Correction of Hyperkalemia in Dogs with Chronic Kidney Disease Consuming Commercial Renal Therapeutic Diets by a Potassium‐Reduced Home‐Prepared Diet

Background: Hyperkalemia occurs in dogs with chronic kidney disease (CKD). Objectives: (1) To determine the incidence of hyperkalemia in dogs with CKD, (2) to determine the proportion of hyperkalemic dogs that required modification of dietary potassium intake, (3) to evaluate the response to dietary modification. Methods: The hospital database was reviewed retrospectively to identify dogs with CKD and persistent (>5.3 mmol/L on at least 3 occasions) or severe (K ≥ 6.5 mmol/L) hyperkalemia while consuming a therapeutic renal diet. Records of dogs with hyperkalemia that were prescribed a home‐prepared, potassium‐reduced diet were evaluated further. Response was evaluated by changes in body weight, BCS, and serum potassium concentration. Results: One hundred and fifty‐two dogs were diagnosed with CKD, of which 47% had ≥1 documented episode of hyperkalemia, 25% had ≥3 episodes of hyperkalemia, and 16% had ≥1 episodes of severe hyperkalemia (K > 6.5 mmol/L). Twenty‐six dogs (17.2%) with CKD and hyperkalemia were prescribed a potassium‐reduced, home‐prepared diet. The potassium concentration of all hyperkalemic dogs on therapeutic diets (potassium content, 1.6 ± 0.23 g/1,000 kcal of metabolizable energy [ME]) was 6.5 ± 0.5 mmol/L but decreased significantly to 5.1 ± 0.5 mmol/L in 18 dogs available for follow‐up in response to the dietary modification (0.91 ± 0.14 g/1,000 kcal of ME, P < .001). Potassium concentration normalized in all but 1 dog. Conclusions and Clinical Importance: Hyperkalemia is a potential complication of CKD. In a subset of CKD dogs, hyperkalemia can be associated with commercial renal diets and could restrict use of these diets. Appropriately formulated, potassium‐reduced, diets are an effective alternative to correct hyperkalemia.     

Hyponatremia and hyperkalemia associated with idiopathic or experimentally induced chylothorax in four dogs

Two dogs with idiopathic chylothorax and 2 dogs with experimentally induced (ie, ligation of the cranial vena cava) chylothorax were treated by intermittent thoracic drainage. Of these 4 dogs, 3 that did not have evidence of renal failure had normal or near-normal serum sodium and potassium concentrations before thoracic drainage began, and all 3 developed repeatedly marked hyponatremia and hyperkalemia during thoracic drainage. Another dog became weak and depressed, ostensibly because of hyperkalemia. Serum sodium and potassium concentrations in 1 dog with spontaneous chylothorax returned to normal after chylothorax resolved and thoracic drainage was stopped. The other 3 dogs died or were euthanatized, and the effect of stopping thoracic drainage could not be evaluated. In 3 dogs in which it was measured, normal-to-high plasma cortisol concentration was observed before and after adrenocorticotropin administration, and 2 dogs also had hyperaldosteronemia. Hyponatremia was hypothesized to be caused by sodium loss via thoracic drainage whereas hyperkalemia may have been multifactorial in origin, but probably was attributable, at least, in part to decreased renal potassium clearance.     

Severe whipworm infection in the dog

Three dogs with trichuriosis were presented because of depression, anorexia and severe dehydration following a period of chronic diarrhoea, Systemic signs attributable to hypovolaemia and acid-base and electrolyte disturbances resolved following intravenous fluid therapy, although diarrhoea persisted until appropriate anthelmintics were administered. Whipworm infection may sometimes give rise to a life-threatening dehydration syndrome associated with hyponatremia, metabolic acidosis and hyperkalemia.     

Effects of asphyxia and potassium on canine and feline electrocardiograms.

