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Basics ⬇

Outline

BASICS

Definition!!navigator!!

Substantial and permanent decrease in GFR.

Pathophysiology!!navigator!!

  • Usually a consequence of GN or CIN
  • Impaired urine-concentrating ability (i.e. isosthenuria) occurs when more than two-thirds of nephron function is lost
  • Azotemia develops after loss of more than three-fourths of nephron function
  • Disturbances in fluid, electrolyte, and acid–base homeostasis are less severe than with AKI/ARF, but the loss of renal function is irreversible

Systems Affected!!navigator!!

  • Renal/urologic—failure
  • Endocrine/metabolic—disturbances in electrolyte and acid–base homeostasis; decreased erythropoietin production
  • GI—inappetence, possible diarrhea, and increased risk of ulcers
  • Nervous/neuromuscular—occasional ataxia or dementia in severe CKD; tremors or muscle fasciculations may accompany metabolic disturbances
  • Hemic/lymphatic/immune—platelet dysfunction, increased susceptibility to infection, anemia

Genetics!!navigator!!

N/A

Incidence/Prevalence!!navigator!!

Reported to be 0.12%.

Geographic Distribution!!navigator!!

N/A

Signalment!!navigator!!

Breed Predilections

  • May be more common in Clydesdales
  • A heritable form of PKD may occur in Arabians and Paints

Mean Age and Range

Older horses (>15 years) are at greater risk (prevalence 0.5%); however, this may reflect more extensive investigation of valuable animals.

Signs!!navigator!!

Historical Findings

  • Insidious-onset lethargy, partial anorexia, and weight loss
  • Ventral edema and mild polyuria and polydipsia (with clear-appearing urine)
  • At an earlier stage, decreased performance

Physical Examination Findings

  • Weight loss, poor hair coat, mild lethargy, reduced appetite, edema, excessive dental tartar, and uremic odor in the oral cavity may be found
  • Affected horses usually are not dehydrated
  • Voided urine usually is clear and pale yellow
  • Rectal examination may reveal a small, firm left kidney with an irregular surface and, rarely, ureteral distention due to obstruction with uroliths
  • With endstage disease, anuria may develop with anorexia, and more marked lethargy may be accompanied by ataxia, hypermetria, and mental obtundation

Causes!!navigator!!

  • Immune-mediated GN initiated by chronic infections (e.g. equine infectious anemia, streptococcal diseases) or autoimmune disease
  • CIN encompasses all non-GN causes and may be a sequela to ischemic or nephrotoxic AKI/ARF
  • Less commonly, ascending infections may lead to bilateral pyelonephritis and nephrolithiasis and/or ureterolithiasis
  • Long-term use of NSAIDs with medullary necrosis and nephrolithiasis
  • Amyloidosis and renal neoplasia—rare
  • In horses <5 years of age and with no history of medical problems, anomalies of development—renal hypoplasia or dysplasia; PKD

Risk Factors!!navigator!!

  • Previous episodes of AKI/ARF or UTI
  • Prior medical or surgical diseases, especially when treatment included aminoglycoside antibiotics and NSAIDs
  • Long-term use of NSAIDs
  • CKD may develop months to years after nephrotoxin-induced AKI

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

  • All disorders that may lead to lethargy, partial anorexia, and weight loss
  • AKI/ARF—supported by an underlying disease process producing renal ischemia or recent/concurrent exposure to nephrotoxic agents
  • Postrenal failure—supported by stranguria, anuria, or uroperitoneum

CBC/Biochemistry/Urinalysis!!navigator!!

