Mann, 2012). ...
Poster
This retrospective case analysis shows the prevalence of phosphorus and protein excess in the feeding history of dogs and cats with and without CRI.
... The allowance for adult dogs is close to the minimum requirement that just prevents phosphorus deficiency (9). Low versus high phosphorus intake reduces the progression of experimental chronic kidney disease in cats (10) and dogs (11). It is conceivable that low dietary phosphorus curbs chronic kidney disease (12), which typically develops in senior cats and dogs. ...
Research
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Life-stage petfood Canine and feline life-stage nutrition, as opposed to one complete diet for all ages, can be justified. Requirements of nutrients are greater for growth than for the maintenance phase. Thus, an all-life-stage diet contains nutrient levels higher than needed by adult animals. Worth noticing, phosphorus intakes required for growth might jeopardize kidney health in senior animals. Furthermore, there is suggestive evidence that adult animals, rather than their growing counterparts, benefit from extra intakes of vitamin E and EPA (eicosapentaenoic acid). Most petfood lines consist of puppy/kitten, adult and senior foods. However, few lines take into account the relationship between age and nutrient requirements, in combination with adjusting nutrient supply to age-related disease.
... Each food was recommended for all life stages. Indirect evidence suggests that the above-average protein and phosphorus levels enhance the development of chronic kidney disease in senior dogs (5,6). The high calcium concentrations may induce skeletal disease (osteochondrosis) in growing dogs of large breeds (7). ...
Research
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Raw frozen and freeze-dried dog foods have no demonstrable health effects
... The foods with above-average calcium levels may induce skeletal disease (osteochondrosis) in young growing dogs of large breeds (5) for which FEDIAF advises a maximum calcium content of 1.0 g/MJ. Indirect evidence indicates that the foods' high phosphorus load enhances the development of chronic kidney disease in older dogs (6). ...
Research
Full-text available
Meat-first and high-protein petfoods " Meat-first should neither mislead purchasers nor compromise pet health " Many dog and cat owners want to feed their pets a meat-based diet with plentiful animal protein. They look for foods that are meat-first in their ingredient listings. Pro-actively, various petfood labels highlight a meat species as first ingredient. Meat-first does not guarantee a sizeable proportion of animal protein, whereas meat-first, high-protein foods can have health drawbacks. Meats in petfood Caregivers who believe that dogs and cats are designed to consume meat for optimum health seem not to consider that their pets require specific nutrients rather than specific ingredients. There is no objective evidence that complete and balanced, meat-based and meatless foods have differential health effects. This leaves unimpeded that meat type and content claims on petfood should be transparent. Numerous ingredient lists declare the name of a warm-blooded land animal species without denoting meat. The declarations concern fresh or preserved, fleshy parts, organs, viscera and/or carcass derivatives. The claims " rich in " , " high in " or " with extra X " require that the food contains at least 14% X. When X is included in the product name, the minimum amount must be 26%. Animal material abounding in water could add little to the food's nutrient content. Dry, grain-based foods normally contain more than 14% preserved animal materials referred to as dried, dehydrated or meal. Listing ingredients In accordance with the basic formula, the petfood label must list the ingredients in descending order by weight, but with a tolerance of ± 15%. The inclusion percentages are not disclosed, except for ingredients highlighted in the labeling. Although moist animal parts tend to rank higher, they could contribute little nutrition as their water fraction of up to 75% is without nutrients. This applies to wet diets and dry foods produced with wet animal ingredients. The recipes of dry foods can be designed legally so that an animal component heads the ingredient list (1, 2). The rehydration method ranks the ingredients with their original water content. Thus, dry animal material mounts, passes other ingredients and may become number one. Alternatively, recipes can be steered toward meat-first by splitting starchy ingredients into different processing forms, fractions or crop varieties. High-protein, low-carb foods Natural, grain-free foods that emphasize meats as ingredients often bear the captions biologically appropriate, evolutionary, ancestral or instinctive. For such dry, extruded foods, meat-first and recommended for dogs of all life stages, the composition was computed. Six foods state the first ingredient by animal species only. One food does so with meat or organs as noun and two foods
... Hyperphosphatemia reduces survival in animals with renal disease and is associated with renal secondary hyperparathyroidism; 26,27 therefore, in dogs with experimental kidney disease, diets containing elevated protein, but reduced phosphorus, were as benefi cial as those with reduced protein and phosphorus. 28 Commercial renal diets provide more protein (25-55 g/1000 kcal for canine diets) than the recommended allowance for adult dogs (ie, > 25 g/1000 kcal). 2 • When consumed in appropriate amounts, they should not cause amino acid defi ciencies. • Dogs and cats fed these diets have median survival times 2× greater than those fed maintenance diets. ...
... Consistent with this, animals fed HPD developed increased plasma Pi (Fig 2A) with subsequent kidney fibrosis, connective tissue calcification and mononuclear cell infiltration [27][28][29][30], mirroring the findings in present study. Conversely, restricting dietary Pi prevented renal injury and failure in experimental models of kidney disease [15,28,37,38]. These data strongly suggest that excessive Pi is intrinsically linked to renal diseases and that HPD is a valid and powerful approach to characterize how abnormalities in this key electrolyte cause disease. ...
Article
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Tubulo-interstitial fibrosis is a common, destructive endpoint for a variety of kidney diseases. Fibrosis is well correlated with the loss of kidney function in both humans and rodents. The identification of modulators of fibrosis could provide novel therapeutic approaches to reducing disease progression or severity. Here, we show that the peptidyl-prolyl isomerase Pin1 is an important molecular contributor that facilitates renal fibrosis in a well-characterized animal model. While wild-type mice fed a high phosphate diet (HPD) for 8-12 weeks developed calcium deposition, macrophage infiltration and extracellular matrix (ECM) accumulation in the kidney interstitium, Pin1 null mice showed significantly less pathology. The serum Pi in both WT and KO mice were significantly increased by the HPD, but the serum Ca was slightly decreased in KO compared to WT. In addition, both WT and KO HPD mice had less weight gain but exhibited normal organ mass (kidney, lung, spleen, liver and heart). Unexpectedly, renal function was not initially impaired in either genotype irrespective of the HPD. Our results suggest that diet containing high Pi induces rapid renal fibrosis before a significant impact on renal function and that Pin1 plays an important role in the fibrotic process.
