What is the difference between leukocytes and nitrite




















When both test results were combined using a logistic regression analysis, the area under the curve of the combination of both tests was 0. Furthermore, addition of age as a diagnostic variable to both tests resulted in a minimal increase of the area under the curve to 0. The positive and negative predictive values of the LE test were less than those of the nitrite test, and addition of the results of the LE test to those of the nitrite test did not substantially improve the predictive values.

The missing nitrite and LE test data may be secondary to the fact that, according to the general practitioner guidelines in The Netherlands, the LE test should not be performed when results of the nitrite test are positive [ 4 ]. Another disadvantage of the nitrite test is that the causative microorganism and its antibiotic susceptibility are not known.

However, in our study, the majority of the cultured bacteria were gram-negative bacteria, suggesting that empirical therapy can be started in men without symptoms of complicated UTI, pending culture results.

The general practitioner guidelines recommend starting empirical antibiotic therapy in women with symptoms indicative of UTI when nitrite test results are positive [ 4 ]. Therefore, we suggest that, after a positive nitrite test result, empirical therapy be started, pending results of the urine culture.

Further studies are warranted to evaluate empirical therapy for male UTI. In men, UTIs become increasingly frequent with age and functional disability [ 10 , 11 ], but bacteriuria in elderly men tends to be intermittent, episodic, and more complex to diagnose [ 11 ].

However, when the nitrite test yields negative results, a UTI cannot be excluded, and urine samples should be further investigated by culture, without start of empirical therapy. Financial support. Dutch Working Party on Antibiotic Policy. Potential conflicts of interest. All authors: no conflicts. Google Scholar. Oxford University Press is a department of the University of Oxford.

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Volume Article Contents Abstract. Oxford Academic. Alfons G. Sita Nys. Ellen E. Annelies Verbon. Reprints or correspondence: Dr. Select Format Select format. Permissions Icon Permissions. Primary glomerulonephritis. Focal segmental glomerulonephritis. Mesangioproliferative glomerulonephritis. Postinfectious glomerulonephritis. Rapidly progressive glomerulonephritis.

Secondary glomerulonephritis. Hemolytic-uremic syndrome. Systemic lupus nephritis. Thrombotic thrombocytopenic purpura. Renal causes. Arteriovenous malformation.

Loin pain-hematuria syndrome. Malignant hypertension. Medullary sponge kidney. Metabolic causes. Papillary necrosis. Polycystic kidney disease.

Renal artery embolism. Renal vein thrombosis. Sickle cell disease or trait. Tubulointerstitial causes. Vascular cause. Urologic causes. Benign prostatic hyperplasia. Cancer kidney, ureteral, bladder, prostate, and urethral. Schistosoma haematobium infection.

Other causes. Drugs e. Trauma e. Adapted with permission from Ahmed Z, Lee J. Asymptomatic urinary abnormalities. Hematuria and proteinuria. Med Clin North Am ; Glomerular hematuria typically is associated with significant proteinuria, erythrocyte casts, and dysmorphic RBCs. However, 20 percent of patients with biopsy-proven glomerulonephritis present with hematuria alone. Nonglomerular hematuria is secondary to tubulointerstitial, renovascular, or metabolic disorders.

Like glomerular hematuria, it often is associated with significant proteinuria; however, there are no associated dysmorphic RBCs or erythrocyte casts. Further evaluation of patients with glomerular and nonglomerular hematuria should include determination of renal function and hour urinary protein or spot urinary protein-creatinine ratio. Urologic causes of hematuria include tumors, calculi, and infections. Urologic hematuria is distinguished from other etiologies by the absence of proteinuria, dysmorphic RBCs, and erythrocyte casts.

Exercise-induced hematuria is a relatively common, benign condition that often is associated with long-distance running. Results of repeat urinalysis after 48 to 72 hours should be negative in patients with this condition.

In healthy persons, the glomerular capillary wall is permeable only to substances with a molecular weight of less than 20, Daltons. Once filtered, low—molecular-weight proteins are reabsorbed and metabolized by the proximal tubule cells. Normal urinary proteins include albumin, serum globulins, and proteins secreted by the nephron. Proteinuria is defined as urinary protein excretion of more than mg per day 10 to 20 mg per dL and is the hallmark of renal disease.

Microalbuminuria is defined as the excretion of 30 to mg of protein per day and is a sign of early renal disease, particularly in diabetic patients. Dipstick tests for trace amounts of protein yield positive results at concentrations of 5 to 10 mg per dL—lower than the threshold for clinically significant proteinuria.

Proteinuria can be classified as transient or persistent Table 5. Congestive heart failure. Emotional stress. Orthostatic postural proteinuria. Primary glomerular causes. IgA nephropathy i.

IgM nephropathy. Membranoproliferative glomerulonephritis. Membranous nephropathy. Minimal change disease. Secondary glomerular causes. Collagen vascular diseases e.

Diabetes mellitus. Infections e. Malignancies e. Sickle cell disease. Tubular causes. Fanconi syndrome. Heavy metal ingestion. Hypertensive nephrosclerosis. Interstitial nephritis. Overflow causes. Multiple myeloma. Persistent proteinuria is divided into three general categories: glomerular, tubular, and overflow. In glomerular proteinuria, the most common type, albumin is the primary urinary protein.

Tubular proteinuria results when malfunctioning tubule cells no longer metabolize or reabsorb normally filtered protein. In this condition, low—molecular-weight proteins predominate over albumin and rarely exceed 2 g per day. In overflow proteinuria, low—molecular-weight proteins overwhelm the ability of the tubules to reabsorb filtered proteins.

