Slide 1: toxic nephritis تنفيذ : د.فراس خلف الغراوي
باشراف :الاستاذ الدكتور محسن الروضان INTRODUCTION : INTRODUCTION The kidneys are particularly vulnerable to endogenous & exogenous toxins because they receive a large proportion of total cardiac output and because substance are concentrated in the kidney for excretion. ETIOLOGY : ETIOLOGY Most cases of nephrosis are caused by the direct action of toxins but hemodynamic changes may contribute to the pathogenesis. TOXINS : TOXINS Metals Antimicrobials Vitamins TOXINS : TOXINS Anthelmintics Monensin aldrin TOXINS : TOXINS Oxalate poisoning Naphthalenes Oxalate poisoning TOXINS : TOXINS Hyperoxaluria Tannins Unidentified toxin TOXINS : TOXINS TOXINS : TOXINS NSAIDs
(phenylbutazone & flunixin
Megalumine) Toxemias NSAIDs PATHOGENESIS : PATHOGENESIS Obstruction to the flow of glomerular filtrate through the tubules as a result of interstitial edema &intraluminal casts.if thers sufficient tubular damage there may be back leakage of glomerular filtrate in to the interstitium. Acute
nephrosis Direct toxin effect on glom- eruli, which dec- reases glome- rular filtration the combined effect is oliguria & uremia PATHOGENESIS : PATHOGENESIS Polyuria SUBACUTE. Impaired tubular
resorption of solutes
and fluids CLINICAL FINDINGS : CLINICAL FINDINGS Colic and stranguria Oliguria & proteinuria uremia Polyuria CLINICAL SIGNS : CLINICAL SIGNS Depression 1 Dehydration 2 Anorexia 3 Hypothermia 4 CLINICAL SIGNS : CLINICAL SIGNS ↓or ↑HR &weak pulse 5 6 7 8 Diarrhea hypocalcemia bleeding diathesis CLINICAL PATHOLOGY : CLINICAL PATHOLOGY *In acute tubular nephrosis, urinalysis abnormalities are usually pre- sent before serum urea and creatinine concentration are increased
Proteinuria , glucosuria , enzymuria and hematuria are initial changes on urinlysis in experimental toxic nephrosis .
*The earliest indication of tubular epithelial damage is the detection tubular enzyme GGT in urine.
*Hypoproteinemia may be present.
*In acute renal disease in horse hypercalcemia and hypophosph- atemia can be present.
*In the chronic stage the urine is isosthenuric and may or may not contain protein .
*Azotemia occur when uremia is present.
*Ultrasongraphically renal changes are seen in foals receiving high daily doses of phyenylbutazone. NECROPSY FINDINGS : NECROPSY FINDINGS In acute cases the kidney is swollen and wet on the cut surface and edema , especially of perirenal tissues may be apparent.
Histologicaly there is necrosis and desquamation of tubular epithelium and hyaline casts are present in the dilated tubule.
In phenylbutazon poisoning the renal lesion is specifically a renal medullarly necrosis .
Ulcer in all or any part of the alimentary tract from the mouth to the colon if phenylbutazone was administered orally. DIFFERENTIAL DIAGNOSIS : DIFFERENTIAL DIAGNOSIS *Clinical differentiation from acute GN is difficult but clinical signs of involvement of other organs in the toxic process may be present a combination of polyuria .
Combination of polyuria & glucosuria is an uncommon finding in large animal & is usually caused by nephrosis.
*Occasional cases of D.M have been recorded in horse and cattle.
*Case of cushing syndrum (CHRONIC HYPERADRENO -CORTICISM)in horse are more common but this includes characteristic signs of polyuria, ,glucosuria,debilitetion, hirsutism,polyphagia and hyperglycemia.
*Diarrhea in terminal stage of uremia in horse can be confused with other case of diarrhea. It requires a blood urea and urinalysis for differentiation. TREATMENT : TREATMENT Treatment should be directed at general supportive care for acute renal disease.
If the toxin is identified , it should be removed .
Treatment for specific toxins may be available .
Hemodialysis was used successfully to treat a foal with presumed oxytetracycline nephrotoxicosis. Slide 19: DR.FIRAS KHALEF ALGHARAWYI Thank You