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equine renal


Acute renal failure (ARF) in horses is most likely caused by exposure to nephrotoxins or as a consequence of hypoperfusion or ischemia of the kidney.
The most common pathologic lesion with ARF is acute tubular necrosis (ATN).
Administration of aminoglycosides is likely the most common cause of ATN in horses.
Neomycin is the most nephrotoxic of the aminoglycosides, followed by gentamicin, kanamycin and amikacin, which all have similar levels of toxicity.
Streptomycin is the least nephrotoxic.
This group of antibiotics exert toxicity by accumulating within the proximal tubular epithelial cells.
It is believed that aminoglycosides are filtered at the glomerulus in to the urine and enter the proximal tubular cell via the urine.
Once toxic amounts have accumulated within the tubular epithelial cell, cellular metabolic processes are disrupted which leads to cell swelling, cellular death and sloughing of the epithelial cell into the tubular lumen. Release of lysosomal enzymes and intracellular accumulation of calcium are
Most cases of aminoglycoside toxicity are not the result of overdosing or use in an azotemic patient, but rather the repeated doses and duration of administration leading to accumulation of drug within the tubular epithelial cells.
The healthy kidney may tolerate a single major overdose (ie ten times the normal amount) without detrimental effects.
Toxicity is almost always the cumulative effect of repeated administration of aminoglycosides.
Prolonged administration of aminoglycoside antibiotics without monitoring of trough concentrations or serum creatinine (Cr) concentration is a common history with aminoglycoside nephrotoxicity in the horse.
Gentamicin and amikacin may be used for extended periods (> 10 days) if the patient is adequately hydrated and appropriate trough concentrations and Cr concentration are maintained.
It should be noted that only minor increases in Cr (03mg/dl) may indicated potential toxicity.
Sick foals may be at greater risk for aminoglycoside toxicity, not because the neonatal kidney is more susceptible, but more likely due to prolonged duration of treatment related to septicemia.
When aminoglycosides are administered to high-risk patients, it is imperative volume deficits are replaced and serum Cr and trough levels monitored closely.
Aminoglycoside toxicity rarely occurs in patients that are receiving appropriate fluid therapy.
Increased urinary fractional excretions of Na+ that accompany fluid dieresis have a protective effect on the kidney, while conditions of hypokalemia and hypocalcemia may predispose to ATN by decreasing urine output.
Administration of oral e-lytes (Na+, Cl-, K+) daily to horses undergoing aminoglycoside therapy will encourage water consumption and subsequent diuresis.
Once daily dosing of aminoglycosides is important to reduce the risk of nephrotoxicity while still ensuring appropriate therapeutic response.
It is important to remember the risk of toxicity is related to its cumulative effects, therefore, in the azotemic patient, it is not necessary to delay the initial dose of antimicrobial administration as long as rehydration of the patient is ensured.
Aminoglycoside toxicity should be considered in any horse that becomes depressed and inappetent while being treated with aminoglycosides or within a few days following discontinuation of therapy.
Renal failure may occur even after the drug has been discontinued, making continued monitoring of renal function for 2-4 days advisable in high risk patients.
Polyuria and stranguria may be observed before the onset of depression and anorexia.
A tentative diagnosis is based on clinical signs, historical use of aminoglycosides and laboratory support.
ATN in the horse is evidenced by presence of enzymuria and cylinduria, as well as azotemia.
ARF related to ATN typically manifests as non-oliguric to polyuric renal failure and outcome is favorable as long as the duration of ARF is not prolonged and the underlying disease processes can be corrected. Therapies such as peritoneal and pleural dialysis, plasmapheresis and hemodialysis have not proven
Additional toxic nephropathies to consider in the horse include vasomotor nephropathy, pigment nephropathy, NSAID therapy, Vitamin D toxicity, heavy metal ingestion, acorn poisoning and leptospirosis.
Vasomotor nephropathy results from any condition that causes sustained marked hypotension or release of endogenous pressor agents (ie cortisol).
Hemorrhagic shock, severe intravascular volume deficit (ie enterocolitis), septic shock, and coagulopathy are important risk factors for vasomotor ARF in horses.
Pigment nephropathy in the horse typically occurs following episodes of rhabdomyolysis which are prolonged or associated with concurrent dehydration.
