Urinary Tract Diseases in Horses

Urinary Tract Diseases in Horses

• Common presenting signs of kidney disease include:
  • Polyuria/polydipsia (PU/PD)
  • Oliguria/anuria (decreased urine output)
  • Lethargy and inappetence
  • Poor performance

Acute Renal Failure/ Acute Kidney Failure

• Pathophysiology:
  • Most acute kidney injury (AKI) is due to acute tubular necrosis (ATN)
  • ATN caused by death and shedding of tubular epithelial cells, obstructing tubular lumen and preventing urine output from blocked nephrons
  • ATN can be caused by toxic insults (including drugs) or ischemia

ATN Caused by Toxic Insult

• Different toxins affect the kidneys differently:
  • Proximal convoluted tubule (PCT) and cortex are most affected by toxic insult due to higher blood flow
  • Aminoglycosides, NSAIDs, and oxytetracyclines are common nephrotoxic drugs

ATN Caused by Ischemia

• Loop of Henle and medulla are most affected by ischemia:
  • These areas receive the least blood flow

History of Acute Renal Failure

• Common causes:
  • Administration of nephrotoxic drugs
  • Primary diseases causing renal hypoperfusion or ischemia
  • Combination of both factors
  • Exposure to other renal toxins

Aminoglycosides and Kidney Toxicity

• Toxicosis is almost always due to repeated administration:
  • Frequent dosing is more nephrotoxic than single high doses
  • Aminoglycoside uptake is a saturation process, making single large doses less nephrotoxic

NSAIDs and Kidney Toxicity

• Excessive doses or prolonged treatment increase the risk of ATN:
  • Combining NSAIDs with hypovolemic patients is especially risky
  • NSAIDs can be nephrotoxic even in horses with pre-existing renal issues

Other Causes of Acute Renal Toxicosis

• Pigment nephropathy:
  • Can be caused by hemoglobin or myoglobin
  • Tubular obstruction and direct toxic effect of pigments
• Heavy metals, acorn poisoning, and other drugs:
  • Drugs like oxytetracycline, polymyxin B, and others can cause kidney toxicity

Vasomotor Nephropathy

• Renal artery constriction reduces blood flow to the kidneys, leading to acute ischemic necrosis:
  • This can be caused by various factors

Biochemistry in Acute Renal Failure

• Increased creatinine is the most reliable indicator of kidney function
• Increased blood urea nitrogen (BUN) can be affected by diet and gut microbe activity

Urine Analysis in Acute Renal Failure

• Urine specific gravity (USG):
  • Decreased ability to concentrate urine is a sign of AKI
• Dipstick:
  • May be normal even with AKI
• Sediment:
  • Casts may not be seen due to alkaline pH
  • Cells, pigments (hemoglobin, myoglobin), and hematuria may be present

Treatment of Acute Renal Failure

• IV fluids:
  • The main treatment
  • Correct electrolyte and acid-base abnormalities
• Diuretics (furosemide) may be helpful in oliguria/anuria:
  • Given after 12-24 hours of IV fluid therapy
• Monitor PCV, TP, body weight, urine output, USG, BP and central venous pressure (CVP) :
  • Assess fluid status and treatment effectiveness
• Aim to improve kidney function by reducing creatinine levels

Prevention of Renal Failure/ Acute Kidney Injury

• Closely monitor patients receiving nephrotoxic medications:
  • Monitor creatinine and use therapeutic drug monitoring for aminoglycosides
• Use oxytetracycline cautiously in foals:
  • Slow administration, administer with IV fluids, and avoid consecutive day administration

Chronic Renal Failure/ Chronic Kidney Disease

• Irreversible and progressive decline in glomerular filtration rate:
  • Glomerular or tubulointerstitial in origin (one often leads to the other)

Common Presenting Complaints/ History of CKD

• Weight loss, PU/PD, and poor performance:
  • History of previous AKI or administration of nephrotoxic drugs may be present

Physical Exam in CKD

• Non-specific findings:
  • Dental tartar, especially in male canines
  • Mild ventral edema associated with excess sodium retention

Clinical Pathology in CKD

• Plasma:
  • Azotemia (increased BUN and creatinine)
  • Hypercalcemia (decreased calcium excretion due to kidney dysfunction)
  • Hypermagnesemia (may be present)
  • Acid-base normal unless end-stage CKD
  • Isosthenuria ( inability to concentrate urine)
• Urine:
  • Proteinuria (glomerular disease)
  • Hematuria and pyuria (pyelonephritis, less common)
  • Clear urine due to lack of crystals and mucus
  • Opaque urine due to mucus and crystals may appear unusually clear

Causes of CKD

• Chronic Interstitial Nephritis:
  • Sequela to acute tubular necrosis or other kidney disease
  • Fibrosis may develop
• Pyelonephritis:
  • Rare, often concurrent with nephroliths/ureteroliths and sluggish urine flow
  • Risk factors include lower urinary tract (LUT) disease
• Proliferative glomerulonephritis:
  • Type III hypersensitivity response leads to immune complex deposition in glomerular membranes
• Other causes include:
  • Amyloidosis
  • Polycystic kidneys
  • Congenital renal dysplasia
  • Neoplasia

Diagnosis of CKD

• Biochemistry, urinalysis, ultrasound, and biopsy (always US guided):
  • Biopsy is always right to avoid penetrating the spleen
• Cystoscopy and culture (C&S) for pyelonephritis:
  • Looking for differences in urine flow from each ureter

Treatment/ Management of CKD

• Acute exacerbations:
  • Treat as AKI
• Stable CKD:
  • Ensure adequate hydration
  • Salt supplementation as needed (not if edema)
  • Good quality diet with moderate protein intake
  • Monitor kidney function
• End stage CKD:
  • Maintain appetite and caloric intake
  • Prevent weight loss
• Pyelonephritis:
  • Prolonged course of antimicrobial therapy based on C&S
  • Use drugs excreted in urine

