What each pad measures, and where it can mislead

The blood pad detects heme peroxidase-like activity. It reacts to intact erythrocytes, to free hemoglobin released from lysed cells, and to myoglobin. A blood-positive result with RBCs seen on sediment fits hematuria. A blood-positive result with absent or sparse RBCs supports a pigment or lysed-cell explanation and cannot by itself distinguish hemoglobin from myoglobin. Hypochlorite contamination or microbial peroxidase can produce a false positive, and captopril can reduce the pad's sensitivity.

The protein pad works on the protein-error-of-indicators principle and is more sensitive to albumin than to mucoproteins or globulins, so a negative or low protein pad does not exclude a non-albumin proteinuria. Visible blood can elevate the protein result on its own, and transient protein increases can follow exercise, dehydration, infection, or fever. When the pad result does not fit the clinical picture, a local algorithm may call for sulfosalicylic acid precipitation or a quantitative protein or albumin method rather than trusting the pad alone. Quantitative urine albumin-to-creatinine ratio (ACR) is categorized by KDIGO as A1 below 30 mg/g, A2 30 to 299 mg/g, and A3 at least 300 mg/g in adults, and an elevated random ACR should be confirmed with a first-morning midstream specimen before it drives a clinical decision.

Nitrite and leukocyte esterase (LE) are both indirect infection markers, not a culture result. The nitrite pad detects nitrite generated from dietary nitrate by some bacterial species; it does not detect bacteria directly, and it needs meaningful bladder incubation time (roughly 4 hours or more on this strip family) to accumulate a detectable amount. A negative nitrite does not rule out bacteriuria: short dwell time, low dietary nitrate, or a non-nitrate-reducing organism can all produce a negative result in a genuinely infected specimen. LE reflects granulocytic esterase and supports pyuria, not infection by itself; high glucose, cephalexin, cephalothin, oxalic acid, or tetracycline can blunt the LE reaction, while vaginal discharge can cause a false positive.

The glucose pad uses glucose oxidase and peroxidase and is specific for glucose rather than a general reducing substance; ketones can reduce its sensitivity at low glucose concentrations. Because renal glucose threshold varies between people, a urine glucose result has to be read against a contemporaneous blood glucose rather than against a fixed cutoff. The bilirubin pad uses a diazo reaction and the urobilinogen pad uses the Ehrlich reaction; both analytes degrade in urine left at room temperature and exposed to light, so a delayed, light-exposed negative cannot exclude prior bilirubin or urobilinogen. Formalin can cause a false-negative urobilinogen, and sulfonamides can create an Ehrlich-reactive interference that mimics a positive.

Specific gravity (SG) is measured differently by each of three common methods: the dipstick estimates ionic concentration through a polyelectrolyte reaction, refractometry estimates refractive index, and osmometry measures particle concentration directly. A study of 504 urine specimens found that both dipstick and refractometer SG correlated only approximately with osmolality, because pathological urine constituents shift each method differently; when the distinction matters clinically, osmolality is the better concentration measurement. Highly buffered alkaline urine can drive dipstick SG low, moderate protein can drive it high, and nonionic substances such as glucose can make the dipstick disagree with a refractometer on the same specimen.

Before ranking a physiological cause, rule out a pad-specific interference or a specimen-timing effect, because several of the mismatches above are built into how the method works, not into the patient.