Renal Failure:

• The kidneys excrete the end products of tissue metabolism (except for carbon dioxide), and maintain fluid, electrolyte, and acid-base balance, by varying the volume of water and the concentration of solutes in the urine.
• A partial loss of function is described as renal insufficiency. When the kidneys can no longer regulate body fluid and solute composition, renal failure occurs.
• Renal failure is of 2 types; Acute renal failure and chronic renal failure

Etiology:

Etiology of renal failure, renal insufficiency and uremia can be divided into 3 categories; pre-renal, renal and post-renal

Pre-renal causes:

• Congestive heart failure and acute circulatory failure
• Inadequate circulating blood volume; dehydration, hemorrhage, loss of fluid and electrolytes
• Occlusion of renal arteries by disease
• Expansion of vascular bed shock

Renal Causes:

• Glomerulonephritis
• Amyloidosis
• Pyelonephritis, embolic nephritis
• Interstitial nephritis
• Nephrotoxins; metals, plant toxins, organic chemicals like ethylene glycol, chloroform, CTC, antibiotics; gentamicin, amphotericin B, Sulphonamides

Post-renal causes:

• Complete obstruction of urinary tract by vesical or urethral calculus
• Bilateral urethral obstruction by transitional cell carcinoma located in trigone of bladder
• Internal rupture of any part of urinary tract such as bladder, ureter or urethra

Pathogenesis:

Damage to glomerular epithelium destroys its selective permeability and permits passage of proteins into glomerular filtrate

Due to loss of plasma protein, glomerular filtration completely ceases off

Due to decreased glomerular filtration, metabolic waste also starts to accumulate within kidneys

Urea starts to gets into saliva and creatinine is almost entirely excreted by kidney

Phosphate and sulphate retention occurs as result of reduced glomerular filtration resulting to metabolic acidosis in renal insufficiency

There is loss of tubular resorptive function due to continuous loss of sodium and chloride

Continuous loss of large amount of solute diuresis causes clinical dehydration

Terminal stage of renal failure is cumulative effect of impaired renal excretory and homeostatic functions

Acute renal failure is result of acute circulatory disturbances in kidneys as in case of renal ischemia, injury to glomerular epithelium by toxins. While chronic renal failure is progressive loss of kidney function due to circulatory disturbances or due to disease of kidneys. Onset of ARF is rapid while onset of CRF or CKD is gradual.

Clinical Signs:

Diagnosis:

Acute renal failure should be differentiated with CRF. ARF is reversible condition.

• Based on history and clinical findings
• Based on physical examination; hypothermia, dehydration, buccal ulceration, palpation reveals enlarged kidney with pain in case of acute renal failure. In CRF, palpation reveals small, firm, nodular kidney.
• Laboratory findings:
  • CBC: leukocytosis, monocytosis, increased hematocrit value,
  • Serum biochemistry: hyperproteinemia, increased BUN, creatinine, phosphorus and potassium level, decreased Ca level
  • Metabolic acidosis
  • Urinalysis; high specific gravity of urine, presence of white blood cells casts indicates inflammatory changes
  • Urine culture to detect presence of bacteria
  • Serological test to detect antibody against leptospirosis, ehrlichiosis, dirofilariasis, etc
• Radiographic examination
• Ultrasonography
• Renal biopsy

Treatment and Management of Renal Failure:

Acute Renal Failure:

