Received: 26 April 2024 Accepted: 26 April 2024

DOI: 10.1111/jvim.17101

CONSENSUS STATEMENT

Consensus Statements of the European College of Equine Internal Medicine (ECEIM) provide the veterinary community with up-to-date informa-
tion on the pathophysiology, diagnosis, and treatment of clinically important animal diseases. The ECEIM Board oversees selection of relevant
topics, identification of panel members for each topic with the expertise to draft the statements, and other aspects of assuring the integrity of the
process. The statements are derived from evidence-based medicine whenever possible and the panel offers interpretive comments when such
evidence is inadequate or contradictory. A draft is prepared by the panel, followed by solicitation of input by the ECEIM membership which may
be incorporated into the statement. It is then submitted to the Journal of Veterinary Internal Medicine, where it is edited prior to publication. The
authors are solely responsible for the content of the statements.

ECEIM consensus statement on equine kidney disease

Gaby van Galen 1,2 | Thomas J. Divers 3 | Victoria Savage 4 |

Harold C. Schott II 5 | Natalia Siwinska 6
1
Goulburn Valley Equine Hospital, Congupna, Victoria, Australia
2
Sydney School of Veterinary Science, University of Sydney, Sydney, New South Wales, Australia
3
College of Veterinary Medicine, Cornell University, Ithaca, New York, USA
4
Three Counties Equine Hospital, Gloucestershire, United Kingdom
5
College of Veterinary Medicine, Michigan State University, East Lansing, Michigan, USA
6
Faculty of Veterinary Medicine, Wroclaw University of Environmental and Life Sciences, Wroclaw, Poland

Correspondence
Gaby van Galen, Goulburn Valley Equine Abstract
Hospital, Congupna, VIC, Australia.
The aim of this consensus statement is to summarize and appraise scientific evidence
Email: gaby@equinespecialists.eu
and combine this with the clinical experience of a panel of experts to optimize recom-
mendations on how to recognize and manage kidney disease in horses.

KEYWORDS
acute kidney injury, chronic kidney disease, horse, renal

1 | AZOTEMIA excretion, with urinary tract obstruction or rupture) should be differ-

entiated. Prerenal causes for azotemia are frequently mentioned;
Azotemia is the term for increased blood concentrations of urea, however, in the panelists' opinions, many are linked with inflammatory
serum creatinine (sCr), and other nonprotein nitrogenous substances. changes, toxic insults, or associated with acute kidney injury (AKI).
Prerenal (decreased renal blood flow [RBF], e.g., dehydration, hypovo- Furthermore, there is a continuum between prerenal and renal azote-
lemic shock, cardiac failure), renal (decreased glomerular filtration rate mia, where poor perfusion eventually leads to intrinsic kidney
[GFR] caused by renal injury), or postrenal azotemia (failure of damage.

Abbreviations: 99mTc, 99-metastable technetium; AKI, acute kidney injury; ARF, acute renal failure; BUN, blood urea nitrogen; CKD, chronic kidney disease; CRF, chronic renal failure; DTPA,
diethylenetriaminopentaacetic acid; ESKD, end-stage kidney disease; FE, fractional excretion; GFR, glomerular filtration rate; GN, glomerulonephritis; IRH, idiopathic renal hematuria; IRIS,
International Renal Interest Society; IVFT, intravenous fluid treatment; NSAIDs, nonsteroidal anti-inflammatory drugs; PD, polydipsia; PPID, pituitary pars intermedia dysfunction; PU, polyuria;
RBF, renal blood flow; RTA, renal tubular acidosis; sCr, serum creatinine; SDMA, symmetric dimethylarginine; USG, urine specific gravity.

This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any
medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
© 2024 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals LLC on behalf of American College of Veterinary Internal Medicine.

2008 wileyonlinelibrary.com/journal/jvim J Vet Intern Med. 2024;38:2008–2025.

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VAN GALEN ET AL. 2009

In horses sCr is freely filtered by the glomerulus and is neither (IVFT) should be commenced before, or soon after, administration of
reabsorbed nor secreted.1 Therefore, sCr is inversely proportional to potentially nephrotoxic drugs. The panelists agree that clinical judgment
GFR and a functional marker. In advanced disease, a small decrease in should be used to decide if benefits of prompt administration of a poten-
GFR results in a large sCr increase. In early renal disease, a large tially nephrotoxic compound before initiating fluid treatment outweigh
decrease in GFR results in only a small sCr increase, and sCr does not the risk of AKI. Simultaneous use of several nephrotoxic drugs increases
increase above reference limits until GFR is reduced by nearly 75%.2 the risk of AKI. In noncritically ill human patients, escalating the burden
As creatinine is formed by muscle, heavily muscled animals can have of nephrotoxic drugs from 2 to 3 more than doubles the risk of develop-
sCr values above reference limits.3,4 In humans, production of creati- ing AKI, and 25% of those receiving 3 or more develop AKI.29
5
nine is reduced in sepsis. This has not been demonstrated in horses
but could limit detection of AKI in critically ill horses. Other causes
Because of the multifactorial influences on blood urea nitrogen AKI can be caused by immune-mediated glomerular barrier injury
(BUN), including dietary protein and protein metabolism, BUN is a (e.g., purpura hemorrhagica), idiosyncratic hypersensitivity reactions
less specific estimator of GFR and has not been found useful to causing acute interstitial nephritis, Actinobacillus spp. infections in
diagnose AKI. foals,30 and leptospirosis.31

