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Acute renal failure in the dog

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Category: Schede
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  • Disciplina: Medicina d'urgenza
  • Specie: Cane

Acute renal failure (ARF) is a potentially reversible clinical condition characterized by the sudden inability of the kidneys to carry out their excretory, metabolic and endocrine functions. The aetiopathogenesis of ARF can be classified on the basis of the disease process into pre-renal, renal or post-renal.

Pre-renal ARF is characterized by a decrease in the glomerular filtration rate (GFR), caused by haemodynamic imbalances due to decreased renal blood flow or increased peripheral vascular resistance. When the mean arterial pressure is less than 60 mmHg renal perfusion is compromised and this, if not diagnosed and promptly treated, can cause ARF. In patients with haemodynamic imbalances (e.g., dehydration, decompensated hypovolaemic shock  an adequate mean arterial pressure must be restored as quickly as possible and maintained above 70 mmHg.

The use of non-steroidal anti-inflammatory drugs or ACE-inhibitors in patients with hyopotension can worsen renal perfusion and compromise the function of the kidneys. Non-steroidal anti-inflammatory drugs reduce the production of prostaglandins (including the vasoactive ones responsible for maintaining glomerular perfusion), thereby decreasing glomerular blood flow which may reduce the GFR. ACE-inhibitors block the production of angiotensin II and the inactivation of bradykinin, causing glomerular vasoconstriction and a possible reduction of GFR. Prolonged renal hypoperfusion can lead to ischaemic damage to cells which in turn can cause ARF. 

The most common causes of pre-renal azotaemia are:

  • dehydration;
  • uncompensated hypovolaemic shock;
  • a protein-rich diet;
  • post-prandial azotaemia;
  • fever;
  • burns;
  • gastrointestinal bleeding;
  • vasculitis;
  • pancreatitis;
  • heat shock;
  • liver failure;
  • gastric dilatation-volvulus.

Renal ARF, as a result of damage to one or more of the functional components of the kidney, can be caused by:

  • ischaemic nephrosis (e.g., acute tubular necrosis, progression of pre-renal ARF, thrombosis, stenosis, disseminated intravascular coagulation);
  • nephrotoxicity (e.g., NSAID, ACE-inhibitors, ethylene glycol; ingestion of lilies, grapes, or raisins; antibiotics; allopurinol; cimetidine; amphotericin B);
  • primary kidney diseases (e.g., infections, renal neoplasms, immune-mediated lesions);
  • systemic disorders with renal lesions (e.g., feline infectious peritonitis; Lyme disease, babesiosis, leishmaniasis, pancreatitis, neoplasms).

Post-renal ARF can be caused by obstructions or rupture of the upper or lower urinary tract:

 

SIGNS AND SYMPTOMS

 The signs and symptoms that can be found in patients with ARF include:

  • anorexia;
  • vomiting;
  • sensorial depression;
  • dehydration;
  • hypovolaemia;
  • oliguria/anuria;
  • hyperkalaemia (when the concentration of potassium in the blood increases, the cell membrane depolarises compromising the conduction of the nerve impulse because of excessive excitation, the hyperpolarisation can be manifested by: weakness, flaccid paralysis, hyporeflexia, respiratory failure, gastrointestinal hypomotility, ileus and, in the more severe forms, bradycardia and cardiac arrest);
  • metabolic acidosis during ARF this can be manifested by: tachypnoea, arrhythmias, hypotension, pulmonary congestion and insulin resistance;
  • anorexia associated with the ingestion of urea can produce: nausea, vomiting, halitosis, stomatitis, gastritis, gastrointestinal ulcers, diarrhoea and haematemesis;
  • cardiovascular complications (e.g., arrhythmias, heart failure, cardiomegaly);
  • pulmonary complications (e.g., pulmonary oedema, pleural effusion, pneumonia, pulmonary thromboembolism);
  • neuromuscular disorders (e.g., apathy, lethargy, tremors, seizures).