• Before initiating treatment, results of blood values of BUN, creatinine, PCV, T.P.K, phosphorus, calcium etc. should be interpreted to know renal status.
• Specific therapy includes removal of etiological agent causing condition.
• In case of cardiac failure, digoxin therapy is recommended to control heart rate and cardiac output.
• In case of hemorrhage, hemorrhage should be controlled through correcting damage in arteries, veins causing hemorrhage. Vit. K injection is given to control excess hemorrhage.
• In case of toxin ingested or exposure, toxin removal through specific measure such as gastric lavage, induction of emesis and antidotal therapy should be done.
• In case of obstruction in any part of urinary tract, obstruction should be cleared either through surgical incision or catheterization to evacuate urine.
• In case of anemia or ARF due to blood loss, whole blood transfusion is required.
• In case of bacterial infection, antibiotic therapy should be adopted. Penicillin @ 25,900-40,000 units/kg, b.wt. I/V at 8 hours’ interval for 2 weeks.
• Fluid therapy should be made based on degree of dehydration. Cardiac conditions should be judged prior to fluid therapy. If condition is normal, patient should be rehydrated through I.V fluid for 2-6 hours.
• Most often RL solution is used. Mixture of 2 parts of 5% dextrose and one part RL is suggested. In case of hypokalaemia, 0.9% will be fluid of choice.
• Diuresis should be induced using mannitol. Mannitol 20-25% @ 0.25-0.5 gm/kg, b.wt. through slow IV. If urine passes, dose should be continued every 6-8 hours’ interval during 24 hours’ treatment.
• In no urine output, dose of mannitol should be repeated every 15 minutes upto a total dose of 1.5gm/kg.
• If still there is no urine output, dextrose 20% should be used @25-65 ml/kg at rate of 2ml/min. then dose should be followed @1ml/minute after 15 minutes. If diuresis occurs, then 10% dextrose should be used during next 24 hours. If no diuresis occurs, fluid should be withdrawn.
• To improve blood circulation, vasodilators should be used. Dopamine @ 2-3mcg/kg/min in NS should be given as constant IV drop along with furosemide drip @ 1mg/kg/hour
• For correcting vomiting, gastric protectants; Sucralfate @0.5-1.0 gm orally may be given TID
• For correcting acidosis, initially sodium bicarbonate @8-12 mg/kg, BID-TID. Dose should be adjusted depending on pH of blood.
• For correcting hyperphosphotaemia, diet should contain less phosphorus. Intestinal phosphate binder such as aluminium hydroxide, aluminium carbonate, calcium carbonate, calcium acetate @ 30-90 mg/kg/day should be administered.
• For correction of non-regenerative anemia, anabolic steroids should be used. Testosterone dipropionate @10-15 mg/day/dog. Stanozol @ 25-50 mg, IM weekly in dogs and 0.5-2mg orally, BID or @ 10-25 mg, IM weekly in cats.
• Uraemic gastritis may occur in both acute and chronic kidney failure. It can be controlled by using metoclopramide, cimetidine @10mg/kg, b.wt. BID, IV. For oral administration, it can be given @ 5mg/kg, BID

Chronic Renal Failure:

• Protein intake should be reduced but not restricted totally. First class protein containing all essential amino acid should be provided.
• Carbohydrate and fat in ratio of 3:1 should be provided. It helps to overcome ketoacidosis. Sweetened cream is good source of energy for dogs suffering from CRF
• Vitamin-B should be supplemented, since there is deficiency of it due to anorexia.
• Large volume of fluid produce diuretic effect and reduce effect of diuretics. 5% dextrose followed by 10% dextrose should be provided.
• Foodstuff containing potassium (coconut water) may be given. In case of hyperkalaemia, calcium gluconate @ 10ml, I.V for dog followed by slow IV of following:
  • 10% dextrose or 5% dextrose- 300 ml
  • 5% sodium bicarbonate- 100 ml
  • 50% glucose- 100ml
  • Regular insulin- 20 units
• Metabolic acidosis should be corrected by administration of sodium bicarbonate @3-6gm orally for dog.
• Dialysis may be required when kidney starts to fail completely.
• Salt intake should be minimized gradually over a period of 14 days

Monitoring protocol of CRF patient:

• Body weight and hydration status should be monitored at least once daily
• Serum protein and hematocrit values should be evaluated at least at 3 days’ interval
• BUN and serum creatinine values should be determined daily at first stages.
• Urine output should be monitored.