2 | R E N A L SY N D R O M E S 2.1.3 | Diagnosis

2.1 | Acute kidney injury Clinical signs of AKI are often difficult to discern from signs from the
primary disease. Careful attention to urine output must be paid to
AKI represents a continuum of inapparent nephron injury or loss to detect oliguria (<0.5 mL/kg/h). Inappetence and lethargy persisting
acute renal failure (ARF). longer than expected as the primary disease resolves should raise sus-
picion. Neurological signs (uremic encephalopathy) are occasionally
seen with severe azotemia.32
2.1.1 | Prevalence In human and small animal medicine, scoring systems have been
developed to document AKI based on sCr and urine output.33-35 The
Prevalence studies in horses are lacking; however, estimates are that Veterinary Acute Kidney Injury system has been applied to hospitalized
3% to 23% of a hospitalized population are affected (published6 and horses (Table 2).6 Although unvalidated, the panelists consider scoring
unpublished data from panelists). systems worth implementing in practice with a focus on detecting small
increases in sCr from baseline even when it remains within reference ranges.
Electrolyte abnormalities are not present in all cases with AKI but
2.1.2 | Risk factors are common in ARF, especially hyponatremia and hypochloremia.
Marked hyperkalemia is seen in peracute oliguric/anuric ARF, postre-
Decreased renal blood flow and hypoxia nal obstruction, or uroabdomen. Calcium and phosphorus concentra-
The kidney is particularly susceptible to ischemic injury, especially the tions are variable.
less perfused medulla. Hypotension, dehydration, hypovolemia, or ane- Measurement of urine output is challenging in adult horses. Col-
mia are risk factors for AKI because of decreased RBF and hypoxia. lection of a urine sample before IVFT can be helpful to evaluate renal
function. With adequate tubular function, urine specific gravity (USG)
Systemic inflammatory response syndrome is increased (>1.035) in hypovolemic states. In ARF, concentrating
Systemic inflammation accompanying sepsis and endotoxemia ability can be lost and urine becomes dilute (USG <1.020) despite
can result in hypotensive injury, renal microcirculatory dysfunction, hypovolemia. Urinalysis can identify microscopic hematuria, casts and
thrombotic injury, infarction, fibrin deposition, and renal cortical glucosuria.
7,8
necrosis in horses. Panelists do not consider renal rectal palpation a reliable diagnos-
tic tool. Renal ultrasonography is often unremarkable with AKI (see
Nephrotoxicity Imaging 3.3). Renal biopsy results rarely alter management of ARF,
Nephrotoxic agents described in horses include aminoglycosides, oxy- and biopsy is not recommended by the panelists.
tetracycline, bisphosphonates, and nonsteroidal anti-inflammatory
drugs (NSAIDs). Many other medications, including omeprazole and
hydroxyethyl starches, are nephrotoxic in humans; however, there is 2.1.4 | Treatment
currently no evidence for this in horses. Endogenous nephrotoxins,
such as myoglobin and hemoglobin, can also induce AKI (Table 1).26,27 Initial treatment focuses on correcting the primary disorder. Intrave-
As recognized in humans,28 foals and geriatric horses are likely at nous fluid treatment is the therapeutic cornerstone to normalize intra-
greater risk for nephrotoxic AKI. With hypovolemia, IV fluid treatment vascular volume and blood pressure, and subsequently RBF and GFR
 19391676, 2024, 4, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/jvim.17101 by Test, Wiley Online Library on [03/09/2025]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
2010 VAN GALEN ET AL.

TABLE 1 Evidence for potential nephrotoxic agents commonly used in equine practice.

Panel recommendation,
Mechanism of Evidence of nephrotoxicity Evidence of nephrotoxicity other than cautious use in at
Agent nephrotoxicity in humans in horses risk patients
Aminoglycosides Accumulation in proximal Risk factors include age, Reported.12 Dosing
tubular cells. Caused by hypovolemia, preexisting schedules should be
sustained drug exposure renal dysfunction, altered in neonates.13,14
(frequent dosing), not combination with
individual high doses.9 furosemide.10 Gentamicin
is more nephrotoxic than
amikacin.11
Oxytetracycline Unknown Rare AKI caused by high dose for Evaluate sCr before
flexural limb deformities in administration of high
foals15 and normal doses to foals.
antimicrobial doses in
adults.
NSAIDs Inhibition of COX blocks Uncommon In healthy horses, NSAIDS, especially
renal autoregulatory phenylbutazone induced phenylbutazone should be
response to hypoperfusion. medullary crest necrosis avoided in at risk horses.
Causing medullary crest with prolonged
necrosis and interstitial supraphysiological doses16
nephritis. and AKI with normal
doses.17,18 COX2 selective
drugs carry a similar19,20 to
lower risk for
nephrotoxicity.18
Bisphosphonates Proximal tubule Reported AKI reported and may be Evaluate sCr before use.
degeneration, segmental more common with Caution with concurrent
glomerulosclerosis and concurrent NSAIDs.21 NSAIDs.
apoptosis.
Polymyxin B Accumulation in proximal Reported. No longer Reported in hospitalized Avoid concurrent
tubular cells causes acute recommended for sepsis. horses and when aminoglycosides.
tubular necrosis. coadministered with
gentamicin.22,23
Vitamin D Hypercalcemia and renal Reported Toxicity observed in horses Avoid supplementation in at
mineralization. fed grain diets high in risk horses.
cholecalciferol.24
Vitamin K3 Renal tubular nephrosis. Observed, not used in Toxicity observed clinically Avoid use.
humans. and induced
experimentally when
administered at
recommended doses.25

Note: Antimicrobial stewardship should be considered when selecting antimicrobials.

Abbreviations: AKI, acute kidney injury; COX, cyclooxygenase; NSAID, nonsteroidal anti-inflammatory drug; sCr, serum creatinine.

T A B L E 2 Veterinary Acute Kidney Injury (VAKI) scoring system Within the initial 24 to 72 hours of treatment of reversible AKI,
for horses (unvalidated).6 sCr can be expected to decrease by 30% to 50%. With nephrotoxic
Change in serum creatinine from baseline AKI panelists have observed that it can take longer for sCr to decline.
Stage (baseline = 100%) Urine output during IVFT should be observed. For anuric or oliguric
0 <150% cases, the aim of IVFT is to induce diuresis and polyuria. Failure to
1 150%-199% or absolute increase of >0.3 mg/dL produce urine within 12 hours after IVFT is considered a “red flag” for
(>26.5 μmol/L) oliguria and patients should be evaluated for obstructive disorders.
2 200%-299% With oliguria unrelated to obstruction, use of a diuretic agent can be
3 300% or absolute increase to >4.0 mg/dL (>354 μmol/L) considered (Table 3). A furosemide challenge test can be performed in
a euvolemic AKI patient. In human medicine, this test is a predictor of
AKI severity and outcome.43 No further doses are advised unless a
(see Principles Intravenous Fluid Therapy). For persistent hypotension favorable response with urine production is witnessed. Mannitol is no
after adequate fluid replacement, inotropes and vasopressors can be longer recommended as it can be nephrotoxic. Supportive evidence
used (Table 3). for dopamine agonists is weak. Other than IVFT, all other medical
 TABLE 3 Therapies to consider for oliguric/anuric acute renal failure.
VAN

Consensus for use in Consensus for use in

Drug Dose Mechanism of action Evidence in humans Evidence in horses Adverse effects foals adult horses
Diuretics
GALEN ET AL.

Furosemide Bolus 0.5-2 mg/kg Decreases sodium, Induces diuresis but Unavailable. High dose can be Single high dose Single high dose
IV/IM q2h-q6h or chloride, and without clinical nephrotoxic. furosemide test is furosemide test is
CRI 0.25-2 mg/kg/h potassium tubular benefit in AKI. Increase in sCr can 1st-line treatment of 1st-line treatment of
reabsorption. occur through normotensive foals normotensive adults
tubuloglomerular with anuria/oliguria. with anuria/oliguria.
feedback.
Electrolyte
disturbances.
Single high dose
advised (furosemide
test; 2 mg/kg). No
further doses unless
good response. If
positive response
switch to CRI.
Mannitol 0.25-1 g/kg IV q4h- Increases osmotic Associated with Unavailable. Osmotic renal tubular Not recommended. Not recommended.
q6h (20% solution). pressure in renal increased risk of injury.
tubules. AKI.
Inotropes / vasopressors
Dobutamine 2–20 μg/kg/min Beta-1 agonist: Beneficial effect on Increased blood Arrhythmias 1st-line treatment for Common treatment
inotropic effect. renal function for pressure.36 hypotension despite for anesthesia
cardiorenal IVFT, and for induced
syndrome. anesthesia induced hypotension.
hypotension.
Not witnessed.a Can be used in
selected
hypotensive
nonanesthetized
adults. Limited.a
Norepinephrine 0.2-0.3 μg/kg/min Alpha-1 agonist: Recommended for Increased blood Arrhythmias Common treatment Possible vasopressor,
peripheral treatment and pressure in for hypotension especially for
vasoconstriction. prevention of AKI in anesthetized despite IVFT and distributive shock.
humans with horses37 and dobutamine. Usually
distributive shock. critically ill foals.38 in conjunction with
Improved renal dobutamine.
function in healthy Interchangeable
foals.39 No evidence with AVP.
in standing horses.