Further evaluation of persistent proteinuria usually includes determination of hour urinary protein excretion or spot urinary protein-creatinine ratio, microscopic examination of the urinary sediment, urinary protein electrophoresis, and assessment of renal function.

Glucose normally is filtered by the glomerulus, but it is almost completely reabsorbed in the proximal tubule. Glycosuria occurs when the filtered load of glucose exceeds the ability of the tubule to reabsorb it i. Ketones, products of body fat metabolism, normally are not found in urine. Dipstick reagents detect acetic acid through a reaction with sodium nitroprusside or nitro-ferricyanide and glycine.

Ketonuria most commonly is associated with uncontrolled diabetes, but it also can occur during pregnancy, carbohydrate-free diets, and starvation. Nitrites normally are not found in urine but result when bacteria reduce urinary nitrates to nitrites. Many gram-negative and some gram-positive organisms are capable of this conversion, and a positive dipstick nitrite test indicates that these organisms are present in significant numbers i.

This test is specific but not highly sensitive. Thus, a positive result is helpful, but a negative result does not rule out UTI. After one week of exposure, one third of strips give false-positive results, and after two weeks, three fourths give false-positive results. Leukocyte esterase is produced by neutrophils and may signal pyuria associated with UTI. Leukocyte casts in the urinary sediment can help localize the area of inflammation to the kidney.

Organisms such as Chlamydia and Ureaplasma urealyticum should be considered in patients with pyuria and negative cultures. Other causes of sterile pyuria include balanitis, urethritis, tuberculosis, bladder tumors, viral infections, nephrolithiasis, foreign bodies, exercise, glomerulonephritis, and corticosteroid and cyclophosphamide Cytoxan use. Urine normally does not contain detectable amounts of bilirubin.

Unconjugated bilirubin is water insoluble and cannot pass through the glomerulus; conjugated bilirubin is water soluble and indicates further evaluation for liver dysfunction and biliary obstruction when it is detected in the urine. Normal urine contains only small amounts of urobilinogen, the end product of conjugated bilirubin after it has passed through the bile ducts and been metabolized in the intestine.

Urobilinogen is reabsorbed into the portal circulation, and a small amount eventually is filtered by the glomerulus. Hemolysis and hepatocellular disease can elevate urobilinogen levels, and antibiotic use and bile duct obstruction can decrease urobilinogen levels. Microscopic examination is an indispensable part of urinalysis; the identification of casts, cells, crystals, and bacteria aids in the diagnosis of a variety of conditions. To prepare a urine specimen for microscopic analysis, a fresh sample of 10 to 15 mL of urine should be centrifuged at 1, to 3, rpm for five minutes.

The supernatant then is decanted and the sediment resuspended in the remaining liquid. Leukocytes may be seen under low- and high-power magnification Figure 1. Squamous epithelial cells arrows and leukocytes X.

Epithelial cells often are present in the urinary sediment. Squamous epithelial cells are large and irregularly shaped, with a small nucleus and fine granular cytoplasm; their presence suggests contamination. The presence of transitional epithelial cells is normal.

These cells are smaller and rounder than squamous cells, and they have larger nuclei. The presence of renal tubule cells indicates significant renal pathology Figure 2. Erythrocytes are best visualized under high-power magnification. Dysmorphic erythrocytes, which have odd shapes because of their passage through an abnormal glomerulus, suggest glomerular disease. Casts in the urinary sediment may be used to localize disease to a specific location in the genitourinary tract Table 6.

Their cylindrical shape reflects the tubule in which they were formed and is retained when the casts are washed away. Take a sample halfway through urinating. The initial stream of urine may be contaminated by skin bacteria, so taking a sample this way also reduces the risk of a misleading outcome. Leukocytes are white blood cells. They are heavily involved in immune responses that protect people from infection.

There are several types of white blood cell. The two main leukocytes are phagocytes and lymphocytes. Phagocytes are produced in the bone marrow. Their job is to engulf foreign particles, such as bacteria or parasites. This means surrounding, absorbing, and destroying a particle.

Lymphocytes are the white blood cells that recognize foreign particles based on previous encounters. Lymphocytes produce antibodies. These bind to foreign particles and allow the immune system to remember them later on, should the same infection occur. There are other types of leukocyte. Cytotoxic white blood cells, for example, can kill other cells. A doctor will often carry out urinalysis during pregnancy to check for leukocytes.

This is the same test that confirms a bladder or kidney infection. This checks for certain pregnancy-related conditions too. One of these is preeclampsia , or high blood pressure during pregnancy. Protein in the urine and a raised blood pressure reading can indicate preeclampsia. UTIs are common during pregnancy, and doctors will often find leukocytes in the urine that suggest the presence of an infection.

However, some women who are pregnant have a bacterial infection in the urine without symptoms. A UTI can affect the upper and lower urinary tracts, the kidneys, the bladder, urethra, and prostate.

Most UTIs cause manageable infections that an individual can treat with antibiotics. The doctor may prescribe a range of different antibiotics, although they will only prescribe certain antibiotics to women during pregnancy.

More severe or serious infections with complications, such as abscesses, kidney involvement, or any infections that occur during pregnancy, may need more intensive treatment, including hospitalization. The doctor may need to change the course of antibiotic drugs once the bacteria are identified. Certain bacteria can only be treated with specific antibiotics.



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