  • Normal to low packed cell volume (attributed to decreased serum erythropoietin concentration and shortened RBC life span), platelets normal to decreased
  • Increased BUN (100–250 mg/dL; 36–89 mmol/L) and Cr (2.0–20 mg/dL; 177–1768 μmol/L); BUN:Cr ratio usually >10; Cr usually >5.0 mg/dL (440 μmol/L) with horses presented for chronic ill thrift
  • Variable hyponatremia, hypochloremia, and hyperkalemia—less severe than with AKI/ARF
  • Hypercalcemia and hypophosphatemia are unique to horses
  • Mild to moderate hypoalbuminemia, hypertriglyceridemia, and hypercholesterolemia
  • Mild to moderate metabolic acidosis may accompany endstage disease
  • USG—isosthenuria (1.008–1.014) is a hallmark feature
  • GN—moderate to marked proteinuria that may increase USG to 1.020
  • Urine sediment is relatively devoid of crystals, but otherwise may be unremarkable. Increased RBCs support lithiasis or neoplasia, and increased leukocytes support UTI

Other Laboratory Tests!!navigator!!

  • Increased fractional clearances of sodium and chloride with advanced disease
  • Increased urine protein–urine creatinine ratio (>2:1) supports GN
  • Quantitative urine culture and antimicrobial sensitivity even in the absence of pyuria
  • Coagulation panel when performing renal biopsy or investigating GN (decreased antithrombin III)

Imaging!!navigator!!

Transabdominal and Transrectal Ultrasonography

  • Kidneys may be small (diameter <6 cm; length <12 cm), with irregular surfaces
  • Increased parenchymal echogenicity (similar to that of the spleen), loss of detail of corticomedullary junction
  • Nephrolithiasis/ureterolithiasis and variable hydronephrosis may be detected
  • Multiple cystic structures may be found with PKD or pyelonephritis

Urethroscopy/Cystoscopy

  • Useful with suspected obstructive disease or pyelonephritis
  • Urine samples may be collected from each ureter by catheterization

Other Diagnostic Procedures!!navigator!!

GFR

Measuring changes in GFR, by plotting the inverse of Cr over time, may be the most accurate way to follow the progressive decrease in renal function.

Biopsy

  • Percutaneous renal biopsy with routine histopathology, immunohistochemistry, and electron microscopy of the sample may provide information regarding cause (GN versus CIN) but rarely affects prognosis or progression of CKD
  • Pursue biopsy with caution, because life-threatening hemorrhage can be a complication

Blood Pressure

Serial measurement of blood pressure may reveal persistent hypertension and support for use of antihypertensive medications, especially in cases of GN with proteinuria.

Pathologic Findings!!navigator!!

Gross

  • Firm, shrunken, pale kidneys, with irregular surfaces and narrowed cortices
  • Renal capsule is often adhered to underlying parenchyma
  • See chapters Urolithiasis and Urinary tract infection (UTI)
  • Enlarged kidneys with multiple cysts are found with PKD

Histopathologic

  • Variable glomerular, tubular, and interstitial changes
  • Endstage CKD may preclude categorization of the initiating cause

Treatment ⬆ ⬇

Outline

TREATMENT

Appropriate Health Care!!navigator!!

Inpatient/outpatient medical management.

Nursing Care!!navigator!!

Fluid Therapy

  • With stable CKD short-term diuresis with IV fluid therapy is rarely beneficial and may carry an increased risk of thrombophlebitis
  • IV fluid therapy can be pursued to rule out AKI/ARF or acute-on-chronic disease—5% dextrose or isotonic (0.9%) saline at 1.5–2-fold the maintenance rate for 24–48 h with daily assessment of changes in body weight, BUN and Cr, serum electrolyte concentrations, and USG
  • Increased urine output and decreased azotemia should occur in patients with AKI/ARF or acute-on-chronic disease
  • Horses with more severe CKD typically gain weight and develop edema, with little decrease in magnitude of azotemia

Oral Electrolyte Supplementation

With serum bicarbonate <20 mEq/L, 30 g of sodium bicarbonate may be administered once or twice daily.

Activity!!navigator!!

When clinical signs are mild and the horse's attitude is good, light exercise can be continued.

Diet!!navigator!!

