Relation of endogenous Heinz bodies to disease and anemia in cats: 120 cases (1978-1987)

Disease diagnosis, age, sex, and selected hematologic variables were evaluated retrospectively in a population of feline patients with high number of circulating Heinz bodies. By comparing these cats with a control population and results of additional hematologic investigation on a subsample of the cats, we tested the hypotheses that endogenous Heinz body formation is increased in specific disease states and that endogenous Heinz bodies may contribute to anemia. There was strong correlation between diabetes mellitus, hyperthyroidism, and lymphoma and Heinz body formation. Diabetic cats, in particular, consistently had marked Heinz body formation. These diseases together accounted for nearly 40% of cats with Heinz body formation, but for less than 12% of cats of the control group. The PCV of cats with Heinz bodies (29.77 +/- 9.32%) was significantly (P less than 0.001) lower than that of control cats (35.33 +/- 8.08%). Polychromasia and punctate reticulocyte number were slightly increased in cats with Heinz body formation and correlated significantly (P less than 0.001) with PCV. A subsample of 13 of the cats had significant (P less than 0.006) inverse correlation between Heinz body percentage and erythrocyte reduced glutathione (GSH) concentration. Mean GSH concentration was significantly lower in cats with Heinz bodies, compared with that in a random cat population (5.28 +/- 1.67 mumol/g of hemoglobin vs 7.06 +/- 2.10 mumol/g of hemoglobin), in which GSH values followed normal distribution. Cats with Heinz body formation were older, and were more likely to be spayed.     

Corpuscular oxidation in newborn crossbred calves naturally infected with Theileria annulata

Erythrocytic lipid peroxidation has been implicated as a cause of anemia in Theileria annulata infection in cattle. The present study aimed to evaluate oxidative damage of membrane lipids and proteins in addition to hemoglobin (Hb) as three criterions of erythrocyte oxidation and their relation to erythrocyte deformability and anemia of newborn crossbred calves (Friesian × Egyptian Balady breed) naturally infected with T. annulata. Twenty-five T. annulata-infected calves (aged 20-30 days) along with 15 age matched healthy controls were used. Percentage of parasitemia varied from 12% to 63% (34.76 ± 3.05%). In comparison to controls, infected calves showed increased levels (P<0.001) of lipid peroxidation (malondialdehyde; MDA, 52%) and protein oxidation (protein carbonyls; PCs, 132%) in erythrocyte membrane as well as increased values of Hb oxidation (methemoglobin; MetHb, 186%), corpuscular osmotic fragility (15.1%) and hemolysis (free Hb; 195.5%). Parasitemia was positively correlated with MDA (r=0.41, P=0.039), PCs (r=0.45, P=0.023) and MetHb (r=0.40, P=0.042). Also, percent of erythrocytic deformability (echinocytosis) was positively correlated with MDA (r=0.49, P=0.013) and PCs (r=0.63, P<0.001). On the other hand, erythrocytic packed cell volume was negatively correlated with MDA (r=-0.44, P=0.028), PCs (r=-0.72, P<0.001) and MetHb (r=-0.42, P=0.037). In conclusion, T. annulata infection is associated with a parasitic burden-dependant oxidative damage to the erythrocyte membrane protein and lipid contents in addition to Hb. This oxidative damage is linked to the morphological changes of the erythrocyte and may act as mechanisms contribute to pathogenesis of anemia in T. annulata infection in newborn calves.     