In order to make the diagnosis of ARF, a thorough history must be taken (e.g., lifestyle, drugs, diet) and then the animal must undergo a careful clinical examination and laboratory and instrumental investigations (e.g., measurement of blood pressure, ultrasonography). The history can pick up anuria, oliguria, sensorial depression, for one or more days, apathy, vomiting, diarrhoea, dysorexia, anorexia, urinary tenesmus (in the post-renal forms), assumption of toxic substances and tachypnoea (compensatory respiratory alkalosis). Possible findings of the general clinical examination are dehydration, sensorial depression, halitosis, hypothermia, congested mucosae, prolonged filling time (hypovolaemia, vasoconstriction), tachycardia, bradycardia, weak pulse, hyperdynamic pulse, bladder distension and weight loss (acute exacerbation of chronic renal failure).

 

DIAGNOSIS

Independently of the site of the lesion, the diagnosis of ARF involves laboratory examinations (full blood count, biochemical profile, blood-gas analyses, full urinalysis including urine cultures, and possibly serological studies), diagnostic imaging techniques (e.g., radiology, ultrasonography, particularly in forms suspected to be due to obstruction) and the measurement of blood pressure. An electrocardiographic evaluation should be performed in all hyperkalaemic patients: hyperkalaemia-associated arrhythmias are not correlated with a particular level of potassium, but depend on individual sensitivity to the change in the concentration of this electrolyte. In order to be able to give the correct treatment based on objective data, the laboratory examinations must be repeated daily (at least the biochemical profile and blood-gas analyses with electrolytes).

The most common laboratory alterations during ARF are increased blood levels of creatinine, urea, phosphate and potassium, while there may be a decrease in the specific gravity of the urine and low blood levels of calcium, bicarbonate, total proteins and albumin. The risk factors for or disorders which can predispose to or promote the progression of renal damage are: pre-existing kidney disease, advanced age, dehydration, hypovolaemia, hypotension, sepsis, systemic diseases, assumption of nephrotoxic vasoactive drugs and intoxication. In cases of ARF it is essential that the diagnosis is made early and that the treatment is started promptly, in particular because the condition can be reversible and the patient may regain an excellent quality of life. 

 

TREATMENT

In cases of pre-renal or renal ARF efforts must be made to restore diuresis quickly. The 24-hour urine production should be measured, preferably with a closed system, but if this is not possible by estimating urine output by weighing the sleeper pads before and after they are changed. Diuresis is promoted in oliguric patients by intravenous hydration or by restoring efficient circulation, if necessary. In this first stage it is, therefore, essential to measure the blood pressure and administer fluid therapy to bring the blood pressure to an acceptable level. If the patient does not produce urine after it has been rehydrated or its circulation restored, it should be given a first intravenous bolus of a balanced crystalloid solution (e.g., Ringer’s lactate solution or Normosol R) at a dose of 20 ml/kg in 15-20 minutes. Before giving bolus fluid therapy to normotensive or hypertensive patients, it is good practice to measure the central venous pressure (CVP) in order to avoid circulatory overload, which is responsible for pulmonary oedema and congestion. Bolus fluid therapy must be administered under close haemodynamic monitoring in patients whose CVP is 12-14 cmH2O or greater. If the patient does not urinate within about 30 minutes of administering the first fluid bolus of 20 ml, a second bolus of the same volume can be given together with an intravenous injection of 2-5 mg/kg furosemide. If both these trials fail to produce active diuresis, the patient can be given a bolus of mannitol 18% at the dose of 0.25-1 g/kg i.v.

When fluid therapy and the above mentioned drugs have not managed to promote diuresis in the dog, an attempt to induce urine production can be made by giving dopamine as a constant rate infusion at a dose of 1-3 mg/kg/min i.v. If urine is not produced within 3 hours after the administration of mannitol, furosemide and dopamine, the whole protocol can be repeated from the start. If the patient begins to urinate after the pharmacological treatment, mannitol 18% at a dose of 0.5 mg/kg can be given by intravenous bolus injections over 15-20 minutes every 3 hours, until normalisation or to the greatest achievable reduction in blood urea and creatinine; this treatment may require several days (2-5 days). When giving repeated boluses of mannitol, the CVP must be monitored continuously, whereas electrolytes, acid-base balance and total proteins must be monitored at least once a day. Metabolic acidosis tends to resolve after fluid therapy with balanced solutions. If the serum pH is less than 7.1 and the serum bicarbonate is below 14 mEq/L following fluid therapy, treatment with sodium bicarbonate (NaHCO3) can be considered. The dose is calculated using the following formula:

NaHCO3  =  Body weight (kg) x 0.3 x (desired NaHCO3 – patient’s NaHCO3) 

Usually a quarter of the calculated dose is administered very slowly, over 20-30 minutes, and then at least 30 minutes later blood gases are analysed again to determine the efficacy of the treatment. Animals which must be given NaHCO3 must be capable of adequate ventilation in order to avoid a paradoxical acidosis as a result of inability to eliminate the excess CO2 produced by the administration of bicarbonate.

