Toxic nephritis

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Firas K. Jassim BVMS DVM Supervision Prof. Dr. Mohsen Alrodhan


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University of Al Qadisiyia College of Veterinary Medicine Veterinary Internal Medicine & Prevention branch Firas K. Jassim BVMS DVM Supervision Prof. Dr. Mohsen Alrodhan

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toxic nephritis


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 Most cases of nephrosis are caused by the direct action of toxins but hemodynamic changes may contribute to the pathogenesis.

Drugs that induce toxic nephritis :

Drugs that induce toxic nephritis


TOXINS 1 Mercury,ars- Enic,cadmium,selenium,organic copper compounds 2 1-Aminoglycosides 2-tetracycline 3-sulfonamides 3 vitamin K3 vitaminD2 Metals Antimicrobials Vitamins


TOXINS 4 Benzimidazole Thiabendazole 5 In Ruminants 6 Low-level poisoning in goats Anthelmintics Monensin aldrin


TOXINS 7 Highly chlorinated naphthalenes 8 Oxalate in Plant.Oxalate in fungi ( penicillium spp &mushroom) 9 Oxalate in ethylene glycol or ascorbic acid which is amet- abolic precursor to oxalate. Oxalate poisoning Naphthalenes Oxalate poisoning


TOXINS 10 Primary hyperoxaluria due to inherited metabolic defect in bf master calves. 11 Tannins in the foliage of oak trees and acorns . 12 Amaranthus retroflexus in pigs and cattle Narthecium asiaticum in fed to cattle Isotropis Forrestii in ruminants . Hyperoxaluria Tannins Unidentified toxin


TOXINS 13 Mycotoxins, ochratoxins and Citrinins, fumonisins in ruminants. 14 Ingestion of Lophy-rotoma interrupta (sawfly) larvae by cattle . 15 Cantharidin in horses following ingestion of dead blister beetles in alfalfa hay and hay products


TOXINS 16 Most nonspecific endogenous or exogenous toxemias cause some degree of temporary nephrosis . 17 NSAIDs ( phenylbutazone & flunixin Megalumine) Toxemias NSAIDs


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 Polyuria SUBACUTE. Impaired tubular resorption of solutes and fluids


CLINICAL FINDINGS preacute acute chronic Colic and stranguria Oliguria & proteinuria uremia Polyuria


CLINICAL SIGNS Depression 1 Dehydration 2 Anorexia 3 Hypothermia 4


CLINICAL SIGNS ↓ or ↑HR &weak pulse 5 6 7 8 Diarrhea hypocalcemia bleeding diathesis


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 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 * 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 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.

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