Association between naturally occurring chronic kidney disease and feline immunodeficiency virus infection status in cats

Joanna D. WhiteFaculty of Veterinary Science, University of Sydney, NSW, Australia.

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Richard MalikCentre for Veterinary Education, University of Sydney, NSW, Australia.

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Jacqueline M. NorrisFaculty of Veterinary Science, University of Sydney, NSW, Australia.

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Nicholas MalikidesNovartis Animal Health Pty Ltd Australia, 245 Western Rd, Kemps Creek, NSW 2178, Australia.

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Abstract

Objective—To investigate the association between naturally occurring chronic kidney disease (CKD) and FIV infection status in cats in Australia.

Design—Case-control study.

Animals—73 cats with CKD and 69 cats without historical, physical, or clinicopathologic evidence of CKD.

Procedures—Cats were tested for serum antibodies against FIV glycoprotein 40 (gp40) by use of an immunomigration assay. Information regarding age, breed (purebred or domestic), and sex was obtained from medical records. Analysis was performed on data from cats stratified into 2 age categories (< 11 years old and ≥ 11 years old). Univariable and then multivariable analyses were performed to investigate the relationship between CKD and the study variable (FIV infection), the latter analysis accounting for breed (purebred or domestic), sex, and veterinary hospital of origin.

Results—Results of multivariable analysis revealed that younger cats with CKD (< 11 years old) were significantly more likely to have positive test results for serum antibodies against FIV gp40 than were cats without CKD. No significant associations were found between CKD and FIV infection, breed, sex, or hospital of origin among older (≥ 11 years old) cats in the multivariable analysis.

Conclusions and Clinical Relevance—Among cats < 11 years of age, those with CKD were significantly more likely to have positive test results for serum antibodies against FIV gp40 than were cats without CKD. It cannot be definitively established from results of this study whether infection with FIV preceded the development of CKD, and the role, if any, of FIV in the establishment or progression of CKD remains to be determined.

Abstract

Objective—To investigate the association between naturally occurring chronic kidney disease (CKD) and FIV infection status in cats in Australia.

Design—Case-control study.

Animals—73 cats with CKD and 69 cats without historical, physical, or clinicopathologic evidence of CKD.

Procedures—Cats were tested for serum antibodies against FIV glycoprotein 40 (gp40) by use of an immunomigration assay. Information regarding age, breed (purebred or domestic), and sex was obtained from medical records. Analysis was performed on data from cats stratified into 2 age categories (< 11 years old and ≥ 11 years old). Univariable and then multivariable analyses were performed to investigate the relationship between CKD and the study variable (FIV infection), the latter analysis accounting for breed (purebred or domestic), sex, and veterinary hospital of origin.

Results—Results of multivariable analysis revealed that younger cats with CKD (< 11 years old) were significantly more likely to have positive test results for serum antibodies against FIV gp40 than were cats without CKD. No significant associations were found between CKD and FIV infection, breed, sex, or hospital of origin among older (≥ 11 years old) cats in the multivariable analysis.

Conclusions and Clinical Relevance—Among cats < 11 years of age, those with CKD were significantly more likely to have positive test results for serum antibodies against FIV gp40 than were cats without CKD. It cannot be definitively established from results of this study whether infection with FIV preceded the development of CKD, and the role, if any, of FIV in the establishment or progression of CKD remains to be determined.

Chronic kidney disease is a common syndrome typically of older cats that results in well-described physical and clinicopathologic abnormalities.1 Many specific causes of kidney disease have been determined; however, in most cats, the disease progresses slowly and the inciting cause or causes are rarely identified. One proposed cause of CKD, at least in young male cats, is infection with FIV. This assertion is based on evidence suggesting that CKD may occur more frequently in young, male cats2; FIV infection has an increased prevalence in male cats and infection with FIV has been associated with clinicopathologic and other indicators of kidney disease.3–7

The strength of evidence for a relationship between FIV infection and CKD varies and generally is derived from populations of cats with or without FIV infection rather than from cats with or without CKD. In 155 cats naturally infected with FIV, azotemia and proteinuria were more common than these findings were in age-matched cats not infected with FIV.8 In Western Australia, results of a survey in which cats had blood samples taken as part of diagnostic testing for a range of various conditions revealed that cats seropositive for antibodies against FIV were 3 times as likely to be azotemic and twice as likely to have small kidneys than were cats seronegative for antibodies against FIV.6 Although not definitive, both abnormalities (ie, azotemia and small kidneys) are consistent with a diagnosis of CKD. In contrast, results of a survey of 213 healthy and sick cats revealed no significant difference in BUN and serum creatinine concentrations between cats seropositive and seronegative for antibodies against FIV.9 A limitation of both studies6,9 was that prerenal causes of azotemia were not excluded.