(Continues)
2011

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 2012

TABLE 3 (Continued)

Consensus for use in Consensus for use in

Drug Dose Mechanism of action Evidence in humans Evidence in horses Adverse effects foals adult horses
Not witnessed.a None in
nonanesthetized
adults.a

Arginine 0.1-2.5 mU/kg/min Increase water Similar effect to Increased blood Arrhythmias, Treatment for Possible vasopressor,
vasopressin reabsorption in norepinephrine for pressure and urine hyponatremia hypotension despite especially for
(AVP) distal tubule and treatment and output in IVFT and distributive shock.
collecting duct. prevention of AKI in hypotensive foals.38 dobutamine. Usually
Vasoconstriction at humans with in conjunction with
high doses. distributive shock. dobutamine.
Interchangeable
with
norepinephrine.
Not witnessed.a None in
nonanesthetized
adults.a
Fenoldopam 0.04 mg/kg/min Selective dopamine Not recommended for Increased urine output Potential treatment for Potential treatment for
mesylate (D1) agonist: renal treating/preventing in healthy foals.40 normotensive foals normotensive adults
vasodilation. AKI. No additional with anuria/oliguria. with anuria/oliguria.
benefit to renal
function when
combined to
norepinephrine.39
Limited.a None (cost-
prohibitive)a
Low-dose 1–5 μg/kg/min Renal dopamine Not recommended for Increased renal blood Arrhythmias 2nd-line treatment 2nd-line treatment
dopamine receptors-agonist: treating/preventing flow and urine after unsuccessful after unsuccessful
renal vasodilation AKI. production in furosemide furosemide
and natriuresis. healthy horses.41 challenge in challenge in
normotensive foals normotensive adults
with anuria/oliguria. with anuria/oliguria.
Anecdotal clinical Not witnessed.a Some have moderate Some have moderate
success in adult experience.a experience.a
horses with oliguric
ARF. Oliguria may
return when
VAN

discontinued.
GALEN ET AL.

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VAN GALEN ET AL. 2013

treatments for AKI remain unproven because no drug has obtained

Potential treatment for

normotensive adults

Potential prophylactic
Consensus for use in
evidence of improving outcome of AKI/ARF in human clinical trials. In
equine medicine, large trials are unlikely, but case reports on treating
oliguric ARF can give guidance to treatment decisions.

treatment.
adult horses

with ARF.
If oliguric ARF cannot be converted to polyuria, renal replacement

None.a

None.a
(dialysis) can be considered in select cases.15,44 Peritoneal dialysis has
been described45-47; its therapeutic success can be questioned in
some of these cases as urination was present before dialysis,47
Potential treatment for

Potential prophylactic
normotensive foals
Consensus for use in

however, high aminoglycoside concentrations and azotemia were

1 has experience.a effectively reduced.46 The panelists recommend consideration of peri-

treatment.
with ARF.

toneal dialysis in select cases with persistent oliguria and high blood

Abbreviations: AKI, acute kidney injury; ARF, acute renal failure; AVP, arginine vasopressin; CRI, continuous rate infusion; IVFT, IV fluid treatment; sCr, serum creatinine.
concentrations of nephrotoxic drugs despite appropriate IVFT. How-

None.a
foals

ever, the procedure can be challenging, lead to complications and

should only be performed in a hospital setting.
nervous signs.42

nervous signs.42
tachypnoea and

tachypnoea and
Adverse effects

2.1.5 | Prognosis
tachycardia,

tachycardia,
Dose-related

Dose-related

Azotemia has been identified as a poor prognostic indicator when identi-

fied secondary to many conditions48-50 but is often disregarded as
“prerenal” instead of being an indicator of AKI. As equine intensive
horses.42 Anecdotal

care expands, AKI will likely be increasingly recognized as an

Evidence in horses

Induced diuresis in

success treating

outcome-limiting factor. In humans, early detection of AKI, before

oliguric ARF in
healthy adult

progression to ARF and need for dialysis, improves patient outcome.29

Unavailable.
neonates.

Although there are no data for horses, panelists agree that early detec-
tion of AKI likely improves outcome and failure to recognize and manage
AKI early can result in ARF.
Prognosis is largely dependent on success in treating the primary
Lowers sCr in pediatric

dose helped prevent

urine production or
Evidence in humans

disease process. Severe increases in sCr do not necessarily equate to a

patients with AKI

with severe birth

Prophylactic single
improvement of

AKI in neonates

poor prognosis, and panelists have observed that response to IVFT is

but without

a better prognostic indicator. If within 72 hours of starting treatment,

outcome.

asphyxia.

the patient is producing adequate urine and sCr is decreasing, progno-

sis can be favorable.51 Horses with persistent azotemia that remain
oliguric or anuric have a guarded to poor prognosis. Prognosis is grave
for uremic encephalopathy.32
Mechanism of action

shorter acting than

Final sCr may not be reached until 2 to 6 months postinjury, as

vasoconstrictor.

vasoconstrictor.
Less potent and
Afferent arteriole

Afferent arteriole
theophylline.

remaining functional nephrons hypertrophy. If sCr returns to near nor-

mal, the horse likely has sufficient renal function for a relatively
normal and athletic lifespan. Despite clinical recovery, affected horses
may have residual structural damage and decreased function, which can
reduce their tolerance to future insults, and which can eventually progress
to chronic kidney disease (CKD).52 Based on personal observations of
2–5 mg/kg slow IV

1 of the panelists on response to treatment in horses with ARF,

8 mg/kg IV q12h

approximately 60% recover, 30% are euthanized and 10% improve

q8h-q12h

but develop CKD.

Dose
(Continued)

Adenosine antagonists

2.1.6 | Prevention
Panelists' experience.
Aminophylline

Theophylline

In at risk patients, sCr concentration should be closely monitored, primary

TABLE 3

disease and hypovolemia and hypotension corrected as soon as possible,

Drug

nephrotoxic drugs used cautiously, and simultaneous use of several neph-

rotoxic drugs avoided.
a
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2014 VAN GALEN ET AL.

