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Successful nutritional management of a 21-year-old Quarter Horse gelding

with acute renal failure

Article · May 2016

DOI: 10.1136/vetreccr-2016-000309

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1
Laboratory of Animal
Nutrition, Faculty of Veterinary
Medicine, Ghent University,
Merelbeke, Belgium
2
Department of Large Animal
Internal Medicine, Faculty of
Veterinary Medicine, Ghent
University, Merelbeke, Belgium
Correspondence to
Veerle Ludmilla
Vandendriessche, veerle.
vandendriessche@ugent.be
Received 3 March 2016
Revised 25 April 2016
Accepted 26 April 2016
To cite:
Vandendriessche VL,
Dufourni A, van Loon G,
et al. Vet Rec Case Rep
Published online: [please
include Day Month Year]
doi:10.1136/vetreccr-2016-
000309
Vandendriessche VL, et al. Vet Rec Case Rep 2016;4:e000309. doi:10.1136/vetreccr-2016-000309
HORSES AND OTHER EQUIDS
Successful nutritional management of a 21-year-old
Quarter Horse gelding with acute renal failure
Veerle Ludmilla Vandendriessche,1 Alexander Dufourni,2 Gunther van Loon,2
Myriam Hesta1
SUMMARY
A 21-year-old Quarter Horse gelding was diagnosed
with acute renal failure after an acute kidney injury.
Upon discharge a nutritional recommendation was given
with the aim to minimise risk for chronic renal failure
development by optimally supporting kidney function.
A ration was designed to achieve weight gain, to
decrease retention of renal toxic solutes from protein
catabolism by limiting protein intake, to avoid gastric
ulcer development by limiting sugar and starch intake
per meal to 1.5 g/kg of ideal bodyweight, to supply ω-3
polyunsaturated fatty acids for their kidney protective
properties and restrict dietary calcium uptake to avoid
hypercalcaemia development. Three months after
implementing the recommendation the horse’s ideal
bodyweight was reached, muscle mass was regained and
its renal blood parameters were normalised. Biannual
blood checks with a nutritional recommendation to
maintain bodyweight in a healthy horse were applied
hereafter.
BACKGROUND
Few case reports have been published on horses
with acute renal failure (ARF) (Markel and others
1984, Rebhun and others 1984, Divers and others
1987, 1992, Gallatin and others 2005, Thompson
and others 2011), none of them supply any detail
on the nutritional support during hospitalisation or
after discharge if the horse survived. After acute
kidney injury (AKI), regeneration of tubular cells is
required. Therefore, to facilitate the healing
process and to avoid further development into a
more permanent state of chronic renal failure
(CRF) it is advisable to optimally support remain-
ing kidney function in the months following an
AKI. Prevalence and mortality of ARF is unre-
ported in horses although ARF develops after an
AKI if renal hypoperfusion is not timely recognised
and treated (Geor 2007). In comparison to human
beings and companion animals, where extensive lit-
erature is available on dietary management of renal
failure, information on horses is very scarce
(Wambacq and Hesta 2015). However, in the
authors’ opinion, correct nutritional therapy can
optimally support remaining kidney function;
prevent malnutrition; attenuate inflammatory
responses and oxidative stress; and re-establish an
appropriate immune status as described in human
beings (Martínez and others 2011). Thus evolution
to CRF, which reduces life expectancy and quality
of life (Schott 2007), can be avoided. Distributing
nutritional knowledge regarding equine dietary
Veterinary Record Case Reports
management of renal failure to veterinarians is thus
crucial to helping them treat and manage these par-
ticular patients.
CASE PRESENTATION
A 21-year-old Quarter Horse gelding presented in
autumn with a three-week history of weight loss,
partial anorexia for five days and lethargy. The
owners were referred to the Department of Large
Animal Internal Medicine (Ghent University,
Belgium) for further workup the day after the refer-
ring veterinarian performed a clinical and complete
blood examination. The results indicated azotaemia
and increased liver parameters (Table 1) and
therapy with Phytovet Hetaren was initiated (50 ml
once daily orally). The owners kept the horse on a
meagre meadow of 1.5 ha every day of the week,
day and night with one other horse and two
Shetland ponies. The meadow was completely sur-
rounded by oaks and might have contained other
poisonous plants. Haylage was available ad libitum
in a hayrack and the horse received 635 g of barley
concentrate (Mijten) with 500 g of carrots and one
apple once daily. In addition, it received several
supplements once daily because of navicular disease
and osteoarthritis: 12 g methyl sulfonyl methane
(PharmaHorse), 12 g glucosamine sulfate 2KCL
(PharmaHorse) and 20 g Harpagophytum procum-
bens (Simicur International). It also received 30
drops Echinacea Forte (Physalis) and some garlic
powder. The horse did not perform any exercise.
No abnormalities were found when an equine
dentist examined its teeth without sedation five
months before referral. The horse was dewormed
with Furexel Combi (Merial, ivermectine plus
praziquantel) two months before referral.
INVESTIGATIONS
Upon presentation at the clinic, the horse had a body-
weight (BW) of 443 kg. Clinical examination revealed
a systolic crescendo murmur of 2–3/6 with second
degree atrioventricular block, mildly icteric sclera and
mild muscle wasting. The horse was not dehydrated
and had no diarrhoea. Results outside of the reference
range in the blood work and urine analysis can be
found in Table 1. No abnormalities were found on
abdominal ultrasonographic examination. Faecal
examination revealed a faecal egg count of zero.
DIFFERENTIAL DIAGNOSIS
Some liver parameters were above the reference
range but ammonia and clotting times were
normal. After general examination, abdominal
1
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Veterinary Record Case Reports

