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Plants generally incorporate combined nitrogen into organic compounds, whereas animals eliminate the surplus nitrogen of metabolized compounds chiefly as Ammonia, urea or uric acid. The two processes connect nitrogen chemistry to the organism's carbon supply, water economy and environment.

Roots take up nitrate and ammonium from their surroundings. Nitrate must be reduced before its nitrogen can be incorporated in the usual amino form: nitrate reductase produces nitrite, and nitrite reductase produces ammonium. The balanced reduction, written without implying a single elementary reaction, isReducing equivalents and energy must be supplied by metabolism; nitrate is not simply deposited unchanged inside every protein.

In the modern biochemical account, glutamine synthetase incorporates ammonium into glutamine, using ATP; glutamate synthase transfers that nitrogen to a carbon skeleton derived from 2-Oxoglutarate, producing glutamate. Further transfer and synthesis distribute nitrogen into other amino acids, proteins, nucleotides and other cell constituents. Carbon metabolism therefore provides both energy and skeletons for nitrogen assimilation. These named enzymes and reactions explain the process today; they were not a completed molecular scheme in 1864.^[ref]

Ordinary higher-plant cells do not themselves reduce atmospheric molecular nitrogen merely because the gas surrounds the leaves. Biological nitrogen fixation is performed by particular microorganisms; symbiotic associations can supply fixed nitrogen to a host plant. The later elucidation of root-nodule symbiosis should be distinguished from what the examiner could have expected. Organic nitrogen can also be taken up in suitable circumstances, so nitrate and ammonium are important routes rather than an exhaustive prohibition on every other source.^[ref]

A useful assimilation experiment grows comparable seedlings in a defined medium containing all required minerals except combined nitrogen, with parallel nitrate- or ammonium-supplied cultures. Initial seed reserves, contaminating nitrogen, water and microbial growth must be allowed for. Growth and final nitrogen content are more informative than green appearance alone. A plant initially growing in a nitrogen-free solution may simply be consuming seed reserves; that observation does not demonstrate fixation of atmospheric nitrogen.

Animals obtain most of their nitrogen from organic food. Amino acid metabolism separates nitrogen handling from oxidation or reuse of the carbon skeleton. Free Ammonia is toxic at high concentrations, and mammals convert much of their waste nitrogen into urea in the liver; the kidneys then eliminate it in urine. Uric acid is also produced from purine breakdown. Renal ammonium excretion has a separate important connection with acid-base balance. Urea formation and urinary excretion are different processes in different organs.^[ref]

Many aquatic animals can release Ammonia directly into abundant surrounding water. Birds, many reptiles and many insects eliminate much nitrogen as relatively insoluble uric acid, conserving water; mammals generally depend more on soluble urea. These are broad physiological strategies with exceptions, not a rule that all animals have human urine. Faecal nitrogen includes unabsorbed food as well as endogenous material, while smaller losses can occur through skin and secretions. For a stated interval the accounting identity isPositive retention during growth and negative balance during tissue loss need not be errors of excretion. Nitrogen is redistributed or lost in compounds; it is not simply breathed out as all the atmospheric nitrogen passing through the lungs.

Urine microscopy can identify the kind and possible site of urinary disease, directing further investigation and cause-specific treatment; a sediment finding alone is seldom a prescription. This is a general methods question. No particular specimen, microscopic field or patient result is supplied.

Examine a fresh, properly collected sample, noting collection and storage conditions. After gentle mixing, examine a standardised sediment with a microscope: a low-power objective helps find urinary casts, while higher power characterises cells, bacteria and crystals. A centrifuge concentrates sediment when that method is used, but excessive delay or unsuitable processing can destroy cells and casts or generate crystals after collection. Interpret findings with symptoms, urine chemistry and kidney function; a dirty container or vaginal contamination can otherwise mimic urinary disease.^[ref]

Red blood cells indicate haematuria, whose source may be anywhere along the tract. Red blood cell casts or convincing dysmorphic red blood cells support a glomerular origin and justify assessment for glomerulonephritis, including renal function, proteinuria and appropriate referral. They do not establish a particular immunological cause. Isomorphic red blood cells with pain may suggest a stone; persistent unexplained haematuria also requires assessment for other urinary pathology. A historically tempting order to give an astringent would not address these different mechanisms.^[ref]

Many white blood cells, with compatible symptoms and bacteria, support urinary tract infection; obtain a suitable bacterial culture when indicated and select an antibiotic according to the clinical syndrome and susceptibility. Contamination or asymptomatic bacteriuria is not equivalent to symptomatic infection. White blood cell casts favour an intrarenal process such as pyelonephritis or interstitial nephritis, so the treatment cannot be inferred from pus alone. Numerous squamous epithelial cells instead raise concern about collection quality.^[ref]

Renal tubular epithelial cells and granular casts can support tubular injury; fatty elements together with marked proteinuria suggest a nephrotic process. These findings direct assessment of kidney disease, fluid balance and potentially nephrotoxic exposures. A few hyaline casts may occur without a specific kidney disease. Casts are moulds formed within renal tubules; that origin is why they can localise a finding more effectively than free cells.^[ref]

Urinary crystals must be interpreted with urine acidity, concentration and the time after collection. Uric acid or calcium oxalate crystals can suggest a stone-forming environment but do not prove an obstructing stone or justify an unrestricted alkali prescription. Hexagonal cystine crystals raise a different metabolic question. Infection-associated phosphate stones require attention to the associated infection as well as stone management. Modern decisions combine stone analysis, imaging and metabolic assessment; hydration, urinary alkalinisation or other measures depend on the confirmed disorder. Microscopy does not by itself measure glucose, albumin loss or renal filtration, so these require separate tests.^[ref]