Kidney Function.pdf

7/29/2019 Kidney Function.pdf

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Kidney Function


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Kidney

The kidney is primarily concerned in the

elimination of nitrogenous waste productsthat one might think of it purely as anexcretory organ. The kidney should not beviewed only as an organ which removes end

products of metabolism and other wasteproducts of foreign substance dissolved inthe plasma but, also make continuousadjustments in the concentration of normalconstituents in the plasma regulatory.


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THE GENERAL FUNCTIONS OF THE

KIDNEYS:

ELIMINATION OF METABOLIC WASTEPRODUCTS THROUGH THE FORMATIONOF URINEREGULATION OF THE PLASMA ANDWATER VOLUME.

REGULATION OF IONIC EQUILIBRIUMMAINTENANCE OF ACID BASE BALANCEENDOCRINE FUNCTION


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THREE MAJOR GROUPS OF KIDNEY

FUNCTION TESTS:

TEST MEASURING GLOMERULAR

FILTRATION RATE (GFR)TEST MEASURING RENAL BLOOD FLOWTEST MEASURING TUBULAR FUNCTION


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TEST MEASURING GLOMERULAR

FILTRATION RATE

Tests which measure the rate of glomerular

filtration- are generally called CLEARANCES


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TYPES OF CLEARANCE

CREATININE CLEARANCE TEST

Creatinine occurring through metabolic productionis eliminated from the plasma by glomerular filtration and therefore a measurement of its rateof clearance affords a measure of the process.

Normal Values: 107-139 ml/min


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TYPES OF CLEARANCE

INULIN CLEARANCE TESTS

Inulin freely passes the glomeruli but is neither secreted nor reabsorbed by the nephric tubules. Considered to be the most accurate measure of

GFR.

Normal value: 250 ml/min. - men (due to larger renal mass) ; 110 mi/min - women


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TYPES OF CLEARANCE

UREA CLEARANCE TEST

Urea is freely filtered by the glomeruli but variablyreasbsorbed in the tubules depending upon thetransit time (rate of urine flow along the course of nephric tubules) of urea filtrate


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TOTAL NON-PROTEIN NITROGEN

PROCESS

DIGESTION PROCEDURE:

KJELDAHL DIGESTION PROCESSThe nitrogen ion in the PFF of the specimen inconverted to ammonia using hot concentrated sulfuricacid in the presence of a catalyst (copper sulfate,selenium oxide or mercuric- sulfate)


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MEASUREMENT OF AMMONIA:

NESSLERIZATION The ammonia formed when it reacts with the

Nessler's reagent (double iodide of potassiumand mercury, K 2Hg 2I2) in the presence of acolloidal stabilizer (gum ghatti) forms a colloidalsuspension of dimercuric ammonium iodide

(NH2Hg

2l2), which is said to be yellow in color, if nitrogen is present in low to moderate

concentration, and orange brown, if nitrogen ispresent in high concentration


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MEASUREMENT OF AMMONIA:

BERTHELOT'S REACTION

The ammonia formed reacts with phenol andalkaline hypochlorite using sodium nitroprussideas catalyst to form indophenoi blue.


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BLOOD UREA NITROGEN (BUN)

Urea is the principal waste of proteincatabolism.In severe liver damage, levels of ureadecreases. It is also the first metabolite toincrease in kidney disease,

It is used as a screening test for kidneydisease.Urea is readily removed by dialysis.


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BLOOD UREA NITROGEN

DETERMINATION:

ENZYMATIC AND NESSLERIZATION

Urea in the PFF is made to react with ureaseglycerol extract in the presence of buffer andheat-forming ammonium carbonate which is thenreacted with Nessler's reagent to form a yellowdimercuric ammonium iodide.


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BLOOD UREA NITROGEN

DETERMINATION:

Urea is hydrolyzed to ammonium carbonate

by urease and ammonia reacts with phenoland sodium hypochlorite in an alkalinemedium forming a blue indophenol.


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BLOOD UREA NITROGEN

DETERMINATION:

ENZYMATIC AND ACID TITRATION

Urea is hydrolyzed by urease forming ammoniawhich is then titrated with a weak acid.a. Van Slyke Cullenb. Urograph


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BLOOD UREA NITROGEN

DETERMINATION:

DIRECT MEASUREMENT OF UREA

DiacetyI Monoxime Method (DAM)Urea is made to react with diacetyl monoxime toproduce a yellow diaxine derivative (Fearon's reaction).

Arsenic thiosemicarbazide is added to enhance color formation and to exclude protein interference.


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CONSIDERATION IN BUN

DETERMINATION

The determination is affected by high protein diet,hydration and other physiologic functions.

Whole blood should be deproteinized to eliminateinterferences of hemoglobin. Ammonium-containing anticoagulants arecontraindicated in enzymatic methods.Sodium fluoride inhibits the action of urease.Upon prolonged standing, ammonia concentrationin the sample rises 2-3 times the original value dueto enzymatic deamination of labile amide likeglutamine.