The relationship between FIV infection and CKD is further supported by findings in studies8,10 in which cats experimentally infected with FIV were more likely to have evidence of renal disease (ie, higher serum creatinine concentration and proteinuria) than were cats without FIV infection. However, most of the biochemical variables in cats infected with FIV remained within the reference range.10 Furthermore, in a study4 on histologic evaluation of renal tissue from cats with naturally occurring FIV infections, 6 of 15 cats were azotemic and proteinuric. Histopathologic findings for 12 of the 15 cats included segmental glomerulosclerosis, glomerular capillary collapse, increased mesangial matrix, and tubular dilatation.4 Additionally, FIV antigen (protein 24) was detected within tubular, glomerular, or interstitial cells in 13 of the 15 cats.5 Other histologic changes described in renal tissue from naturally and experimentally infected cats include glomerulosclerosis and microcystic tubular dilation.8 The purpose of the study reported here was to investigate the potential relationship between naturally occurring CKD and FIV infection status in cats in Australia.

Materials and Methods

Animals—A hospital-based case-control study involving 73 cats with confirmed CKD (cases) and 69 cats without historical, physical, or clinicopathologic evidence of CKD (controls) was performed. Informed consent was obtained from owners of cats, and the study protocol was conducted in accordance with institutional animal care and use guidelines.

Veterinary hospitals—Two hospitals were involved. Hospital A was a primary accession, feline-only practice. Hospital B was both a primary accession and referral practice (Appendix). To obtain demographic information on each veterinary hospital, the signalment of all cats attending each hospital between January 2001 and November 2003 was obtained from clinical records. Each patient was only counted once regardless of the number of visits made to the hospital during this time frame. For consistency, age was classified as age at first visit for both hospitals and was rounded to the nearest whole number in years. Because hospital A had a substantially larger number of consultations for kittens, only cats ≥ 6 months old were included.

Case and control definition and selection—All cats in the study were privately owned. Cats were recruited before the introduction of FIV vaccination into Australia. Cases were defined as cats with confirmed CKD, namely consistent historical and physical findings together with serum creatinine concentration above relevant reference range and urine specific gravity ≤ 1.035. Cats were selected for inclusion if they visited the veterinary hospital between October 2002 and November 2003, thereby including both incident and prevalent cases. Cases included both hospitalized cats and outpatients. To ensure as homogenous a disease entity as possible, cats with renomegaly were included only if findings on histologic evaluation were available to exclude specific causes of kidney disease such as lymphosarcoma and polycystic kidney disease.

Cats were defined as controls if the recorded history, physical findings, serum creatinine concentration (ie, < 180 mol/L), and urinary specific gravity (ie, ≥ 1.035) were consistent with adequate kidney function. All cats that visited the veterinary hospitals between October 2002 and November 2003 that had a known serum creatinine concentration and urine specific gravity were eligible for inclusion as control cats. Potential control cats were excluded if there was a record of proteinuria, a bacterial urinary tract infection, hypertension or hypokalemia not attributable to another cause, or untreated hyperthyroidism or if the clinical records indicated the cat developed CKD over the subsequent 2 years (ie, up until 2006).

Data collection—Clinical records for all case cats and control cats were obtained from the respective veterinary hospitals and assessed by 1 author (JDW). Information regarding age, sex, breed (purebred or domestic), and medical history was tabulated. Ages were rounded to the nearest whole year. Cats were excluded if the records were incomplete. Similar numbers of case cats and control cats were recruited from each hospital. Testing for FIV infection was performed prior to determination of cat status (ie, case cat vs control cat). The author (JDW) was blinded to FIV infection status during the classification of cats as case and control cats.

FIV testing—Blood samples (0.5 to 3.0 mL) from each cat that fulfilled the case or control selection criteria were collected into a serum separator or EDTA tubes and centrifuged at 12,000 × g for 10 minutes. Serum or plasma was harvested, divided into 300-μL aliquots, transferred into 1.5-mL microcentrifuge tubes, and stored at −20°C (–4°F) prior to testing. Testing for FIV infection was performed in batches by trained personnel according to the manufacturer's instructions. Each serum or plasma sample was allowed to reach room temperature (approx 23°C) before testing for antibodies against FIV glycoprotein 40 by use of a commercial kit.a In this study, cats with positive test results for serum antibodies against FIV glycoprotein 40 were referred to as FIV-positive cats, and those with negative test results were referred to as FIV-negative cats.