Intravenous sodium bicarbonate is often suggested in human increased glomerular barrier permeability characterized by proteinuria
medicine to protect against pigment nephrosis through urine alkalini- and microscopic (and occasionally macroscopic) hematuria. Focal glo-
zation; however, it has not been shown to be superior to IVFT without merular disease is a common histopathologic finding consequent to
sodium bicarbonate.53 To limit the risk for aminoglycoside induced subclinical glomerular injury; however, progression to CRF remains
AKI, IV, or PO calcium (feeding alfalfa or other legume hays can be a rare.61 Panelists have observed that GN can occur in patients with
practical way to increase calcium intake) and vitamin C administration infectious disease or vasculitis syndromes but remain unrecognized
54,55
have been described. These treatments are not well documented, because of lack of azotemia unless urinalysis is performed revealing
are not routinely used by the panelists, and no consensus was reached hematuria and proteinuria.
about them.
Infiltrative causes
Infiltrative causes of CKD include neoplasia (lymphoma, carcinoma),62
2.2 | Chronic kidney disease nephroblastoma, amyloidosis, and Halicephalobus gingivalis.63 Occa-
sionally these can lead to CRF.
CKD is an irreversible, progressive disease of the kidneys, with a dura-
tion greater than 3 months. The International Renal Interest Society End-stage kidney disease
(IRIS) has developed a staging system for CKD for dogs and cats based End-stage kidney disease (ESKD) describes the final stages of CKD
on sCr, and a similar system been suggested for horses (Table 4).56 where kidneys are pale, shrunken, and firm, with an irregular surface and
adherent capsule. It is often impossible to determine the inciting cause.

2.2.1 | Causes
2.2.2 | Diagnosis
Anomalies of development
Congenital disorders include renal agenesis, hypoplasia, dysplasia, and CKD can be subclinical. The most common clinical signs of CKD pro-
polycystic kidney disease. Affected equids are born with decreased gressing into CRF are loss of body condition (86%) and mild to moder-
renal functional reserve and are at increased risk of developing ate polyuria and polydipsia (PU/PD; 42%).57 Accumulation of dental
chronic renal failure (CRF).57 tartar, especially on canine teeth, gingivitis, oral and gastro-intestinal
ulcers, and decreased performance are other possible findings. Hyper-
Chronic interstitial nephritis tension can be present64 and panelists recommend measurement of
Tubulointerstitial disease is usually a consequence of acute tubular necro- indirect blood pressure. Ventral edema may be noted with GN.
sis secondary to ischemia or nephrotoxicity8 and rarely also develops as Subclinical stages can be detected incidentally. Most horses usu-
adverse drug reaction. Subsequent loss of vasculature around tubules ally have moderate to severe azotemia (IRIS stages III and IV) when
coupled with cell cycle arrest can lead to progressive interstitial fibro- clinical signs are initially recognized. Sodium and chloride concentra-
sis.52 CKD may not be recognized for months to years after prior AKI. tions are often mildly decreased. Hypercalcemia is unique to horses65
Chronic interstitial nephritis (CIN) can also be caused by ascend- and diet dependent; high values can return to normal within days of
ing urinary tract infection resulting in pyelonephritis. changing from legume to grass hay.66 Concurrent hypophosphatemia
Nephrolithiasis is commonly found with CIN. Equine nephroliths are is common and not caused by renal secondary hyperparathyroidism.65
almost exclusively composed of calcium carbonate. These crystals can Mild anemia is commonly observed in CKD. Although there is cur-
be found in collecting ducts of normal equine kidneys but can deposit rently no equine literature, based on other species this is most likely
and grow at sites of renal parenchymal damage and form nephroliths, multifactorial in nature because of blood loss, decreased erythrocyte
which are rarely obstructive. Thus, unlike nephrolithiasis in humans in survival time, nutritional deficiencies, and decreased erythropoietin
which obstructive calcium oxalate stones are often the primary prob- production. Proteinuria can cause hypoproteinemia and hypoalbumi-
lem, the panelists consider nephroliths in horses a consequence nemia. Isosthenuria (USG, 1.008-1.014) is a hallmark of CKD, although
of CKD, rather than the inciting cause. However, when bilateral proteinuria can increase USG.
obstructive disease occurs after calcification of necrotic renal papillae Small renal size and irregular surface are not always apparent
and lodging of the stones in the ureters (ureterolithiasis) this can on rectal palpation. Enlarged ureters can sometimes be palpated
result in chronic interference to urine flow and has been associated with ureteroliths. Ultrasound is useful for evaluation of CKD (see
58,59
with renal failure. Imaging 3.3).

Glomerulonephritis
Glomerulonephritis (GN) is initiated by immune-mediated inflammation 2.2.3 | Treatment
consequent to deposition of immune complexes along the glomerular
barrier. It is commonly recognized with chronic infectious disease CKD is an irreversible process characterized by progressive decline in
(e.g., Streptococcus equi60 and equine infectious anemia virus), but auto- GFR and rise in sCr.29,52 IVFT is unlikely to reduce azotemia unless there
immune glomerular damage can also occur. Glomerulonephritis causes is an AKI component or dehydration exacerbating CKD (see Principles of
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VAN GALEN ET AL. 2015

TABLE 4 An equine chronic kidney disease staging system, based on the small animal International Renal Interest Society (IRIS) staging
system.

Stage Serum creatinine concentration Azotemia Clinical signs of uremia

Normal <180 μmol/L No Absent
(<2.0 mg/dL)
1 <180 μmol/l No Some renal abnormalities are present, such as
inadequate urinary concentrating ability,
abnormalities in urinalysis, abnormal renal palpation
or imaging, increasing creatinine in serial samples.
(<2.0 mg/dL)
2 180-250 μmol/L Mild Mild or absent
(2.0-3.0 mg/dL)
3 251-450 μmol/L Moderate Early Stage 3: absent
Late Stage 3: mild to moderate
(3.1-5.0 mg/dL)
4 >450 μmol/L Severe Moderate to severe
(>6.0 mg/dL)