... 47 In cats with more profound nephron loss, hyperperfusion of enlarged glomeruli 33 may cause podocyte damage and loss, resulting in the lesion of focal segmental glomerulosclerosis. Compared with dogs, 40,74,75 secondary glomerulosclerosis in the remnant kidney model is comparatively mild in cats 73 and in spontaneous feline CKD focal segmental glomerulosclerosis, when present, similarly affects relatively few glomeruli and only a small portion of the capillary tuft. 47 Varying proportions of glomeruli in cats with CKD are decreased in size and are globally sclerotic or obsolescent. ...
Article
Chronic kidney disease (CKD) is the most common metabolic disease of domesticated cats, with most affected cats being geriatric (>12 years of age). The prevalence of CKD in cats exceeds that observed in dogs, and the frequency of the diagnosis of CKD in cats has increased in recent decades. Typical histologic features include interstitial inflammation, tubular atrophy, and fibrosis with secondary glomerulosclerosis. In contrast to people and dogs, primary glomerulopathies with marked proteinuria are remarkably rare findings in cats. Although a variety of primary renal diseases have been implicated, the disease is idiopathic in most cats. Tubulointerstitial changes, including fibrosis, are present in the early stages of feline CKD and become more severe in advanced disease. A variety of factors-including aging, ischemia, comorbid conditions, phosphorus overload, and routine vaccinations-have been implicated as factors that could contribute to the initiation of this disease in affected cats. Factors that are related to progression of established CKD, which occurs in some but not all cats, include dietary phosphorus intake, magnitude of proteinuria, and anemia. Renal fibrosis, a common histologic feature of aged feline kidneys, interferes with the normal relationship between peritubular capillaries and renal tubules. Experimentally, renal ischemia results in morphologic changes similar to those observed in spontaneous CKD. Renal hypoxia, perhaps episodic, may play a role in the initiation and progression of this disease.
... Bei Katzen, die an CKD leiden, wird häufig eine Hypokaliämie beobachtet (DOW und FETTMAN, 1992;DIBARTOLA et al., 1993 (FINCO et al., 1992;BLOCK et al., 1998). ...
... Reduced protein intake compromises the urinary acid excretion by decreasing renal ammoniagenesis and serum urea nitrogen and P concentration 9 . NaHCO3 or potassium citrate should be cautiously supplemented at a dosage of 8-12 mEq/Kg to minimize metabolic acidosis and lessen the stimulus for renal ammoniagenesis. ...
... 7 The data regarding phosphorus restriction appear more convincing. 3 Specific management recommendations based on stages of disease have recently been made. 8 Use of a diet restricted in phosphorus, but not in protein, is recommended for dogs that are azotemic but not uremic. ...
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32 Modifying the diet is an important component of the medical management of chronic renal failure (CRF) in dogs. Protein, sodium, and phosphorus contents of such diets are restricted, and the level of B-complex vitamins is increased. These diets also offer a high energy density from non-protein sources and are often high in fat. A study using a commercial canned diet designed for dogs with CRF indicates that increases in total cholesterol associated with high den-sity lipoproteins are unlikely to be atherogenic or to promote glomeruloscle-rosis; this suggests that using high levels of fat to increase non-protein energy is not detrimental to the CRF patient. Some eicosanoids also play an impor-tant role in renal disease; for example, supplementation with dietary fish oils has been shown to be beneficial in some animal models of renal disease. A study compared urinary eicosanoid concentrations in normal dogs to those in dogs with CRF; the impact of safflower oil or menhaden fish oil was evaluat-ed. Safflower oil significantly increased glomerular filtration rate, which could be of short-term benefit to the patient.
... Tryfonidou et al. (2003) demonstraram em filhotes de raças gigantes que a reabsorção renal de fósforo inorgânico é maior que a de filhotes de raças pequenas, explicando a retenção orgânica de P e a elevação da fosfatemia verificadas em animais alimentados com excesso de P. Acredita-se que ao redor de 25% dos cães idosos apresentem algum comprometimento da função renal (Crowell e Finco, 1975;Debraekeleer et al., 1999), de modo que a ingestão excessiva de P deve ser evitada para animais nessa faixa etária. Redução da progressão da doença renal, aumento da qualidade e expectativa de vida e regularização das alterações bioquímicas relativas à insuficiência renal crônica foram conseguidas com dietas que apresentavam ao redor de 0,4% de P (Kronfeld, 1994;Finco et al., 1992), valor correspondente a apenas 25% da concentração média encontrada nas rações avaliadas neste trabalho. ...
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Fortynine food products for adult or juvenile dogs, commercially available in Jaboticabal, São Paulo, Brazil, were tested for nutrient composition. The products were divided into three categories: low-cost, standard and super-premium. In that order, average compositions for adult foods were 16.9%, 20.9% and 27.8% protein, 9.7%, 10.5% and 15% fat, 6.4%, 2.9% and 1.1% fiber, and 1.9%, 1.9% and 1.4% calcium. For puppy foods, the average compositions of standard and super-premium foods were 26.1% and 31% protein, 10.8% and 15.2% fat, 2.6% and 2.4% fiber, 2.1% and 1.7% Ca, and 1.6% and 1.3% P, respectively. The percentages of products whose published label values were in disagreement with laboratory results were: super-premium products for puppies, 80% for Ca and 60% for fat; standard products for puppies, 28.6% for protein and 57.2% for Ca; low-cost products for adults, 44% for fiber and 33% for protein; standard products for adults, 33% for fat and 50% for Ca; super-premium products for adults, 50% for calcium and 33% for fat. Products with nutritional shortcomings were found, such as insufficient protein content and too high levels of fiber, calcium, and phosphorus.
