Three things I learned: acute renal failure

My late cat Lily, with some FAKE lilies, to illustrate the point that lilies (the real ones) are a common cause of acute renal failure in cats. All parts of the plant are toxic, so if you want to buy a bunch of flowers for a cat owner, ask your florist for an arrangement that does not contain lilies. OR grab some fakies. They last forever.

Dr Graham Swinney gave a fantastic webinar on behalf of the ASAVA last night on acute renal failure (ARF) in dogs and cats. (If you're not a member of the ASAVA you are missing out, the webinar program this year is fantastic - you do need to be a member of the Australian Veterinary Association to join).

I like the way he broke it down. Kidneys are major players (I feel like I should be writing playas for the benefit of any younger readers) in body function, eliminating waste products, excreting drugs, regulating water and electrolyte balance and producing hormones like EPO. So kidney failure is kind of a big deal.

The good news is that we have two of them (kidneys that is). Renal disease can be structural or functional, but doesn’t tend to result in azotaemia until 75% of nephron function is lost (loss of urine concentration tends to occur earlier, i.e. when 2/3 of renal function is lost). (That's NOT a good reason to sell one on the internet. Incidentally, selling BOTH kidneys on the internet is a certified Dumb Way to Die).

Essentially there are three potential outcomes of ARF: 1) complete recovery; 2) chronic renal disease; 3) death. Best outcomes are achieved when ARF is detected early.

There are four stages of ARF.

1. Initiation – can last for hours to a day, the first injury to the kidney. We need to recognise this phase to maximise chances of recovery.  Trouble is that affected animals often do not illustrate clinical signs during this period, meaning that we can miss an option to intervene when our treatment is likely to be most effective.
2. Extension – hypoxia and inflammatory disease cause damage which may or may not be reversible. This phase can last days. (The proximal convoluted tubule and loop of Henle are particularly sensitive to hypoxic injury as these are very metabolically active).
3. Maintenance – renal changes are irreversible; at this stage removal of the underlying cause doesn’t necessarily improve the outcome. This stage can last days to weeks.
4. Recovery – repair and regeneration, may take months and may not be complete.

In many ways the distinction between ARF and chronic renal failure is one of time. ARF is caused by a sudden reduction in glomerular filtration rate (GFR) resulting in azotaemia.

Chronic kidney disease = reduction in GFR & azotaemia due to a renal disorder that has been present for at least 2 months. ARF is rapidly progressive although there is a chance of complete recovery if caught early. CRF is usually slowly progressive but its irreversible.

The two big categories of causes of ARF are

1. Ischaemic injury
2. Toxicity

Ischaemic injury can occur with hypotension, cardiac failure, thromboembolic disease etc.

Thousands of toxins can damage the kidneys. These include drugs that are commonly used therapeutically such as some antimicrobials, antifungals, chemotherapeutic agents, diuretics, ACE inhibitors, as well as diagnostic agents such as contrast.

Endogenous substances such as haemoglobin, myoglobin and even bilirubin can also be hard on the kidneys. Infectious agents (especially agents causing leptospirosis and bacterial pyelonephritis) and immune complexes can cause acute renal injury.

Other potential toxins include ethylene glycol and herbicides such as paraquat.

Clinical signs of acute renal failure vary from classic lethargy, inappetance, vomiting, polyuria and polydipsia to hyphema and/or blindness (secondary to hypertension), neurological signs (uraemic encephalopathy) and even respiratory signs (vasculitis leading to pulmonary oedema).

A detailed history is helpful in determining the potential underlying cause, e.g. access to a toxin such as lilies, grapes, ethylene glycol, medication prescribed for the owner or another animal.

It is important to assess the patient’s hydration status and body condition, the presence of a bladder (is there an obstruction?) and renal palpation, fundic examination and blood pressure measurement, rectal examination to rule out anal sac masses (which may be causing ARF due to profound hypercalcaemia) and in some cases palpate pelvic urethral obstruction, as this can help determine whether the patient has ARF or CRF and even the underlying cause.

The work up will help rule out treatable causes. Thus a CBC/MBA/UA, urine culture and sensitivity (even in the light of a bland sediment), cytology and even biopsy can help rule in/out pre and post renal causes and determine the presence of treatable disease (e.g. lymphoma, pyelonephritis). An ACTH stim can help rule out Addison's which can clinically look like ARF.

According to Dr Swinney, a patient with mild to moderate azotaemia and severe clinical signs is more likely to have ARF, while a patient with severe azotaemia and mild clinical signs is more likely to have CRF (the latter have more time to adapt).

And ARF doesn’t have a monopoly on renomegaly – you can also get enlarged kidneys from polycystic kidney disease, perinephric pseudocysts, haematomas, hydronephrosis, FIP, and compensatory hypertrophy. So don't be thinking that bilaterally big kidneys = acute renal failure.

A rather large polycystic human kidney. Note loads of cysts replacing most of the parenchyma. Not much room for functional nephrons there.

One of the most important points Dr Swinney made was the need to calculate the fluid deficit and replace it – often over 2-3 hours, as while that hypotension remains renal damage continues. As he said, these are not patients you simple put on 2x maintenance and leave for a day. So if you have a 50kg dog which is 10% dehydrated and you give 3 litres of fluids, the renal injury will continue.

Once the patient is better hydrated Dr Swinney considers using mannitol or frusemide to promote urine production where required. Other supportive care includes gastroprotectants such as H2 blockers or proton pump inhibitors, anti-emetics, oxygen support in hypoxaemic animals and nutritional support.