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Management of renal disease in dog

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Management of renal disease in dog

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Management of renal disease in dog

  1. 1. Dr Ajay Katoch Assistant Professor, Veterinary Medicine
  2. 2. Introduction The kidneys are responsible for the excretion of nitrogenous and other metabolic waste products and for the regulation of water, electrolyte and acid-base balance
  3. 3.  The kidney has a biosynthetic role, and is involved in the production of renin, erythropoietin, prostaglandins and Vitamin D3  Gluconeogenesis under conditions of starvation and is an important site for degradation of some peptide hormones
  4. 4. Essential terminology Renal disease Renal failure Azotemia Uremia
  5. 5. Renal disease Implies the presence of histological lesions in the kidney but does not specify any degree of renal dysfunction
  6. 6. Renal failure  Inability of the kidney to maintain the homeostasis leading to :  The buildup of the nitrogenous waste in blood (azotemia)  The loss of urine concentrating ability  Disturbances of fluid, electrolyte, and acid-base balance  75% of the total nephron population has become non-functional
  7. 7. Azotemia Increased concentration of non- protein nitrogenous waste products (e.g. urea, creatinine) in the blood
  8. 8. Uremia Uremia is the poly systemic toxic syndrome, which develops with the progression of renal failure and is characterized by the presence of clinical signs in association with azotemia
  9. 9. Toxic Substances accumulating in uremia Sr. No. ACCUMULATING SUBSTANCE ADVERSE EFFECTS 1. Urea Weakness, anorexia, vomiting, glucose intolerance, bleeding disorder 2. Guanidine compounds: 1. Guanidine 2. Dimethyl guanidine 3. Creatinine 4. Cretine 5. Guanidinoacetic acid Weight loss, platelet function defect 6.Guanidinosuccinic acid Interfere with platelet factor III 3. Aliphatic amines: Dimethylamine Trimethylamine Uraemic breath odour, encephalopathy
  10. 10. Sr.No Accumulating substance Adverse effects 4. Polyamine : i. Spermine ii. Spermidine Spermidine reduces erythropoiesis 5. Peptides and polypeptide hormones Accumulate due to reduced excretion or increased secretion occurs as compensating response to renal failure 6. Parathyroid hormone Osteodystrophy, nephrotoxicity, impaired erythropoiesis, cardiotoxicity 7. Insulin Hyperinsulinism may lead to islet exhaustion and diabetes mellitus 8. Glucagon Insulin resistance/ glucose intolerance
  11. 11. Sr. No. Accumulating substance Adverse effects 9. Growth hormone Insulin resistance/ glucose intolrence 10. Gastrin Hypergastrinaemia contribute to gastritis 11. Myoinositol Neuropathy 12. Ribonuclease Impaired erythropoeisis, decreased cellular proliferation 13. Cyclic adenosine monophosphate (cAMP) Abnormal platelet function 14. Derivative of aromatic amino acids: i. Trptophan ii. Tyrosine iii. phenylalanine Anorexia
  12. 12. Renal failure Acute renal failure Chronic renal failure
  13. 13. Acute renal failure Acute renal failure (ARF) describes a sudden reduction in renal function associated with a sudden decrease in the glomerular filtration rate (GFR) and the rapid development of azotemia and uremia
  14. 14. Causes Pre renal (functional ) Shock Dehydration Heart failure Hypoadrenocorticism Thrombosis of the renal artery or massive blood loss
  15. 15. Renal intrinsic ( structural) Acute tubular necrosis Ischemia Toxin Tubular factors
  16. 16. Renal intrinsic ( structural) Acute interstitial Necrosis Inflammation Oedema
  17. 17. Renal intrinsic ( structural) Glomerulonephritis Damage to intrinsic mechanisms
  18. 18. Post renal (obstructive) Urolithiasis Neoplasm Herniation Damage to lower urinary tract Anatomical abnormalities
  19. 19. Some Nephrotoxins causing renal damage  Ethylene glycol (in antifreeze)  Antibiotics: Amino glycosides, Tetracycline, Cyclosporin  Chemotherapeutics: Amphotericin B, cis- platinum, Doxorubicin  Heavy metals: Lead, Thallium, Zinc, Arsenic, Mercury  Hypercalcemia: Malignancies, Hyperparathyroid, Vitamin D toxicity  Other causes: Carbon tetrachloride, Chloroform, Iodinated contrast media
  20. 20. Clinical signs of ARF Hyperkalemia Nausea/Vomition Pulmonary edema
  21. 21. Clinical signs of ARF Ascites Dehydration
  22. 22. Clinical signs of ARF Encephalopathy Kidney pain Oliguria