TABLE 1: Results of laboratory data

Day 0 3 7 12 112 135 Reference range

Blood:
BUN (mmol/l) 9.16 7.1 7.49 6.2 4.28–9.64
Creatine (mmol/l) 292 320 260 269 147.6 148 79.56–176.8
Creatine kinase (IU/l) 427 247 119–287
AST (IU/l) 464 300 251 138–409
ALP (IU/l) 371 357 221 86–285
LDH (IU/l) 473 1026 588 162–412
GGT (IU/l) 52 68 22 8–22
Bile acids (mmol/l) 141 4 6 ≤ 12
Bilirubin total (mmol/l) 134.1 41 98.7 8.55–39.33
Leucocytes (cells/ml) 12450 7180 5000–10000
Total protein (g/l) 65 58 55 52 58 58–77
Albumin (g/l) 23 23–36
Ammonia (mg/dl) < l.o.d. 13–108
APTT (s) 40 30–65
PTT (s) 12 8–14
Urine
Source Voiding Voiding
Colour Yellow Yellow Yellow
Appearance Turbid Clear Clear
SG 1.041 1.005 1.020–1.050
pH 9 8 7–9
Proteins (mg/dl) 784 21 <10
Glucose ++++ + Negative
Leucocytes +++ - Negative
Bacteria +++ Negative
Creatine (mmol/l) 204.9 229.7 71–194
GGT (IU/l) 252 67 0–87
GGT/creatine (IU/g) 123 29 0–25
PCR leptospirosis Negative Negative
Bold text highlights parameters out of reference range.
Data reference range for clinical chemistry from Smith 2002; data reference range of urine analysis from internal laboratory, Ghent University
ALP, alkaline phosphatase; APTT, activated partial thromboplastin time; AST, aspartate aminotransferase; BUN, blood urea nitrogen; GGT, γ glutamyltransferase; IU, international unit;
l.o.d., limit of detection; LDH, lactate dehydrogenase; PTT, prothrombin time; SG, specific gravity