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Each nephron is a functional unit composed of a glomerulus and its associated renal tubule, and the kidneys are composed of thousands of nephrons. Glomerular filtration rate is defined as the total filtration rate of both kidneys. The kidneys receive 20–25% of the cardiac output, and the major sites of resistance to blood flow are the afferent and efferent arterioles. The majority of renal blood flow is distributed to the renal cortex, while the remaining blood flow is distributed between the outer medulla and inner medulla. Normal daily urine output (UOP) ranges from 20 to 40mL/kg in dogs and cats. There are four broad categories of UOP associated with renal failure: anuric, oliguric, nonoliguric, and polyuric. Acute kidney injury can be caused by hemodynamic disturbances, intrinsic parenchymal damage, postrenal disorders, or by a combination of these.
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Background Withholding food is often recommended before collection of blood for routine biochemical analysis in dogs despite a paucity of evidence to support this requirement. Objectives To compare measurements of selected biochemical analytes collected before and after feeding in clinically healthy dogs. Animals One hundred clinically healthy staff‐ and student‐owned dogs weighing ≥15 kg. Methods Prospective observational study. Food was withheld from the dogs for 10‐26 hours. Preprandial serum was collected, and then dogs were fed their usual food at an amount equivalent to at least 2/3 resting energy requirement (RER). Selected serum analytes were measured at 2‐, 4‐, 6‐, and 8‐hours postprandially. The proportion of postprandial values that exceeded either the reported allowable total error (TEa), or for symmetric dimethylarginine (SDMA), the reference change value (RCV), was determined. As neither TEa nor RCV is available for lipase, comparison was made to the high end of the reference interval (RI). Results The proportion of dogs with at least 1 postprandial measurement that exceeded the TEa or RCV was 92/100 for triglycerides, 66/100 for blood urea nitrogen (BUN), 46/100 for phosphorus, 17/100 for glucose, 9/100 for bilirubin, 5/100 for SDMA, 2/100 for creatinine, and 0/100 for cholesterol and albumin. Postprandial lipase never exceeded the RI in dogs with normal fasted lipase. Conclusions and Clinical Importance Withholding food is generally not necessary before performing routine biochemical analysis in clinically healthy dogs. Withholding food might be helpful to limit variability in analytes impacted by feeding, such as triglycerides and phosphorus.
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Proteinuria can be caused by prerenal, postrenal, and primary renal disorders. The finding of proteinuria provides a diagnostic clue for disorders of the upper and lower urinary tract. A detailed review of the molecular structures and functions of the glomerular basement membrane (GBM), including GBM assembly, maintenance, and repair, is available for the interested reader. Proteinuria may be classified as prerenal, renal, or postrenal in etiology. Renal proteinuria develops long before overt loss of excretory renal function is identified in humans with a variety of glomerular diseases. Protein in urine can be measured by qualitative, semiquantitative, or quantitative methods. It appears that longstanding proteinuria of glomerular origin can lead to further glomerular injury, tubular damage, tubulointerstitial inflammation, and progressive nephron loss. Systemic hypertension from any cause can be associated with glomerular proteinuria. The finding of increased amounts of proteins in the urine provides important diagnostic clues to the nature of underlying kidney and systemic diseases.
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The nutritional management of canine and feline chronic kidney disease and protein-losing nephropathy is discussed. Special attention is paid to assessment of body composition (body weight, body condition score, and muscle condition score) and the dysrexia that often occurs with kidney disease. Various nutrients of concern are discussed and specific dietary options are provided.
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Elevated concentrations of serum phosphate are linked with progression and increased case fatality rate in animals and humans with chronic kidney disease. Elevated concentrations of serum phosphate can be a risk factor for development of renal and cardiovascular diseases or osteoporosis in previously healthy people. In rodents, an excess intake of dietary phosphorus combined with an inverse dietary calcium : phosphorus ratio (<1 : 1) contributes to renal calcification. Renal injury also has occured in cats fed experimental diets supplemented with highly soluble phosphate salts, especially in diets with inverse calcium : phosphorus ratios. However, not all phosphorus sources contribute similarly to this effect. This review, which focuses on cats, summarizes the published evidence regarding phosphorus metabolism and homeostasis, including the relative impact of different dietary phosphorus sources, and their impact on the kidneys. No data currently shows that commercial cat foods induce renal injury. However, some diets contain high amounts of phosphorus relative to recommendations and some have inverse Ca : P ratios and so could increase the risk for development of kidney disease. While limiting the use of highly soluble phosphates appears to be important, there are insufficient data to support a specific upper limit for phosphate intake. This review also proposes areas where additional research is needed in order to strengthen conclusions and recommendations regarding dietary phosphorus for cats.
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A serum calcium-phosphorus (sCaPP) product was assessed for prediction of survival in dogs affected with chronic kidney disease (CKD). Dogs (N = 150) were retrospectively studied and followed up to determine their lifespan using 25 healthy dogs as controls. Blood and urine analyses were performed and blood pressure was measured. The dogs were divided into groups according to sCaPP (higher or lower than 70 mg²/dL²) and International Renal Interest Society (IRIS) stage (IRIS 1-4). Shorter survival was observed with sCaPP > 70 mg²/dL² compared to dogs with sCaPP < 70 mg²/dL² [45.48 days (range: 5.8 to 149 days) versus 505.40 days (range: 113.31 to 539.52 days), mean (95% confidence interval); P ≤ 0.001 respectively]. Similarly, dogs with advanced IRIS stages showed higher levels of sCaPP [mean (95% confidence interval) in mg²/dL²; IRIS 1: 42.83 (range: 29.58 to 62.10); IRIS 2: 63.18 (range: 46.34 to 90.09); IRIS 3: 95.57 (range: 88.34 to 127.19); IRIS 4: 130.38 (range: 125.16 to 153.52)], accompanied by lower survival rates. Therefore, sCaPP could represent a valuable tool in the prognosis of canine CKD. Copyright and/or publishing rights held by the Canadian Veterinary Medical Association.