Source: Olsen and van Galen.56

Intravenous Fluid Therapy). Free access to fresh water is essential. L), many maintain a fair attitude, appetite, and body condition. Once sCr
Patients with GN may benefit from corticosteroids. Based on positive exceeds this level, the progression rate typically accelerates and signs of
effects in people with CKD, treatment with an angiotensin converting uremia become apparent. Each horse should be managed on an individual
enzyme inhibitor (benazepril 1 mg/kg PO; ramipril 0.8 mg/kg PO) basis until humane euthanasia becomes necessary.
could potentially help control blood pressure, attenuate proteinuria,
and slow renal fibrosis in horses.67 The panelists consider that nephro-
lith removal is not indicated unless they are a focus of persistent sepsis, a 2.3 | Pyelonephritis
suspected source of pain, or obstruct urine flow. Erythropoietin adminis-
tration is not recommended for anemic patients. Pyelonephritis is uncommon in horses and is a hematogenous or
Maintaining appetite and body condition is the goal for management ascending bacterial infection of the renal pelvis and parenchyma. Pre-
of horses with CKD. Access to good quality pasture, increasing carbo- disposing factors are mechanical obstruction or functional impair-
hydrate intake, and adding fat to the diet can increase caloric intake. ments of urine flow and cases occur after urolithiasis, recurrent
Panelists suggest allowing adequate protein access based on monitor- cystitis, bladder paralysis, ectopic ureter, lower urinary tract neoplasia,
ing of BUN, BUN/sCr ratio, and serum total protein concentrations. urinary surgery, and foaling injury to the urethra. Unilateral pyelone-
Salt supplementation beyond a normal diet is not recommended by phritis is more common than bilateral.
the panelists, as there is no evidence of efficacy, it could exacerbate Organisms isolated include Escherichia coli, Proteus spp., Klebsiella
edema and hypertension and lead to an increase in sCr as observed in spp., Enterobacter spp., Streptococcus spp., Staphylococcus spp., Pseu-
other species.68 For patients with edema or hypertension, a restricted domonas aeruginosa, and Corynebacterium spp.72-76
salt diet is recommended. With hypercalcemia, low calcium feeds are Clinical signs include fever, inappetence, lethargy, and weight
recommended (grass hay instead of alfalfa). Omega-3 fatty acids69 loss. Renal hemorrhage,75 sepsis,72 renal failure,76 and death can
and vitamin E70 slow progression of CKD in humans and small ani- occur. Increased inflammatory markers are common. SCr can be
mals, but benefits are unknown for horses. Quality pasture is an excel- increased or within reference ranges when disease is unilateral. Renal
lent source of omega-3 fatty acids and of vitamin E. Many equine ultrasonography may demonstrate a dilated renal pelvis, distortion of
food supplements for renal support are commercially available; there the renal parenchyma, and nephroliths. Cystoscopy can assess the
is no evidence of their benefit. In humans with CKD, regular exercise gross appearance of urine flowing from each ureter and allows ure-
is associated with improved health outcomes.71 teral urine collection. Urinalysis (including bacteriology and cytology)
can confirm infection and whether the disease is unilateral or bilateral.
Empirical antimicrobial choices should consider stewardship,
2.2.4 | Prognosis urinary drug concentrations, and nephrotoxicity. Trimethoprim-
sulfonamides are the treatment of choice.35,43 Ongoing treatment should
Progressive loss of nephron function with CKD precludes successful be guided by culture and susceptibility results. Long-term antimicrobial
long-term treatment. Many horses with early CKD can continue in perfor- treatment is often required and can be discontinued after negative
mance, breeding or as companion animals for months to years. In the pan- culture results and resolution of clinical signs and blood work abnor-
elists' experience, as long as sCr remains <4 to 5 mg/dL (<350-440 μmol/ malities. Panelists recommend repeating a urine culture 2 weeks after
 19391676, 2024, 4, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/jvim.17101 by Test, Wiley Online Library on [03/09/2025]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
2016 VAN GALEN ET AL.

discontinuation of treatment. When treatment of unilateral, nonazote- dysfunction causing urinary loss of glucose, phosphate, uric acid,
mic, pyelonephritis is unsuccessful, nephrectomy is indicated. amino acids and protein) are also described in horses.80,81 RTA occurs
Prognosis ranges from guarded to favorable and depends on as a primary disorder, or secondary to kidney injury, systemic diseases,
underlying cause, concurrent nephrolithiasis (often difficult to cure), or drug administration.
and extent of renal damage. The predominant clinical features, regardless of type, include anorexia,
lethargy, and weakness associated with severe metabolic acidosis. If the
condition is chronic, weight loss occurs. The nearly pathognomonic
2.4 | Renal hematuria serum chemistry findings include metabolic acidosis and hyperchloremia
with a normal anion gap.79 Azotemia is sometimes noted because of
Hematuria most commonly originates from the lower urinary tract. dehydration or a predisposing renal injury. Serum potassium concentra-
Hematuria originating from the upper urinary tract can be a tion is frequently low.79 Some cases have increased serum parathyroid
consequence of lithiasis, pyelonephritis, neoplasia, drug toxicity hormone and 25-hydoxyvitamin D concentrations.79 Urine is often
(NSAIDs), idiopathic renal hematuria (IRH), and occasionally intense alkalotic (7.5-9), despite metabolic acidosis, although some cases have
exercise. acidic urine. Bicarbonate or ammonium chloride challenge tests are
Idiopathic renal hematuria is characterized by sudden onset of used in humans and dogs to determine the RTA type but are rarely
gross hematuria. Arabian or part-Arabian horses are over-represented, used in horses because treatment is identical.
suggesting a genetic predisposition.77,78 Hematuria can resolve spon- Initial treatment should focus on correcting metabolic acidosis by
taneously but can be followed by recurrent hemorrhage months to administering IV sodium bicarbonate.79 Hypokalemia should be trea-
years later. A diagnosis is made by exclusion of systemic disease, coa- ted with potassium chloride supplementation; further decreases
gulopathy and other causes of hematuria. Small neoplastic masses can can occur during sodium bicarbonate administration. Most
be difficult or impossible to diagnose antemortem and can also cause horses with RTA have a favorable clinical response within 24 to
renal hemorrhage. Cystoscopy confirms that hematuria originates 72 hours to treatment.4 Treatment can then be changed to oral
from the upper urinary tract and whether hemorrhage is unilateral or sodium bicarbonate, with or without potassium chloride supple-
bilateral. Treatment is supportive for acute blood loss. With mentation depending on appetite and serum potassium concentra-
severe hematuria of unilateral origin, a nephrectomy can be consid- tion. Duration of treatment is unpredictable, but many require
ered. However, in some of the panelists' experience, hematuria from treatment for months.79 RTA can recur, especially with ongoing
the contralateral kidney can develop within days postprocedure. renal disease.79

2.5 | Renal tubular acidosis 2.6 | Renal causes for PU/PD

Renal tubular acidosis (RTA) is a rare disorder categorized as Type I PU/PD is not common in horses, except for temporary iatrogenic
(impaired hydrogen excretion by the distal tubule) and Type II causes and pituitary pars intermedia dysfunction (PPID). Physiological
(impaired reabsorption of bicarbonate by the proximal tubule).79 Type causes of PD (>100 mL/kg/day) are hot weather, intense exercise,
IV (impaired excretion of potassium), a mixture of Type I and Type II, and lactation. Physiological causes of PU are excessive dietary salt
and Fanconi syndrome (Type II RTA with widespread proximal tubular consumption, or iatrogenic causes such as administration of