ultrasonographic examination and evaluation of blood values,
deviations in liver values were more likely secondary to an
underlying pathology. The increased total bilirubin and accom-
panying icteric sclera could be explained by the partial anorexia
at the time of examination (Smith 2002). Additional tests,
including urine analysis were performed to obtain more infor-
mation. A primary renal problem, either acute and/or more
chronic, was assumed due to azotaemia with a blood urea nitro-
gen (BUN)/creatine ratio of 17:1 and a prominent metabolic
acidosis. Urine was collected by covering the preputium with a
sterile glove. Since urine analysis (Table 1) revealed a possible
urinary tract infection (leucocytosis, glucosuria and proteinuria),
urine culture with sensitivity testing was performed. Horses
with CRF tend to have isosthenuric urine (1.008–1.014 specific
gravity (SG)), mild to moderate anaemia ( packed cell volume
(PCV) 20–30 per cent), hypercalcaemia, hypoproteinaemia and
hypoalbuminemia (Smith 2002). Since this horse had a normal
SG of 1.041, normal PCV of 43.7 per cent, normal total protein
of 65 g/l and normal serum calcium (1.49 mmol/l) but an
increased urine γ glutamyltransferase/creatine ratio of 123 (indi-
cative for tubular damage) (Tate and Meister 1985, Blasco and
others 2011), it was diagnosed with AKI. AKI can be caused by
nephrotoxins and/or vasomotor nephropathies. Nephrotoxicity
can be caused by aminoglycosides, pigments, NSAIDs, hypervi-
taminosis D, heavy metals, acorns, leptospirosis and
tetracyclines. Renal hypoperfusion or renal ischaemia can be
caused by haemorrhagic shock, severe intravascular volume
deficit, septic shock, coagulopathies and adverse drug reactions
(Smith 2002). Metabolic acidosis can be caused by diabetic
ketoacidosis, lactic acidosis (heavy exercise or hypoxia), CRF,
diarrhoea, toxic agents (methanol, ethylene glycol or aspirin) or
as compensation for respiratory alkalosis (Smith 2002). It can be
concluded in this horse that the metabolic acidosis was a result
of decreased renal bicarbonate reabsorption and decreased acid
excretion (sulfates, phosphates, urates and hippurates) because
of its acutely reduced kidney function (Hamm and others
2015). However, a definite cause for the development of AKI
could not be diagnosed. Although, intake of acorns could have
been a possible cause, the horse did not exhibit clinical signs
typically seen with acorn poisoning such as colic and diarrhoea
due to colitis (Smith and others 2015).
TREATMENT
Initially, the horse’s general condition and appetite were good.
However, its metabolic acidosis and overall condition gradually
worsened by day 2 of hospitalisation. Its metabolic acidosis was
followed up through regular blood examinations and corrected
with HCO3- supplementation (day 3 to day 7) to the constant
rate infusion by adding 40 g of NaHCO3 to one litre of saline.
From day eight on, bicarbonate was administered orally in a