The effects of asphyxia and potassium on the electrocardiogram (ECG), lead II, were recorded from dogs and cats anesthetized with sodium pentobarbital and halothane. Electrocardiographic recordings were made during control periods, during asphyxia (occluded endotracheal tube), during infusion of an isotonic KCl solution and during infusion of an isotonic NaCl solution. Arterial and venous blood gas partial pressures (PaCO2, PvCO2, PaO2 and and PvO2), plasma Na+ and K+ concentrations, heart rate and mean arterial blood pressure were measured during control periods, asphyxia and during the periods of infusion. The vagi were severed to assess the effect of vagal tone on the ECG changes. The characteristic ECG changes during asphyxia and the electrolyte imbalances resulting from infusion of isotonic KCl and NaCl were determined during sodium pentobarbital and halothane anesthesia in both dogs and cats. The combination of halothane and high PCO2 caused cardiac arrhythmias. Spontaneous recovery from ventricular fibrillation, as a result of hyperkalemia, was recorded from cats. Disappearance of the P waves, which is characteristic of hyperkalemia, was infrequent in this study and the U waves associated with hypokalemia were not found. Severing the vagi did not alter the ECG changes characteristic of asphyxia, hyperkalemia and hypokalemia. It was found that asphyxia and infusion of fluids high or low in potassium can produce ECG changes in both dogs and cats that can be correlated with blood gas partial pressure changes or plasma potassium concentrations.     

Electrocardiographic assessment of hyperkalemia in dogs and cats

Objective: To determine if electrocardiogram (ECG) changes induced by hyperkalemia in clinical patients correspond with previously reported changes in experimental animals. Design: Prospective clinical study. Setting: Two private practice 24‐hour emergency and critical care facilities. Animals: Fifteen dogs and 22 cats with serum potassium levels >5.5 mEq/L. Interventions: None. Measurements: The following data were collected when hyperkalemia was documented: ECG (n=37), sodium and chloride (mEq/L) (n=35), total magnesium (mg/dL) (n=18), total calcium (mg/dL) (n=30), and venous pH (n=18). Animals were divided into five groups based on severity of hyperkalemia and ECG interpretation included rate, rhythm and P‐QRS‐T evaluation. Main Results: Twenty‐two of 37 (59%) of the ECGs were normal or revealed abnormalities that have not been previously described in conjunction with hyperkalemia. In dogs, there was no correlation (r=0) between potassium blood levels and heart rate (n=15). There was weak correlation (r=0.40; P=0.06) between potassium blood levels and heart rate in cats (n=22). The correlation was stronger (r=0.64; P<0.05) when data were compared in cats with serum potassium level >8.5 mEq/L (Groups 4 and Group 5; n=11). Conclusions: ECGs obtained from ill dogs and cats with hyperkalemia are inconsistent with ECGs from experimentally induced hyperkalemia. It is difficult to determine the clinical relevance of heart rate differences between cats with serum potassium levels >8.5 mEq/L and animals with experimentally induced hyperkalemia; this may be due to the presence of other biochemical abnormalities in diseased animals.     

Combined hyponatremia and hyperkalemia mimicking acute hypoadrenocorticism in three pregnant dogs

Differential diagnoses for hyponatremia with concurrent hyperkalemia should include hypoadrenocorticism. Renal failure, chylothorax, and gastrointestinal tract disorders may also cause abnormally low serum sodium:potassium ratios. The ACTH stimulation test is the gold standard for diagnosis of hypoadrenocorticism.     

Clinicopathologic findings resembling hypoadrenocorticism in dogs with primary gastrointestinal disease

Nine dogs with primary gastrointestinal disease had clinical and laboratory findings resembling hypoadrenocorticism. The dogs had histories of anorexia, weakness or lethargy, diarrhea, vomiting, and weight loss. Hypothermia, dehydration, and emaciation also were detected on physical examination. Hyponatremia, hyperkalemia, and abnormally low Na/K ratios were found on laboratory evaluation, but results of ACTH-response tests were not compatible with hypoadrenocorticism. The primary diagnoses were trichuriasis and salmonellosis in 2 dogs, trichuriasis in 5 dogs, and perforated duodenal ulcer in 2 dogs. Most dogs responded to medical or surgical treatment of their primary gastrointestinal disease, and the original electrolyte abnormalities resolved. These findings emphasize the importance of the ACTH-response test in the diagnostic evaluation of dogs with clinicopathologic findings similar to those of hypoadrenocorticism.     

Muscle cramps in two standard poodles with hypoadrenocorticism

Two standard poodles were evaluated for painful, episodic muscle cramps affecting their thoracic and pelvic limbs. Both dogs had been diagnosed with hypoadrenocorticism and were being treated with fludrocortisone acetate and prednisone when evaluated for muscle cramps. However, the muscle cramping started approximately 1 month prior to the diagnosis of hypoadrenocorticism. Findings on general physical examination included lethargy and dehydration. Neurological examination was normal between episodes. Serum biochemical abnormalities included hyperalbuminemia, azotemia, hyponatremia, hypochloremia, and hyperkalemia. Altering treatment to desoxycorticosterone pivalate resolved the electrolyte abnormalities and the episodes of muscle cramping in both dogs. The authors conclude that hypoadrenocorticism can be associated with episodes of painful muscle cramping in standard poodles.     