Hemolysis (leading to increased amounts of intravascular hemoglobin pigment) is a less common cause of ATN in horses, although likely the most common etiology is red maple leaf toxicity.
Administration of NSAIDs may result in ATN and ARF following prolonged duration or in dehydrated horses.
The lesion produced by NSAID toxicity is medullary or papillary crest necrosis, which may be manifested as gross hematuria.
Renal prostaglandins (PGE2 and PGI2) are important vasodilatory agents necessary during periods of renal hypoperfusion.
The presence of renal PG’s is 7-10 fold greater in medullary tissue.
It is not surprising to find lesions associated with NSAID toxicity primarily associated with the renal medullary crest.
Administration of NSAIDs to dehydrated and volume depleted patients increases the risk of ATN.
Vitamin D toxicity is most commonly associated with ingestion of plants with increased amounts of vitamin D metabolitites (ie Cestrum diurnum).
Heavy metal ingestion is also a very rare cause of ATN in horses. Ingestion of mercury, cadmium, zinc, arsenic and lead may all lead to
Diagnosis is confirmed by measuring increased concentrations of the metals in blood and tissue.
Acorn toxicity is primarily a disease of cattle, but horses may be affected on rare occasions.
Leptospirosis may also be considered as a differential for ATN and ARF when vasomotor nephropathy can be ruled out and without historical support of nephrotoxin administration.
Diagnosis of ARF in the horse begins with clinical suspicion of more marked anorexia and depression than should be expected due to the primary disease process, as well as confirmation of history and potential exposure to nephrotoxins.
Patients that fail to produce urine within 6-12 hours of initiating fluid therapy should also raise concern for ARF.
Diagnosis of ARF is confirmed by laboratory results.
ARF increase in Cr (up to 5-15 mg/dl) is typically greater than that for BUN (50-100 mg/dl), resulting in a BUN/Cr ratio less than 10:1.
The triad of e-lyte abnormalities include hyponatremia, hypochloremia, and hyperkalemia is consistent with ARF, as well as hypocalcemia, hyperphosphatemia and metabolic acidosis, which may also be detected.
Urinalysis should be performed on all horses in which ARF is suspected.
Documentation of isosthenuria (urine specific gravity 1008-1012) or lack of concentration of urine (<1020) in the face of dehydration and azotemia are supportive of ARF.
Microscopic hematuria may be present ARF.
Evidence of proximal tubular damage including ezymuria and glucosuria are supportive.
The presence of proteinuria indicates glomerular damage as well.
Urine sediment in ARF reveals casts and increased numbers of RBCs and leukocytes, and the number of crystals may be decreased (decreased calcium carbonate crystals).
Increased fractional excretions of urinary sodium, chloride and phosphorus are common findings ARF.
Because IV fluid administration will augment the fractional excretions of e-lytes, it is necessary to obtain urine for examination prior to the inititation of IV fluids.
The most accurate assessment of renal function involves measuring glomerular filtration rate (GFR).
In the clinical setting, GFR assessment may be performed using timed urine collections (with inulin and creatinine clearances) as well as nuclear scintigraphy.
Use of scintigraphy may be performed prior to nephrectomy to determine GFR of the kidneys prior to unilateral nephrectomy.
Renal biopsy is more commonly performed to determine glomerular injury and tubular necrosis.
With acute renal failure the diagnosis is typically obvious related to historical factors, but may be indicated in cases of ARF for which exposure to nephrotoxins or other underlying primary disease process is not apparent.
Renal biopsy should be approached cautiously because life-threatening hemorrhage is a potential complication.
Biopsy of the right kidney is most commonly performed with ultrasonographic guidance.
Renal tissue should be submitted for histopathology as well as culture and sensitivity.
Unfortunately, patient response to therapy may be the most obvious determinant of degree of injury.
General principles of therapy ARF for horses are similar to those for humans and small animals.
Initial treatment should always focus on judicious fluid therapy to replace volume deficits and correct e-lyte and acid base abnormalities. The magnitude of
The fluid therapy of choice is typically 0.9pct NaCl, as hyperkalemia is often present.
Following replacement of volume and corrections of e-lyte imbalances, careful attepts should be made to determine whether the patient is oliguric or non-oliguric (polyuric).
The prognosis appears more favorable for polyuric renal failure than oliguric failure.
