| Chemistry: | ||
| Test | Result | Reference |
| Glucose | NEG | <> |
| Protein | NEG | <> |
| Bilirubin | NEG | <> |
| Urobilinogen | <2.0 | <> |
| pH | 6.0 | <> |
| Blood | NEG | <> |
| Ketone | NEG | <> |
| Nitrite | NEG | <> |
| Leukocytes | NEG | <> |
| Clarity | CLEAR | <> |
| Specific Gravity | 1.02 | <> |
| Color | Yellow | <> |
| Microscopy: | ||
| Test | Result | Reference |
| Red Blood Cell | 2 /HPF | <> |
| White Blood Cell | 1 /HPF | <> |
| Mucous | TRACE |
First, look at GLUCOSE to determine if the pt is DIABETIC. Is glucose level 3+ or 4+?
If pt is not diabetic, and GLUCOSE is 1+, reduced sugar. If GLUCOSE is 3+, check glucose serum.
Also look at NITRITE or LEUKOCYTE to see if there's an infection(+ may be infection)
Look at KETONE for dehydration. 3+ or 4+ KETONE in starvation
If PROTEIN is around 3 g, check for kidney problem
pH should be a little acidic, but if it is alkaline, then check for kidney stone. Urine becomes more acidic as it is waiting for analysis
If BILIRUBIN results in (+), then the pt may have liver problem or taking medication that results in higher BILIRUBIN level
UROBILINOGEN less than 2.0 is normal. If it is > 4, the liver is bypassing hepatic circulation.
Urine being CLOUDY may be due to pH going down(normal) while sitting out waiting for analysis, or it amy also be due to squamous epithelial cells or sediment
SPECIFIC GRAVITY is concentration of urine
BLOOD (+) may be hematuria
PROTEIN (+) may be proteinuria
when they occur separately it's not a problem
But if they occur together, check for glomerular nephritis
Glomerular Disease
HEMATURIA - +3
PROTEINURIA - >= 3.5g
Type II hypersensitivity reaction Ab+ Ag Reaction
HEMATURIA - KIDNEY DISEASE
HEMOPTYSIS(GOOD PASTURE) - LUNG DISEASE
Wegenar Glomerulonephritis
HEMATURIA + HEMOPTYSIS + SINOPULMONARY => kidney, vascular, lung
Nephrotic Syndrome (Adult = membranous, kid minimal change disease, lipoid nephrosis)
HEMATURIA (24 hrs Hme profu >= 3.5 g)
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Bilirubin is a yellow breakdown product of normal heme catabolism. Its levels are elevated in certain diseases and it is responsible for the yellow color of bruises.
Bilirubin is formed when red blood cells die and their hemoglobin is broken down within the macrophages to heme and globins. The heme is further degraded to Fe2+, carbon monoxide and bilirubin via the intermediate compound biliverdin. Since bilirubin is poorly soluble in water, it is carried to the liver and bound to albumin. Bilirubin is made water-soluble in the liver by conjugation with glucuronic acid. Conjugated bilirubin, or bilirubinglucuronide, moves into the bile canaliculi of the liver and then to the gall bladder. When stimulated by eating, bile (including the conjugated bilirubin) is excreted into the small intestine. In the later portions of the small intestine (ileum) and the colon, about half of the bilirubinglucuronide is converted into urobilinogen. Urobilinogen is either reabsorbed or converted by the presence of oxygen to stercobilin. The stercobilin and remaining bilirubinglucuronide are excreted in the feces. These two metabolites of bilirubin are what give feces their characteristic brown color. Small amounts of urobilinogen remaining in the blood are filtered by the kidneys, ending up in the urine as urobilin. This bilirubin metabolite gives urine its characteristic yellow color.
In diseases where too much hemoglobin is broken down or the removal of bilirubin does not function properly, the accumulating bilirubin in the body causes jaundice.
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Urobilinogen is a colourless product of bilirubin reduction. It is formed in the intestines by bacterial action. Part of it is resorbed and returned to the liver, while the rest is excreted in faeces. Trace amounts can be detected in urine.
The urobilinogen test detects impaired liver function by measuring urine levels of urobilinogen, the colorless, water-soluble product that results from the reduction of bilirubin by intestinal bacteria. Absent or altered urobilinogen levels can indicate hepatic damage or dysfunction. Increased urine urobilinogen levels may indicate hemolysis of red blood cells.
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Hematuria
In medicine, hematuria (or "haematuria") is the presence of blood in the urine. It is a sign of a large number of diseases of the kidneys and the urinary tract, ranging from trivial to lethal.
Occasionally "hemoglobinuria" is used synonymously, although more precisely it refers only to hemoglobin in the urine.