Centrally acting antiemetics, such as metoclopramide 0.1-0.45 mg/kg t.i.d. i.v. or i.m., can be used for the treatment of gastrointestinal symptoms. Metoclopramide also controls the activity of the chemoceptor trigger zone, which is stimulated by uraemic toxins. If this thrice daily dosing is not effective, the drug can be administered as a constant rate infusion at a dose of 0.01-0.02 mg/kg/hour i.v. (in the dog and cat). Metoclopramide, being an antagonist of dopamine receptors, should not be administered to subjects receiving treatment with the vasoactive drug. Anti-H2 drugs can be used to protect the gastric mucosa from erosion caused by uraemic toxins (ranitidine 1-2 mg/kg s.i.d., famotidine 0.5-1 mg/kgs.i.d., cimetidine 2.5-5 mg/kg b.i.d.); these drugs can be used alone or in combination with gastroprotectants such as sucralfate 40 mg/kg b.i.d. or  t.i.d., per os or diosmectite 15-3 g b.i.d. or  t.i.d., per os.

Once the patient’s vital parameters, and possibly also diuresis, have been restored, all the diagnostic investigations necessary to identify the cause of the ARF should be carried out. Patients with ARF are usually given antibiotic cover, also in the absence of apparent infection, because even a venous access can become an entry route for numerous bacteria in a critically ill patient. A rigorously aseptic technique must be used during the establishment of the venous access, whether central or peripheral. The introduction of cannulas and catheters is the one of the most common causes of iatrogenic infections in intensive care units, particularly in cases in which toxins increase a patient’s susceptibility to infections. In the absence of specific indications, broad-spectrum antibiotics are used (e.g., cephalexin 20-30 mg/kg  b.i.d., per os,  ceftriaxone 20 mg s.i.d. i.v.).

In the case of suspected or diagnosed leptospirosis, the affected animal should initially be given high doses of penicillin (penicillin G 25,000-40,000 IU/kg/12 hours i.m. or i.v. or ceftriaxone or cefotaxime). After the acute phase, the treatment can be changed to doxycycline at a dose of 2.5 mg/kg b.i.d. per os for 3 weeks, since this antibiotic is able to control the leptospira in the blood and, if present, in the urine. Most cases of pyelonephritis are caused by E. coli and require treatment with antibiotics active against Gram-negative bacteria, selected after cultures and an antibiogram; while waiting for the results of the cultures and antibiogram, an affected animal can be administered ceftriaxone at a dose of 20 mg/kgs.i.d. orb.i.d. i.v. given that this is not a nephrotoxic drug;  nephrotoxic antibiotics  (e.g., aminoglycosides and tetracycline) should not be used in this situation.

Anorexia is commonly present in all forms of ARF and to avoid protein catabolism developing as the result of a worsening azotaemia, effective nutritional support should be established as early as possible. The method of choice for anorexic patients with ARF is enteral nutrition through a naso-oesophageal or nasogastric tube, while a oesophagostomy tube can be placed in chronic cases, in particular in cats. In some cases, when it is not possible to supply all the necessary calories with forced enteral nutrition, it may be useful to add parenteral nutrition. The diets must be energy-rich, with a low content of proteins, which must be of good quality. Since uraemia can cause thrombocytopenia, it increases the risk of bleeding, so animals that must undergo interventions or surgical operations (e.g., renal biopsies or insertion of a tube for parenteral nutrition) must also be monitored by coagulation tests. In most cases, coagulation parameters and platelet counts are not sensitive to the increased urea and so the results of the tests are within the norm; in doubtful cases the blood mucosal bleeding time can be evaluated). If the treatment fails to induce effective diuresis and life-threatening imbalances persist (e.g., hyperkalaemia, overhydration), or when the hyperazotaemia does not respond to medical treatment, dialysis must be considered.

 

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