This section of chapter 61 pretty much reiterates the information in the VCNA article. I think it puts it in more succinct terms which is why I like this article a little bit better than the previous one.

The presence of acanthocytes on a blood film is not uncommon with liver disease. The liver is important in lipid metabolism and therefore its dysfunction can result in alterations in red cell membrane lipids causing a change in the red cell shape.

Again don’t worry about the isozymes. Liver and bone are the important ones in the dog and cat. Corticosteroid induced is also somewhat important and the dog and that is pointed out later in this section.

Don’t worry about figure one. It is a little more of an extensive work up for a mildly increased ALT than most practitioners will do.

Please don’t memorize this list of drugs. It will be always available to you when you need it.

This is a very important concept. Don’t be misled into trying to determine reversibility based on the magnitude of increase in a liver enzyme. Yes, irreversible change or less extensive injury can cause a more mild increase but it’s not predictable.

Do not worry about these isozymes.

This section on reference intervals and biologic variation is interesting and helpful. But don’t concentrate on the information here. The important thing to remember is that for many of the test such as the enzymes have significant biologic variation. Reference intervals may be wide and therefore we don’t just look at if it is over the reference interval, we actually look at how much increase is there to see if it’s significant.

This is where addision's comes in to the picture. These patients are usually volume depleted due to renal water and sodium loss. And, sodium is usually lost in excess of water. Addision's patients are usually hypoosmolar and hyponatremic. Addison's and diuretics are the most common cause of hyposomolar hyponatremia.

In reality, it is not the metabolites of ethylene glycol that contribute to the osmol gap, it is the unmetabolized ethylene glycol. In fact, the serum concentration of etheylene glycol hyas a direct linear relationship with the osmol gap.

The mechanisms behind the types of hyponatremia are complex and can be difficult to understand. The take home for this section is to understand hyponatremia that results from either translocation of water from the cells into the ECF (hyperosmolar hyponatremia, most commonly seen with marked hyperglycemia of diabetes mellitus) and the hypoosmolar hyponatremia seen with Addison's where sodium and water are both lost with the sodium loss exceeding the water loss.

As a rule of thumb, in chronic conditions, rapidly trying to correct an abnormality is an invitation to doom. Examples, rapidly decreased a markedly increased serum glucose or sodium concentration or rapidly correct a severe hyponatremia. Or as you will learn in GI, trying to correct a marked calorie deficient in a starving patient (refeeding syndrome).

Very important point! Slow a steady is best for correcting a marked hypernatremia.

Most laboratories can measure urine sodium. That said, it is not commonly done. Differentiating the causes of hyponatremia can be determined based on clinical findings and looking at the serum osmolality.

This is an important explanation of the term "free water". When first learning about these concepts, you might want to use the full term "solute-free" water.

remember the idiogenic osmols that the brain is really good at creating.

These should be the primary differentials, a defect in thirst sensation does happen with CNS disease but is much less common than lack of access to water or the physical inability to drink.

One thing to remember, Urine Specific Gravity is an indirect indicator of urine osmolality. So hyposthenuric urine in the face of hypertonicity and polyuria should prompt investigation for primary (central) or nephrogenic diabetes insipidus.

this is a very important point. These dogs must have access to water. If not, they will become dehydrated because they usually have medullary washout due to renal sodium loss over time.

Don't let this diagram confuse you. The entire descending limb of the loop of Henle is impermeable to Na and Cl while being permeable to water.

Please disregard this statement. Dr. Klimecki and I think that there may be some confusion about how the loop diruetics work. Its a bit too in the weeds for our discussion.

Like all things there is a spectrum. As with ability to concentrate urine, in early renal disease the kidney will retain the ability to dilute urine until sufficient loss of nephrons results in loss of that function. However, we don't have a "range of inadequate dilution" comparative to "range of inadequate concentration" so, in general we say that the kidneys still have sufficient renal mass if they can dilute to 1.006 or less.

You will likely not see this phenomenon because of the newer technology used in most reference laboratories. That said, if you have a patient with marked hyperproteinemia or hyperlipemia and hyponatremia, it is important to reach out to your reference laboratory to ask if their method of electrolyte measurement is affected by these two components.

A terminology comment: Na+ is not an enzyme. Sodium is an electrolyte. BUN and Creatinine are not "kidney enzymes" they are waste products. You may see these terms used every now and then but, it is best not to use enzyme for anything but an enzyme. ALT, AST, GGT, ALP, Amylase, Lipase are enzymes. The rest of the things we measure in a chemistry are not enzymes.

This is an excellent table to help understand the clinical disease/syndromes that can affect urine concentration. It organizes the clinical situation based on what mechanism for dilution or concentration is being disrupted.

we didn't discuss this action of ADH as much as the action of ADH on the collecting duct.

Remember that angiotensin II stimulate release of ADH by the hypothalamus.

The neurons are very good at creating idiogenic osmoles to protect from dehydration. The problem is, the idiogenic osmoles don't go away very quickly. How might is impact the rate at which you would want to reduce a patients glucose concentration when you have hyperosmolar hyperglycemia? This same phenomenon can occur with severe chronic dehydration.

This should all sound pretty familiar!

This is a very important concept to understand. In the example in Figure 6, glucose is an impermeant solute in the diabetic dog (remember that insulin is needed for glucose to enter most cells.) Glucose does not move freely between intracellular and extracellular fluid compartments unless insulin is present. What two tissues do not require insulin for glucose uptake? Brain and liver.