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Meat in kibble petfood Quite some dog and cat owners feed dry kibble because of convenience and economy while believing that meat-based diets are the natural and healthy way. They look for kibble foods with meat as the number one, most abundant ingredient. However, both character and quantitative impact of the first meaty ingredient are difficult to assess. Compared to dry ingredients, moist ones generally contribute less nutrition as their considerable water fraction is without nutrients. High-meat dry foods usually contain rendered meal rather than meat. Rendering involves cooking of slaughter by-products, thereby separating fat, and drying the remaining material into poultry, meat or fish meal. Certain petfood marketing and advertising, rating sites and online writings disseminate that animal meal is unnatural and unhealthy. This has fueled the dry market segments of raw freeze-dried, raw-infused kibble and raw-included kibble products. As the three product groups are manufactured foods, raw is a contradiction in terms: it cannot stand for unprocessed, unprepared or fresh. Raw-infused dry foods represent a combination of kibble plus freeze-dried meat(y) pieces. The ingredient panels of raw-included kibbles normally list both (fresh) meat and animal meal. A few kibble foods tout the absence of (poultry) by-product or animal meal, implying that fresh is superior to rendered. Both the meal and meat(y) ingredients pass the extrusion cooking and drying procedures to finish dry kibbles. Animal meal is rendered and meaty constituents also undergo various forms of pretreatment. The two types of animal ingredients have highly variable qualities that are not given by the food's ingredient list. For details owners should contact the manufacturer. There is no evidence that well-formulated meal-and meat-based foods have differential effects on pet health. Meal and meat Rendered meals are universally used as protein sources for extruded dry petfood. In the ingredient lists, the word meal has prefixes such as animal, by-product, meat, poultry or fish. Meals are also named by species origin (chicken, duck, beef, lamb, salmon etc), with or without meal as noun. Meals are derived from tissues of farm mammals and fowl, exclusive of avoidable hair or feathers. By-products refer to clean carcass parts other than meat: muscle with accompanying structures. Raw-included kibble foods are made by introducing wet animal ingredients into the extruder barrel. Commonly used insertion forms are refrigerated, pumpable meaty slurries. The protein level in the final food may be increased by supplementing slurries with (partially) dehydrated or hydrolysed, concentrated animal ingredients. Other insertion forms are cooked slurry or ground frozen meaty blocks. Details of the methods and materials are not found in end-product communications. Ingredient list
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In cats with chronic kidney disease (CKD), the most common histopathologic finding is tubulointerstitial inflammation and fibrosis. However, these changes reflect a nonspecific response of the kidney to any inciting injury. The risk of developing CKD is likely to reflect the composite effects of genetic predisposition, aging, and environmental and individual factors that affect renal function over the course of a cat's life. However, there is still little information available to determine exactly which individual risk factors predispose a cat to develop CKD. Although many cats diagnosed with CKD have stable disease for years, some cats show overtly progressive disease.
Chapter
The parathyroid glands generally consist of four small oval disks with a diameter of 1 to 5 mm. The two largest parathyroids arise from the fourth branchial pouches and remain almost stationary during embryonic development, accounting for their final location at the cranial pole of the thyroid (Fig. 9–1). Two smaller parathyroids are usually located beneath the thyroid capsule, embedded at various depths near the caudal thyroid pole. They develop from the third branchial pouches in association with the thymus; migration with the descent of the thymus may give rise to ectopic parathyroid tissue.
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Nephron is a functional unit composed of a glomerulus and its associated renal tubule, and the kidneys are composed of thousands of nephrons. The kidneys have an intrinsic ability to autoregulate blood flow, permitting a relatively constant blood flow despite variations in arterial perfusion pressure. Glomerular filtration rate (GFR) and renal blood flow (RBF) are maintained when mean arterial pressure ranges between 80 and 180 mmHg. Acute kidney injury is characterized by an insult to the kidneys that results in a rapid decline in GFR, with the resultant accumulation of nitrogenous waste products such as blood urea nitrogen (BUN) and creatinine. The use of proper, established dosages for drugs is essential. Diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), ACE inhibitors, and other vasodilator drugs should be used with caution in patients with suspected hypovolemia or renal disease.
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A 7-year-old spayed female English Cocker Spaniel dog presented with polyuria (PU), polydipsia (PD), intermittent vomiting, and weight loss. Physical examination revealed pale, tacky mucous membranes and severe emaciation. Hematological and biochemical examinations revealed moderate normocytic normochromic non-regenerative anemia and moderate azotemia. Abdominal ultrasonography demonstrated bilaterally small lumpy-bumpy kidneys with hyperechoic parenchyma as well as loss of renal corticomedullary junction. Based on clinical history and examinations, the dog was diagnosed with chronic kidney disease (CKD). The dog was treated with supportive care including fluid therapy, phosphate-binding agent, and histamine H2-receptor antagonist. Darbepoetin Alfa was administered to control renal secondary non-regenerative anemia. Prescribed diet with low-protein and low-phosphorus was fed to alleviate CKD signs. Further, dietary probiotics were supplemented. This case demonstrates that oral probiotic supplementation helped reduce blood urea-nitrogen (BUN) levels. This case indicates that dietary probiotics can be a potential alternative therapeutic agent for management of renal failure.