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CONSIDERATION IN BUN

DETERMINATION

NORMAL VALUE: 7-18 mg/dL (2.5 - 6.4

mmol/L)CONVERSION FACTOR: 0.357


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CLINICAL SIGNIFICANCE:

Pre-renal causes - conditions in which

circulation through the kidneys is lessefficient than usual. Hemorrhage (blood loss) Cardiac decompression

Increased protein catabolism Heatstroke (Dehydration) Burns (Fluid loss)


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Renal causes - characterized by the

presence of lesions on the parenchymaitself (tubular injury). Chronic nephritis Acute glomerulonephritis (AGN)

Polycystic kidney Nephroschlerosis Tubular necrosis


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Post-renal causes - due to the obstruction in

the-urinary-tract due to: Stones Prostatic enlargement Tumors


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AZOTEMIA - ("azo) - nitrogen containing a-

biochemical abnormality that refers to anincrease in BUN and creatinine levels whichis largely related to decrease glomerular filtration.


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UREMIA - defined as the increased in ureaand creatinine (azotemia) with accompanyingclinical signs and symptoms of renal failurelike: Metabolic acidosis due to failure of the kidneys to

eliminate acidic products of metabolism Hyperkalemia due to failure of potassium

excretion Generalized edema due to water retention


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CREATININE

Creatinine is the principal waste product of

muscular metabolism derived mainly fromcreatine (alpha-methyl guanidoacetic acid).It is synthesized form three amino acids(methionine, arginine and lysine)


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CREATININE DETERMINATION:

Creatinase Method

Available on Ektachem analyzer whereincreatinine is hydrolyzed to N-methyldantolin andammonia by creatinase. The ammonia is thenmade to react with alpha-ketoglutarate andNADH in the presence of glutamatedehydrogenase forming glutamate and NAD.The decrease in NADH is followedfluorometrically.


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CREATININE DETERMINATION:

Creatinine Aminohydrolase Method

Creatinine is hydrolyzed'to creatineby,creatinine aminohydrolase followed by aseries of coupled enzyme reactions in whichcreatine reacts with creatinine kinase, pyruvatekinase, and !actate dehydrogebase, culminatingin the oxidation of the NADH.


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DIRECT JAFFE REACTION METHODS

It is the formation of red tautomer of creatinine picrate when creatinine in serum ismade to react with a freshly preparedalkaline sodium picrate solution (alkalinepicrate - Jaffe reagent).


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Creatinine Determination

NORMAL VALUE: 0.6 - 1.2 mg/dL (53-106umol/L)CONVERSION FACTOR: 88.4


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Aside from renal diseases, it is also elevatedin myopathies like: Muscular dystrophies Familial periodic paralysis Myasthenia gravis

Dermatomyositis


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BLOOD URIC ACID (BUA)

Uric acid is the major end product of purinemetabolism formed in the liver and intestinalmucosa from xanthine by the action of xanthine oxidase.


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Normally, 89% of the filtered UA isreabsorbed.It is relatively insolubleWhen it accumulates, it may be deposited inthe joints (tophi) or in the genitourinary tractsas uric acid stones.


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DETERMINATION

DIRECT REDOX METHODS Uric acid is oxidized to allantoin and C02 by

phosphotungstic acid reagent (proteinprecipitant and color reagent in alkaline solution.In the process of phosphotungstic acid isreduced to tungsten blue


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DETERMINATION

ENZYMATIC METHOD (BLAUNCH andKOCK or URICASE METHOD)

Differential or Absorption Spectrophotometry Uric acid is destroyed by the action of uricase to

form carbon dioxide and allantoin. Since uricacid has a maximum.absorption peak at 290-

293 nm, white allantoin has no absorption at thispoint, the decrease in the absorbance ispositively related to the uric acid present in thesample


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CONSIDERATION IN BUA

DETERMINATION:

Uric acid is stable for several days at room'temperature and longer if refrigerated

Addition of thymol increases its stability to bacterialdestruction.

Any of the common anticoagulants, can be usedexcept for potassium oxalate which formspotassium phosphotungstate promoting turbidity.Purine like foods like legumes, visceral organs andothers may affect uric acid assay


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DETERMINATION

NORMAL VALUES:

4.0 - 8.5 mg/dL(0.25 - 0.50 mmol/L) men2.7 - 7.3 mg/dl (0.16 - 0.43 mmol/L) - women


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CLINICAL SIGINIFCANCE:

Gout - a defect in uric acid metabolismwhich causes an excess of the acid andsalts to accumulate in the bloodstream and

joints.


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Chronic alcoholism increases uric acid inthe bloodstream because alcohol inhibits itsexcretion.


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Leukemia and other malignant conditionsdue to increased turnover of nucleoproteins


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Uric acid levels are elevated in decreasedrenal functions either due to over productionof uric acid or decreased rate.of excretion.


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Fatal poisoning with chloroform andmethanol, excessive exposure to X-raysand radioactive radiators, due to excessivecell breakdown and nucleic acid catabolism


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Genetic disease such as: Lesch-Nyhansyndrome and Von Gierke's disease


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AMMONIA

Ammonia determinations contribute very littleor none at all in renal impairment.It has its significance in impending hepaticcoma and terminal stages of hepaticcirrhosis.


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AMINO ACIDS

Quantitative amino acid determinations areimportant in congenital renal disorder wherein aminoaciduria resuIts.


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CREATINE

Synthesized from amino acid arginine,methionine, and glycine. It is increased inmuscular dystrophies.


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TESTS MEASURING TUBULAR

FUNCTIONS

EXCRETORY TEST: Para-amino Hippurate Test (PAH) or Diodrast

Test Phenolsufophthalein (PSP) Dye Excretion Test


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TESTS MEASURING TUBULAR

FUNCTIONS

CONCENTRATION TEST Specific gravity Osmolality Fishberg Concentration Test

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