Heinz body hemolytic anemia associated with high plasma zinc concentration in a dog

Acute zinc toxicosis from the ingestion of pennies was diagnosed in a dog with Heinz body hemolytic anemia (PCV = 14%), leukocytosis (51,000 cells/ml) with a left shift (3,060 band neutrophils; 37,740 segmented neutrophils) and monocytosis (4,080 cells/ml), azotemia (BUN = 60 mg/dl), bilirubinemia (total bilirubin = 5.3 mg/dl), hypokalemia (3.0 mEq/L), high serum alkaline phosphatase activity (691 U/L), high total plasma solids (8.1 g/dl), hemoglobinuria, and proteinuria. Despite aggressive medical treatment, renal failure ensued, and the dog died of cardiac arrest. The clinical signs, clinical course, and laboratory findings in this dog were similar to what has been reported in other cases of acute zinc toxicosis in dogs, with the exception of a history of generalized seizures and the findings of Heinz bodies. Although a causative relationship between plasma zinc values and Heinz body formation cannot be proven, their association suggests that oxidative damage to erythrocyte hemoglobin and cell membrane proteins may be involved in the pathogenesis of zinc-induced hemolysis.     

Antioxidant prevention of Heinz body formation and oxidative injury in cats

OBJECTIVE: To determine the effectiveness of 3 antioxidants in preventing Heinz body anemia in cats. DESIGN: Prospective study. ANIMALS: 44 specific-pathogen-free healthy cats. PROCEDURE: Cats were housed individually, divided randomly into 4 groups, and given the following orally every 12 hours: empty gelcaps (control cats), N-acetylcysteine (NAC, 100 mg/kg of body weight), vitamin E (d,l-alpha-tocopherol; 400 IU), or ascorbate (250 mg). After 2 weeks, Heinz bodies were induced by dietary onion powder (OP; 1% or 3% of dry matter) or propylene glycol (PG, 8% wt/vol in drinking water) for an additional 3 weeks. Intake of treated water or food was recorded daily. Body weight, PCV, Heinz body and reticulocyte percentages, reduced glutathione concentration, and total antioxidant status were measured twice weekly in all cats. RESULTS: Heinz body percentage and degree of anemia did not differ significantly among cats receiving antioxidants and control cats except in cats that ingested water containing PG, in which antioxidant supplementation was associated with a decrease in water intake. Of cats that were fed a diet that contained OP, cats that received NAC had significantly higher reduced glutathione concentrations, compared with other cats in the experiment. Total antioxidant status did not consistently correlate with antioxidant supplementation or type of oxidant administered (ie, OP or PG). CONCLUSIONS AND CLINICAL RELEVANCE: Although the effect of antioxidant supplementation on Heinz body anemia in cats was minimal, antioxidants may have subclinical biochemical effects such as GSH sparing that may be important against milder forms of oxidative stress.     

S-adenosylmethionine (SAMe) in a feline acetaminophen model of oxidative injury

S-adenosylmethionine (SAMe) is reported to have hepatoprotective and antioxidant functions. Acetaminophen (paracetamol) was used to induce oxidative damage in cats, and to then determine the effect of SAMe treatment on erythrocyte morphology, PCV, liver histopathology, thiobarbituate reacting substances (TBARS), reduced glutathione (GSH), and oxidised glutathione (GSSG).Cats receiving acetaminophen had a significant increase in methemoglobin and Heinz body production. A significant effect for the interaction of time and treatment was found for Heinz body production and changes in PCV. No significant changes were found in blood or hepatic TBARS. Blood GSH increased significantly in all cats, while the blood GSH:GSSG ratio tended to increase the most in cats given acetaminophen only. The hepatic GSH:GSSG ratio tended to increase in cats given SAMe and decrease in cats given acetaminophen, but this effect was not significant. SAMe protected erythrocytes from oxidative damage by limiting Heinz body formation and erythrocyte destruction and maybe useful in treating acetaminophen toxicity.     

