Acute Renal Failure
Introduction
Acute renal failure is rapidly progressive but may be reversible. It can result from pre-renal, intra-renal or post-renal factors.
- Prerenal factors include ischaemia and reduced renal perfusion
- Renal factors include acute interstitial nephritis and
- Postrenal factors include lower urinary tract obstruction.
Clinical signs include oliguria or anuria, vomiting and anorexia; blood sample analysis shows azotaemia.
On presentation is it important to establish two things:
(1) Whether the renal failure is acute or chronic as they present very similarly but have very different treatment protocols and prognoses.
(2) Whether the renal failure is pre-renal, renal or post-renal
Acute Renal Failure is a syndrome caused by the acute failure of haemodynamic, filtration and excetory functions in the kidney. This results in the accumulation of uraemic toxins and the dysregulation of acid-base, fluid and electrolyte balances.
Aetiology
This section only covers the intrinsic causes or ARF, as pre- and post-renal failure are very different disease processes.
Toxic injury s the most common cause. Toxins such as aminoglycosides, ethylene glycol, NSAIDs, easter lillies and ACE-inhibitors can all cause renal failure. Some toxic agents act directly on tubular cells, some act on the haemodynamics of the kidney, whilst others cause damage by precipitating within the tubules.
Ischaemic injury is also common, especially following hospitalisation. It is therefore essential to monitor the fluid therapy requirements of hospital patients, especially peri- and post-operatively to prevent pre-renal azotaemia and subsequent ischaemia.
Tubulointerstital disease resulting in inflammation and oedema can also cause acute renal failure. This is normally precipitated by infections (pyelonephritis and leptospirosis), autoimmune reactions and allergy.
Pathogenesis
- A reduction in GFR is caused by the decreased in surface area or conductivity of glomerular capillaries (resulting in a drop in the ultra-filtration coefficient)
- Epithelial cells and debris obstruct the tubules. Toxin precipitates may contribute to this
- Tubular fluid leaks out of the tubules and across the epithelium, back into the interstitium - causing a drop in GFR
- Ischaemic injury to the peripheral medulla occurs due to intra-renal vasoconstriction
Clinical Signs
The most significant information can be gleaned from the history. It is important to ask the owners about toxin ingestion and urine production.
Clinical exams normally reveals fairly non-specific signs such as:
- Dehydration
- Lethargy
- Malaise
- Vomiting
There may also be evidence of swollen or painful kidneys abdominal palpation, an increased or decreased heart rate, hypothermia and oral ulceration or signs of a concurrent disease.
Diagnosis
The most suggestive sign of severe acute renal failure is oliguria or anuria. It does not occur in all cases so should not be completely relied on for diagnosis.
As mentioned it is important to differentiate ARF from decomensated CRF, as ARF is potentially reversible with aggressive therapy. The only diagnostic test that can achieve this is biopsy, but due to the high level of risk involved in an already sick animal this is normally not performed. Instead the following factors can be used by the clinician to guide diagnosis:
(1) History
With ARF there may be a history of ingestion of or access to toxins/nephrotoxic drugs, and oliguria. Cats with CRF normally have a history of chronic weight loss, anorexia and PU/PD.
(2) Clinical Exam
ARF cats tend to have a good body condition score, and healthy skin and coat. CRF cases have a poor body condition score and a dull/scruffy coat.
(3) Renal Parameters - palpation, ultrasound, radiography
The kidneys in ARF cats are normal sized or enlarged, and normally painful. In CRF, the kidneys are shrunken, firm and non-painful
(4) Other
The presence of secondary renal hyperparathyroidism and non regenerative anaemia is suggestive of CRF
Secondly the type of azotaemia must be identified:
(1) Pre-renal
Caused by severe dehydration, shock or any other pathology that results in poor renal perfusion. In these cases USG is >1.035 in the cat and >1.030 in the dog before fluid therapy. There should be no evidence of inflammation and urine sodium concentrations are low. Diagnosis is confirmed by a rapid and dramatic response to fluid therapy.
(2) Renal
This is caused by a direct insult to the kidney, with intrinsic damage. In these cases azotaemia is present, and urine specific gravity is between 1.007 and 1.025. There may be evident of inflammation in the urine sediment and a high sodium content. There is only a minimal response to fluid therapy.
(3) Post-renal
Post-renal failure is caused by an obstruction or rupture with in the urinary system. This is normally identifiable following a thorough history and physical exam.
Treatment
The aim of treatment is to support the patient whilst the tubules repair.
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