2 Vandendriessche VL, et al. Vet Rec Case Rep 2016;4:e000309. doi:10.1136/vetreccr-2016-000309

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TABLE 2: Results of blood haematology and ionograms during hospitalisation
Day 0 2 4 6
PCV (%) 36 36 36 35
BE (mEq/l) −6.8 −8.8 −5.7 −4.8
Na+ (mmol/l) 133 127 129 128
K+ (mmol/l) 2.5 3.1 3.1
Ca++ (mmol/l) 1.5 1.5 1.5 1.4
pH 7.2 7.2 7.28
HCO-3 17 20.8 21.9
Data reference range from internal laboratory, Ghent University
BE, base excess; PCV, packed cell volume
gradually decreasing amount corresponding to the amount of
blood bicarbonate (5×10 g NaHCO3 for five days, then 3×10 g
on day 13 and 1×10 g on day 14). Results of follow-up blood
examinations to correct metabolic acidosis can be found in
Table 2. Because a urinary tract infection was suspected, antibio-
tics were commenced for seven days on day 5 of hospitalisation:
trimethoprim-sulfadoxide was given at 2.5 mg trimethoprim
and 12.5 mg sulfadoxine per kg BW intravenously (Borgal 24
per cent). Additionally, NSAIDs were administered intravenously
for three days at 2.2 mg Flunixin meglumine per kg BW
(Emdofluxin 50 per cent). Results of the urine culture revealed
presence of Streptococcus species and Staphylococcus interme-
dius, which were responsive to trimethoprim/sulfamethoxazole.
During hospitalisation, the horse was offered a variety of
foods five times daily to stimulate appetite: hay and haylage,
carrots and a handful of concentrate. Amounts are unknown
and variable upon the person giving the food. Because appetite
gradually decreased, fluid therapy was supplemented with 30
per cent glucose. Glucose supplementation was discontinued by
day 10.
Upon discharge, metabolic acidosis had completely normal-
ised but kidney function was not restored yet, thus the horse
was diagnosed with ARF. Since there was a risk for CRF devel-
opment if insufficient kidney function improvement would
occur in the months following discharge, the Department of
Nutrition was contacted for nutritional advice. The aim of the
nutritional support was to unburden remaining functional
kidney cells, to achieve weight gain, to ensure appetite and to
minimise the risk of CRF development. The horse weighed
436 kg and had a body condition score (BCS) of 3/9 on the
Henneke scale (1983) (underweight) with mild muscle wasting.
Based on the information provided by the owner from a nutri-
tional history form about feeding and management at home, a
nutritional evaluation was made. The horse had a 10 per cent
energy deficit to maintain actual BW, a crude protein (CP)
intake of 1.62 g/kg BW, a sugar and starch intake of 1.8 g/per kg
BW/meal, a calcium intake of 28.7 g/day and a sodium intake of
11.19 g/day. Taking into account recommendations for animals
with CRF, the following advice (daily amounts) was given:
unlimited pasture access; 7.5 kg haylage preferably late cut;
100 mL vegetable oil (corn oil); 300 g beet pulp (Pavo
Speedibeet) weighed dry; 1.4 kg cornflakes; 30 mL ω-3 rich oil
(Cavalor OilMega); 75 g ration balancer (Cavalor NutriPlus);
240 g diet supplement (Boehringer Pronutrin); and 15 g of a
Vitamin C supplement. Unfortunately, the owners were only
able to supply two meals a day. The aim of the nutritional rec-
ommendation was to increase the weight of the horse and to
optimise BCS by supplying 25 per cent more energy than
required for maintenance. Furthermore, it had to supply
Vandendriessche VL, et al. Vet Rec Case Rep 2016;4:e000309. doi:10.1136/vetreccr-2016-000309
Veterinary Record Case Reports
8 10 12 Reference range
36 36 38 30–46
−2.3 0.3 5.4 −5 to +5
129 128 133 135–150
2.5 3.6 2.8 3.0–5.9
1.5 1.5 1.3 1.4–1.7
7.33 7.37 7.35–7.45
23.7 25.8 31.7 28.6±1.9
sufficient proteins for physiological purposes without supplying
excessive protein; to provide additional ω-3 polyunsaturated
fatty acids (PUFAs) and vitamin C; and to limit the uptake of
salt and calcium. The horse went home with the advice to only
supply pasture and hay or haylage, preferably from a late cut,
awaiting the personalised nutritional advice. The nutritional
advice was given seven days after discharge and the
owners started introducing the new ingredients gradually. Since
no adverse reactions occurred in this transition period, the
horse received its full ration 10 days later. Energy and
protein requirements were calculated using the Centraal
Veevoeder Bureau (CVB) guidelines (2013) for an estimated
ideal BW (iBW) of 485 kg. Every macroelement and microele-
ment in the diet was individually verified using National
Research Council (NRC) guidelines (2007) to ascertain adequate
intakes and to avoid toxic levels. Details of the ration can be
found in Fig 1.
OUTCOME AND FOLLOW-UP
Three months after discharge, a complete veterinary check-up
was performed by the referring veterinarian. The following
results were obtained: a measured BW of 485 kg (Carroll and
Huntington 1988), its BCS was 4/9 (Henneke and others 1983)
and its muscle condition score (Freeman and others 2011) was
normal. Blood results can be found in Table 1 (day 112): creat-
ine levels had normalised; total protein and albumin concentra-
tions were below the reference range even though muscle mass
had increased. All specific liver values were within the reference
range except for total bilirubin. Icterus was not present. The
appetite of the horse was very good. Since the horse’s kidney
function seemed to have normalised, protein intake was tempor-
arily increased by gradually adding alfalfa pellets to the existing
nutritional recommendation (Fig 2). Main changes were an
increased protein intake from 0.95 g CP/kg iBW/day to 1.5 g
CP/kg iBW/day and an increased calcium intake from 32 g/day
to 78 g/day. Blood work was performed two weeks after the
nutritional change to verify the effect of these adjustments (day
135): there were no elevations in BUN or creatine levels but
serum total protein concentration had increased. Based on these
results the nutritional recommendation was adjusted to achieve
weight maintenance in a healthy horse (Fig 3).
DISCUSSION
Before going into detail on the nutritional choices that were
made, two of the medical decisions that have been made during
the hospitalisation period warrant further explanation. First, the
supplementation of fluids with additional glucose will be dis-
cussed. When a negative energy balance is present because of
decreased feed intake, production of non-esterified fatty acids
3
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Veterinary Record Case Reports