Erythrocyte pathology and mechanisms of Heinz body-mediated hemolysis in cats

Despite the frequency of both oxidant drug-induced and spontaneous Heinz body formation in cats, the cellular and biochemical mechanisms by which Heinz bodies result in red blood cell (RBC) destruction and hemolytic anemia in this species remain unknown. Feline spleens are non-sinusoidal and inefficient at removing Heinz body-containing RBC from the circulation; therefore, alternative mechanisms must be involved in accelerated RBC destruction. Propylene glycol (PG) ingestion causes dose-dependent Heinz body formation and decreased RBC survival in cats. We investigated several aspects of Heinz body-containing RBC from three cats ingesting diets that provided 8.0 g PG/kg body weight for up to 3 weeks, in order to characterize cellular lesions that are associated with the presence of Heinz bodies and that might contribute to chronic, accelerated RBC destruction, as well as to gain insight into the mechanism by which PG induces Heinz body formation. Erythrocytes with PG-induced Heinz bodies had decreased levels of reduced glutathione and adenosine triphosphate and reduced deformability. There was no change in hemoglobin isoelectric focusing or membrane lipid peroxidation. Electrophoretic patterns of Heinz body-containing RBC membranes were significantly altered, and membrane surface charge distribution was disturbed. Progressively protruding Heinz bodies suggested that extrusion of Heinz bodies may be a means of cell healing and/or destruction in the absence of splenic pitting. When compared to results obtained using RBC from cats treated with the oxidant drug phenylhydrazine, significant differences were noted in packed cell volume, turbidity index, membrane heme, and morphologic appearance of Heinz bodies. Our results indicate that multiple cellular abnormalities develop in RBC with PG-induced Heinz bodies that do not cause acute hemolysis but that may shorten RBC survival. Propylene glycol-induced Heinz bodies provide an ideal model for studying the chronic effects of Heinz bodies on RBC structure and function and may be useful in understanding the mechanisms of formation and the consequences of endogenous Heinz bodies in cats.     

Antioxidant status and biomarkers of oxidative stress in cats with diabetes mellitus

Increasing evidence implicates oxidative damage in the progression and pathologic complications of human diabetics. This study assessed antioxidant status and oxidative stress in cats with diabetes mellitus (DM). Antioxidant status was measured in diabetic (n = 10) and control (n = 10) cats by HPLC of vitamin E isomers, reduced (GSH) and oxidized glutathione (GSSG), and calculation of the GSH:GSSG ratio. Biomarkers of protein, lipid and DNA peroxidation (fructosamine, isoprostanes and Comet assay, respectively), and neutrophil function evaluated oxidative stress. Correlation between glycemic control and antioxidant status/ oxidative stress was also investigated. A diabetic index was generated using clinical signs, body condition score, insulin dose, fructosamine, fasted blood glucose and urinary glucose and ketones. Alpha tocopherol was increased (DM = 0.11 μg/mL, controls = 0.06 μg/mL; p = 0.0012) and gamma tocopherol was decreased (DM = 0.03 μg/mL, controls = 0.05 μg/mL; p = 0.0065) in diabetic vs. control cats. There was no difference in the GSH:GSH ratio between groups. Predictably, fructosamine was greater in diabetic vs. control cats (DM = 447 μmol/L, controls = 204 μmol/L; p < 0.0001). Antioxidant status/oxidative stress was not associated with glycaemic control in diabetic cats. Despite strong association of DM with oxidative stress in humans, this simple relationship is not found in diabetic cats. They have both increased and decreased parameters of systemic oxidative stress compared with control cats. This may be due to higher levels of antioxidants in feline therapeutic diets, the relatively short duration of disease in cats compared with humans, or other factors.     