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This article describes nutritional assessment for geriatric patients and addresses some nutrient sensitive conditions common in older dogs and cats. The goal of completing a nutritional assessment is to identify the presence and significance of factors that put patients at risk for malnutrition. Dietary recommendations for geriatric patients should take into account the needs of the patient and client preferences as well as economics. Changes in feeding management should be considered a part of total patient management. As with any aspect of medical management, the patient should be reevaluated at appropriate intervals to assure achievement of desired results.
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Chronic kidney disease (CKD) is a common medical condition of ageing cats. In most cases the underlying aetiology is unknown, but the most frequently reported pathological diagnosis is renal tubulointerstitial fibrosis. Renal fibrosis, characterised by extensive accumulation of extra-cellular matrix within the interstitium, is thought to be the final common pathway for all kidney diseases and is the pathological lesion best correlated with function in both humans and cats. As a convergent pathway, renal fibrosis provides an ideal target for the treatment of CKD and knowledge of the underlying fibrotic process is essential for the future development of novel therapies. There are many mediators and mechanisms of renal fibrosis reported in the literature, of which only a few have been investigated in the cat. This article reviews the process of renal fibrosis and discusses the most commonly cited mediators and mechanisms of progressive renal injury, with particular focus on the potential significance to feline CKD.
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Standard therapy forms the basic foundation for care of dogs with glomerular disease, as it is herein recommended for use in all affected animals regardless of causation of the disease. Consensus recommendations target the evaluation and management of proteinuria, inhibition of the renin-angiotensin-aldosterone system, modification in dietary intake with special consideration for those nutrients with renal effects, diagnosis and treatment of systemic hypertension, and evaluation and management of body fluid volume status in dogs with glomerular disease.
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There is strong scientific evidence to support the use of dietary management in chronic kidney disease (CKD) in dogs (Roudebush and others 2010) and prepared therapeutic diets are available, however, veterinarians are often asked to endorse homemade diets instead. Homemade recipes are usually computer-generated (Remillard and Crane 2010), and to the authors knowledge, feeding trials to establish that they are complete and suitable for long-term feeding have not been conducted, nor have controlled, randomised clinical trials to prove efficacy in dogs with CKD. Recipes for home-prepared diets intended for dogs with CKD have been evaluated using computer software (Larsen and others 2012), and it was concluded that they result in highly variable and often inappropriate diets, and that many recipes would not meet the nutritional and clinical needs of individual patients. Variability in content could also occur depending on raw ingredients selected for inclusion and methodology used to make the food. Study hypothesis: Homemade rations prepared by several people in accordance with a set recipe would have similar content making them reliable for the management of canine CKD. Aim: To determine whether veterinary nurses following a homemade recipe would construct diets with similar analyses. Six veterinary nurses were asked to prepare a homemade diet according to a formula with a declared analysis (Table 1) that has been widely distributed and recommended by veterinarians for dogs with CKD (Elliott and …
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Dietary protein exerts a significant calciuretic effect. A twofold increase in protein at constant levels of calcium and phosphorus intakes causes a 50% increase in urinary calcium. The protein-induced hypercalciuria results primarily from decreased fractional renal tubular reabsorption of calcium associated with catabolism of excess sulfur amino acids and the resultant urinary excretion of acid and sulfate. A protein-induced elevation in glomerular filtration rate also contributes to the calciuresis. Dietary phosphorus also modifies the calciuretic effect of proteins, as it increases renal tubular reabsorption of calcium and thereby exerts a hypocalciuretic effect. Consequently, a soy-based diet was able to maintain calcium balance at a calcium intake of 457 mg/day in spite of a protein intake of 90 g, presumably due to the lower level of sulfur amino acids in the soy diet and to the 1450 mg phosphorus which accompanied the soy protein.
Chapter
The majority of patients with chronic renal failure (CRF) undergoing hemodialysis treatment is shown to have hypertriglyceridemia and a high frequency of premature morbidity and mortality from cardiovascular disease1.
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A chronic renal disease was induced by 5/6 nephrectomy in young adult Wistar albino male rats. Groups of 3 rats were killed at varying time intervals from 10 to 50 weeks after nephrectomy, and the glomerular structure was studied by light and electron microscopy. By light microscopy, increase in glomerular size and hypertrophy of the visceral glomerular epithelial cells were evident as early as the tenth week. Significant degree of glomerular hyalinization started on the 25th week and gradually became more extensive in involvement towards the 50th week. By electron miscroscopy, the hypertrophied glomerular epithelia showed many osmiophilic bodies and vacuoles in their cytoplasm and fusion of foot processes. Beginning on the 30th week, increase of the mesangial matrix was quite evident, and endothelial and epithelial cells disappeared from the areas where the increase was prominent. The increased matrix gradually encroached and occluded capillary lumina and Bowman's space, leading to a formation of obsolescent glomeruli. Whether or not these glomerular changes are due to the glomerular hyperfiltration which has been known to occur after 5/6 nephrectomy remains to be elucidated.