---------------------------------------------------------------------------Proteinuria (from protein and urine) means the presence of an excess of serum proteins in the urine. The protein in the urine often causes the urine to become foamy although foamy urine may also be caused by bilirubin in the urine (bilirubinuria)[1],retrograde ejaculation[2], pneumaturia (air bubbles in the urine) due to a fistula[3], or drugs such as pyridium[4]. Proteinuria is often diagnosed by a simple dipstick test although it is possible for the test to give a false negative even with nephrotic range proteinuria if the urine is dilute[5]. False negatives may also occur if the protein in the urine is composed mainly globulins or Bence-Jones Proteins because the reagent on the test strips,Bromphenol blue, is highly specific for albumin [6][7]. Anyone with foamy urine should be more thoroughly evaluated with more sensitive tests such as a 24-hour urine collection test or Protein electrophoresis even if the dipstick is negative for protein to completely rule out proteinuria[8][9].
Proteinuria may be a sign of renal (kidney) damage. Since serum proteins are readily reabsorbed from urine, the presence of excess protein indicates either an insufficiency of absorption or impaired filtration. Diabetics usually suffer from damaged nephrons and develop proteinuria.
With severe proteinuria, general hypoproteinemia can develop which results in diminished oncotic pressure. Symptoms of diminished oncotic pressure may include ascites, edema, and hydrothorax.
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A glomerulus is a capillary tuft surrounded by Bowman's capsule in nephrons of the vertebrate kidney. It receives its blood supply from an afferent arteriole of the renal circulation, and empties into an efferent arteriole. The resistance of the arterioles results in high pressure in the glomerulus aiding the process of ultrafiltration where fluids and soluble materials in the blood are forced out of the capillaries and into Bowman's capsule. The rate at which blood is filtered through the glomeruli is the glomerular filtration rate (GFR), measurements of which are often used to determine renal function.
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| Glomerulus. | |
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Nephritis is inflammation of the kidney. The word comes from the Greek nephro- meaning "of the kidney" and -itis meaning "inflammation". The two most common causes of nephritis are infection or an auto-immune process.
Symptoms
Nephritis has the effect of damaging and closing up the microscopic filters in the kidney. This means that in addition to various toxic waste products, the inflamed kidney filters out important proteins (larger molecules) from the blood. Therefore the characteristic symptom of nephritis is proteinuria — meaning the excessive removal of protein from the blood and its excretion in urine.
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Nephrosis is an old term for non-inflammatory disease of the kidneys, now called nephropathy.
Nephropathy refers to damage to or disease of the kidney. An older term for this is nephrosis.
One cause of nephropathy is the long term usage of analgesics. The pain medicines which can cause kidney problems include aspirin, acetaminophen, and nonsteroidal anti-inflammatory drugs, or NSAIDs. This form of nephropathy is "chronic analgesic nephritis," a chronic inflammatory change characterized by loss and atrophy of tubules and interstitial fibrosis and inflammation (BRS Pathology, 2nd edition).
Specifically, long term use of the analgesic phenacetin has been linked to renal papillary necrosis (necrotizing papillitis).
A second possible cause of nephropathy is due to decreased function of Xanthine Oxidase in the Purine degredation pathway. Xanthine Oxidase will degrade hypoxanthine to xanthine and then to Uric Acid. Because Xanthine is not very soluable in water an increase in Xanthine will form crystals (which can lead to kidney stones) and result in damage of the kidney. Drugs like Allopurinol that are used to inhibit Zanthine Oxidase can therefore cause possible nephropathy.
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Nephrotic syndrome is a disorder where the kidneys have been damaged, causing them to leak protein from the blood into the urine. It is a fairly benign disease when it occurs in childhood, but may lead on to chronic renal failure, especially in adults, or be a sign of an underlying serious disease such as systemic lupus erythematosus or a malignancy.
Signs and symptoms
- The most common sign is excess fluid in the body. This may take several forms:
- Puffiness around the eyes, characteristically in the morning.
- Edema over the legs which is pitting (i.e. leaves a little pit when the fluid is pressed out, which resolves over a few seconds).
- Fluid in the pleural cavity causing pleural effusion.
- Fluid in the peritoneal cavity causing ascites.
- Renal failure
- Hypertension (rarely)
- Some patients may notice foamy urine, due to a lowering of the specific gravity by the high amount of proteinuria. Actual urinary complaints such as hematuria or oliguria are uncommon, and are seen commonly in nephritic syndrome.
Laboratory Findings
- Proteinuria (Nephrotic syndrome is arbitrarily defined as urinary protein loss of greater than 3.5 g/day)
- Hypoalbuminemia
- High levels of cholesterol (hypercholesterolemia), specifically elevated LDL, usually with concomitantly elevated VLDL
- Lipiduria
- Coagulation abnormalities: renal vein thrombosis more common than thrombosis in nonrenal circulation.
- Lower Back pain, usually in the kidney or bladder area.