Contribution of propylene glycol-induced Heinz body formation to anemia in cats

Propylene glycol (PG) is a common preservative and source of synthetic carbohydrates in soft-moist pet foods. Propylene glycol was fed to cats for 5 weeks at concentrations found in commercial diets (1.6 g/kg of body weight; 12% of diet on a dry-weight basis) and for 3 weeks at concentrations exceeding usual intake (8 g/kg; 41% of diet). There was a dose-dependent increase in Heinz body percentage to 28% in cats fed the low dose of PG and to 92% in cats fed the high dose. Erythrocyte half-life, measured using [14C]-cyanate hemoglobin (Hb), decreased significantly (P less than 0.05) by 18.8% and 60% in cats fed the low and high PG doses, respectively. The PCV in cats fed the low dose was unaffected, whereas cats fed the high dose had a mean (+/- SEM) decrease in PCV from 33.5 +/- 1.05% to 26.3 +/- 1.45%, accompanied by punctate reticulocytosis and bone marrow erythroid hyperplasia. A dose-dependent increase in iron pigment was found in the liver and spleen of all cats. In cats fed the low dose of PG, erythrocyte reduced glutathione concentration actually increased from 7.02 +/- 0.56 to 9.74 +/- 0.69 mumol/g of Hb, but decreased to 2.96 +/- 0.27 mumol/g of Hb in cats fed the high dose. There was no significant increase in methemoglobin concentration. These results indicated that PG cannot be considered innocuous even at concentrations consumed by cats eating commercial diets. Heinz body-induced acceleration of RBC destruction develops in a dose-dependent manner, so that cats with greater food intake, ie, lactating queens and nursing kittens, are at greater risk for development of PG-induced Heinz body hemolytic anemia.     

Scanning electron microscopy of Heinz bodies in feline erythrocytes.

Whole blood and partially lysed blood films from 5 cats having 20 to 91% of the erythrocytes containing Heinz bodies were examined, using the light microscope and the scanning electron microscope. Heinz bodies were detected in the intact erythrocytes from 3 of the cats as abruptly elevated and distinctly demarcated protuberances in various shapes, sizes, and locations. The Heinz bodies were located just beneath the cell membrane either centrally or near the cell margin and varied in their projectional magnitude. Brilliant cresyl blue staining of blood of these 3 cats revealed prominent Heinz bodies within, and projecting from, the erythrocytes. In contrast, Heinz bodies were not identified on scanning electron microscopy of intact erythrocytes of the remaining 2 cats even though Heinz bodies were found on their blood films stained with brilliant cresyl blue. Scanning electron microscopy of partially lysed blood smears of all 5 cats revealed Heinz bodies of various sizes in the erythrocyte ghosts. Furthermore, blood smears from the 3 cats having distinct Heinz bodies in intact erythrocytes revealed small dense intracellular granules distributed singly or coalesced in small clumps. Further aggregation of these clumps was assumed to result in the formation of a single large Heinz body. The 3-dimensional nature of Heinz bodies was clearly apparent in lysed blood smears.     

Hematologic abnormalities associated with chronic acetaminophen administration in a dog

Large numbers of eccentrocytes (erythrocytes with hemoglobin contracted to one side of the cell) were seen on a stained blood smear from a Dachshund with compensated hemolytic anemia. The 7-kg dog had been given 325 mg of acetaminophen orally once daily for 6 weeks by the client, because the dog exhibited signs attributed to abdominal pain. More than half of the erythrocytes contained small Heinz bodies visualized after methyl violet staining. The methemoglobin content was 6.4% (normal less than 2%) when measured 16 hours after the last acetaminophen tablet was given. High serum alanin transaminase and alkaline phosphatase activities and hyperbilirubinuria were measured. All abnormal laboratory findings were attributable to acetaminophen-induced oxidative damage to erythrocytes and hepatocytes.     

Serum insulin-like growth factor-I concentration in cats with diabetes mellitus and acromegaly