Lower Urinary Tract Disease in Foals - Bladder Rupture

• Urinary bladder rupture is the most common urinary tract issue in foals:
  • The dorsal bladder wall is most commonly affected
• Healthy foals:
  • Typically present within the first few days of life
• Sick foals:
  • Often recumbent, not emptying bladder, dull, lethargic, and have abdominal distension

Clinical Signs of Bladder Rupture

• Dullness, lethargy, stranguria, loss of interest in nursing, abdominal distension, and tail flagging
• May struggle to urinate or urinate frequently

Diagnosis of Bladder Rupture

• Clinical signs, abdominal ultrasound ( large volume of peritoneal fluid, SI loops and mesentery, +/- rupture site), and plasma electrolytes
• Hyponatremia, hypochloremia, hyperkalemia, and azotemia are common:
  • Electrolyte abnormalities may be harder to detect in foals on IV fluids
• ECG in severe hyperkalemia and peritoneal fluid analysis (peritoneal fluid creatinine greater than or equal to twice plasma creatinine)

Treatment of Bladder Rupture

• Surgical repair:
  • The most common treatment
  • Bladder ruptures do not typically heal on their own
• Stabilization is crucial before anesthesia:
  • Correction of electrolyte abnormalities (especially hyperkalemia and sodium)
  • Address cardiovascular compromise
  • Treat underlying disease (sepsis)
  • Peritoneal drainage may be effective until stabilization

Addressing Hyperkalemia

• IV fluids (Hartman's is preferred) and dextrose:
  • Dextrose helps create an endogenous insulin response, driving potassium intracellularly
• If hyperkalemia is severe (> 8 mmol/L) and ECG changes are present, use calcium gluconate and exogenous insulin:
  • Calcium gluconate helps restore normal resting membrane potential
  • Insulin drives potassium intracellularly

Colic by Signalment

• Horses are prone to colic due to their hindgut fermentative system, domestication practices, and gastrointestinal tract design:
  • Large fermentative gut, inability to eructate, dietary changes, housing and management changes, and a vulnerable bowel design

Causes of Abdominal Pain in Horses

• Gastrointestinal pain:
  • Caused by issues in the stomach, small intestine, large colon, small colon, and rectum
  • Can result from abnormal gas production, obstruction, ischemia, or inflammation
• Obstruction:
  • Functional: impaired motility
  • Physical:
    • Intraluminal: feed impaction, foreign material
    • Extraluminal: volvulus, lipoma
• Ischemia (strangulation):
  • Extraluminal obstruction
• Inflammation:
  • Enteritis and peritonitis

Colic by Signalment

• Age, breed, sex, and other factors can influence colic risk:
  • Arabians are prone to enteroliths, miniature ponies to faecoliths in the small colon, and females are more at risk of uterine torsion, ovarian problems, and pregnancy complications

Interpretation of Pain in Foals

• Mild pain:
  • Restlessness, attempts to pass manure, tail swishing, straining to urinate, and lack of nursing
• Severe pain:
  • Lying down, rolling, bruxism, reflux from nares, sweating, no response to analgesia, and loss of milk let down in mares

Physical Exam in Foals

• Normal foal parameters are different from adults:
  • Resting heart rate and respiratory rate are higher
• Signs suggesting a surgical lesion:
  • Tachycardia (>120 bpm), absence of fever, abdominal distension, inability to control pain, and supportive ultrasound findings

Colic Issues Specific to Foals

• Meconium impaction:
  • Often passes within the first 24 hours
• Ileus associated with pinworms:
  • Strongyloides westeri can cause irritation and colic in young foals
• Gasterophilus spp. (bots):
  • Larvae reside in the stomach, causing minor issues
• Ascarids:
  • Roundworms that can cause significant disease in foals

Anthelmintic Resistance

• Constant exposure to anthelmintics:
  • Lead to resistance through selection for resistant parasites
• Parasites retain resistance genes:
  • Passed on to offspring
• Selective deworming is recommended in adult horses to reduce resistance

Selective Deworming

• Used to prevent anthelmintic resistance in small strongyles:
  • Perform fecal egg counts (FECs) to identify high and moderate shedders
  • Low shedders (<150 EPG) often do not require deworming
  • Moderate shedders (150-500 EPG) may be dewormed depending on farm situation
  • High shedders (>500 EPG) should be dewormed

FECRTs

• FECRTs (fecal egg count reduction tests) are used to assess the level of resistance on a farm:
  • Conducted every 2-3 years
  • A reduction of >90% indicates no significant resistance
  • 80-90% reduction suggests possible resistance

Goals of Selective Deworming

• Prevent parasitic disease and pasture contamination while preserving refugia:
  • Refugia are parasites that are not exposed to anthelmintics
  • Refugia helps to mitigate the emergence of resistance
• Refugia can be found in horses that are not dewormed, in encysted larvae, and in the environment:
  • These parasites contribute to the overall parasite diversity and can help delay the development of resistance

How FEC Results are Interpreted

• Low shedders (<150 EPG):
  • Not a cause for concern
• Moderate shedders (150-500 EPG):
  • May be dewormed depending on farm situation
• High shedders (> 500 EPG):
  • Deworming is recommended

How to Identify Resistance on a Farm

• Perform FECRTs on at least 6 horses :
  • Use the results to assess the level of resistance and guide deworming practices

Explore the critical aspects of urinary tract diseases, focusing on acute renal failure and acute tubular necrosis in horses. Understand the common signs, pathophysiology, and the effects of toxic insults and ischemia on kidney health. This quiz is designed for veterinary students and equine health professionals.