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Fluid therapy for ketoacidosis and renal failure (Proceedings)

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Apr 01, 2009

When presented with animals with evidence of renal dysfunction (as evidenced by elevated serum creatinine concentration), there are a few considerations. One is whether the abnormal lab test represents functional impairment only; meaning that at this moment the animal has an abnormally high serum creatinine concentration in spite of an adequate mass of functional renal tissue. This is typically because the kidneys are not receiving enough blood flow to maintain normal plasma concentrations of compounds excreted by the kidney (a process that produces the phenomenon of 'pre-renal azotemia'), or has lower urinary obstruction, or has uroabdomen. Another consideration is whether or not the kidneys are sustaining acute, active damage by some disease process such as toxicity, infection, thrombosis, outflow obstruction, or others that will require specific therapy intended to remove the cause. Another is whether or not there is impaired renal blood flow subsequent to circulatory problems (or lower urinary obstruction) that is sufficiently severe to cause collateral damage to the kidney by ischemia. Yet another is whether systemic illness that may be causing renal hypoperfusion is damaging the kidney by other mechanisms – for example, severe sepsis, wherein the kidneys do suffer from underperfusion but the organ injury and tubular epithelial apoptosis is being driven by many other factors (mostly associated with inflammation) as well. And finally, what was the baseline level of health of the kidney – if the patient with acute renal injury began the illness with a functional renal mass that was 20% of what it was 5 years earlier, that animal has less potential for recovery of adequate function compared to what it would have had at the younger age. This is especially pertinent in animals that present sick (uremic) with chronic renal disease (CRD), as they often have had chronic, insidious, compensated loss and all it took to make them symptomatic was a tiny acute further reduction in function.

Some specific points

1. Fluid therapy is essential to prevent or limit ischemic injury in vulnerable kidneys. In the face of hypovolemia or other causes of poor circulation, healthy young kidneys have enormous biological reserve to maintain function, and if pushed to extremis with ischemia can sustain a large amount of tubular epithelial loss and still do their job. But, if the kidneys have limited biological reserve – for example overwhelming acute nephron loss or senescent kidneys in geriatrics or chronically diseased kidneys - they are more likely to fail both *functionally* (as defined by reduced glomerular filtration rate [GFR]) and are perhaps also more likely to develop temporary or permanent *nephron loss* (due to epithelial apoptosis or necrosis, depending on the situation) when renal blood flow is compromised.

2. The only therapeutic effect of fluid therapy is to restore and maintain renal perfusion. Fluids do nothing else. When indicated to correct hypovolemia, fluid therapy can be life saving as no other treatment is as effective at preventing or limiting acute ischemic injury. However, unless hypovolemia is present fluids will not prevent kidney injury due to most nephrotoxins, and, once renal blood flow is restored, extra fluid will not provide any 'extra' renal benefit. So prompt recognition of impaired renal blood flow (assumed to be present in an animal with clinical signs of hypovolemia) and RAPID restoration of extracellular fluid and renal blood flow are huge, but once extracellular fluid volume and plasma volume are restored fluid therapy goals should immediately shift toward simply maintaining homeostasis.

3. Drug therapy for acute renal failure is a mixed bag. Although drug therapy of any specific cause of acute renal injury is essential (e.g., antibiotics for pyelonephritis or leptospirosis, 4MP to prevent conversion of ethylene glycol to oxalate), there are no great drug therapies to limit renal injury from poor perfusion, sepsis, or other shock syndromes. The only serious exception to this is drug therapy for circulatory support: in the world of critical care, restoring renal blood flow often requires drug therapy on top of fluid therapy to restore renal perfusion (for example, dobutamine and norepinephrine to animals with septic shock). Diuretics do not prevent acute renal injury and do nothing to help renal function. For all the interest in drugs like calcium channel blockers, dopamine receptor agonists and the like there is currently no good evidence to suggest that these have even a tiny fraction of the benefit of fluids and circulation support. Dopamine does not preserve renal tissue (and is a very weak diuretic).