Retrospective analysis of dietary management of hyperphosphatemia in cats with CKD

Jonathan Elliott

Introduction

The renal research clinic at the Royal Veterinary College has used Royal Canin diets as part of its protocol for the management of chronic kidney disease (CKD) in cats since 2003. This brief report provides some descriptive retrospective analysis of the use of the diets, focusing particularly on the management of hyperphosphatemia in cats with CKD.

Methods

Cats diagnosed with CKD presenting to the Royal Veterinary College Feline Renal Research Clinics between January 2003 and September 2007 were included in the study. The standard criteria for diagnosis of CKD applied were persistence of azotemia (plasma creatinine concentration >177 ?mol/L) normally associated urine specific gravity <1.035. Persistence of azotemia was based on two blood samples taken at least two weeks apart.

Figure 1. Radiograph of a cat with severe CKD and marked secondary renal hyperparathyroidism (1).
a. Lateral radiograph of the proximal humerus
b. Antero-proximal view of the tibia. Note the cystic lesions in both long bones leading to thinning of the cortices.

All cats were offered both dried and wet versions of the diet supplied through the WALTHAM Centre for Pet Nutrition. The diet was dispensed normally at the second visit to the clinic when the diagnosis of CKD was confirmed on the basis of persistent azotemia. In cases diagnosed with systemic arterial hypertension, medical treatment of this problem was instituted and the response to antihypertensive medication established prior to commencing dietary therapy. Cats diagnosed with hyperthyroidism were also treated before dietary therapy (Figure 1). Most hyperthyroid cats were not azotemic when first diagnosed but plasma creatinine concentrations became elevated as they were made euthyroid with either medical or surgical treatment. Cats made euthyroid by surgical treatment are included with all other cats with CKD. Cats on chronic medical treatment for their hyperthyroidism were considered as a separate group since medical treatment in our clinics generally provides less consistent control of the hyperthyroid state.

Table 1. The distribution of cats in the four groups according their feeding regime

Group	N	Age (years)	IRIS Stage (creatinine; ?mol/L)
100%	19	15.1±4.2	236.0±65.4 Stage 2 - 14 Stage 3 - 5 Stage 4 - 0
Part diet	118	14.1±3.5	238.7±74.5 Stage 2 - 88 Stage 3 - 27 Stage 4 - 4
Non-diet	20	15.1±3.0	236.0±60.6 Stage 2 - 15 Stage 3 - 5 Stage 4 - 0
Hyperthyroid (medical tx)	36	16.0±2.6	229.7± 57.8 Stage 2 - 29 Stage 3 - 6 Stage 4 - 1

Data presented are mean values ± 1SD.

The case data extracted from our database were categorized into four groups according to the dietary treatment used and the way in which hyperthyroidism was managed. These groups were:

1. Cats which were fed Feline Low Phosphorus (FLP) diet as their only food
2. Cats which were fed FLP diet as a proportion of their daily ration
3. Cats which continued to eat their standard maintenance food
4. Cats that were hyperthyroid where this problem was managed medically and where control of phosphate intake was attempted with dietary therapy.

The response to dietary therapy was assessed by serial measurement of plasma phosphate concentration. Cats were seen 4 to 6 weeks after their diet was changed and then at 2 to 3 monthly intervals. Data were extracted from our database at the first re-check and then after 4 to 6 months of treatment.

Results

A total of 193 cats were diagnosed with CKD and offered renal clinical diet over the time period studied. These consisted of 146 cats in Stage 2 CKD (plasma creatinine 177-249 ?mol/L), 42 in Stage 3 (plasma creatinine 250 to 439 ?mol/L) and 5 in Stage 4 (plasma creatinine >440 ?mol/L). Seventy four of the 193 cases considered sufficiently hypertensive to require amlodipine treatment.

Owners were encouraged to gradually introduce the clinical diet over a period of 1 to 2 weeks and to feed as much of the clinical diet as was acceptable to the cat. As can be seen from Table 1, 19 of the 193 cats ate the diet as their only source of food. The majority of cases accepted the diet as a proportion of their ration although it is not possible from our records to say precisely what proportion this represented. In the case of 20 cats, the owners were unwilling or unable to feed the clinical diet.