  • Access to fresh water at all times
  • The ideal diet provides adequate caloric intake without excessive protein intake
  • Offering a variety of concentrate feeds, bran mash, and access to good quality pasture is the recommended diet. Grass hay is preferred to alfalfa owing to the higher protein and calcium content of the latter; however, if appetite for grass hay is poor, feed alfalfa
  • Supplementation with fat effectively increases caloric intake
  • Supplement omega-3 fatty acids (flax seed, fresh grass pasture) and antioxidants (vitamins C and E)

Surgical Considerations!!navigator!!

Surgery is only required for acute-on-chronic disease due to obstructive urolithiasis.

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

Contraindications!!navigator!!

  • NSAIDs may exacerbate renal hypoperfusion and the decline in GFR
  • Avoid all nephrotoxic medications unless specifically indicated for a concurrent disease process, and then modify dosage accordingly

Precautions!!navigator!!

Discontinue oral electrolyte supplementation if it produces or exacerbates edema.

Possible Interactions!!navigator!!

N/A

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

  • Monitor response to fluid therapy closely—as little as 40 mL/kg of IV fluids (20 L to a 500 kg horse) may produce pulmonary edema in oliguric/anuric patients
  • Assess clinical status (emphasizing attitude and appetite), edema formation, body weight, and magnitude of azotemia at least monthly during the initial few months of supportive care and every 2–3 months thereafter
  • Assess electrolyte and acid–basis status whenever changes in clinical status are noted

Prevention/Avoidance!!navigator!!

  • Anticipate compromised renal function in patients with other diseases or prolonged anesthesia and surgery; minimize dehydration and potential renal damage
  • Ensure adequate hydration status in patients receiving nephrotoxic medications
  • Avoid use of NSAIDs unless necessary

Possible Complications!!navigator!!

  • Pulmonary and peripheral edema with fluid therapy
  • Increased risk of thrombophlebitis with IV fluid therapy
  • Oral and GI ulceration or GI bleeding
  • Signs of neurologic impairment—ataxia, mental obtundation

Expected Course and Prognosis!!navigator!!

  • Issue a poor prognosis and consider euthanasia for horses that are emaciated, anuric, or have Cr >10 mg/dL (850 µmol/L) at initial evaluation
  • Issue a guarded prognosis for short-term survival for horses with Cr of 5–10 mg/dL (440–850 µmol/L) at initial evaluation
  • Issue a fair prognosis for short-term survival for horses with Cr <5 mg/dL (440 µmol/L) that are in good body condition at initial evaluation
  • Horses with GN typically have a poorer prognosis and more rapid decline in renal function than horses with CIN

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Associated Conditions!!navigator!!

Hypertension

Age-Related Factors!!navigator!!

In horses <5 years of age, CKD may be due to a developmental anomaly—renal hypoplasia or dysplasia.

Pregnancy/Fertility/Breeding!!navigator!!

Pregnant mares may be at increased risk of UTI. Mares with CKD have successfully carried foals to term but the prognosis for a viable foal is guarded.

Synonyms!!navigator!!

  • Chronic renal failure
  • Kidney failure

Abbreviations!!navigator!!

  • AKI = acute kidney injury
  • ARF = acute renal failure
  • BUN = blood urea nitrogen
  • CIN = chronic interstitial nephritis
  • CKD = chronic kidney disease
  • Cr = creatinine
  • GFR = glomerular filtration rate
  • GI = gastrointestinal
  • GN = glomerulonephritis
  • NSAID = nonsteroidal anti-inflammatory drug
  • PKD = polycystic kidney disease
  • RBC = red blood cell
  • USG = urinary specific gravity
  • UTI = urinary tract infection

Suggested Reading ⬆ ⬇

McLeland S. Diseases of the equine urinary system. Vet Clin North Am Equine Pract 2015;31(2):377–387.

Author(s) ⬆ ⬇

Author: Harold C. Schott II

Consulting Editor: Valérie Picandet

Additional Further Reading ⬆

Click here for Additional Further Reading