FIG 1: Composition of the nutritional recommendation given after discharge. Energy requirements were calculated using Centraal Veevoeder
Bureau (CVB) guidelines (2013). Every single nutrient present in the ration has been verified to fulfil National Research Council (NRC) (2007)
requirements for maintenance but only a selection of relevant nutrients is illustrated to keep the figure clear. Additionally, the nutrients with
amounts above 100 per cent of NRC requirements were verified to not exceed NRC (2007) toxicity levels. Abbreviations: EWpa, energy requirement
horse; VREp, digestible crude protein

(NEFAs) is stimulated. When the liver is not able to process all
the NEFAs, triglycerides will accumulate in the serum (Smith
2002). Ideally, serum triglycerides should be determined and
followed up in a horse with decreased appetite to tailor its
therapy. However, due to budget limitations this could not be
performed. Additionally, the amounts of glucose administered
did not supply sufficient energy to counteract a negative energy
balance.
The second medical decision the authors will discuss is the
administration of NSAIDs to a horse with known reduced
kidney function. The administration of NSAIDs was deemed
necessary because a urinary tract infection was suspected. Since
the horse was well hydrated through fluid therapy and NSAID
administration was only for three days, known nephrotoxic
effects of NSAID administration (Stillman and Schlesinger
1990) were negligible in this case.
The main goal of nutritional therapy for horses with renal
failure, whether acute or chronic, is to maintain BW, to stimulate
appetite, to avoid muscle loss and to assure quality of life (Geor
and others 2013). To accomplish these goals, the diet of the
horse should be individually tailored and adapted over time
while taking into account results of regular blood work and clin-
ical investigations (Schott 2007).
In small animals, management of renal failure includes a diet
with, among other properties, protein content below 20 per
cent of metabolisable energy since this increases life expectancy
and delays progression of the disease (Roudebush and others
2010). Clinical studies on the dietary effects on progression of
renal failure are not available in horses for the moment.
Therefore, to formulate a diet for horses, extrapolating knowl-
edge from other species is required. Thus, the diet aimed to
limit excess protein intake. Reduced renal function results in

FIG 2: Composition of the nutritional recommendation given at day 112. Energy requirements were calculated using Centraal Veevoeder Bureau
(CVB) guidelines (2013). Every single nutrient present in the ration has been verified to fulfil National Research Council (NRC) (2007) requirements
for maintenance but only a selection of relevant nutrients is illustrated to keep the figure clear. Additionally, the nutrients with amounts above 100
per cent of NRC requirements, were verified to not exceed NRC (2007) toxicity levels. Abbreviations: EWpa, energy requirement horse; VREp,
digestible crude protein.