BACKGROUND: Serum insulin-like growth factor-I (IGF-I) has been used in place of serum growth hormone quantification for identifying acromegaly in diabetic cats. The utility of IGF-I as a screening test for acromegaly has not been critically evaluated. This retrospective study was performed to evaluate the usefulness of serum IGF-I concentration for identifying acromegaly. HYPOTHESIS: Serum IGF-I is a useful screening test for acromegaly in diabetic cats. ANIMALS: A review was made of the medical records of 74 diabetic cats that had serum IGF-I quantified. The diabetes was classified as well controlled (15 cats), poorly controlled because of problems with the insulin treatment regimen, concurrent disease, or both (40), or poorly controlled with clinical findings consistent with acromegaly (19). METHODS: A review of medical records was made. RESULTS: Serum IGF-I concentration was significantly (P < .0001) increased in acromegalic diabetic cats, compared with well-controlled and poorly controlled diabetic cats. Sensitivity and specificity for serum IGF-I concentration were 84% (95%/ confidence interval [CI] = 60.4-96.6%) and 92% (95% CI = 81.3-97.2%), respectively. There was no significant correlation between serum IGF-I concentration and duration of insulin treatment (r = 0.23, P = .089), insulin dosage (r = 0.14, P = .30), age (r = 0.16, P = .12), and pituitary volume (r = 0.40, P = .11), but a modest correlation was found between serum IGF-I concentration and body weight (r = 0.48, P < .0001). CONCLUSIONS AND CLINICAL IMPORTANCE: Results support the use of serum IGF-I concentration as a screening test for acromegaly in diabetic cats that have clinical findings supportive of the disease.     

Experimental onion-induced hemolytic anemia in dogs

Within one day following a single oral dose of dehydrated onions, dogs were found to have large numbers of Heinz bodies within erythrocytes. The percentage of erythrocytes that contained Heinz bodies increased slightly to a maximum on day 3 and then declined. The turbidity index increased more gradually with a maximal value on day 4. Erythrocytes with hemoglobin contracted to one side of the cell (eccentrocytes) also appeared after onion feeding. Eccentrocytes are believed to result from a direct injury to the erythrocyte membrane. As with Heinz body-containing cells, the percentages of eccentrocytes present declined as anemia developed. The packed cell volume began to decrease one day after onion administration. A mean decrease of 19 percentage points was reached by day 5. The most anemic dogs had evidence of intravascular hemolysis. Reticulocytosis was first observed five days after onion administration. A slight increase in methemoglobin content was measured four hours after onion administration. No significant changes in erythrocyte reduced glutathione concentration were measured. Transient neutrophilia occurred concomitant with the peak reticulocyte response.     

Hematologic alterations in adult cats fed 6 or 12% propylene glycol.

Cat foods containing propylene glycol (PG) induce Heinz body formation in feline erythrocytes. To further study the hematologic importance of dietary PG, 21 adult cats were allotted to 3 groups of 7 each and fed diets containing 0, 6, or 12% PG on a dry-weight basis. Cats fed PG had a dose-related increase in Heinz bodies within 2 weeks, and the increase persisted throughout the study. Although only slight changes occurred in PCV, hemoglobin concentration, and RBC count, punctate reticulocytes were significantly increased in the group fed 12% PG. Mean RBC survival was decreased in the groups fed 6 or 12% PG by 30 and 55%, respectively, compared with the control group. These data indicate that PG-containing diets cause a dose-dependent erythrocyte destruction, even when fed at concentrations as low as 6%.     

Effect of diet on Heinz body formation in kittens

Heinz body formation was examined in kittens, in response to consumption of a variety of diets. A commercial salmon-based diet containing 16.5 mg of nitrite, 39 mg of histamine, and 210,000 IU of vitamin A/kg of diet (dry-matter basis) was found to induce Heinz body formation. Purified experimental diets--containing nitrite up to 405 mg/kg; histamine, 50 mg/kg; histamine 50 mg/kg plus nitrite, 45 mg/kg; or vitamin A, 250,000 IU/kg--failed to induce Heinz body formation. The effect of propylene glycol (PG) on Heinz body formation was examined by giving groups of 6 kittens purified diets containing 5 or 10% PG for 12 weeks. Two additional kittens were fed a commercial soft-moist diet containing PG for 12 weeks. All kittens fed PG developed Heinz bodies, with peak values for erythrocytes containing Heinz bodies being: 28% for kittens of the 10% PG group; 20% for kittens of the 5% PG group; and 36% for kittens of the soft-moist diet group. Kittens did not develop anemia or methemoglobinemia. Heinz body percentage required 6 to 8 weeks to decrease to the pretreatment value of less than 1% after diets containing PG were discontinued. 51Chromium-labeled erythrocytes were used to evaluate erythrocyte survival in 4 kittens of the 10% PG-fed group and in 4 control kittens. Kittens with Heinz body formation induced by 10% PG had significantly (P less than 0.001) decreased erythrocyte-survival, compared with that for controls, with half-life of 8.3 days for kittens of the PG group, compared with 12.6 days for kittens of the control group.     