Abnormalities of serum electrolyte concentrations in dogs with hypoadrenocorticism

BACKGROUND: The sensitivity and specificity of the sodium to potassium ratio (Na:K ratio) as a cutoff for recommendation of an adrenocorticotropic hormone (ACTH) stimulation test in dogs suspected of having hypoadrenocorticism (HA) is unknown. Additionally, abnormalities in plasma ionized calcium (iCa2+) and ionized magnesium (iMg2+) concentrations and venous pH of dogs with HA are incompletely documented. OBJECTIVES: To define the sensitivity and specificity of the Na:K ratio as a diagnostic aid for HA in dogs and to examine for associations between venous pH and the Na:K ratio, iCa2+ concentration, or iMg2+ concentration in dogs with HA. ANIMALS: Seventy-six dogs with HA and 200 dogs randomly selected from the general hospital population. METHODS: Retrospective study. Dogs were included in the study if results of an ACTH stimulation test confirmed a diagnosis of HA, the dog had a serum sodium concentration below the reference range or a serum potassium concentration above the reference range, and the dog was treated with mineralocorticoids. Receiver operating curve analysis was used to determine optimal cutoffs of sensitivity and specificity for the Na:K ratio in diagnosing HA. RESULTS: Use of Na:K ratios of 27 or 28 classified 95% of dogs correctly as diseased or not diseased. The sensitivity of a Na:K ratio of 28 was 93% (CI, 85-98%) and that of 27 was 89% (CI, 80-95%). The specificity of a Na:K ratio of 28 was 96% (CI, 92-98%) and that of 27 was 97% (CI, 93- 99%). The sensitivity and specificity of a Na:K ratio of 24 were 79% (95% CI, 67-86%) and 100% (98%, CI, 97%-100%), respectively. CONCLUSIONS AND CLINICAL IMPORTANCE: Na:K ratios of 27 or 28 identify the highest percentage of dogs with suspected mineralocorticoid and glucocorticoid deficiency correctly. In dogs with a Na:K ratio of 24 or less, the likelihood of confirming a diagnosis of HA with an ACTH stimulation test is high.     

Low ratios of sodium to potassium in the serum of 238 dogs

Serum sodium:potassium (Na:K) ratios are often reported in biochemical studies of dogs, although their value has not been assessed. The aims of this study were to identify diseases associated with a low Na:K ratio in dogs and to compare their prevalence with the prevalence in dogs from the same referral hospital with normal Na:K ratios. A total of 238 dogs with a Na:K ratio less than 27 were identified from medical records. Sample contamination with edta was suspected in 74 cases (31 per cent) and these and two cases that had been supplemented with potassium were removed from the analysis. The remaining 162 cases and 147 control dogs were divided into five categories depending on the organ system affected. Among the cases there were significantly more in the endocrine category than among the control dogs. Hypoadrenocorticism was the most single common cause of a low Na:K ratio and affected 27 (16.7 per cent) of the cases. Other clinical problems associated with low Na:K ratios included different urogenital, cardiorespiratory and gastrointestinal diseases.     

Nursing sickness in lactating mink (Mustela vison). II. Pathophysiology and changes in body fluid composition.

An investigation of the pathophysiological characteristics of nursing sickness in mink was carried out as a follow-up study of a previous epidemiological survey at a Danish fur research farm during the 1989 breeding season. In a total of 48 nursing females of the Standard Black and Pastel type, concentrations of several pertinent biochemical constituents of whole blood, plasma, urine and skeletal muscle were determined in order to identify nutritional and metabolic factors involved in the origin and development of the disease. Compared to the reference data obtained in 17 apparently normal lactating dams the findings in 31 females suffering from nursing sickness presented varying clinical and biochemical signs of progressive dehydration and emaciation: aldosteronism, hypovolemia, hyponatremia, hyperkalemia (in the face of muscle potassium depletion), hyperglycemia and azotemic acidemia. Neither ketosis nor severe lactacidemia was observed. The urine was almost devoid of sodium and chloride, and urinary potassium concentration diminished by approximately 50%. The concentrating ability of the kidneys was reduced to less than one third of the maximum value. The results were consistent with severe dehydration and emaciation due to heavy losses of energy, water and body mass along with increasing milk production. The progressive nature of the disease supported the hypothesis that nursing sickness is due to the combined effects of heavy milk production and excessive tissue catabolism along with reduced or ceased dietary intake, and maybe increasing environmental stress. In the advanced stage of the disease coma and death appear to be the inevitable outcome of the metabolic strains for continuing milk production.     