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FIG 3: Composition of the nutritional recommendation given at day 135. Energy requirements were calculated using Centraal Veevoeder Bureau
(CVB) guidelines (2013). Every single nutrient present in the ration has been verified to fulfil National Research Council (NRC) (2007) requirements
for maintenance but only a selection of relevant nutrients is illustrated to keep the figure clear. Additionally, the nutrients with amounts above 100
per cent of NRC requirements, were verified to not exceed NRC (2007) toxicity levels. Abbreviations: EWpa, energy requirement horse; VREp,
digestible crude protein.

retention of many toxic solutes from protein catabolism, which,
when combined, cause lethargy, altered mentation, decreased
appetite and a number of other adverse effects like halitosis and
gastrointestinal ulcerations (Vanholder and Glorieux 2003). A
reasonable goal for protein intake in horses with renal failure is
1–1.5 g CP/kg iBW/day (Geor and others 2013) and the advised
ration contained 0.95 g CP/kg iBW/day. Since the horse also had
pasture access, total protein intake will have been higher than
calculated for the ration alone. However, pictures of the pasture
in wintertime revealed very limited availability of grass. Hay or
haylage of late cut typically contains less protein than early cut
(CVB 2013). Therefore, owners were encouraged to supply late
cut hay or haylage. Follow-up of blood serum values for BUN,
creatine, albumin and total protein are necessary to evaluate the
adequacy of protein intake and to tailor each individual case.
Follow-up blood work of this horse (day 112) indicated that
despite having regained muscle mass, serum total protein and
albumin were below the reference range. This could be
explained by either a shortage in supply or continued urinary
protein losses. Ideally, a sterile urine sample should be taken to
verify proteinuria evolution. However, sedation or catheterisa-
tion is required for this and owners did not allow either of these
procedures. Since the serum total protein concentration
improved after increasing the protein intake through the diet
(day 135), it can be concluded that the protein content of the
initial recommendation was too low to support muscle gain and
replenish depleted protein storage simultaneously.
The ration also contained beet pulp, which is rich in pectins
and thus in fibre and is relatively rich in energy but contains
little protein (Sauvant and others 2004). The additional benefit
of this product is the supply of extra fluids to promote diuresis.
A disadvantage, however, is that it also supplies extra calcium to
the diet. Compared with the contribution of calcium from the
roughage and the supplement in this ration, the amount of
calcium added by the beet pulp was negligible.
To supply additional energy and increase palatability, use of a
palatable concentrate was warranted. This concentrate, however,
should contribute minimally to additional dietary protein. On
the other hand, quantities supplied should avoid excessive sugar
and starch intake per meal. Cornflakes were chosen because
they are very palatable, provide energy mainly through starch
and contain less protein compared with other grains (CVB
2013). Because owners were only able to feed two meals a day,
cornflake supplementation had to be limited to 1.4 kg, which
resulted in a sugar and starch intake of 1.45 g/kg iBW/meal.
This was well below the recommended safe intake of 2 g/
kg iBW/meal (Julliand and others 2006). When supplying sugar
and starch below this reference, occurrence of adverse reactions
like development of diarrhoea, colic, laminitis and gastric ulcers
can be avoided (Geor and others 2013).
Because this horse required extra energy to achieve weight
gain, supplementation with oil was necessary. The supplementa-
tion of ω-3 fatty acids to the diet of human beings and small
animals has been shown to improve renal function, to decrease
loss of proteins through the urine and to decrease mortality
(Fassett and others 2010, Roudebush and others 2010). For
horses, however, there are no clinical trials on dosage or the
beneficial effects. Nonetheless, a comparative approach would
warrant the use of ingredients rich in α-linolenic acid (ALA) like
linseed oil (contains 57 g ALA per 100 ml) and pasture.
Therefore, the ration was supplemented with a commercially
available oil (Cavalor OilMega), which contains linseed oil.
Patients with renal failure suffer from ongoing membrane
damage by oxygen radicals contributing to the progressive
nature. Supplementation with antioxidants has been demon-
strated to reduce oxidative stress and creatine concentrations in
dogs with CRF (Brown 2008). Whether antioxidant administra-
tion in horses with renal disease would be beneficial is
unknown, but since this horse had limited access to fresh grass
from which antioxidants can be derived (Geor and others
2013), vitamin C was added to supply 30 mg/kg iBW (Kolb and
others 1983). Vitamin E is also an important antioxidant and
was supplied above the recommendation of 1 IU/kg iBW plus
1 IU/ml of oil added to the diet (Harris 1999). This would
require a dietary vitamin E content of at least 615 IU. This
horse received 900 IU.
In contrast to other species that develop hyperphosphataemia
with progressing renal failure, horses tend to develop