A retrospective study of serum β-hydroxybutyric acid in 215 ill cats: clinical signs, laboratory findings and diagnoses

Serum concentrations of β-hydroxybutyric acid (sBHBA) are increased in cats with diabetes mellitus (DM), diabetic ketoacidosis (DKA) and hepatic lipidosis (HL). This study assessed sBHBA as a diagnostic tool in 215 consecutively-enrolled ill cats in the general population in a veterinary hospital. At the time of presentation, sBHBA was within the reference range in 158/215 (73.5%) cats (median 0.27; range 0.00-0.49 mmol/L) and elevated in 57/215 (26.5%) cats (median 0.87; range 0.51-21.45 mmol/L). Compared to cats with normal sBHBA, those with increased sBHBA had higher frequencies of anorexia, weight loss, icterus, polyuria/polydipsia, hyperbilirubinaemia, hypertriglyceridaemia, pancreatitis, HL, DM and DKA. They had higher concentrations of bilirubin and triglycerides and lower concentrations of potassium, chloride and total protein. There were positive correlations (P<0.01) between sBHBA and urinary glucose (r=0.42) and ketones (r=0.76), but there were no group differences in dipstick levels of urinary ketones. Cats with DM/DKA and with HL had significantly higher sBHBA compared to other cats. Receiver operator characteristics analysis of sBHBA as a predictor of HL showed that sBHBA was a good predictor of HL. Increased sBHBA occurs frequently in ill cats and provides useful diagnostic information, especially in DM/DKA and HL.     

Effects of propylene glycol-containing diets on acetaminophen-induced methemoglobinemia in cats

Soft-moist cat foods contain 7 to 13% propylene glycol (PG) on a dry-weight basis. These diets induce Heinz body formation in feline RBC. In this study, we evaluated cats on a control diet and on a commercial diet containing 8.3% PG. All cats on the PG diet developed an increase in the number of circulating Heinz bodies. We then administered acetaminophen to cats on each diet to determine whether RBC from cats on PG diets were more susceptible to oxidant stress. Methemoglobin concentrations were significantly greater in cats in PG diets after acetaminophen administration. These data indicate that RBC from cats fed PG diets are more susceptible to oxidative stress.     

Hematologic changes associated with the appearance of eccentrocytes after intragastric administration of garlic extract to dogs

OBJECTIVE: To determine whether dogs given garlic extract developed hemolytic anemia and to establish the hematologic characteristics induced experimentally by intragastric administration of garlic extract. ANIMALS: 8 healthy adult mixed-breed dogs. PROCEDURE: 4 dogs were given 1.25 ml of garlic extract/kg of body weight (5 g of whole garlic/kg) intragastrically once a day for 7 days. The remaining 4 control dogs received water instead of garlic extract. Complete blood counts were performed, and methemoglobin and erythrocyte-reduced glutathione concentrations, percentage of erythrocytes with Heinz bodies, and percentage of eccentrocytes were determined before and for 30 days after administration of the first dose of garlic extract. Ultrastructural analysis of eccentrocytes was performed. RESULTS: Compared with initial values, erythrocyte count, Hct, and hemoglobin concentration decreased to a minimum value on days 9 to 11 in dogs given garlic extract. Heinz body formation, an increase in erythrocyte-reduced glutathione concentration, and eccentrocytes were also detected in these dogs. However, no dog developed hemolytic anemia. CONCLUSIONS AND CLINICAL RELEVANCE: The constituents of garlic have the potential to oxidize erythrocyte membranes and hemoglobin, inducing hemolysis associated with the appearance of eccentrocytes in dogs. Thus, foods containing garlic should not be fed to dogs. Eccentrocytosis appears to be a major diagnostic feature of garlic-induced hemolysis in dogs.     