Statistical analysis—Cats were grouped according to age, around the median age of all cats in this study (< 11 years and ≥ 11 years). This cut point ensured similar numbers of cats in both groups and that the median age of case cats and control cats were within 2 years of each other. All analyses were performed on the 2 groups independently by use of a commercial software package.b Descriptive statistics including age, sex, breed, hospital, and FIV infection status were calculated for all case cats and control cats. Univariable logistic regression analysis was performed for the categorical variables (ie, FIV infection status, sex, hospital, and breed), with CKD as the outcome variable. All of the variables were then fitted into a multivariable logistic regression model to evaluate the potential relationship between CKD and FIV, adjusting for the potential confounders (ie, sex, breed, and hospital). All potential 2-way interaction terms between the study variables were evaluated. Each interaction term, in turn, was added to the base model of all variables and included if significant (P < 0.05). The base model then comprised all study variables and all significant 2-way interactions. A backward elimination technique was subsequently used to determine the final model. Each nonsignificant variable was removed individually, and the effect on the odds ratio for FIV was evaluated. If the removal of a variable resulted in a > 10% change in the odds ratio for FIV, it was considered a potential confounder and its relationship with CKD and FIV further assessed.

Results

Descriptive statistics—There were 73 case cats (41 females and 32 males). Ages ranged from 3.5 to 21 years old. Forty-two case cats were from hospital A, and 31 were from hospital B; 25 were purebred cats, and 48 were domestic cats. Of the 73 case cats, 12 (16%; 4 females and 8 males) were FIV-positive cats.

There were 69 control cats (24 females and 45 males). Ages ranged from 3 months to 18 years old. Forty-two control cats were from hospital A, and 27 were from hospital B; 26 were purebred cats, and 43 were domestic cats. Of the 69 control cats, 6 (9%; 2 females and 4 males) were FIV-positive cats.

In the stratified analysis, among cats < 11 years old, there were 17 case cats (median age, 8 years old) and 50 control cats (median age, 6 years old). In comparison, among cats ≥ 11 years old, there were 56 case cats (median age, 15 years old) and 19 control cats (median age, 13 years old).

Univariable logistic analysis—Cats < 11 years old with CKD were significantly more likely to be FIV-positive cats (P = 0.010) and to be from hospital B (P = 0.014; Table 1). Older cats with CKD (≥ 11 years old) were significantly more likely to be purebred cats (P = 0.041) and to be from hospital A (P = 0.041; Table 2).

Table 1—

Univariable analysis results of the association of FIV, sex, hospital of origin, and breed with CKD in 67 cats < 11 years of age.

VariableStatusNo. of case catsNo. of control catsUnadjusted OR95% CIP value
FIVPositive52101.7–580.010
Negative1248
SexMale11360.710.22–2.30.57
Female614
HospitalA6350.230.073–0750.014
B1115
BreedPurebred4240.330.10–1.20.085
Domestic1326

CI = Confidence interval. OR = Odds ratio.

Table 2—

Univariable analysis results of the association of FIV, sex, hospital of origin, and breed with CKD in 75 cats ≥ 11 years of age.

VariableStatusNo. of case catsNo. of control catsUnadjusted OR95% CIP value
FIVPositive740.540.14–2.10.37
Negative4915
SexMale2190.670.23–1.90.45
Female3510
HospitalA3673.11.1–9.10.041
B2012
BreedPurebred2125.11.1–240.041
Domestic3517

See Table 1 for key.

Multivariable regression analysis—For younger cats (< 11 years old), none of the 2-way interaction terms added to the initial multivariable model were significant (Table 3). After backward elimination, FIV infection status was significantly associated with CKD. Cats < 11 years old with CKD were significantly (P = 0.010) more likely to be FIV-positive cats than cats without CKD (odds ratio, 10.0; 95% confidence interval, 1.7 to 58).

Table 3—

Initial multivariable model for the association of FIV, sex, hospital of origin, and breed with CKD in 67 cats < 11 years of age.