Article
Abnormalities in the function of the central nervous system exist in chronic renal failure (CRF) and some of these derangements may be related to excess parathyroid hormone (PTH) which causes a rise in brain calcium. The latter may affect metabolism of neurotransmitters such as norepinephrine (NE) in brain synaptosomes. We measured NE content, uptake and release in brain synaptosomes of CRF rats and studied whether excess PTH affects these parameters. Synaptosomes from rats with 21 days of CRF compared to those from normal animals have higher calcium content (11.4 +/- 0.92 vs. 7.1 +/- 0.50 nmol/mg protein, P less than 0.01) and lower Na-K ATPase activity (6.5 +/- 0.81 vs. 11.4 +/- 0.76 mumol Pi/mg protein/hr, P less than 0.01). NE content (11.0 +/- 0.60 vs. 13.6 +/- 0.55 pmol/mg protein/hr, P less than 0.01), uptake (46 +/- 4.5 vs. 110 +/- 5.9 pmol/mg protein times 50 min, P less than 0.01) and release (2.0 +/- 0.2 vs. 5.1 +/- 0.47 pmol/mg protein times 10 min, P less than 0.01). Parathyroidectomy (PTX) in CRF rats kept normocalcemic reversed these abnormalities in brain synaptosomes; indeed calcium content, Na-K ATPase activity and NE content, uptake and release in synaptosomes from PTX-CRF rats were not different from those seen in normal rats.(ABSTRACT TRUNCATED AT 400 WORDS)
Article
Compensatory growth of the kidney (CRG), the growth response on the part of the remaining renal tissue following loss of some of it, has been the subject of numerous symposia and reviews. Rather than limiting this review to a simple marshalling of experimental results, I have sought an overview of CRG as a process which is but one of a number of growth responses of the kidney and of other organs as well.
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Twelve male cats were fed 2 diets that differed in the source of P. In diet 1 (14% P), 62.7% of P originated from poultry, meat, and fish meal, and the remainder from other organic ingredients of food. In diet 6 (1.6% P), 63.5% of P was derived from neutral monobasic/dibasic salts, and the remainder from other organic ingredients of the food. The P intake was nearly the same with both diets, but there was a significant ( P < 0.05) difference between diets in the percentage of ingested P that was excreted in the urine (14.7 ± 5.3% for diet 1; 34.9 ± 8.4% for diet 2), and in 6-day urinary P excretion (774 ± 290 mg for diet 1; 2,004 ± 556 mg for diet 2). The P concentrations in urine samples obtained by cystocentesis after cats ate were significantly ( P < 0.05) higher when cats were fed diet 2 than when those same cats were fed diet 1. Plasma P concentrations increased after ingestion of diet 2, but were unchanged after ingestion of diet 1. Seemingly, urinary excretion of P was markedly influenced by dietary composition. Diets with the same P content have potential for different biologic effects because of differences m availability of P.
Article
Renal failure was induced in 15 normal Beagle dogs by ligation of approximately 5/6 of the renal arteries of the left kidney and contralateral nephrectomy in order to determine how: (a) 11/12 reduction in total renal mass influences urine protein excretion and renal morphology in dogs, and (b) dietary protein intake influences renal function, urine protein excretion, and renal morphology in canine renal failure. Dogs were fed a reduced protein diet for 12 weeks after induction of renal failure, while compensatory renal hypertrophy developed. Renal function was then evaluated and dogs were distributed into 2 groups with approximately equal degrees of renal dysfunction. One group was fed a high protein diet (42% protein) and a second group was fed moderately restricted protein diets (18% protein). After 8 weeks, renal function, magnitude of proteinuria, and renal morphology were re-evaluated. Inulin clearance increased in all dogs fed the 42% protein diet and 3 of 10 dogs fed the 18% protein diets. Proteinuria was significantly greater in dogs fed the high protein diet than dogs fed the reduced protein diets. Compared with previously nephrectomized contralateral control kidneys, glomerular sclerosis and renal interstitial lesions had developed in all dogs, regardless of severity of renal dysfunction or diet fed. Although reduced dietary protein intake did not prevent development of renal lesions, renal lesions were significantly more severe in the 5 dogs fed the 42% protein diet and 3 dogs fed the 18% protein diets in which inulin clearance increased, than in 7 dogs fed the reduced protein diets in which inulin clearance did not increase.
Article
Following 5/6 nephrectomy, 18 rats were fed a normal diet. After 30 days, serum creatinine (SCr), urine protein excretion and urine volume were increased compared to pre-nephrectomy (0.27 +/- 0.1 vs. 1.62 +/- 0.6 mg/deciliter, 17.0 +/- 10.3 vs. 257.6 +/- 13.4 mg/24 hr, and 16.6 +/- 4.4 vs. 39.2 +/- 11.7 ml/24 hr, respectively, all P less than 0.001). At this time, when serum phosphorus (SPi) and serum calcium (SCa2+) were normal, the rats were separated into two groups, matched and paired by body weight and SCr, and housed separately in metabolic cages. Animals of one group ingested a normal diet supplemented with dihydroxyaluminum aminoacetate (DHAAA), 15 g%, to induce phosphate depletion (PD). The second group ingested the same diet supplemented with 7.5% glycine and was the phosphate replete (PR) group. All rats were pair fed throughout the study to maintain similar caloric, protein, carbohydrate, vitamin, and mineral intakes. At six weeks after separation, SPi was decreased in PD vs. PR group (2.85 +/- 0.8 vs. 6.71 +/- 1.2 mg/deciliter, P less than 0.001) and SCa2+ was increased in the PD group (11.98 +/- 0.7 vs. 10.03 +/- 0.7 mg/deciliter, P less than 0.001). Urine urea nitrogen, body weight, and sodium, potassium and solute excretion were similar between the groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Article
It has been proposed that ingestion of large amounts of dietary protein leads to sustained renal hyperperfusion and progressive glomerulosclerosis in rats. This hypothesis was tested in dogs, with 75% reduction in renal mass, maintained for 4 years on either 56, 27, or 19% dietary protein. Twelve of 21 dogs survived 4 years, and death due to renal failure was not correlated to diet. Dogs fed 56 and 27% protein had increased GFR and CPAH before and after reduction of renal mass compared to the 19% group. A pattern of deterioration of renal function, including proteinuria, was not found in any diet group. Nine of 11 dogs, fed 56, 27, or 19% protein had minimal glomerular lesions, including mesangial proliferation, GBM irregularities, adhesions, and sclerosis. Two other dogs, fed 56% protein, had more severe glomerular lesions. No significant ultrastructural differences were found in glomeruli among the three diet groups. These results do not support the hypothesis that high protein feeding had a significant adverse effect on either renal function of morphology in dogs with 75% nephrectomy.
