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Incoming links: Renal Glucosuria by Merck Manual Professional Edition
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.[ref]
Albuminuria by the National Kidney Foundation. Causes: temporary and persistent albuminuria; importance of repeat testing
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.[ref]
Albuminuria: Albumin in the Urine by NIDDK. Detection: urine albumin measurement and albumin-to-creatinine ratio
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.[ref]
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
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.[ref]
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
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. “Pus in urine” neither localises every lesion nor proves an ordinary bacterial infection.
The significance of glycosuria and albuminuria depends on persistence, amount, mechanism and accompanying findings. The older words “sugar” and “albumen” do not guarantee that a nineteenth-century test identified one particular molecule.
For urinary sugar, distinguish the following situations:
- In diabetes, an excessive filtered glucose load can exceed recovery by the proximal tubule. Persistent glycosuria with measured hyperglycaemia, thirst, excessive urination and loss of body mass has much greater diagnostic significance than one weak urinary reaction.
- Transient hyperglycaemia during acute stress or illness can produce transient glycosuria. Changes after a large carbohydrate load depend on the individual's renal handling; a positive sample does not by itself establish chronic diabetes.
- In renal glycosuria, impaired tubular recovery permits loss despite an ordinary blood glucose level. This may be an isolated inherited trait or accompany wider proximal tubule dysfunction, as in Fanconi syndrome or tubular injury. Pregnancy can also lower the effective threshold for urinary loss.
- A specimen can contain other reducing substances, including sugars other than glucose. A general reducing test therefore needs chemical confirmation before its result is labelled glycosuria.
Modern glucose-specific assays and concurrent blood glucose measurements distinguish excess filtered load from reduced recovery.[ref]
Glucosuria in Clinical Methods. Technique, nonspecific copper reduction; Basic Science, glucose load, tubular defects and pregnancy
[ref]Renal Glucosuria by Merck Manual Professional Edition. Definition and causes, isolated transport defect versus generalized tubular dysfunction
For “albumen”, the principal pathological groups are injury to the glomerular filtration barrier in glomerulonephritis, renal amyloidosis, diabetic kidney disease and other glomerular diseases; changes associated with heart failure and renal venous congestion; and pregnancy-associated injury such as pre-eclampsia. Fever and severe exertion may produce transient proteinuria, while orthostatic proteinuria can disappear during recumbency. Impaired tubular recovery chiefly increases smaller urinary proteins; it should not automatically be called a selective loss of serum albumin.[ref]
Proteinuria by Merck Manual Professional Edition. Pathophysiology; Etiology; functional and orthostatic proteinuria
A collected specimen can also receive blood plasma proteins from haematuria or inflammatory material below the filtering apparatus. Moreover, immunoglobulin light chains in multiple myeloma can give a positive general protein test without being serum albumin. Historical heat and acid precipitation tested a physical property of material in a tube, not a modern molecular diagnosis.[ref]
Proteinuria in Clinical Methods. Technique and Basic Science, precipitation versus protein identification
[ref]The diagnostic value consequently rises with reproducibility and coherent accompanying evidence. Persistent heavy albuminuria, especially with oedema and abnormal sediment, strongly suggests significant renal disease; red blood cell casts support a renal rather than merely lower-tract source of bleeding. Repeated urinalysis, sediment microscopy and a urine albumin-to-creatinine ratio help quantify and localize the problem.[ref]
Albuminuria: Albumin in the Urine by NIDDK. Detection by dipstick and urine albumin and creatinine measurement
Coexisting glycosuria and albuminuria may reflect diabetes with renal injury, or another combination of mechanisms. Neither their coexistence nor either isolated result is sufficient to establish the whole diagnosis.