SDH is a cytoplasmic enzyme, and it acts as a catalyst in the conversion of sorbitol to fructose.

       SDH activity is low, and the majority comes from the hepatocyte.

       SDH is a “leakage” enzyme released when hepatocytes are damaged.

       Thus, SDH is considered a specific indicator of liver damage, especially acute damage.

       SDH has a short half‐life (hours), so serum concentrations fall quickly.It is generally not increased in chronic liver disease.

       It is a labile enzyme, and its activity decreases with time.However, it is stable in serum for up to five hours when refrigerated.

       Reference range: 1–8 U/l.

       Increased TBIL in serum is an indicator of hepatic dysfunction, hemolysis, or reduced feed intake.

       TBIL may be subdivided into unconjugated (indirect) bilirubin, and conjugated (direct) bilirubin.

       The reference range for the horse is 21–57 μmol/l for TBIL; 2–10 μmol/l for conjugated bilirubin, and 18–52 μmol/l for unconjugated bilirubin.

       Hepatic dysfunction causes both indirect and direct concentrations to rise.If direct is greater than 8% of total, liver disease should be suspected as a contributor to the increase.

       Biliary obstruction (e.g. cholelithiasis) increases the direct to indirect ratio.

       Hemolysis raises the serum indirect concentration.

       Reduced feed intake raises the serum indirect concentration as a result of slowed clearance of bilirubin from the blood rather than from its overproduction. However, the cause is uncertain.Ligandin, a protein responsible for bilirubin uptake into the liver may be decreased in the fasting horse, as has been demonstrated in rats.Free fatty acids may play a role in fasting hyperbilirubinemia, and horses develop significant hyperlipidemia during fasting. This may result in competition for carrier proteins.Increases in unconjugated bilirubin occur after 12 hours of fasting.

       Neonates have higher bilirubin values due to immaturity of liver processing.This can lead to kernicterus, resulting from unconjugated bilirubin causing neurologic damage. However, this condition is extremely rare in foals, and may be more likely to occur in a foal with neonatal isoerythrolysis.

       Bile acids are synthesized and secreted by the liver.

       Bile acids are removed from the portal blood by hepatocytes, and SBA concentrations increase as hepatic function decreases.

       Increase in SBA concentration is an indicator of hepatic dysfunction.

       Reference range: 0–20 μmol/l.

       Bile acids are not affected by fasting.

       Only a single blood sample is required instead of pre‐ and post‐feeding samples, as bile is released continuously because the horse lacks a gallbladder.

       Increased BUN and or Cr indicates that the horse suffers from either pre‐renal, renal, or post‐renal azotemia.

       Reference range for BUN is 4.2–8.9 mmol/l and for Cr is 80–130 μmol/l.

       In contrast to urea nitrogen, Cr is not reabsorbed within the tubules, so serum Cr concentrations provide a more accurate measurement of glomerular filtration rate (GFR) than does BUN.

       Neonates have higher Cr values, and the value declines over the first week of life.

       Occurs when the increases in BUN and Cr results from a decrease in renal blood flow and the associated decrease in GFR.

        Significant (>75%) decreases in GFR are required before the BUN is increased, especially early in disease.Most commonly results from dehydration and circulatory shock.

       When renal function is adequate (pre‐renal), azotemia is accompanied by a urine specific gravity (USG) > 1.025.This indicates that the kidney has the ability to concentrate the urine.

       Uroperitoneum secondary to bladder rupture in foals also causes pre‐renal azotemia.

       Occurs when the GFR is low due to acute or chronic kidney injury.

       BUN may be low because less of the filtered urea is re‐absorbed in the proximal tubule.

       Serum Cr increases as filtration decreases.

       Diagnosed by concurrently measuring the USG.The presence of azotemia in a patient that cannot concentrate their urine (USG < 1.020) indicates kidney injury.

       Is associated with mechanical (e.g. uroliths) or functional (e.g. neurogenic bladder dysfunction) obstruction of the urinary tract.

       It is uncommon in horses.

       Blood consists of plasma and solid components.

       Plasma comprises about 55% of the blood volume.

       Plasma contains about 90% water, and the remaining 10% consists of ions, proteins, dissolved gases (primarily nitrogen, oxygen, and carbon dioxide), nutrients, and wastes.

       Total protein reference range for adult horse: 6.5–7.5 g/dl.Plasma protein value is approximately 0.3–0.5 g/dl greater than serum protein.

       The proteins in plasma include the globulins, albumin, fibrinogen, and coagulation factors.

       A hand‐held refractometer can be used to measure total solids, which are an estimate of total protein; however, the readings can be affected by other substances in the plasma.This is because refractometer scales are calibrated against normal serum, and values of many non‐protein solutes (e.g. electrolytes) vary in the population.Thus, it may be prudent to evaluate albumin and globulin concentrations separately in some disease states.

       Albumin is the main protein present in plasma.

       The reference range is 2.7–3.7 g/dl.

       Its main function is the regulation of the colloidal osmotic pressure