F I G U R E 1 Diagnostic approach to
polyuria/polydipsia (PU/PD). CFR, chronic
renal failure; DI, diabetes insipidus; PPID,
pituitary pars intermedia dysfunction; sCr,
serum creatinine concentration; USG,
urinary specific gravity.
 19391676, 2024, 4, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/jvim.17101 by Test, Wiley Online Library on [03/09/2025]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
VAN GALEN ET AL. 2017

alpha2-agonists, corticosteroids, glucose, diuretics, and IVFT. Patho- however, catheterization can lead to ascending infection. Treatment
logical causes of PU/PD are as follows: of foals with AKI should focus on maintaining effective circulatory
volume and RBF without fluid overload while correcting acid-base
1. Psychogenic polydipsia: The most common cause and typically the and serum electrolyte abnormalities and allowing renal tissue time
most dramatic PU/PD. to repair (see Principles of Intravenous Fluid Therapy; and Table 3).
2. Chronic kidney disease. In neonates with ARF and persistent oliguria, panelists find dialysis
3. Diabetes insipidus (DI): Neurogenic DI (vasopressin deficiency) or more feasible than in adult horses.31 Panelists consider AKI affected
nephrogenic DI (vasopressin insensitivity of collecting ducts). foals at risk for developing CKD later in life.52
4. Diabetes mellitus (DM): Chronic hyperglycemia leading to gluco- Failure to urinate, azotemia, or both do not equate to AKI in all
suria. Primary DM is rare in horses. neonates. Congenital abnormalities, uroperitoneum or a dysfunc-
5. PPID: The mechanism of PU/PD in PPID is currently unclear. tional bladder as a component of perinatal asphyxia syndrome can
Overall, 31% of PPID horses had PU/PD in 1 study82; however, be confused with oliguria because of ARF. Spurious hypercreatini-
this is likely underreported. nemia reflects placental insufficiency or maternal renal failure, with
6. Sepsis and endotoxemia. in-utero fetal accumulation of nitrogenous products.88 Azotemia, at
7. Hepatic insufficiency: Although described in literature and anec- times with sCr up to 20 mg/dL (1770 μmol/L), is found with this
dotally reported, panelists have not recognized this as a cause syndrome. As the foal's kidney function is normal, electrolyte concen-
of PU/PD. trations are normal in spurious hypercreatininemia, and sCr typically
drops without IVFT by >50% in the first 24 hours providing the foal is
Medullary washout is a commonly described phenomenon with adequately nursing. Although the term “spurious” is used to describe
PU/PD and could occur after psychogenic polydipsia, IVFT, or sep- this syndrome, panelists consider this syndrome to include a range
sis. The panelists are unaware of documentation of medullary of mild to severe azotemia. Therefore, they suggest a new name
washout in horses because of inability of measuring medullary focusing on pathophysiology: “materno-placental induced neonatal
osmolality. azotemia.”
The diagnostic approach to PU/PD includes blood and urine ana- Further investigation of oliguria and azotemia in neonates
lyses and water deprivation tests (Figure 1). includes transabdominal ultrasonography (renal presence, size and
Psychogenic polydipsia is treated by water intake restriction, slow structure, bladder size, free abdominal fluid volume), serum biochem-
feeding, and reducing boredom. Neurogenic DI has been treated with istry, and urinalysis. An increased BUN relative to sCr can be caused
hormone replacement (desmopressin acetate),83,84 but there are no by increased gastrointestinal protein absorption with gastrointestinal
reports of treatment of nephrogenic DI in horses. ulceration or enterocolitis.
Regardless of cause, azotemia in sick foals has been associated with
lower survival rates,89,90 although in the panelists experience many azo-
2.7 | Foal specific renal problems temic foals can be managed with favorable outcomes.

Neonatal kidneys receive less RBF than adult kidneys, although

being a larger percent body mass.85 However, GFR is similar to that 3 | DI AGN OS TIC S
of adult horses.86 In normal foals, BUN and sCr are variable and
often above the adult reference range at birth but return to adult 3.1 | Conventional diagnostics
reference ranges within 24 to 72 hours. Low BUN and sCr values are
normal in nursing foals because of high fluid intake. Urination is SCr remains the recommended biochemical test to estimate GFR;
expected within 12 hours of birth. Initial USG is variable, but urine BUN is unreliable. SCr results should be interpreted based on lab-
rapidly becomes hyposthenuric (<1.008). Urine pH is neutral and oratory reference ranges, body condition, age, breed and sex of
passive transfer of colostral antibodies can cause proteinuria in the the horse.
first 24 to 72 hours. Stall side urinalysis can be performed with reagent test strips and
AKI in foals follows similar principles as in adults. It can occur as refractometer analysis (USG). In select cases biochemical testing (pro-
isolated organ dysfunction, secondary to sepsis, periparturient hyp- tein, creatinine, gamma-glutamyl transferase), as well as microscopic
oxia, nephrotoxicity, or a combination of these factors. Foals can be sediment evaluation, can be pursued (Table 5).
lethargic, with fluid retention resulting in subcutaneous edema, most Fractional excretions (FE) assess tubular reabsorption of electro-
commonly in axillary or inguinal regions. In humans, a higher propor- lytes.91 When azotemia is present, normal sodium and chloride FE
tion of oliguric/anuric AKI is seen in neonates than adults, and the support a prerenal cause, whereas higher values occur with tubular
panelists also recognize this in horses. Electrolyte derangements in dysfunction. Fractional excretions have limited diagnostic value once
foals with ARF are more common and often more severe than in adults IVFT has started.
and severe hyponatremia can result in encephalopathy.87 Measuring
urine output is feasible via a closed urinary collection system; FEel ¼ Uel =Pel  PCr =UCr  100%,
 19391676, 2024, 4, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/jvim.17101 by Test, Wiley Online Library on [03/09/2025]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
2018 VAN GALEN ET AL.

