Abnormal results can be determined by the following:

Hyaline casts are increased in number with renal disease and transiently with exercise, fever, heart failure, or treatment with diuretics.

Granular casts are seen in pyelonephritis, tubular interstitial disease, renal transplant rejection, and chroniclead poisoning. Coarsely granular casts occur with hematuria in cases of renal papillary necrosis.

Fatty casts result when fatty (lipid) material is incorporated into the cast matrix from lipid-laden renal tubular cells. Usually they are associated with visible fat droplets containing triglycerides or cholesterol esters. Fatty casts are seen in the condition of heavy proteinuria and high serum lipids, that is, nephrotic syndrome.

Red cell casts are see in many diseases affecting the glomerulus, (for example, IgA nephropathy, lupus nephritis, Goodpasture's syndrome, sickle cell anemia, and malignant hypertension), or as a result of bleeding into the kidney (renal infarction). When stasis has occurred in the nephron, a red cell cast may degenerate and appear in the urine as a reddish-brown, coarsely granular cast, called a blood or hemoglobin cast.

White blood cell casts are more common in interstitial cell kidney disease, since WBCs usually enter the renal tubules from the interstitium (that is, between tubular epithelial cells). Diseases associated with WBC casts include interstitial inflammation, pyelonephritis, and lupus nephritis.

Renal tubular epithelial cell casts reflect damage to the renal tubules. They are seen in renal tubular necrosis (for example, caused by nephrotoxic drugs, heavy metal poisoning, or ethylene glycol), viral disease (for example, CMV nephritis), and with acutetransplant rejection.

Waxy casts are associated with tubular inflammation and degeneration. They probably represent an evolutionary product of some other type of cast that has changed form over time. These casts are associated with chronic renal failure and renal transplant rejection.

Cast formation is increased when larger-than-normal amounts of plasma proteins enter the tubules. Usually the excess protein is urine albumin, but globulins, such as the Bence-Jones protein (light chains immunoglobulins), and hemoglobin or myoglobin can increase cast formation. See Bence-Jones protein (quantitative)

Additional conditions under which the test may be performed:

• Acute nephritic syndrome
• Chronic glomerulonephritis
• Complicated UTI (pyelonephritis)
• Necrotizing vasculitis
• Post-streptococcal GN
• Primary amyloid
• Rapidly progressive (crescentic) glomerulonephritis
• Rhabdomyolysis
• Secondary systemic amyloid
• Systemic lupus erythematosus

Casts are reported as part of the normal microscopic examination of urinary sediment (that is, the material that gets centrifuged to the bottom of the tube). Casts are formed as translucent, colorless gels from protein in the tubules of nephrons.

In normal urine, there is a very small amount of protein, less than 150 mg/day. Urine albumin and small globulins derived from plasma comprise two-thirds of the protein in urine. The other one-third is comprised of Tamm-Horsfall protein, a glycoprotein that is secreted by renal tubular cells. It is thought that Tamm-Horsfall protein forms the matrix of all casts (although other proteins can subsequently contribute).

Under certain conditions, this protein forms a meshwork of fibrils that can trap cells, cell fragments, or granular material. Cast formation increases with lower pH and where there is stasis (decreased flow of urinary filtrate) or obstruction of the nephron by cells or cell debris.

Casts begin to disintegrate in dilute and alkaline urine, or in the presence of bacteria, which probably contribute to a decreasing acidity. The size and shape of casts depends on the site of formation. Large casts are seen in dilated tubules or with stasis in collecting ducts. Thin casts occur in tubules compressed by swollen interstitial tissue or because of disintegration.

Note: mg/day = milligrams per day