With simple observation during the initial 12-24 hours of therapy, it is easily determined if the horse is passing the expected amount of urine. Oliguric patients will
In the oliguric renal failure patient edema may also develop.
In patients with pre-renal azotemia (azotemia not related to primary renal function), the degree of azotemia should decrease by 50pct within the initial 24 hours of therapy, as compared to ARF where the Cr will remain unchanged or even increase within this time period.
In severely systemically ill patients (especially those with vasomotor nephropathy), monitoring systemic blood pressure may confirm restoration of blood pressure, as there are some patients that may remain hypotensive as the IV fluid may be accumulating extravascularly as edema.
Measurement of central venous pressure (CVP) is also a non-invasive method of monitoring patient response to volume administration.
CVP is measured with a manometer and IV catheter in the jugular vein of the horse.
A patient receiving IV fluids with a negative CVP or CVP < 8 cmH2O most likely has not received adequate volume to restore deficits.
The patient receiving IV fluids with a CVP > 8cmH2O is likely volume overloaded and at risk of pulmonary edema.
The volume overload occurs because the kidneys fail to excrete the excess water and e-lytes administered via IV catheter.
Careful monitoring of body weight is an excellent indicator of renal function and disposition of IV fluid administration.
Monitoring of urinary output is possible with placement of indwelling urinary catheter or external collection devices (only possible with stallions/geldings).
In horses that remain oliguric after 12-24 hours of therapy, administration of furosemide (1mg/kg) should be administered every 2-4 hours.
The use of Lasix is often ineffective at increasing renal blood flow, GFR and tubular flow in horses with ARF.
Additional therapies include mannitol and dopamine.
Mannitol is administered at 1mg/kg CRI as a 10-20pct solution.
Dopamine given at 3-7 ug/kg/min.
These drugs, particularly dopamine, should only be administered in the hospital setting due to the potential derangements in systemic blood pressure and metabolic side effects of the therapies.
Most cases of equine ARF are polyuric and these therapies are not necessary,dopamine and mannitol.
In the event the patient remains oliguric after 72 hours of therapy with loop diuretics, mannitol and dopamine the prognosis is grave.
One study showed horses with severe enterocolitis that remain azotemic >72 hours following initiation of therapy were three times as likely to die or be euthanized as the horses without azotemia.
Dialysis therapy has been performed in select patients.
Hemodialysis has been successful in two adult horses and peritoneal dialysis has also had reported success.
The patient that presents with polyuric ARF or if converted from oliguric to polyuric renal failure should receive continued fluid diuresis until the Cr returns to normal or reaches a steady state and the horses attitude and appetite are improved.
A word of caution regarding potassium supplementation, diuresis will promote kaliuresis as well and K+ supplementation is likely necessary. It may be necessary to provide TPN or PPN (dextrose CRI) or enteral nutrition in the
Closely monitoring serum Cr will be important as fluid therapy is slowly discontinued.
In the horse that does not experience complete resolution of azotemia following treatment for ARF (ie some horses Cr may plateau between 2-3 mg/dl), the serum Cr may slowly return to normal over the following months.
The patient that maintains a permanently elevated Cr has likely sustained permanent loss of renal function.
As with many systemic diseases in horses, laminitis is a potential side effect of ARF as well.
Although the mechanisms remain fully unknown, prophylaxis may be an important part of the therapy for patients with ARF in addition to fluid support.
Chronic renal failure (CRF) in the horse is an irreversible disease process characterized by a progressive decline in GFR.
The rate of GRF decline is variable from patient to patient, making the short-term prognosis fair to guarded but the long-term prognosis remains poor.
There are essentially two categories of CRF in the horse primary glomerular disease and primary tubulointerstitial disease.
Primary glomerular diseases which can lead to CRF in horses include glomerulonephritis, nonspecific glomerulopathy, renal glomerular hypoplasia and amyloidosis.
Primary tubulointerstitial diseases causing CRF include incomplete recovery from ATN (ARF), pyelonephritis, nephrolithiasis, hydronephrosis, renal dysplasia, and rarely papillary necrosis these dzs commonly referred to as chronic interstitial nephritis.
Because many horses do not present until later in the course of disease, the primary etiology may be lost and the diagnosis results in end-stage kidney disease.
Proliferative glomerulonephritis indicates increased cellularity of the glomerular tufts as a result of influx of inflammatory cells and proliferation of the mesangium.