  23. 23.  Shock  Disseminated intravascular coagulation (DIC)  Respiratory distress  Neurologic disturbances  Coma and death Other signs include -
  24. 24. Diagnosis  History and clinical signs  Laboratory findings - i. Rising creatinine and urea ii. Rising potassium iii. Acidosis iv. Hyponatraemia v. Hypocalcemia
  25. 25. Management of ARF  Early recognition of disease  Identification and treatment of specific underlying cause  Sodium bicarbonate to correct metabolic acidosis  Provide nutritional support – Non protein calories but high quality protein in limited amount
  26. 26. Management of ARF -  Promote urine output if still anuric.- Frusemide, Mannitol  Dialysis to remove excess fluid & waste products.  Gastric protectants and anti-emetics to alleviate gastrointestinal disturbances
  27. 27. Emergency management of Hyperkalemia TREATMENT MECHANISM & SPEED OF ACTION POSSIBLE ADVERSE EFFECTS 10% calcium gluconate (0.5-1ml/kg) Protect myocardium Immediate and short lived effect Administer IV slowly , overdose can lead to rhythm disturbances Sodium bicarbonate (1-2 mmol/kg) Correct metabolic acidosis so lower plasma K+ 15-30 min to work Overcorrection can lead to hypocalcaemia, tissue hypoxia, paradoxical CSF acidosis Glucose insulin (2gm of glucose 1 unit of soluble insulin per kg) Glucose stimulate endogenous insulin release, insulin stimulate uptake of glucose and K+ 15-30 min to work Insulin may be dangerous in case of Addison’s disease
  28. 28. Chronic renal failure  Chronic renal failure is a relatively common syndrome in older dogs and represents the end stage of a number of renal disease  Clinical signs of CRF are not usually apparent until at least 65% to 75% of renal tissue is destroyed; so early cases often go undetected
  29. 29. Cause Pyelonephritis Chronic nephritis Renal amyloidosis Renal urolithiasisHydronephrosis Primary renal neoplasia Glomerulonephritis
  30. 30. Clinical signs  Polyuria and Polydipsia  Weight loss/loss of muscle mass/poor hair coat  Anorexia with vomition  Weakness, lethargy & depression  Pallor & dryness of mucous membranes  Oral ulceration
  31. 31. Clinical signs  Hypertension  Diarrhoea  Pruritis (itching)  Edema  Anaemia  Neurologic changes
  32. 32. Diagnosis I. History II. Clinical findings III. Laboratory findings:  Urinalysis- Sp. gravity<1.025 Proteinuria, WBC,RBC  Blood- Lymphopenia, Non- regenerative anaemia.
  33. 33. Red blood cast
  34. 34. WBC cast
  35. 35. Diagnosis : IV. Blood Biochemistry:  Blood urea >40mg/dl  Creatinine level > 2mg/dl  Elevated phosphorus level  Elevated Cholesterol  Elevated or decreased calcium level  Acidosis
  36. 36. Diagnosis Radiography Bilateral reduction in size of kidney & radio opaque uroliths
  37. 37. Diagnosis Ultrasound Urolithiasis Polycystic renal disease Hydronephrosis
  38. 38. Management of CRF  Fluid therapy  Dietary restrictions (protein; phosphorus) - Protein intake should be low but first class protein should be provided to prevent tissue breakdown.  Calcium supplements
  39. 39. Management of CRF  Blood pressure treatment: Angiotensin converting enzyme (ace) inhibitors - e.g. enalapril / vasotec  Gastrointestinal protectant  Dialysis  Kidney transplant
  40. 40. Drug to be avoided in RF  Aminoglycosides  Nalidixic acid  Aspirin  Amphotericin  Neomycin  Nitrofurantoin,  Sulphonamides  Tetracycline and Magnesium salt
  41. 41. Acute Vs Chronic failure S.no Parameter Acute Chronic 1. History Perfectly healthy until very recently Weeks to months of polyuria / polydipsia, weight loss & vomition 2 Physical examination Good body condition. Extremely depressed relative to the degree of azotaemia May be cachectic. Tolerates severe azotaemia rather well 3 Kidney size Normal sized or large – may be painful Small & non painful. Chronic disease like renal neoplasia, polycystic kidneys, hydronephrosis
  42. 42. S. no Parameter Acute Chronic a) PCV Anemia is not usually present Non-regenerative anemia b) Potassium, Phosphate and Acid/base Hyperkalaemia, hyperphosphataemia and metabolic acidosis No Hyperkalaemia, Hypokalaemia may occur c) Urinalysis Sediment contains casts, cells, debris etc. Urine sediment is inactive. d) Urine production Anuric or oliguric mainly Polyuric e) Response to therapy Often reversible Irreversible
  43. 43. Breeds prone to Renal Failure Bull terrier Doberman Pinscher
  44. 44. Breeds prone to RF Lhasa Apso Norwegian Elkhound Soft coated wheaten terrier
  45. 45. Breeds prone to RF Standard poodle Cairn terrier Beagle

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