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Veterinary Record Case Reports
hypercalcaemia, which is a pathognomonic finding (Schott and
others 1997). This can be explained by a decreased renal excre-
tion of calcium in horses with reduced renal function together
with an unaltered calcium uptake from the diet since hormonal
regulation of intestinal calcium absorption in horses is poor
(Breidenbach and others 1998). The calcium intake was calcu-
lated to supply maintenance requirements and thus avoided
excessive intakes.
The retention of toxic solutes in human beings with renal
failure and potentially also in horses predispose these patients to
gastrointestinal ulcerations (Vanholder and Glorieux 2003). By
limiting sugar and starch intakes to less than 2 g/kg iBW/meal and
supplying multiple small meals throughout the day (preferably
four to six), the gastric mucosa can be protected. To further
reduce the risk of gastric ulcer development, commercial supple-
ments that contain a pectin-lecithin complex (Pronutrin) could be
used (Venner and others 1999). However, their efficacy in ulcer
development prevention has been questioned in more recent
studies (Sanz and others 2014). Because renal failure is a progres-
sive disease and gastrointestinal ulcerations could develop with
time, a stricter intake of less than 1 g/kg iBW/meal of sugar and
starch (Luthersson and others 2009) should be implemented when
gastric ulcers are diagnosed through endoscopy.
A moderate sodium restriction reduces proteinuria and
decreases blood pressure in patients with CRF (Humalda and
Navis 2014, Roudebush and others 2010). Although blood pres-
sure measurements in horses are not routinely performed and
certainly not in field conditions, moderate sodium restriction
might slow the progression of the disease. Based on NRC
recommendations (2007), this horse would require a minimum
of 9.7 g of sodium. Since the ration supplied 11.71 g, availabil-
ity of a salt lick was discouraged to avoid additional intake.
Because appetite can be precarious in horses with renal
failure, crushed gingerbread cookies can be added to the diet to
stimulate uptake (Jarvis 2009).
In conclusion, for this horse, the blood results of day 135
suggest that the horse has sufficient renal function left to excrete
toxic solutes, and therefore has not developed CRF. It is,
however, impossible to quantify the contribution of this specific
nutritional recommendation to the recovery of kidney function.
It would certainly be interesting to study this in more detail using
more horses and compare normalisation of blood parameters
between those on a CRF diet and those on a maintenance diet.
The elevated bilirubin values require further investigation.
The main goal of nutritional therapy in horses with renal failure
is to maintain BW by achieving sufficient energy intake. Protein
intake should be individually tailored to avoid excessive protein
intake on the one hand and to avoid muscle loss on the other
hand. Caution must be taken not to depend on sugar and starch
alone for energy since this can contribute negatively to the devel-
opment of gastric ulcers. The use of vegetable oils as an energy
source is a safe alternative. Use of antioxidants, ω-3 PUFAs or
sodium restriction has not been clinically proven to delay renal
failure progression in horses, even though other species with renal
failure benefit from these nutritional recommendations.
Contributors VLV is the main contributor with input and corrections from the
coauthors.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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Vandendriessche VL, et al. Vet Rec Case Rep 2016;4:e000309. doi:10.1136/vetreccr-2016-000309 7

 Downloaded from http://vetrecordcasereports.bmj.com/ on June 12, 2016 - Published by group.bmj.com

Successful nutritional management of a

21-year-old Quarter Horse gelding with acute
renal failure
Veerle Ludmilla Vandendriessche, Alexander Dufourni, Gunther van Loon
and Myriam Hesta

Vet Rec Case Rep 2016 4:

doi: 10.1136/vetreccr-2016-000309

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http://vetrecordcasereports.bmj.com/content/4/1/e000309

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Topic Articles on similar topics can be found in the following collections

Collections Education (3)
Horses and other equids (21)
Internal medicine (31)
Nutrition (7)
Renal medicine (8)

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