VariableStatusOR95% CIP value
FIVPositive6.71.1–420.043
Negative
SexMale0.750.2–2.70.66
Female
HospitalA0.330.094–1.20.084
B
BreedPurebred0.510.13–2.00.33
Domestic

See Table 1 for key.

Among cats ≥ 11 years old, no significant relationship was found between CKD and variables in the initial multivariable model (Table 4). None of the 2-way interactions terms added to the multivariable model were significant. After backward elimination, breed and hospital were potential confounding variables and were included in the model. However, in the final model, FIV infection status (P = 0.92), hospital (P = 0.15), and breed (P = 0.093) were not significantly associated with CKD.

Table 4—

Initial multivariable model for the association of FIV, sex, hospital of origin, and breed with CKD in 75 cats ≥ 11 years of age.

VariableStatusOR95% CIP value
FIVPositive1.10.24–4.80.94
Negative
SexMale0.610.19–1.90.40
Female
HospitalA2.3071–7.30.16
B
BreedPurebred4.40.85–220.077
Domestic

See Table 1 for key.

Discussion

Results of this study indicate that among younger cats (< 11 years), those with CKD were significantly more likely to be FIV-positive cats than were younger cats without CKD. There are several possible reasons why an association between CKD and FIV infection occurred only in younger cats in this study. There may have been fewer older FIV-positive cats available to develop CKD. Although the prevalence of FIV infection has been shown to increase with age,11–13 older cats (ie, cats > 10 years old) are often grouped together and the difference in prevalence of FIV infection among these older cats is unknown. In addition, increased mortality rate in cats with FIV infection, compared with cats without FIV infection, has been demonstrated.14 Consequently, it is possible that the prevalence of FIV infection increases with increasing age and then plateaus or declines15 during the years when the risk of CKD is greatest.

Finally, FIV infection may be associated with CKD only in younger cats because of differences in the clinical outcome of FIV infection as a result of host age at the time of infection. There are clear differences in the chronic diseases that develop after experimental induction of FIV infection between neonate, young adult, and older specific pathogen–free cats, and between specific pathogen–free and random-sourced cats, which highlights the role of host factors in disease manifestation in FIV-infected cats.16,17

The exact nature of the association between CKD and FIV infection in younger cats was not established on the basis of the study reported here. However, there are several pathophysiologic mechanisms by which FIV infection may contribute to kidney damage. Many similarities exist between FIV infection in cats and HIV infection in humans; kidney disease is common in humans infected with HIV. Infection with HIV can cause kidney disease by direct and indirect means. Human immunodeficiency virus–associated nephropathy is a specific nephropathy that, if untreated, rapidly progresses to renal failure and has highly characteristic histologic findings. Human immunodeficiency virus–associated nephropathy is a direct consequence of HIV infection of kidney tubular cells and podocytes.18 Kidney diseases indirectly associated with HIV infection include immune-complex glomerulopathies caused by immune dysregulation, opportunistic infections, or anti-HIV antibody immune complexes and thrombotic microangiopathies caused by HIV-mediated damage to endothelial cells.19

Infection with FIV may result in kidney damage through indirect means. As FIV is most likely to be spread among cats by fighting and biting behavior,20 cats with FIV infection are likely to be exposed to a range of potentially nephrotoxic events. In dogs and cats, recurrent infections, hypotension under general anesthesia, and nephrotoxic drugs, including antimicrobials and NSAIDs, especially when combined with hypovolemia and septicemia, are reported causes of renal damage.21–26

Whether FIV infection per se causes kidney damage in cats remains to be determined. Although there is always a substantial difference between establishing an association and clarifying the existence or otherwise of causation, aspects of FIV infection may make proving causality particularly difficult. Many diseases have been associated with an FIV infection status in cats.20,27 However, many of these diseases also commonly occur in cats without FIV infection. It can therefore be difficult to determine whether such associations are coincidental or referable to retroviral-induced immune suppression. For some diseases, such as neurologic diseases28 and lymphosarcoma,29,30 a clear causative role for FIV has been established, whereas for many other diseases, direct associations have not been shown with certainty. Although FIV infection can undoubtedly result in severe disease,31 this is not inevitable in either experimentally or naturally infected cats, at least in the time frames studied,10,32 and the long clinical latency seen in naturally occurring FIV infections in cats means that it may be difficult to identify significant disease associations without a similarly long follow-up. Additionally, the proportion of infected cats that will develop clinical signs of FIV infection is unknown.20 Results of 2 studies from Australia3,33 and 1 from Canada12 reveal similar prevalence of FIV infection among clinically normal cats and sick cats. Additionally, FIV infection in cats did not adversely affect life expectancy during a 10-year period in 1 study from England.34 Even if the association between FIV infection and CKD is determined to be a causal one, only a proportion of CKD in cats would truly be the result of FIV infection, similar to the situation with other chronic conditions such as gingivitis and upper respiratory tract infection.20

