QUARTERLY BEAT / JULY 2022 ///
hypersensitivity or anti-tubular basement membrane antibody. Prognosis usually grave, not commonly diagnosed, requires biopsy. Steroid responsive in people. Acute glomerular nephritis: Relatively rare in horses, manifested as nephrotic syndrome sometime with hematuria and oliguria. Group-C Streptococcal antigen, EIA Ag:Ab complexes along basement membrane or in mesangial area. Associated inflammation results in decreased GFR.
Diagnostics : Similar to that for ARF.
Treatment : All efforts are primarily palliative with the goal of preventing additional complications and minimizing weight loss.
WEBINAR HIGHLIGHTS
Prognosis for CRF : Grave.
PAMELA A. WILKINS, DVM, PHD, DACVIM-LA, DACVECC Equine Medicine and Surgery University of Illinois College of Veterinary Medicine Kidney Disease in Horses
URINARY TRACT INFECTIONS Clinical Signs: Lower urinary tract: Altered urine flow, urine scalding, dysuria, pollakiuria, gross hematuria, urinary calculi at end of urination Clinical signs : Upper urinary tract disease: Fever, weight loss, signs of lower tract disease combined with signs of systemic illness. Diagnostics : Urinalysis: More than 20 organisms/hpf, more than 10 WBC/hpf in a midstream catch sample or catheterized sample highly suggestive of infection, WBC casts, azotemia with pyuria, low SG with signs of upper urinary tract infection, ultrasound chemistry screen, hematology with fibrinogen. Pathogenesis : Neurologic disorders: EPM, EHV-1, Cauda equine neuritis, botulism, etc.), urolithiasis, foaling trauma, poor perineal conformation. Common organisms: E . coli, Proteus spp., Klebsiella spp., Pseudomonas spp. Treatment : Preferably based on sensitivity from positive culture. TMS, penicillin, ceftiofur commonly used with success.
Post-renal AKI: Increase in ureteral pressure for whatever reason decreases GFR and ultimately renal blood flow.
Treatment of Acute Kidney Injury: Initial: Focus on reversing the inciting or underlying causes and correcting any fluid and/or electrolyte imbalances. Prevention is most important in patients at risk of developing ARF: rapidly restore fluid volume, maintain intravascular fluid volume, maintain glomerular filtration, maintain urine production, monitor serum creatinine frequently, perform frequent UA. Once diuresis is achieved, maintain on intravenous fluids at ~40-80 mL/kg/day until creatinine decreases dramatically, then go to 10-20 mL/kg/day until creatinine is normal and/or patients is eating and drinking normally. Prognosis for AKI: Depends on underlying cause, how long present until treatment was initiated and development of complications including diarrhea, thrombophlebitis and laminitis. Severe ischemic failure and acute interstitial nephritis carry the worst prognosis. Postrenal ARF carries the best prognosis. Acute tubular necrosis carries a good prognosis if the basement membrane remained intact. Animals frequently recover, but may not fully regain the ability to concentrate urine. CHRONIC RENAL FAILURE (CRF) Infrequently recognized in horses. Considered a problem of older patients primarily, stallions may be at greater risk. As many as 1/3 of all horses have renal lesions microscopically at time of death. Lack of clinical signs of disease due to large renal reserve as clinical signs do not become apparent until ⅔ to ¾ of functional parenchyma has been lost. Underlying causes may be congenital or acquired. • Congenital causes: renal agenesis, renal hypoplasia, dysplasia, polycystic kidney disease • Acquired disease: ARF or consequent to renal tubular or glomerular injury.
In this VETgirl Large Animal Webinar, “Kidney Disease in Horses,” Dr. Pamela Wilkins, DVM, PhD, DACVIM-LA, DACVECC reviews some of the more common urinary problems of horses in a simple and approachable manner. Learn to understand and interpret the common causes, clinical signs and potential treatments of uremia and renal dysfunction in horses of all ages. These proceedings originally presented at the South African Equine Practitioners Congress.
ACUTE KIDNEY INJURY Usually secondary to some other disease process:
Radiography: Not useful in adults. Nuclear Scintigraphy: Useful in providing information about individual kidney function. Renal biopsy: Provides sometimes useful diagnostic and prognostic information regarding type of renal disease in horses with ARF (glomerulonephritis, interstitial nephritis, tubular necrosis) it is usually reserved for chronic renal failure cases. PATHOPHYSIOLOGY OF AKI Heterogeneity of renal blood flow makes the kidney susceptible to ischemic and toxic insults. Low medullary blood flow supports counter-current circulation generation of concentration gradient to allow concentration of urine. HOWEVER, this results in a large corticomedullary oxygen gradient creating a relatively hypoxic medulla normally. Renal cortex receives about 90% to total renal blood flow, making it particularly susceptible to toxins. Acute tubular necrosis: • Aminoglycoside toxicity: accumulation of drug within the renal cortex. Usually need some degree of decreased renal perfusion also. Mild cases usually associated with non- oliguric ARF and may go unrecognized. • Pigment nephropathy: arguable as to whether pigment (hemoglobin or myoglobin) is direct cause. Principal characteristics are tubule obstruction and reduced renal blood flow (loss of vasodilation tone due to pigment?). Acute interstitial nephritis: More likely to be associated with eosinophiluria and eosinophilia, more likely to be associated with red cells than acute tubular necrosis. Mechanism unclear, possibly associated with delayed cell-mediated
aminoglycoside antimicrobial therapy, NSAID toxicity, acute enterocolitis, exertional rhabdomyolysis or other myopathy, pleuropneumonia, DIC, purpura hemorrhagica, etc. Physical examination findings, clinical signs, complaints include weight loss, dullness, depression, odor, anorexia, polyuria, oliguria, pigmenturia, signs consistent with primary disease. If ARF secondary, pigmenturia: hemoglobin or myoglobin, secondary to intravascular hemolysis (red maple leaf toxicity, DMSO) or rhabdomyolysis. Distinguish from hematuria by centrifugation of urine. DIAGNOSTICS Urinalysis: ARF: renal tubular casts, moderate proteinuria, +/- hematuria, pigmenturia, increased white blood cells. Increased uGGT, increased uGGT:uCr, abnormal fractional electrolyte excretion, isosthenuria in animals not on IV fluids poor prognosis. Serum chemistry analysis: Azotemia: BUN> 20 mg/dl, creatinine > 2.0 mg/dl, Creatinine > 8 mg/dl poor prognosis. Electrolytes: Decreased sodium, decreased chloride in animals not on IV fluid supplementation, calcium can be >13 mg/dl, potassium can be increased. Fractional excretion of electrolytes: Sodium primarily. Need urinary and plasma sodium and creatinine values. Ultrasonography: In AKI kidneys may appear normal or slightly enlarged with little appreciable parenchymal abnormalities. When present, abnormalities include perirenal edema, widening of the renal cortex and loss of a distinct corticomedullary junction.
Parasitic infections: Strongylus vulgaris, Halicephalobus gingivalis (deletrix), Dioctophyma renale, Klossiella equi
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