where Uel, urinary electrolyte concentration, Pel, plasma/serum elec- 3.4 | Renal biopsy
trolyte concentration, UCr, urinary creatinine concentration, PCrsCr.
Normal: Na <1%, Cl <1.7%, and K 24% to 75%. Although renal biopsies have a low reported mortality (0.6%) in
horses, complications were observed in 11.3%, and include colic signs
(likely associated with perirenal hemorrhage) and hematuria. Occa-
3.2 | Novel biomarkers sionally hemorrhage is severe.105 In humans, hypertension is a risk
factor for hemorrhage.106
Data on novel biomarkers of renal function or injury in horses is lim- As compared with humans often suffering from glomerular dis-
ited and restricted to AKI (Table 6). ease for which renal biopsy can yield a definitive diagnosis and prog-
Serum symmetric dimethylarginine (SDMA; a functional bio- nostic information, renal biopsy is rarely helpful in horses with
marker) and sCr concentrations are highly correlated, but superiority of predominantly tubulointerstitial disease. Panelists do not recommend
SDMA over sCr to support changes in GFR in horses has not been docu- renal biopsy for routine evaluation of either AKI or CKD and agree it
mented.93,94 Measurement of SDMA is currently not recommended in should only be performed when information gained from the biopsy could
foals less than 6 months of age because of lack of established reference change patient management or prognosis. Renal biopsy technique is
92
ranges. As SDMA is not affected by muscle mass, it could prove to described elsewhere in detail.105
be more accurate to assess GFR in heavily muscled horses with sCr
above reference ranges.
Biomarkers for glomerular and tubular injury, such as cystatin C,95 4 | T R E A T M E N T A N D P R E V EN T I O N
96 95,97
podocin, neutrophil gelatinase–associated lipocalin and
N-acetyl-β-d-glucosaminidase99 show potential as early indicators of 4.1 | Principles of Intravenous Fluid
kidney injury, but more research is needed, and assays are not com- Therapy (IVFT)
mercially available. No novel biomarkers currently replace conventional
biomarkers of kidney function or injury.92 The goals of IVFT in patients with AKI are (1) to establish and maintain
euhydration, circulatory volume, and RBF, (2) to replace ongoing fluid
loss, and (3) to promote diuresis. In patients with stable CKD, azote-
3.3 | Imaging mia may have been present for weeks to months and diuresis is estab-
lished (polyuria). Therefore, if the patient is drinking adequately, IVFT
With AKI, kidneys may be normal in size (15-18 cm in length for Thor- might not be needed or indicated. Intravenous fluid treatment in horses
oughbreds)100 or enlarged. Abnormalities of parenchymal detail are with CKD is unlikely to reduce azotemia unless there is an AKI component
often not detected but can include diffuse or focal increased echogeni- or dehydration exacerbating CKD.
city of the renal cortex and (rarely) subcapsular edema. With CKD, Fluid selection warrants consideration. In human medicine, 0.9%
especially ESKD, kidneys are usually small, have increased echogenicity, saline remains a common initial choice as it does not contain potas-
and may have nephroliths or cystic cavitation. Doppler assessment of sium. Because hyperkalemia is less common in horses, except for
intrarenal blood flow can be performed, also allowing measurement of foals, polyionic replacement solutions are a reasonable choice. Further-
renal resistive index. Doppler studies are time consuming, require skill, more, the large amount of chloride administered with 0.9% saline can
and results are unlikely to change patient management.101 worsen GFR.107
Nuclear scintigraphy can be performed with radiopharmaceuti- Maintenance rates of IVFT (2-3 mL/kg/h) typically induce
cals labeled with 99-metastable technetium (99mTc). When 99m
Tc is increased output of dilute urine. Thus, unless additional fluid require-
tagged to diethylenetriaminepentaacetic acid (DTPA), both disap- ments are identified, maintenance rates or slightly more are sufficient.
pearance of 99mTc-DTPA activity in serial blood samples and sequen- Overzealous IVFT should be avoided as it can lead to renal interstitial
tial gamma camera images of the kidneys can be used to assess edema, worsening rather than improving RBF and GFR.108,109 Large
GFR.102 Scintigraphy with 99m
Tc tagged to mercaptoacetyltriglycine volume IVFT also presents a large sodium load. Because sodium is
can evaluate individual kidney function in horses with suspected uni- eliminated slower (days) compared to water (minutes to hours), a
lateral disease.103 sodium load can result in edema formation.108,109 It is the panelists
Computed tomography provides excellent anatomical detail. strong opinion that avoidance of fluid overload should receive the same
Patient size and requirement for general anesthesia restrict its use. consideration as providing adequate fluid support.
Endoscopic viewing of the ureteral openings can determine if Panelists agree that in most cases, IVFT is only needed short-term
hematuria or pyuria originates from 1 or both kidneys and ureteral and not until azotemia fully resolves. Once euhydration is achieved,
catheterization allows urine sampling from each kidney. Smaller diam- appetite improves, voluntary drinking returns, and sCr has appreciably
eter endoscopic equipment (6 mm or less outer diameter) allows ure- declined, there is little benefit to continuing IVFT. SCr might not
teroscopy and pyeloscopy. When ureteral orifices are damaged and return to normal values within a few days in all cases, and can even
open, a larger diameter endoscope can sometimes be advanced to the increase slightly after discontinuation of IVFT because of return of
renal pelvis.104 intravascular volume to normal.
 TABLE 5 Urinalysis testing and interpretation.
VAN

Reference Suggestive of (not exhaustive

Parameter Analysis method value Abnormalities Process listing) Next diagnostic step
USG Refractometry Adults: Hyposthenuria (<1.008) Water excretion. Psychogenic polydipsia; WDT, if needed followed by
GALEN ET AL.

1.025-1.040 diabetes insipidus; modified WDT.

Foals: <1.025 medullary washout. Measure plasma AVP
concentration after
negative WDT.
Response to administration of
exogenous AVP.
Isosthenuria No excretion, no concentration. CKD (USG is more variable with Further renal diagnostics.
(1.008–1.014) AKI)
Concentrated (USG may vary; Ability to concentrate urine. Normal renal function or Assess hydration status.
more concentrated than dehydration.
plasma)
pH Reagent strip Adults: 8–9 Aciduria (pH <7) Potassium deficiency and Strenuous exercise; Blood analysis;
Foals: <8 increased excretion hydrogen diet; blood gas analysis;
in distal tubules. Urinary metabolic acidosis (alkaline urine urine culture.
excretion of with severe metabolic acidosis
methylenecyclopropyl acetic can be suggestive of renal
acid (atypical myopathy). tubular acidosis);
Systemic or local acid bacteriuria;
production. anorexia;
atypical myopathy.
Protein Biochemistry analyzer (or <100 mg/dL Proteinuria Damage to glomerular filtration Glomerular injury; Blood analysis;
Urine protein reagent strip) <0.5 membrane; bacterial infection; urine culture;
to creatinine Biochemistry analyzer reduced reabsorption in tubules; hematuria; further diagnostics for
ratio protein excretion. post colostrum absorption; hematuria and glomerular
postexercise; injury.
false reagent strip results.
Glucose Reagent strip or biochemistry Not present Glucosuria Hyperglycemia; Diabetes mellitus; Blood glucose analysis;
analyzer tubular damage. endotoxemia; evaluation of tubular injury.
iatrogenic (glucose/dextrose,
steroids, alpha-2-agonists,
sodium glucose cotransporter
2 inhibitor);
Strenuous exercise.
GGT or Biochemistry analyzer GGT/uCr Enzymuria Leakage from proximal tubular Tubular damage (mostly Evaluation of tubular injury.
GGT to urinary <25 U/g brush border cells. nephrotoxic insults).
creatinine
ratio
RBC Microscopic sediment or reagent 5000 RBC/mL Hematuria Bleeding from urinary tract. Bacterial infection; Further diagnostics of
strip or <5 Microscopic: 10 000-2 500 000 uroliths; hematuria;
RBC/hpf RBC/mL or 10-20/hpf cystitis; urine culture.
2019

(Continues)

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 TABLE 5 (Continued)
2020

Reference Suggestive of (not exhaustive

Parameter Analysis method value Abnormalities Process listing) Next diagnostic step
Note: reagent strips do not Macroscopic: idiopathic renal hemorrhage;
distinguish between >2 500 000-5 000 000 neoplasm;
hemoglobin and myoglobin. RBC/mL or approximately parasite migration;
0.5 mL of blood per liter of iatrogenic (catheterization,
urine nephrotoxic drugs);
strenuous exercise.
Note: red coloration on snow or
shavings can occur
physiologically because of
pyrocatechin.
WBC Microscopic sediment <5 WBC/hpf Pyuria: >5 WBC/hpf Inflammation or infection. Bacterial infection Urine culture;
(pyelonephritis, septic Urinary tract ultrasonography
nephritis); and endoscopy.
Inflammation;
Uroliths;
Neoplasm.
Casts Microscopic sediment Absent Casts formed off the following: Protein and cells aggregate after Renal pathology (tubular/ Further diagnostics of renal
hyaline, tubular damage or high glomerular injury, disease;
myoglobin, concentration. pyelonephritis); blood analysis.
WBC, hematuria;
RBC, pyuria;
tubular epithelial cells. hemolysis;
rhabdomyolysis.
Crystals Microscopic sediment Normal Crystalluria Physiological process. Physiological (crystalluria or If abundant: neurological
visible sedimentation does not examination, endoscopy.
equal presence of a stone or
pyuria).
Less abundant with acidic or
dilute urine.
More abundant in bladder
paralysis syndromes.