In the study reported here, analyses were performed with age of cats stratified into young (< 11 years old) and older (≥ 11 years old) cats because the difference in median age of cats with and without CKD was 7 years, which was considered to be a likely source of noncomparability between case cats and control cats. Findings in other series of cats with naturally occurring CKD suggest that this disease occurs predominantly in older cats.1,2,35,36 This observation was supported in the study reported here by the difficulty in identifying older cats without CKD, which resulted in far fewer numbers of control cats for the older cat group (≥ 11 years). This lack of balance between numbers of case and control cats in the analysis of older cats may have contributed to negative findings for an association between FIV infection and CRD among this age group. Conversely, infection with FIV may influence the progression rather than the cause of CKD, resulting in the development of CKD at a relatively younger age in FIV-positive cats.

Findings in this study did not reveal an association between cats with CKD and whether they were purebred or domestic cats. Similarly, breed predisposition for CKD has not been a consistent finding in other studies.2,35,36

The definition and selection of case animals and control animals are of critical importance in case-control studies. Cats recruited to be control cats in this study also formed part of a concurrent FIV seroprevalence study.3 During this period, blood samples were obtained from as many cats as feasible. When kidney disease was identified, cats were assessed for inclusion as case cats in this and other studies.2 This ensured that cats selected as control cats came from broadly the same population as case cats.

One potential difficulty with the criteria used for the selection of control cats in this study was the necessity for cats to have had blood and urine samples obtained for diagnostic or screening purposes, possibly resulting in a control group of cats that were less healthy than the general hospital population. As infection with FIV has been associated with a wide range of signs of disease,20,27 recruiting a less-than-healthy control group of cats would theoretically result in a selection bias. However, as both hospitals routinely used hematologic analyses as part of health and preanesthetic screening of clinically normal cats, it is unlikely that the control group contained only sick cats. Another consideration regarding the selection of control cats was the difficulty in confirming the absence of CKD. Neither serum creatinine concentrations nor the loss of urine concentrating ability has been sensitive diagnostic tests for a reduction in kidney function in either experimental or naturally occurring kidney disease in cats.37–39 Both this misclassification bias and the described selection bias would theoretically reduce the likelihood of detecting a significant association between CKD and FIV infection.40

This case-control study had several notable limitations. For example, temporality could not be established in this study. Although clinically unlikely, it cannot be disproved from the findings of this study that cats with preexisting CKD are more likely to be exposed to FIV. Both CKD and FIV infection potentially have long latency periods, and although retrospective, hospital-based case-control studies provide a good design for studying such diseases, it was not possible in this study to determine the starting points of each disease on the basis of only time of diagnosis. Follow-up of the control population with FIV infection may be a useful future means of exploring the temporal relationship between FIV infection and CKD.

Another important limitation of this study is the external validity of the findings. Case cats and control cats were selected from only 2 veterinary hospitals in 2 geographically close areas of Sydney. The results, therefore, cannot necessarily be extrapolated to other areas, particularly outer suburban and rural areas or areas with notably different prevalences of FIV infection. However, a significant association between FIV infection and azotemia has also been detected in other Australian and North American cities.6,8 It is also possible that there are important differences between cats that are admitted to veterinary hospitals and the general cat population that cannot be accounted for in a hospital-based study.

Other limitations of this case-control study relate to specific aspects of CKD in cats. It was important that cats included as case cats and control cats had a similar baseline risk of developing CKD, other than the factors under investigation. However, the cause of CKD in cats is typically unknown, and there may be unidentified risk factors for the development of CKD in cats confounding the study results. In addition, although a reasonable number of cats were recruited into the study, the seroprevalence of FIV was low and there were few FIV-positive cats in either the case or control groups. Further studies with larger numbers of cats are required to assess other risk factors for CKD and to confirm the association between young cats with CKD and FIV infection.

Furthermore, in case-control studies, the disease process under study should ideally be as homogenous a disease as possible. Although the final histopathologic diagnosis in cats with CKD is typically tubulointerstitial nephritis, it is unclear whether this represents a single disease or the final pathological process for a variety of disease processes. In the present study, efforts were made to exclude cats suspected of having kidney disease of known etiology (specifically polycystic kidney disease or lymphosarcoma) on the basis of clinical findings and results of histologic evaluation, where available.