Control of plasma phosphate concentration One of the goals of feeding a renal clinical diet is to control plasma phosphate concentration which is used as an indicator of whole body phosphate overload. An international panel of veterinary nephrologists has recommended target plasma phosphate concentrations to aim for at the different stages of CKD. Table 2 presents the data on plasma phosphate concentration in the 4 groups of cats before introduction of the diet (T0), after 4 to 6 weeks of diet therapy (T1) and after 4 to 6 months of therapy (T2). The proportion of cats where the plasma phosphate target concentration relevant to Stage 2 cats was exceeded (>1.45 mmol/L) is indicated in each case.

Plasma phosphate concentrations at diagnosis tended to be lower than we have previously reported (2), probably because we are diagnosing a greater proportion of cats at an earlier stage of their CKD and the practise of feeding geriatric diets (already partially restricted in phosphate) has increased since the 1990s. Overall, feeding the clinical diet reduced the plasma phosphate concentration significantly in all groups and increased the proportion of cats which met the therapeutic target of a plasma phosphate <1.45 mmol/L. Just over a third of cats receiving dietary therapy remained above the target and would therefore benefit from additional therapy to control plasma phosphate concentration (such as intestinal phosphate binding drugs). These tended to be pre-dominantly cats in Stages 3 and 4 CKD.

RETROSPECTIVE ANALYSIS OF DIETARY MANAGEMENT OF HYPERPHOSPHATEMIA IN CATS WITH CKD

Table 2 - Changes in plasma phosphate with time

Group	N	Phosphate (mmol/L) T0 (entry)	N	Phosphate (mmol/L) T1 (4-6 weeks)	N	Phosphate (mmol/L) T2 (4-6 months)
100% diet	19	1.68 ± 0.39^a No>1.45mmol/L 13/19 – 68.4%	19	1.24 ± 0.37^b No>1.45mmol/L 5/19 – 26.3%	16	1.28 ± 0.29^b No>1.45mmol/L 5/16 – 31.3%
Part diet	118	1.70 ± 0.68^a No>1.45mmol/L 74/118 – 62.7%	115	1.47 ± 0.59^b No>1.45mmol/L 43/115 – 37.4%	94	1.48 ± 0.49^b No>1.45mmol/L 34/94 – 36.2%
Non-diet	20	1.51 ± 0.48^a No>1.45mmol/L 10/20 – 50%	18	1.59 ± 0.77^a No>1.45mmol/L 7/18 – 38.9%	17	1.61 ± 0.69^a No>1.45mmol/L 9/17 – 52.9%
Hyperthyroid (medical tx)	36	1.63 ± 0.41^a No>1.45mmol/L 24/37 – 64.9%	35	1.33 ± 0.31^b No>1.45mmol/L 8/36 – 22.2%	24	1.41 ± 0.31^a,b No>1.45mmol/L 9/24 – 37.5%

Data are presented as mean values ± SD. Values bearing different superscript letters within the same row are significantly different from each other (P<0.05; One way analysis of variance with Bonferroni’s pairwise comparison post-hoc test).

Data are presented as mean values ± SD.

Values bearing different superscript letters within the same row are significantly different from each other (P<0.05; One way analysis of variance with Bonferroni’s pairwise comparison post-hoc test).

No change in plasma phosphate concentration was seen in cats where dietary therapy was not possible to institute. Survival and causes of death At the time of analysis of the data, 104 of 193 cats involved in this study had died or been euthanized, 31% of which died of a uremic crisis or progressive uremia. Another 30% have died of unknown causes but it is likely that CKD contributed to the decision to euthanize the animal. The other major cause of death in this study was neoplasia (14.4%). Only 7 of the 19 cases in Group 1 (100% diet group) had died at the time of analysis. Median survival time for the group on the active diet is not yet available as more than 50% of these are still alive. From the part diet fed group the median survival time was 633 days with 67/118 having died. The group that were not fed the diet had a median survival time of 504 days with 10 of the 20 cats having reached the end point.

Conclusion

This uncontrolled retrospective analysis of cats presenting to the Renal Research Clinics at the Royal Veterinary College demonstrates that feeding of renal clinical diets results in effective control of plasma phosphate concentration in about two thirds of cats presenting in Stage 2 and 3 CKD. We thank Royal Canin for their support in this study.

REFERENCES

1. Barber, PJ. Parathyroid gland function in the ageing cat. PhD thesis. University of London 1999.
2. Elliott J, Rawlings JM, Markwell PJ, et al. Survival of cats with naturally occurring renal failure: effect of conventional dietary management. J Small Anim Pract 2000; 41: 235-242.