What is the management approach for chronic renal disease in horses?

Management of Chronic Renal Disease in Horses

Chronic kidney disease (CKD) in horses requires a fundamentally different management approach than in humans, focusing primarily on dietary modification, avoidance of nephrotoxic agents, and supportive care, as there are no validated pharmacological interventions equivalent to SGLT2 inhibitors or ACE inhibitors proven effective in equine CKD. 1

Diagnostic Confirmation and Monitoring

Initial Assessment

• Measure serum creatinine recognizing it only increases after at least 66% of kidney function is lost, making it a late marker of disease 1
• Perform iohexol clearance testing to calculate estimated glomerular filtration rate (eGFR), which provides more accurate assessment of kidney function than creatinine alone 1
• Quantify urine protein content through urine protein-to-creatinine ratio to assess degree of proteinuria 1
• Obtain renal ultrasonography to evaluate kidney size, echogenicity, corticomedullary demarcation, presence of nephroliths, ureteroliths, or hydronephrosis 2

Emerging Biomarkers (Research Stage)

• SDMA, cystatin C, podocin, and NGAL show potential for earlier detection of kidney injury than creatinine, but none are currently validated for routine clinical use in horses 3
• These biomarkers remain investigational and should not replace standard creatinine measurement at this time 3

Identifying Underlying Causes

Determine the specific etiology as this guides prognosis and specific interventions:

• Tubulointerstitial disease and glomerulonephritis are the most common causes 1
• Pyelonephritis requires targeted antimicrobial therapy based on urine culture 1
• Nephrolithiasis and ureterolithiasis may require surgical intervention if causing obstruction 1, 2
• Renal dysplasia carries poor prognosis and is typically diagnosed via ultrasound-guided biopsy 2

Core Management Strategies

Dietary Modifications (Primary Intervention)

Implement protein restriction immediately as this is the cornerstone of slowing CKD progression in horses:

• Reduce dietary protein to 8-10% of total diet (approximately 0.8-1.0 g/kg body weight daily) 1
• Provide high-quality protein sources to minimize nitrogenous waste production while maintaining adequate nutrition 1
• Ensure adequate caloric intake through increased fat and digestible carbohydrates to prevent weight loss 1
• Provide free-choice access to fresh water to support polyuria and prevent dehydration 1

Nephrotoxin Avoidance (Critical)

Eliminate all nephrotoxic medications and compounds:

• Discontinue NSAIDs completely (phenylbutazone, flunixin meglumine) as these directly impair renal blood flow 4
• Avoid aminoglycoside antibiotics (gentamicin, amikacin) which cause tubular necrosis 4
• Do not administer tetracyclines in horses with azotemia as these worsen uremia 4
• Eliminate exposure to heavy metals (mercury, arsenic, lead) and mycotoxins 4
• Avoid vitamin D supplementation which can exacerbate hypercalcemia and soft tissue mineralization 4

Fluid and Electrolyte Management

Monitor and correct fluid balance:

• Ensure constant access to clean water as horses with CKD have obligatory polyuria 1
• Provide oral or IV fluid supplementation during periods of decreased intake or increased losses 4
• Monitor serum electrolytes (sodium, potassium, chloride, calcium, phosphorus) every 2-4 weeks initially, then monthly once stable 4
• Correct metabolic acidosis with oral sodium bicarbonate (50-100 g daily) if venous pH <7.35 or bicarbonate <20 mEq/L 4

Blood Pressure Monitoring

Assess for systemic hypertension:

• Measure blood pressure using tail cuff or facial artery methods, though validated reference ranges for horses with CKD are lacking 4
• Target systolic BP <140 mmHg extrapolating from other species, though equine-specific data is absent 4

Management of Clinical Complications

Weight Loss and Cachexia

• Increase caloric density through added fat (vegetable oil 100-200 mL twice daily) 1
• Offer highly palatable feeds including alfalfa pellets, beet pulp, and senior feeds 1
• Feed smaller, more frequent meals (3-4 times daily) to improve intake 1

Oral and Gastric Ulceration

• Administer omeprazole (2-4 mg/kg PO once daily) for gastric ulcer prophylaxis 1
• Provide soft feeds if oral ulcerations or gingivitis present 1
• Perform dental examination and address tartar buildup and periodontal disease 1

Anemia

• Monitor packed cell volume monthly as anemia develops from decreased erythropoietin production 4
• Consider recombinant human erythropoietin (50-100 IU/kg SC 3 times weekly) though efficacy in horses is unproven and antibody formation may occur 4

Ventral Edema

• Reduce dietary sodium to <1% of diet to minimize fluid retention 1
• Increase protein quality rather than quantity to address hypoalbuminemia 1

Monitoring Schedule

Establish regular reassessment intervals:

• Every 2-4 weeks initially: Serum creatinine, BUN, electrolytes, venous blood gas, body weight 1, 4
• Every 1-3 months once stable: Complete blood count, serum biochemistry, urinalysis with protein quantification 1, 4
• Every 3-6 months: Renal ultrasonography to assess progression 2
• Iohexol clearance testing: Every 6-12 months to objectively measure GFR changes 1

Prognosis and Client Communication

Set realistic expectations:

• Overall prevalence of equine CKD is only 0.12%, making it a rare condition 1
• Prognosis depends on underlying cause: Pyelonephritis may be reversible with treatment, while renal dysplasia is uniformly fatal 1, 2
• Progressive azotemia despite management indicates poor prognosis and warrants discussion of quality of life 1
• Horses may develop acute-on-chronic kidney injury during intercurrent illness, requiring aggressive supportive care 1

Critical Pitfalls to Avoid

• Do not rely solely on creatinine for early detection or monitoring, as it is insensitive until advanced disease 1
• Never administer nephrotoxic drugs even at reduced doses, as horses with CKD have no renal reserve 4
• Avoid excessive protein restriction below 8% of diet, which causes muscle wasting without additional benefit 1
• Do not assume all polyuria/polydipsia is CKD—rule out pituitary pars intermedia dysfunction, psychogenic polydipsia, and diabetes insipidus 1
• Recognize that forebrain signs (rare) indicate severe uremic encephalopathy and poor prognosis 1