Chronic kidney disease is a common problem in cats. Despite recent advances in the prognosis and treatment of cats with CKD, the etiology is typically unknown. Findings in this study reveal that a significant relationship exists between CKD and FIV infection in cats that are < 11 years old, which was not detected in older cats. Infection with FIV may be an important factor to consider in the pathogenesis of CKD in relatively young cats as a result of a direct effect of the virus or immunodysregulation or by contributing to other nephrotoxic events. Further work to confirm the association between CKD in cats and FIV infection in a larger population of younger cats and to elucidate the potential pathophysiologic mechanisms by which FIV infection may contribute to kidney disease is required.

ABBREVIATION

CKD

Chronic kidney disease

a.

Agen FIV Rapid immunomigration test, AGEN Biomedical Ltd, Acacia Ridge, QLD, Australia.

b.

Minitab 15, Minitab Pty Ltd, Sydney, NSW, Australia.

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    Addie DD, Dennis JM, Toth S, et al. Long-term impact on a closed household of pet cats of natural infection with feline coronavirus, feline leukaemia virus and feline immunodeficiency virus. Vet Rec 2000;146:419424.

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    DiBartola SP, Rutgers HC, Zack PM, et al. Clinicopathologic findings associated with chronic renal disease in cats: 74 cases (1973–1984). J Am Vet Med Assoc 1987;190:11961202.

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    Haller M, Rohner K, Müller W, et al. Single-injection inulin clearance for routine measurement of glomerular filtration rate in cats. J Feline Med Surg 2003;5:175181.

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    Gordis L. More on causal inferences: bias, confounding, and interaction. In: Epidemiology. 2nd ed. Philadelphia: WB Saunders Co, 2000;204217.

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Appendix

Background demographic data from the veterinary hospitals included in this study from January 2001 through November 2003.

VariableHospital AHospital B
Number of cats9232,283
Median age (range)5 y (1–21 y)8y (1–24y)
Ratio of males to females1.1:11.03:1
Ratio of domestic to purebred cats1.5:12.3:1

Contributor Notes

Dr. White's present address is the Institute of Veterinary, Animal and Biomedical Sciences, College of Sciences, Massey University, Palmerston North 4474, New Zealand.

Supported by the Australian Companion Animal Health Foundation.

The authors thank Dr. Peter Thompson for assistance with statistical analysis and Drs. Randolph Baral, Melissa Catt, and Erin Bell for assistance in the collection of blood samples.

Address correspondence to Dr. White (J.White@massey.ac.nz).
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    Robertson ID, Robinson WF, Alexander R, et al. Feline immunodeficiency virus and feline leukaemia virus in cats. Aust Vet Pract 1990;20:6669.

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    • Export Citation
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    Addie DD, Dennis JM, Toth S, et al. Long-term impact on a closed household of pet cats of natural infection with feline coronavirus, feline leukaemia virus and feline immunodeficiency virus. Vet Rec 2000;146:419424.

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    • Search Google Scholar
    • Export Citation
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    DiBartola SP, Rutgers HC, Zack PM, et al. Clinicopathologic findings associated with chronic renal disease in cats: 74 cases (1973–1984). J Am Vet Med Assoc 1987;190:11961202.

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    • Export Citation
  • 36.

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    • Search Google Scholar
    • Export Citation
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    Ross LA, Finco DR. Relationship of selected clinical renal function tests to glomerular filtration rate and renal blood flow in cats. Am J Vet Res 1981;42:17041710.

    • Search Google Scholar
    • Export Citation
  • 38.

    Brown SA, Heberman C, Finco DR. Use of plasma clearance of inulin for estimating glomerular filtration rate in cats. Am J Vet Res 1996;57:17021705.

    • Search Google Scholar
    • Export Citation
  • 39.

    Haller M, Rohner K, Müller W, et al. Single-injection inulin clearance for routine measurement of glomerular filtration rate in cats. J Feline Med Surg 2003;5:175181.

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    • Search Google Scholar
    • Export Citation
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    Gordis L. More on causal inferences: bias, confounding, and interaction. In: Epidemiology. 2nd ed. Philadelphia: WB Saunders Co, 2000;204217.

    • Search Google Scholar
    • Export Citation

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