Note: Systemic and lower urinary tract–induced findings are included in this table but are not further discussed in the article.
Abbreviations: AKI, acute kidney injury; AVP, arginine vasopressin; CKD, chronic kidney disease; GGT, gamma-glutamyltransferase; hpf, high powerfield; RBC, red blood cell; USG, urine specific gravity; WBC,
white blood cell; WDT, water deprivation test.
VAN
GALEN ET AL.

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 VAN
GALEN ET AL.

TABLE 6 Novel biomarkers of renal function and injury investigated in horses.92

Availability for
Cause of Sample Evidence in humans and Reference value for commercial/
Biomarker Characteristics increase type small animals Evidence in horses horses clinical use
SDMA Symmetric Endogenous, methylated Renal Serum Early detection of CKD. Higher in azotemic than in Adults: Yes
dimethylarginine form of arginine. dysfunction nonazotemic horses.93 <14-19 μg/dL4,93
or GFR or <0.8 μmol/L94
decrease. Foals:
ND
(>adults)
Cystatin C Cysteine protease Renal Plasma Early detection of AKI. Higher in horses with AKI, ND No
inhibitor. dysfunction /serum and at AKI risk than in
or GFR healthy horses.95
decrease.
Podocin Maintenance protein for Podocyte Urine Promising diagnostic Higher in horses with AKI ND No
glomerular podocytes damage. tool for glomerular than healthy horses.96
(glomerular barrier). diseases.
NGAL Neutrophil Lipocalin protein. Tubular Serum / Early detection of AKI. Increase with azotemia. ND No
gelatinase– damage. urine Indicator of degree of Potential to detect AKI
associated lipocalin damage. earlier than sCr.95,97
MMP-2, Matrix Zinc-dependent Damage to Urine Early detection in some Effectiveness of use not ND No
MMP-9 metalloproteinase 2 proteinases (remodeling tubules or nephropathies. confirmed.98
and 9 extracellular matrix). glomeruli.
NAG N-acetyl-β-d- Lysosomal protein of Tubular Urine Early detection of AKI. Higher in azotemic than in ND No
glucosaminidase proximal tubules. damage. Correlation with nonazotemic horses.99
severity of lesions.

Abbreviations: AKI, acute kidney injury; CKD, chronic kidney disease; GFR, glomerular filtration rate; ND, not determined or lack of sufficient data; sCr, serum creatinine.
2021

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2022 VAN GALEN ET AL.

4.2 | Drug adjustments ACKNOWLEDG MENT

No funding was received for this study. The authors acknowledge the
If drugs that are primarily eliminated or metabolized by the kidney are important work that has been done by other authors on the topic of
used in horses with AKI or CKD, toxic serum and tissue concentra- equine kidney disease.
tions can be reached because of impaired renal function. To avoid sys-
temic or renal toxicity, drug dosage or interval adjustments might be CONFLICT OF INTEREST DECLARATION
indicated. Adjustments are often needed for nephrotoxic drugs and Harold C. Schott, II has accepted funding from IDEXX for research on
occasionally for non-nephrotoxic drugs (e.g., digoxin, amphotericin, symmetric dimethylarginine. No other authors declare a conflict of
enalapril, sotalol, morphine, pregabalin, levetiracetam, acyclovir, and interest.
quinidine).
For concentration dependent antibiotics (aminoglycosides), prolonging OF F-LABEL ANTIMI CROBIAL DECLARATION
the interval between doses to equal the estimated percentage decrease in The authors have taken antimicrobial stewardship principles into
GFR is preferred. For most other potentially toxic drugs, including some account for antimicrobial treatment suggestions in this manuscript
time dependent antibiotics (oxytetracycline), a decrease in dosage is pre- and strongly advise clinicians to consider stewardship for antimicrobial
110 111
ferred. A reduction in a loading dose is rarely recommended. drug selection.
Before adjustments, risk of toxicity without adjustment versus
risk of subtherapeutic dosing, especially for antimicrobials, should be INSTITU TIONAL ANIMAL C AR E AND USE COMMITTEE
considered. Therapeutic drug monitoring can be useful to monitor (IACUC) OR OTHER APPROVAL DECLARATION
plasma drug concentrations, especially when clinical effects or toxicity Authors declare no IACUC or other approval was needed.
are related to plasma drug concentrations (e.g., aminoglycosides).
These adjustments are most appropriate for horses with CKD; rapid HUMAN E THICS APPROVAL DECLARATION
changes in GFR with AKI/ARF make drug adjustments difficult. Authors declare human ethics approval was not needed for this study.

OR CID
4.3 | Limiting further renal damage Gaby van Galen https://orcid.org/0000-0002-0689-7141
Thomas J. Divers https://orcid.org/0000-0001-7125-636X
In patients with existing renal disease, it is important to avoid further Victoria Savage https://orcid.org/0000-0003-0654-8627
insults to the kidney. The panelists recommend avoiding use of poten-
Harold C. Schott II https://orcid.org/0000-0002-7728-5409
tially nephrotoxic drugs (Table 1). Drugs with a similar therapeutic
Natalia Siwinska https://orcid.org/0000-0002-5205-5826
effect but lower nephrotoxicity can sometimes be selected. If nephro-
toxic drugs are needed, not exceeding recommended drug dosages,
RE FE RE NCE S
using the lowest effective dose, shortening duration of use, avoiding
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3. Baxmann AC, Ahmed MS, Marques NC, et al. Influence of muscle
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cious use of NSAIDS, preferring cyclooxygenase-2 selective agents, in serum cystatin C. Clin J Am Soc Nephrol. 2008;3:348-354.
4. Schott HC 2nd, Gallant LR, Coyne M, et al. Symmetric dimethylargi-
patients with CKD if treatment could improve quality of life. There is
nine and creatinine concentrations in serum of healthy draft horses.
weak evidence in humans that misoprostol reduces the risk of NSAID- J Vet Intern Med. 2021;35:1147-1154.
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6. Savage VL, Marr CM, Bailey M, Smith S. Prevalence of acute kidney
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Temporary renal replacement treatment has infrequently been per- 7. Cotovio M, Monreal L, Armengou L, Prada J, Almeida JM, Segura D.
Fibrin deposits and organ failure in newborn foals with severe septi-
formed in horses with unresponsive oliguric/anuric ARF15,44 and will
cemia. J Vet Intern Med. 2008;22:1403-1410.
in the future likely be used in a more expanded manner.
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