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\b[Urinary <albumin>, <glucose> and <leukocytes> represent different abnormalities, and none alone identifies one disease.] A fresh, appropriately collected specimen and confirmation of the constituent are essential before interpreting it.
Persistent <albuminuria> commonly reflects increased passage of <albumin> across an injured <glomerular filtration barrier>. Examples include <glomerulonephritis>, <diabetic kidney disease> and other protein-losing glomerular disorders. Renal vascular congestion and severe systemic illness can also increase excretion. Transient <albuminuria> can accompany fever, strenuous exercise or a <urinary tract infection>; an upright-posture-related pattern may disappear in an early-morning specimen. Blood or inflammatory material added downstream can contribute protein, so a protein-positive specimen need not mean that every protein molecule crossed a diseased <glomerulus>.<Albuminuria by the National Kidney Foundation>[Causes: temporary and persistent albuminuria; importance of repeat testing]{ref}
<Albuminuria> should be distinguished from the broader term <proteinuria>. Reduced tubular recovery and overproduction of other small proteins can produce different urinary protein patterns. A modern urine <albumin>-to-<creatinine> measurement helps quantify albumin loss and reduce the effect of variable dilution.<Albuminuria: Albumin in the Urine by NIDDK>[Detection: urine albumin measurement and albumin-to-creatinine ratio]{ref} The historical “albumen” category does not imply that every old heat or precipitation test was chemically specific for <albumin>.
<Glycosuria> results either from an excessive filtered <glucose> load or reduced renal recovery. <Diabetes> with <hyperglycaemia> is the major systemic example. Transient hyperglycaemic states may also cause it; <renal glycosuria>, pregnancy-related changes and proximal tubular dysfunction can produce <glycosuria> without sustained diabetic <hyperglycaemia>. Modern drugs that deliberately reduce renal <glucose> recovery provide another mechanism, but should not be attributed to 1864 practice.<Renal Glucosuria by Merck Manual Professional Edition>[Definition and etiology: glucose without hyperglycaemia; isolated or associated tubular defects]{ref} <Glucosuria in Clinical Methods>[Chapter 139, Basic Science: excessive filtered load, diminished tubular recovery and pregnancy]{ref} Urinary sugar is therefore a reason to examine <blood glucose>, not proof of one diabetes subtype. Historical reducing-sugar reactions also require care because chemical reduction is not uniquely specific to <glucose>.
“Pus globules” correspond chiefly to <leukocytes>, especially <neutrophils>. <Pyuria> occurs with <cystitis>, <pyelonephritis>, urethral or prostatic infection and suppuration draining into the urinary tract. It can also occur with stones, <urinary tuberculosis>, <interstitial nephritis> and other inflammatory disorders, or through contamination by genital secretions. Previous antimicrobial treatment or organisms not recovered by a routine culture can leave apparently sterile <pyuria>.<Bacterial Urinary Tract Infections by Merck Manual>[Urine testing: leukocytes, casts, noninfective causes and contamination]{ref}<Living Donor Kidney Transplantation Guidelines by the British Transplantation Society and Renal Association (2011)>[§5.13, Pyuria: sterile pyuria and alternative causes]{ref}
A wet sediment examined with a <microscope> can show <leukocytes>, <red blood cells> and <urinary casts>; <urine culture> addresses a different question about detectable organisms. White-cell casts suggest inflammation within the kidney rather than simply pus added in the bladder, but are not unique to bacterial <pyelonephritis>. \b[“Pus in urine” neither localises every lesion nor proves an ordinary bacterial infection.]
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