Dipstick chemical analysis
Urinary pH: The body’s ability to maintain normal acid-base balance is reflected in the urinary pH, typically 5.5-6.5 (normal range: 4.5-8). Infection with any pathogen that produces urease, e.g., Proteus mirabilis and Pseudomonas, can result in a pH >7.0-7.5. An alkaline pH may also indicate a systemic metabolic or respiratory alkalosis. Acid urine (pH <6.0) may occur with high-protein diets or acidosis for a non-kidney-related reason, such as diarrhea, malabsorption, emphysema, and diets high in meat.3 Renal stone formation is related to urinary pH, with phosphate and calcium carbonate stones developing in alkaline urine, and uric acid, cystine, and calcium oxalate stones more often precipitating in acid urine.
Specific gravity: Urine specific gravity, which correlates well with urine osmolality, gives important insight into hydration status and concentrating ability of the kidneys. Specific gravity is usually 1.010-1.025 (normal range: 1.003-1.030) and highest in the morning. A value >1.025 indicates normal concentrating ability. A value >1.035-1.040 suggests possible contamination, very high levels of glucose, or recently received low-molecular-weight dextran or high-density radiopaque dyes. A high specific gravity is also seen in shock, nephrotic syndrome, dehydration, acute glomerulonephritis, heart failure, or liver failure. A low specific gravity may indicate diabetes insipidus, glomerulonephritis, pyelonephritis, or other anomalies that reflect an inability to concentrate urine.
Glucose: Less than 0.1% of glucose filtered by the renal glomerulus appears in urine; the rest is reabsorbed in the proximal tubule until the plasma glucose rises.3 Benign glycosuria may result from a heavy meal or stress. Diabetes mellitus is the major pathologic cause. Other causes include hemochromatosis, hyperthyroidism, Cushing syndrome, steroid therapy, or sudden shock. Renal glycosuria is the rare result of a decreased renal threshold for glucose. Other signs of proximal dysfunction are often seen, including hypophosphatemia, hypouricemia, renal tubular acidosis, and aminoaciduria. Dipsticks using the glucose oxidase reaction can miss other sugars.
Ketones: Ketonuria results when excessive circulating intermediary products of fat metabolism appear in the blood. This most often occurs when fat metabolism is stimulated by inadequate carbohydrate intake or a carbohydrate-metabolism defect. Uncontrolled diabetes mellitus is the most common cause, but other causes include vomiting, diarrhea, acute fever, carbohydrate-free diets, starvation and cachexia, or eclampsia.
Proteins: The major protein found in urine is globulin, followed by albumin. Trace amounts of other proteins may also be found. Dipsticks are most sensitive to albumin and do not detect immunoglobulin light chains or Bence Jones protein. Excretion of >150 mg of protein per day (10-20 mg/dL) is defined as proteinuria and is the hallmark of renal disease.1 Proteinuria may also indicate heart failure, gout, infection, or nephrotoxic drugs. WBC or RBC casts in the urine can yield a positive protein test. Specific tests are needed to quantitate and identify different proteins, including fibrinogen, nucleoproteins, or Bence Jones proteins. Proteinuria may be continuous or intermittent; the latter is more likely caused by physiologic or functional disorders (postural proteinuria, fever, excessive exercise, or emotional stress) than by renal conditions.
Nitrites: A positive nitrite test indicates that bacteria may be present in significant numbers. This test is very specific but not very sensitive. Thus, it is helpful when positive, but a negative test does not rule out UTI. Common organisms, including species of Citrobacter, Escherichia, Pseudomonas, Klebsiella, and Proteus, as well as most Enterobacteriaceae (90%), contain enzymes that reduce urinary nitrates to nitrites. Bacteria without reductases (e.g., enterococci, Streptococcus faecalis) cannot be detected by nitrite testing.4
Leukocyte esterase: The presence of leukocyte esterase, which is produced by neutrophils, has a sensitivity around 75%-95% and a specificity around 65%-95%.5 Testing may be negative in infection because not all patients have significant pyuria (>5 WBCs/high-power field on microscopic examination of centrifuged urine sediment1). Thus, leukocyte esterase testing for UTI has a better positive predictive value for bacteriuria when considered with nitrite testing.1 A negative leukocyte esterase test means that infection is unlikely. Many experts believe that without additional evidence of UTI, microscopic exam and/or urine culture need not be done to rule out significant bacteriuria.
Blood: A sign of damage to the kidney or the urinary tract, hematuria is seen in renal disorders, infectious disease, neoplasms, eclampsia, systemic lupus erythematosus, sickle cell nephropathy, cirrhosis, or urinary tract trauma. Most test strips cannot differentiate among RBCs, hemoglobin, and myoglobin; thus, some care should be taken in interpretation.
RBCs are best detected microscopically. In hemoglobinuria, the serum will be pink or red; in myoglobinuria, the serum is clear.1 Free hemoglobin indicates RBC rupture due to trauma or hemolysis from dilute urine. Hemoglobinuria can be seen whenever blood is in the urine but is greater in transfusion reaction, hemolytic anemia, paroxysmal hemoglobinuria, poisoning, or severe burns. Myoglobinuria may follow traumatic or toxic muscle injury.
Bilirubin: The presence of bilirubin in the urine is an early sign of hepatocellular disease, intra- or extrahepatic biliary obstruction, or hemolysis. Some conjugated bilirubin (about 0.02 mg/dL) appears normally in the urine and increases only if blood levels rise. When liver cells are unable to excrete excess amounts of conjugated bilirubin into the bile or when biliary stasis occurs, bilirubin is secreted into the blood, causing elevated blood and urine levels. Unconjugated bilirubin is not water-soluble and cannot be found in the urine. Conjugated bilirubin, which enters the intestinal tract with bile, forms urobilinogen, which appears in the urine in small amounts (0.1-1.0 mg/dL). This level rises in any condition that increases bilirubin formation or in any hepatic disease that prevents reabsorption of urobilinogen from the portal circulation. These could include destruction of RBCs, as in hemolytic anemias and malaria; hepatitis; portal cirrhosis; or heart failure. Sequential determinations of urinary urobilinogen can help monitor disease progression and response to therapy. Urinary urobilinogen is absent when bilirubin is not excreted into the intestine (bile duct obstruction).