Retrospective evaluation of acute hyperkalemia of unknown origin during general anesthesia in dogs

ObjectiveTo report and characterize cases of acute hyperkalemia of unknown origin in dogs under anesthesia.Study designMulticentric retrospective clinical study.AnimalsMedical records of 19 client-owned dogs that developed acute hyperkalemia during anesthesia.MethodsAnesthetic records of dogs developing acute hyperkalemia from January 2015 to December 2022 were evaluated. Data collected included demographics, duration of anesthesia until the episode, electrolytes and blood gas measurements, electrocardiogram (ECG) abnormalities, drugs used as part of the anesthetic protocol, hyperkalemia treatment and outcome.ResultsA total of 13 cases met the inclusion criteria with documented acute hyperkalemia with no apparent underlying cause during anesthesia. Dogs were [mean ± standard deviation (range)] 6.5 ± 5.0 (3–10) years old and weighed 18.0 ± 14.3 (5.1–40.0) kg. All dogs were administered dexmedetomidine and an opioid as part of the premedication. All dogs had inhalation anesthesia of >60 minutes’ duration. The first clinical sign was bradycardia that was minimally responsive to anticholinergic administration and was often accompanied by moderate/severe hypotension. These signs were rapidly followed by ECG changes compatible with hyperkalemia and/or cardiac arrest. Rapid identification and treatment for hyperkalemia, with or without dexmedetomidine reversal, resulted in survival of 12 dogs and one fatality.Conclusions and clinical relevanceUnknown origin hyperkalemia is a life-threatening complication that can occur during general anesthesia. In healthy dogs, preanesthetic administration of dexmedetomidine in association with an opioid and followed by inhalation anesthesia of more than 1 hour duration may predispose to this complication. A sudden decrease in heart rate >90 minutes after dexmedetomidine administration, or ECG changes, may warrant measurement of blood potassium concentrations.     

Factitious Hyperkalemia in Dogs With Thrombocytosis

To determine the effect of platelet count on the accurate assessment of serum electrolyte concentrations, simultaneous platelet counts and electrolyte determinations were performed on serum and plasma from 40 dogs. Dogs were grouped according to platelet count as follows: thrombocytopenic (less than 150,000/microliters), normal (150,000 to 600,000/microliters), or thrombocytotic (greater than 600,000/microliters). Serum potassium concentration was significantly higher than plasma potassium concentration in normal dogs (mean difference, 0.63 +/- 0.17 mEq/l) and in dogs with thrombocytosis (mean difference, 1.55 +/- 0.73 mEq/l). This difference in potassium concentration between serum and plasma was positively correlated with platelet count (r2 = 0.86). In the blood of dogs with thrombocytosis, the serum-plasma potassium difference was further increased when the time period between blood collection and separation of serum or plasma from cells was lengthened. Differences between serum and plasma concentrations of sodium or chloride were not seen in any platelet group. These results suggest that a portion of the measured serum potassium concentration is released from platelets during the clotting process. In fact, profound elevations in serum potassium concentrations can occur factitiously in dogs with thrombocytosis. Therefore, the actual concentration of potassium in blood is determined more accurately by measuring the plasma concentration rather than the serum concentration of this electrolyte.     

Correlation of spurious potassium elevation and platelet count in dogs

Paired serum and plasma electrolyte determinations were measured on 26 dogs. The difference between plasma and serum electrolyte concentrations was compared to the platelet and leukocyte counts. An increase in serum potassium concentration over plasma potassium concentration was found which correlated linearly with the platelet count. No correlation with white cell count was found. A statistically significant increase in serum sodium concentration over plasma sodium concentration was also noted, however, this change did not correlate with the number of platelets or white cells. It is concluded that thrombocytosis, previously known to cause spurious elevation in serum potassium concentration in humans, can also do so in dogs and, presumably, other species.     