Article
To determine whether the proteinuria, glomerular sclerosis, and decline in glomerular filtration rate (GFR) described in rodents after renal mass reduction develop in another species, 24-hour proteinuria, glomerular structure, and fasting and postfeeding GFR were examined in dogs subjected to seven-eighths reduction in renal mass. All dogs were fed a diet containing 26% protein. Six dogs with a GFR less than 10 ml/min (8% to 17% of control two-kidney GFR) were killed within 6 months after renal mass reduction. Twenty-four-hour urinary protein excretion was modestly although definitely increased (236 +/- 26 mg/24 hr, P less than 0.01). All remnant kidneys demonstrated structural changes of mesangial hyperplasia or focal glomerular sclerosis. Ten dogs with a remnant kidney and early GFRs 16% to 39% of control values were followed for 18 to 39 months. In seven dogs, GFR showed little tendency to decrease with time. In one of them, proteinuria was 106 mg/24 hr with normal-appearing glomeruli at 14 months. In three dogs, proteinuria was progressive, averaging about 1 gm/24 hr at 18 months and 2 gm/24 hr at 24 to 34 months; glomerular pathologic findings progressed from focal mesangial hyperplasia or focal glomerular sclerosis at 8 to 16 months to focal and segmental sclerosis or diffuse glomerular obsolescence at 25 to 34 months; and fasting GFR progressively declined starting at 21 to 24 months after renal mass reduction.(ABSTRACT TRUNCATED AT 250 WORDS)
Article
Healthy mixed-bred dogs of both sexes had renal mass surgically reduced and were allowed 2 to 3 months for hypertrophy of the remnant kidney. They were then allotted into 3 groups with equal renal function and were fed 1 of 3 diets that differed in composition. Group 1 dogs (n = 6) were fed moist food that contained 50% protein, 2.34% Ca, and 1.64% P with a P-binding agent (basic aluminum carbonate gel) added. Group 2 dogs (n = 6) were fed a dry diet that contained 24.5% protein, 1.26% Ca, 1.21% P, and the same P-binding agent as used for group 1. Group 3 dogs (n = 7) were fed a moist diet that contained 16.1% protein, 0.38% Ca, and 0.3% P without a P-binding agent. Each group was fed its diet for 92 days and monitored for responses. Mortality associated with uremia occurred in 2 of 6 group 1 dogs, 0 of 6 group 2 dogs, and in 2 of 7 group 3 dogs. Among survivors, clinical signs were seen in the more azotemic dogs of group 1, but not in dogs of groups 2 and 3. The blood urea nitrogen, plasma P concentrations, and PCV values were most favorable in group 3 and least favorable in group 1. Marked differences between groups were not seen in plasma concentrations of protein, albumin, or Ca or in plasma alkaline phosphatase activity. Values for glomerular filtration rate did not change in any group during the experiment.(ABSTRACT TRUNCATED AT 250 WORDS)
Article
The mechanisms responsible for the adaptive increase in glomerular filtration rate (GFR) following unilateral nephrectomy were studied in mutant Wistar rats having accessible surface glomeruli. Pressures and flows were measured in single glomeruli of the left kidney 2-4 wk after right nephrectomy and in a normal hydropenic control group. Following uninephrectomy, whole kidney GFR and kidney weight increased in proportion (by about 40%); these increases were accompanied by uniform increases in superficial cortical single nephron (SN) GFR and glomerular plasma flow (GPF). As in control rats, filtration pressure equilibrium was observed after uninephrectomy. Mean transcapillary hydraulic pressure difference (ΔP) increased from 34 to 40 mmHg. The ultrafiltration coefficient [K(f)], the product of effective hydraulic permeability and capillary surface area, was determined in uninephrectomized rats under conditions designed to prevent the achievement of filtration pressure equilibrium (2% plasma loading). K(f) was found to be identical, on the average, to the value recently reported for rats with intact kidneys. The findings suggest that the adaptive increase in single nephron glomerular filtration rate (SNGFR), nl/min, following uninephrectomy results primarily from increases in GPF and mean ΔP, with the increase in GPF accounting for approximately three-fourths of the increase in SNGFR.
Article
Myocardiopathy is common in uremia, but its cause in unknown. Excessive entry of calcium in heart cells by catecholamines has been shown to cause necrosis of myocardium. The high blood levels of parathyroid hormone (PTH) in uremia may also enhance entry of calcium into heart cells and exert deleterious effects on the heart. We examined the effect of PTH on rat heart cells grown in culture. Both amino-terminal (1-34) PTH and intact (1-84) PTH, but not the carboxy-terminal (53-84) PTH produced immediate and sustained significant rise in beats per minute and the cells died earlier than control. The effect was reversed if PTH was removed from medium, and was abolished by inactivation of the hormone. There was a dose-response relationship between both moieties of PTH and the rise in heart beats, but the effect of 1-84 PTH was significantly greater than that of 1-34 moiety. PTH stimulated cyclic AMP production within 1 min, and cyclic AMP remained significantly elevated thereafter. The effect of PTH required calcium, was mimicked by calcium ionophore, was prevented by verapamil and was not abolished by alpha- or beta-adrenergic blockers. PTH action was additive to phenylephrine and synergistic with isoproterenol. Sera from uremic parathyroidectomized rats did not effect heart beats, but sera from uremic rats with intact parathyroid glands or from uremic-parathyroidectomized rats treated with PTH had effects similar to PTH. Data indicate that (a) heart cell is a target organ for PTH and may have receptors for the hormone; (b) PTH increases beating rate of heart cells and causes early death of cells; (c) PTH effect appears to be due to calcium entry into heart cells; (d) the locus of action through which PTH induces calcium entry is different from that for catecholamines; and (e) uremic serum has no effect unless it contains PTH. Data suggest that myocardial damage may occur in uremia due to prolonged exposure to very high blood levels of PTH, and assign new dimensions to PTH toxicity in uremia.