The kinetics of hematopoiesis in the light horse III. The hematological response to hemolytic anemia.

The hematological response to acetylphenylhydrazine hemolytic anemia was studied in three standardbred horses. The lifespan of erythrocytes produced during the most severe phase of the anemia were measured with 75-selenomethionine and found to be 144 days as compared to the 139 day lifespan in response to hemorrhagic anemia or 155 days in normal standardbred horses measured previously using the same technique. The erythrocyte counts returned to initial values in 42 days (37, 34 and 54 days) a mean erythrocyte production of 6.4 times 10-12 erythrocytes/day. The mean hemoglobin production was 0.31 gm/kg body weight/day as compared to 0.11 gm Hb/kg/day previously observed in response to hemorrhagic anemia. The mean increase in erythrocyte mean cell volume was 12 mu-3 during the acute response phase to hemolytic anemia in contrast to the absence of a significant increase in the mean cell volume as previously observed during response to hemorrhagic anemia. Free Heinz bodies separated from erythrocytes during the acute phase could not be differentiated from platelets on the hemocytometer counting chamber with standard techniques.     

Hypophosphatemia and Hemolytic Anemia Associated With Diabetes Mellitus and Hepatic Lipidosis in Cats

Hypophosphatemia associated with hemolytic anemia was diagnosed in five cats with diabetes mellitus and in one cat with idiopathic hepatic lipidosis. The hematocrit began decreasing within 24 to 48 hours after documented hypophosphatemia in each case. The anemia resolved in all five surviving cats. Because of the temporal relationship and lack of other detectable causes, hemolytic anemia was presumed to be caused by hypophosphatemia. There were increased Heinz bodies in three of six hypophosphate-mic cats during episodes of hemolysis. Intravenous potassium phosphate administration corrected the hypophosphatemia in four of five cats. The effective dosages of intravenous phosphate ranged from 0.011 to 0.017 mmol of phosphate/kg/h for 6 to 12 hours. Hypocalcemia (5.4 to 8.7 mg/dL) occurred in four of five cats treated with intravenous phosphate; however, only one cat developed clinical signs attributable to hypocalcemia. Based on this retrospective study, we recommend monitoring serum phosphorus concentration every 6 to 12 hours in cats likely to become hypophosphatemic. Treatment of hypophosphatemia in cats is warranted because of the apparent increased susceptibility of cats to hypophosphatemia-induced hemolysis. Cats with severe hypophosphatemia (≤1.5 mg/dL) should be given oral or parenteral phosphate if contraindications do not exist. (Journal of Veterinary Internal Medicine 1993; 7:266–271. Copyright © 1993 by the American College of Veterinary Internal Medicine.)     

The prevalence of microalbuminuria and proteinuria in cats with diabetes mellitus

The prevalence of microalbuminuria (MA) and proteinuria was evaluated in 66 cats with diabetes mellitus (DM), 35 nondiabetic cats with other illness, and 11 healthy nondiabetic cats with use of the E.R.D.-HealthScreen Feline Urine Test. The MA prevalence was higher in the diabetic than in the nondiabetic sick and healthy control cats (70%, 39%, and 18% respectively, P < .0001). In addition, prevalence of proteinuria defined by a protein/creatinine ratio (UPC) > 0.4 was significantly higher in the diabetic cat than in the control cats (70%, 35%, and 9% respectively, P < .0001). There was a significant but weak correlation between the results of MA and UPC (P < .0001, r = 0.43). Our results showed that MA is common in cats with DM. Further studies are required to evaluate the prognostic value of the presence and the severity of MA in cats with DM.