Electrolyte Disturbances in Foals with Severe Rhabdomyolysis

Marked electrolyte abnormalities characterized by profound hyperkalemia, hyponatremia, hypocalcemia, and hyperphosphatemia were noted in 4 neonatal foals with acute rhabdomyolysis and pigmenturia. In 2 foals, rhabdomyolysis developed 4–6 days after admission for dysmaturity, and in 2 foals, rhabdomyolysis was evident on presentation. Rhabdomyolysis was a consequence of selenium deficiency with or without vitamin E deficiency, possibly combined with increased oxidant stress due to sepsis or hypoxia and reperfusion injury after parturition. Foals gained from 7 to 15% of their initial body weight within 48 hours of developing rhabdomyolysis. Three of the foals developed cardiac arrhythmias characterized by spiked T waves and decreased-amplitude P waves. Postmortem examination of 2 foals revealed extensive myodegeneration and renal tubular nephrosis; renal cortical necrosis with myocardial necrosis was noted in 1 foal. Destruction of the major intracellular compartment (intracellular fluid [ICF]) through extensive myonecrosis combined, in some cases, with myoglobinuric renal insufficiency produced major fluid shifts and life-threatening electrolyte derangements. With the major ICF compartment disrupted, hyperkalemia was most effectively treated using mineralocorticoids, loop diuretics, and ion exchange resins to enhance elimination. In addition, IV calcium, glucose, insulin, and sodium bicarbonate were administered, which helped redistribute potassium to the ICE Severe rhabdomyolysis should be included in the differential diagnoses of hyperkalemia, hyponatremia, hypocalcemia, and hyperphosphatemia in neonatal foals.     

Clinical features and heritability of hypoadrenocorticism in Nova Scotia Duck Tolling Retrievers: 25 cases (1994-2006)

OBJECTIVE: To evaluate the clinical features and heritability of naturally occurring hypoadrenocorticism in Nova Scotia Duck Tolling Retrievers (NSDTRs). DESIGN: Retrospective case series. ANIMALS: 25 NSDTRs with hypoadrenocorticism. PROCEDURES: Questionnaires completed by owners of NSDTRs with hypoadrenocorticism and medical records from veterinarians were reviewed for information regarding diagnosis, age at diagnosis, concurrent diseases, age at death, and cause of death. Pedigrees were analyzed for heritability and mode of inheritance of hypoadrenocorticism (including complex segregation analysis of pedigrees of 1,515 dogs). RESULTS: On the basis of results of ACTH stimulation testing, hypoadrenocorticism was diagnosed in 16 female and 9 male NSDTRs (including 6 full siblings). Median age at diagnosis was 2.6 years; the diagnosis was made prior to 2 years of age in 11 dogs. Seventeen dogs had hyponatremia, hyperkalemia, or both, and serum electrolyte concentrations were within reference ranges for 8 dogs at the time of diagnosis. Median survival time after diagnosis for 4 dogs that died or were euthanized as a result of medical causes was 1.6 years. Heritability was calculated at 0.98 with no sex effect, and complex segregation analysis fit a major gene model with an autosomal recessive mode of inheritance. CONCLUSIONS AND CLINICAL RELEVANCE: In NSDTRs, hypoadrenocorticism was diagnosed at an earlier age, compared with published reports of age at diagnosis among the general dog population. Among the study dogs, 32% had no serum electrolyte abnormalities at the time of diagnosis, and the disease appeared to have an autosomal recessive mode of inheritance in the breed.     

Influence of combined angiotensin-converting enzyme inhibitors and spironolactone on serum K, Mg, and Na concentrations in small dogs with degenerative mitral valve disease

ObjectiveTo determine if the administration of an angiotensin-converting enzyme inhibitor (ACEI) plus spironolactone caused hyperkalemia, hypermagnesemia, or hyponatremia in elderly small dogs with degenerative mitral valve disease (MVD).BackgroundACEIs and spironolactone can increase serum potassium and magnesium concentrations and lower serum sodium concentrations. It has been recommended to either not combine these drugs or to do so with caution.Animals, material and methodsFifty client-owned dogs with MVD, left atrial dilation, and without congestive heart failure or azotemia were evaluated retrospectively. Baseline data sets, followed by 1–9 (mean = 2.66) data sets, comprised of serum urea nitrogen (SUN), creatinine, sodium, potassium, and magnesium concentrations, were tabulated. Each dog received an ACEI plus spironolactone for a mean of 23.8 ± 26.6 weeks (range: 2–150) and a median of 15 weeks. No cardiac drugs other than an ACEI and spironolactone were administered during the study period.ResultsThere were no significant differences between baseline and follow-up serum sodium or potassium concentrations. Serum magnesium concentrations increased significantly (p = 0.02) with time >20 weeks compared to baseline.ConclusionsThe combination of an ACEI and spironolactone results in no significant difference between baseline and follow-up serum sodium or potassium concentrations. Although serum magnesium concentrations may increase significantly with time >20 weeks compared to baseline concentrations, hypermagnesemia appears to be rare, mild, and unlikely to be of clinical importance. The combination of an ACEI and spironolactone is safe in elderly small dogs with MVD with normal SUN and creatinine concentrations.     

