AKI and Renal Disease in Large Animals Flashcards
identify and describe the primary etiologies of acute kidney injury in horses, ruminants, and pigs, including toxic, infectious, and hemodynamic causes
- infectious:
-LEPTOSPIROSIS!!
-pylonephritis
-borrelia/lyme nephritis
-streptococcus - inflammatory:
-streptococcus-glomerulonephritis, immune related drug reactions
-type III Ab-antigen complex deposition in glomerular basement membrane: protein losing nephropathy - iatrogenic: general anesthesia, administration of nephrotoxic drugs to renally impaired or dehydrated patient, drug overdose
- idiopathic: diagnosis of exclusion
- toxicity:
-pigmenturia: myoglobin or hemoglobin
-many others in future lectures - acute on chronic kidney disease
describe diagnosis of AKI in horses, ruminants, and pigs
- oliguria (0.5ml.kg.hr) for at least 6 hours (<6L urine/day)
-increase in serum creatinine >0.3mg/dl over baseline in a 24-48 hour window
-azotemia or increase in creatinine - USG (prior to fluid therapy) < 1.025
-UA: absence of casts does not rule out!
-pyuria: consider infectious component
-none to mild proteinuria - rarely electrolyte derangements until ARF/severe
-hypo or hypernatreamia, hypochloridemia, hypocalcemia, hypomagnesemia, hyperkalemia
-all over the place but RARELY see hypercalcemia with AKI - palpation and US rarely helps with diagnosis
-might see enlarged kidneys with perineal edema
goal is to recognize patients at risk BEOFRE there is injury or early in the process
describe risk factors for AKI in LA
- reduced renal blood flow and hypoxia (medulla: lowest perfusion)
- SIRS
- toxicity
-omeprazole - other immune-mediated, infectious
describe SIRS
sepsis inflammatory response syndrome
- reduced renal blood flow and hypoxia-ischemia (esp in medulla, with the lowest perfusion)
-REDUCED CARDIAC OUTPUT: from dehydration, hypovolemia, primary cardiac disease. hypotension leads to renal and splanchnic vasoconstriction in response to shock states - SIRS can result in microcirculatory dysfunction, thrombosis, infarct, fibrin, or cortical necrosis as lesions
- short list of what we see in LA:
-infection
-acute hemorrhage
-enterocolitis
-ischemic bowel
-multiple organ dysfunction/failure
describe the approach to treating and monitoring AKI in LA
- treat underlying condition
- maintain blood pressure and volume
- IV fluid diuresis; CAUTION of fluid overload
- +/- pain management
- avoid nephrotoxic agents
monitoring: difficult in LA!! hard to monitor ins and outs
-PE, PCV,TS, serial creatinine measurements, urine output collection system if possible
-weigh patient if possible q24hr: to check for fluid overload
-HR, RR, thoracic auscultation: will get pulmonary edema before get peripheral edema, more evidence of fluid overload (also crackles, etc.)
-monitor for evidence of peripheral edema to eval if gone too far with fluid therapy
-blood pressure: pressure does NOT equal blood flow!! MAP provides a rough estimate of tissue perfusion but is hard to get accurate indirect measurement in LA
-can try to manage central venous pressure to see trends over time
what are commonly used drugs with nephrotoxic potential?
- NSAIDs
-non-selective COX inhibition: flunixin meglumine, phenylbutazone, meloxicam, ketoprofen
-selective COX-2 inhibition: firocoxib (equioxx) - antibiotics:
-aminoglycosides: IV/IM/SQ (gentamicin > amikacin > streptomycin)
-oxytetracycline: IV/IM/SQ: most nephrotoxic in dehydrated patients
-polymixin B: IV as antiendotoxic therapy - bisphosphonates: treat ortho pathology (navicular syndrome)
-tiludronate and clordronate
risk of AKI increases as number of nephrotoxic drugs administered increases!!!
describe treatment of AKI
- discontinue and avoid nephrotoxic drugs
- IV fluid therapy: cornerstone of treatment, use carefully!!
- diuretics: if anuric or oliguric, use only once euvolemia restored
-furosemide: single high test dose IV (2mg/kg): if favorable response, use as a CRI
–loop diuretic: effects by inhibiting Na-K-2Cl co-transporter in loop of Henle (prevents Na reabsorption and water follows to increase urine production) - pressors: maintain BP >65mmHg MAP
-weak evidence low dose dobutamine - aminophylline- if desperate
-desired effect: afferent arteriolar vasodilation to improve GFR
-MOA: inhibit adenosine = inhibit afferent arteriolar vasoconstriction
no single drug is proven effective in restoring GFR and urine production in LA
what are the goals of AKI treatment in LA?
- response to treatment: in 24-72 hours of reversible AKI expect reduction of sCr by 30-50%
-diuresis and polyuria are the goals for anuria/oliguria - DONT GET GREEDY: don’t fluid overload to try to bring down sCr
-return to baseline creatinine may take months to achieve - approx 60% recover, 30% euth, and 10% improve but develop CKD
describe poor prognostic factors for AKI in LA
KEY: response to IVFT is better prognostic indicator than the magnitude of serum creatinine
- persistent or escalating azotemia in the face of judicious IVFT
- oligoanuria (or anuria) within 12 hours of starting IVFT
- worsened by edema
- some horses can develop laminitis which is obviously bad
describe renal papillary necrosis
- a gross diagnosis from hypovolemia and NSAIDs causing renal medullary ischemia
- histologically: tubular necrosis
- majority of AKI cases due to injury, necrosis, and dysfunction of renal tubular cells (tubulointerstitial diseases)
describe etiology of glomerulonephritis
- rare cause of AKI; causes protein losing nephropathy!!
- horses: equine infectious anemia, STREPTOCOCCAL sp., immune-mediated (IgM)
- cattle: BVDV, trypanosomiasis (case reports)
- swine: classic swine fever/hog cholera, african swine fever
- sheep: finnish lanbrace lambs congenital hypocomplementemia (C3)
-bred out
describe nephrotic syndrome
- hypoalbunemia
- proteinuria (UPC ratio >2:1)
- peripheral edema
- hypertension: hard to document accurately in clinical cases!
-proposed in horses: MAP >90 mmHg
not well documented in large animals