Article
The influence of a maintenance diet containing 44.4% dry weight protein and 2 reduced protein diets containing 8.2% and 17.2% dry weight protein on morbidity, mortality, and renal function of dogs with induced chronic renal failure was studied for 40 weeks. The diets differed in mineral and electrolyte composition in addition to differences in protein, carbohydrate, and fat content. Dogs fed the 44.4% protein diet had a higher mortality (6 of 11) than did dogs fed the 8.2% (1 of 6) or 17.2% (0 of 6) protein diets. Dogs fed the 44.4% protein diet died of uremic complications. An occlusive portal vein thrombus caused death of the nonsurvivor fed the 8.2% protein diet. Clinical signs of uremia were detected only in nonsurvivors fed the 44.4% protein diet. Surviving dogs fed the maintenance diet were less active and had poorer hair than did dogs fed reduced protein diets. Inulin clearance rate and urinary protein excretion were lower in most dogs fed reduced protein diets than in dogs fed the maintenance diet. Despite the greater decrease in renal function, serum urea nitrogen concentrations were markedly lower in dogs fed the 8.2% and 17.2% protein diets than in dogs fed the 44.4% protein diet. Seemingly, the reduced protein renal failure diets were of benefit in preventing or reducing morbidity and mortality associated with the uremic syndrome and in reducing serum urea nitrogen concentrations as compared with that of the higher protein diet. The potential benefits of dietary protein restriction in dogs with chronic renal failure prevailed over potential adverse affects of excessive protein consumption.
Article
Male Sprague-Dawley rats were rendered uremic by surgical removal of 70% of functioning renal mass. This produced a rapid threefold rise in serum creatinine to 0.87 +/- 0.067 (SEM) mg/dl at 2 weeks postoperatively which declined subsequently to a value of 0.64 +/- 0.06 (SEM) and remained stable thereafter for an additional 4 weeks in animals maintained on a diet with normal phosphate content. Increase of dietary phosphate content to 2.2% at 2 weeks after surgery produced a significant and progressive increase in serum creatinine to values fourfold higher than the mean values in comparable partially nephrectomized control animals maintained on a diet with normal phosphate content (P less than 0.001). This deterioration in renal function was associated with extensive nephrocalcinosis, tubular dilatation, cellular necrosis, and marked interstitial inflammation. 3-phosphocitric acid, a compound which has been shown to prevent calcium phosphate crystal growth as well as to prevent in vivo nephrocalcinosis, was very effective in preventing this phosphate-induced deterioration of renal function and in preventing any significant increase in renal calcium content in animals fed a high phosphate diet. This compound was also effective in preventing the renal histologic changes associated with phosphate-induced uremia.
Article
Inhibitors of erythropoiesis have been found in the blood of uremic patients but their nature has not been identified. These patients have excess blood levels of parathyroid hormone (PTH) and it is possible that PTH inhibits erythropoiesis. The present study was undertaken to examine the effect of intact PTH molecules and some of its fragments on human peripheral blood and mouse bone marrow burst-forming units-erythroid (BFU-E), on mouse bone marrow erythroid colony-forming unit (CFU-E), and granulocyte macrophage progenitors (CFU-GM), and evaluate the interaction between PTH and erythropoietin (Ep) on human BFU-E. Intact PTH (1-84 bPTH) in concentrations (7.5-30 U/ml;) comparable to those found in blood of uremic patients produced marked and significant (P less than 0.01) inhibition of BFU-E and mouse marrow GFU-GM, but not of mouse marrow CFU-E. Inactivation of 1-84 bPTH abolished its action on erythropoiesis. Increasing the concentration of Ep in the media from 0.67 to 1.9 U/ml overcame the inhibitory effect of 1-84 bPTH on BFU-E. The N-terminal fragment of PTH (1-34 bPTH) and 53-84 hPTH had no effect on BFU-E. The results demonstrate that (a) either the intact PTH molecule or a C-terminal fragment(s) bigger than 53-84 moiety exerts the inhibitory effect on erythropoiesis, and (b) adequate amounts of Ep can overcome this action of PTH. The data provide one possible pathway for the participation of excess PTH in the genesis of the anemia of uremia.
Article
Micropuncture studies were performed in three groups of male Munich-Wistar rats 1 wk after surgery: group I, eight control rats that underwent laparotomy and were fed a normal diet; group II, nine rats that underwent right nephrectomy and segmental infarction of five-sixths of the left kidney and were fed a normal diet; and group III, seven rats that underwent the same renal ablative procedure and were fed a low protein diet. Single nephron glomerular filtration rate (SNGFR) was higher in the remnant kidney of group II rats compared with group I rats due to higher average values for mean glomerular transcapillary hydraulic pressure difference (delta P) and initial glomerular plasma flow rate (QA) in group II. Glomeruli in remnant kidneys of group II showed striking alterations in morphology, including epithelial cell protein reabsorption droplets, foot process fusion, and mesangial expansion. Group III rats demonstrated a mean SNGFR not statistically different from that of group I, but significantly less than that of group II rats. This lack of absolute hyperfiltration in remnant glomeruli of group III rats relative to group I obtained because QA and delta P did not increase above values found in group I. The glomerular structural lesions seen in group II were also largely attenuated in group III. These studies demonstrate that alterations in glomerular hemodynamics associated with renal ablation are accompanied by structural lesions and suggest that sustained single nephron hyperfiltration may have maladaptive consequences by damaging remnant glomeruli.
Unauthenticated | Downloaded 01/25/24 01:56 PM UTC
Unauthenticated | Downloaded 01/25/24 01:56 PM UTC Nutr 1988 ; 118 :1210-1216.