The inflammatory cellular infiltrate is thought to be deposition of circulating immune complexes along the basement membrane of the glomerulus.
Deposition of immune complexes activates complement and vasculitis ensues (Type III hypersensitivity).
It has been suggested Streptococcal antigens may be the trigger factor for development of proliferative nephropathy, as well as antigens for equine infectious anemia.
It is commonly observed that immune complex deposition along the glomerular basement membrane is much more widely prevalent than indicated by clinical disease.
It is only rarely that proliferative glomerulonephropathy is of clinical significance.
On the other hand, chronic interstitial nephritis (CIN) and fibrosis are the most common cause of CRF in horses.
Tubulointerstitial disease typically develops as a sequela to ATN considequent to exposure to nephrotoxins or vasomotor nephropathy. Additional eitiologies include
While most horses recover completely from the fore-mentioned diseases, there are few that will recover with significant loss of renal function and only later (may be years) develop clinical signs of CIN.
In young horses (< 5 years of age) with indications of CRF congenital anomalies of development must be considered (ie renal hypoplasia, dysplasia, polycystic kidney disease).
The most common clinical sign associated with CRF is weight loss, followed by a small amount of ventral,pectoral edema,PU/PD may be present, but go unnoticed by most owners.
If hematuria (urinary calculi/neoplasia) or pyuria (pyelonephritis) is present, the urine may change enough that owners report it as significant, but this is not common to all horses.
Accumulation of dental tartar, frequently noted on the incisors and canine teeth, melena, and oral ulcers may also be observed in CRF. Growth retardation is common in horses with
Clinicopathologic findings in horses with CRF vary depending upon diet, appetite, and the cause and severity of renal damage. Azotemia, typically >5mg/dl, BUN:Cr ratio >10:1, mild hyperkalemia, hyponatremia, and hypochloremia are
As a result, horses with CRF are encouraged to eat grass hay rather than alfalfa hay to reduce the dietary intake of calcium.
Anemia is often observed related to the decreased erythropoietin produced by the failing kidney.
Horses with glomerular disease may have hypoproteinemia.
Horses with immune-mediated disease or pyelonephritis may have increased globulins.
Urinalysis may also vary depending upon the etiology of CRF.
Urine is typically very dilute with decreased amount of crystals and mucus (most likely due to PU/PD).
Isosthenuria is common, but hematuria and pyuria are less common and dependent upon particular etiologies.
Bacterial culture is recommended in all CRF patients, because pyuria is not always detected, even with septic pyelonephritis.
Diagnosis of CRF is similar for that of ARF.
Rectal exam is important as stones or dilated ureters may be palpable. Ultrasound examination may reveal
Loss of parenchymal echogenicity and corticomedullary distinction is also typical CRF.
Horses with congenital anomalies of the renal system may have kidneys that are misshapen, have variable echogenicity or very small kidneys that may be difficult to locate.
Cystoscopy is useful for visualization of the distal urinary tract, especially when hematuria or dysuria is present.
Measurement of GFR provides the most accurate assessment of renal function.
Biopsy may be useful for determining cause of CRF but due to advanced disease in most patients, biopsy is not remarkable.
In addition, renal biopsy should be approached cautiously and only performed if the result is likely to alter the treatment or prognosis.
In horses with stable CRF, treatment is aimed at management changes to decrease calcium intake, increase Na/Cl intake and if metabolic acidosis is present, the addition of oral NaHCO3- may be warranted.
Treatment for glomerular disease has been unrewarding as immunosuppressive therapy has been of limited benefit.
As CRF progresses, patients lose more and more body condition and nutritional support becomes an issue.
Increasing daily intake of fat calories may be achieved by adding corn oil to the diet (upto16oz/day), as well as adding omega-3 fatty acids (linseed or flaxseed oil) may add calories and slow the progression of CRF.
Ensuring the diet is palatable is first and foremost to stimulate appetite and should not be overlooked.
Prognosis for CRF is largely poor due to the progressive loss of nephron function.
As long as Cr < 5mg/dl and the BUN:Cr ratio <15:1, affected horses may be able to maintain a reasonably good attitude, appetite and body condition.
The emphasis should be placed on maintenance of body condition with humane euthanasia as the end result in most cases of CRF.
Created by: alljacks



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