Relationships between fecal consistency and colonic microstructure and absorptive function in dogs with and without nonspecific dietary sensitivity

OBJECTIVE: To determine relationships between fecal consistency and colonic microstructure and absorptive function in dogs with and without nonspecific dietary sensitivity. ANIMALS: 12 dogs with nonspecific dietary sensitivity (affected) and 9 healthy dogs (controls). PROCEDURE: Affected dogs were fed 4 test diets and control dogs, 3 diets for 4 weeks each in a crossover design. Fecal consistency was assessed daily. At the end of each feeding period, electrolyte and water transport were assessed, and colonic biopsy specimens were obtained for histologic examination and measurement of crypt water uptake by use of confocal microscopy. RESULTS: Feces were consistently looser in affected dogs. In control dogs, we detected net colonic absorption of sodium and chloride and secretion of potassium and bicarbonate. Absorption of sodium and chloride was less in affected dogs, compared with controls, indicating that electrolyte transport was disrupted in affected dogs. This disruption was accentuated during feeding of diets associated with significantly poorer fecal consistency (ie, loose feces). Fecal consistency was inversely correlated with crypt water absorption, which was reduced in affected dogs. Colonic crypts were shorter and less dense in affected dogs fed diets associated with poor fecal consistency, compared with affected dogs fed other diets or with control dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Colonic transport function is a major determinant of fecal consistency in dogs. Dogs with nonspecific dietary sensitivity are particularly susceptible to diet-induced changes in absorptive function. Such changes are associated with damage to colonic microstructure, disrupted electrolyte transport, and failure to dehydrate luminal contents.     

Influence of dietary electrolyte balance, source of added potassium and anticoccidial agents on the performance of male broilers

1. The performance of 1680 male broiler chickens was measured from one to 42 d of age. They were given diets with three (125, 165 and 205 mEq/kg) electrolyte balances (sodium + potassium - chloride), two sources of added potassium (carbonate or sulphate) and two anticoccidial agents (90 mg/kg of either monensin or lasalocid). 2. The dietary treatments had no significant effects on the growth performance of broiler chickens in the starter phase. 3. In the finisher phase, the chickens given the diets containing lasalocid utilised food less efficiently that those given the diets containing monensin. 4. There were significant interactions between dietary electrolyte balance and source of added potassium on body weight gains and food:gain ratios in the finisher phase. In diets with an electrolyte balance of 205 mEq/kg, the inclusion of potassium sulphate instead of potassium carbonate increased body weight gains by 3.4% and reduced food:gain ratios by 4.6%. 5. The body weight gains of chickens given the finisher diets containing lasalocid and added potassium carbonate were reduced by 2.6% compared to those of chickens given the diets containing monensin or added potassium sulphate. 6. The litter moisture content was higher in pens with chickens on the diets with an electrolyte balance of 205 mEq/kg than on the diets with either 125 or 165 mEq/kg. Both lasalocid and potassium sulphate tended to increase the litter moisture content. 7. It may be concluded that the inclusion of 90 mg/kg of either monensin or lasalocid in broiler diets does not alter the balance of electrolytes required for optimum growth performance of broiler chickens.     

Reference limits for urinary fractional excretion of electrolytes in adult non-racing Greyhound dogs

OBJECTIVE: To determine reference limits for urinary fractional excretion of electrolytes in Greyhound dogs. METHODS: Urinary fractional excretion was calculated using a spot clearance method preceded by a 16 to 20 hour fast in 48 Greyhound dogs. Raw data analysed using the bootstrap estimate was used to calculate the reference limits. RESULTS: The observed range for urinary fractional excretion in Greyhound dogs was 0.0 to 0.77% for sodium, 0.9 to 14.7% for potassium, 0 to 0.66% for chloride, 0.03 to 0.22% for calcium and 0.4 to 20.1% for phosphate. Expressed as percentages, the suggested reference limits for fractional excretion in Greyhound dogs are as follows: sodium < or = 0.72, potassium < or = 12.2, chloride < or = 0.55, calcium < or = 0.13 and phosphate < or = 16.5. CLINICAL SIGNIFICANCE: Veterinary practitioners may use these reference limits for urinary electrolyte fractional excretion when investigating renal tubular disease in Greyhound dogs.