Student Publications

Author: Eman Mohamed Ramadan Hassan
Biochemistry Related to Clinical Chemistry
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Clinical Correlations of Amino Acids…………………………..................Page 3
   * Phenylketonuria……………………………………………................Page 3
                * Tyrosinemia and Related Disorders………………………......Page 3
                * Alkaptonuria…………………………………………………Page 3
                * Maple Syrup Urine Disease (MSUD)…………………………Page 3
                * Homocystinuria……………………………………………….Page 4
                * Cystinuria…………………………………………………….Page 4
Clinical Correlations of Plasma Proteins…………………….......................Page 4

  • Prealbumin…………………………………………………....Page 4
  • Albumin……………………………………………………....Page 4
  • Globulins……………………………………………………...Page 4
  • Hemopexin……………………………………………………Page 6
  • Complement…………………………………………………..Page 6
  • Fibrinogen…………………………………………………….Page 6
  • C-Reactive Protein (CRP)…………………………………….Page 6
  • Immunoglobulins (Igُ s)………………………………………Page 6
  • Human Ventricular Myosin Light Chain (HVMLC)…………….Page 6

Total Protein Abnormalities………………………………………......Page 7
   * Hyperproteinemia……………………………………………… .Page 7
   * Hypoproteinemia………………………………………………. .Page 7
Clinical Correlations of Glucose………………………………...........Page 7
   * Factors Determining Blood Glucose Level……………………… Page 7
                  Diabetes Mellitus…………………………………..........Page 8
Liver Function………………………………………………………Page 8
                  Disorders Of The Liver………………………………….Page 8
                  Enzymes in Liver Disease………………………………..Page 9
Clinical Correlations of The Kidney……………………………........Page 10

  • Acute Glomerulonephritis…………………………………….Page 10
  • Chronic  Glomerulonephritis………………………………….Page 10
  • Nephrotic Syndrome………………………………………...Page 10
  • Tubular Diseases…………………………………………….Page 10
  • Urinary Tract Infection/ Obstruction………………………….Page11
  • Renal Calculi………………………………………………...Page11
  • Renal Failure………………………………………………...Page11


Biochemistry Related to Clinical Chemistry

  • Clinical Correlations Of Amino Acids


1- Phenylketonuria
    Phenylketonuria (PKU) occurs in approximately 1 in 14.000 births. The biochemical defect in the classic form of phenylketonuria is a deficiency of the enzyme phenylalanine hydroxylase which catalyzes the conversion of phenylalanine to tyrosine. In the absence of the enzyme, phenylalanine accumulates and is metabolized by an alternate degradative pathway.
   In infants and children with this inherited defect, retarded mental development occurs as a result of the toxic effects on the brain of phenylpyruvate or one of its metabolic by-products. The deterioration of brain function begins in the second or third week of life. Brain damage can be avoided if the disease is detected at birth and the infant is maintained on a diet containing very low levels of phenylalanine. There is a slight reduction in IQ after discontinuation of the diet. The fetal effects of maternal PKU are preventable if the mother is maintained on phenylalanine-restricted diet from before conception through term.
   The reference value for serum phenylalanine is 0.84 to 2.64 mg/dl. Any positive results of the screening test must be verified by measuring serum phenylalanine levels through enzymatic methods using phenylalanine-ammonialyase and a selective electrode using phenylalanine hydroxylase are also available to determine phenylalanine.
2- Tyrosinemia and Related Disorders
     Normally, the major path of tyrosine metabolism involves the removal of an amine group by tyrosine amino transferase forming p-hydroxyphenylpyruvic acid (PHPPA), which is oxidized to homogentisic acid (HGA). Homogentisic acid is metabolized in a series of reactions to fumarate and acetoacetate. The defect in inherited tyrosine abnormalities is a deficiency in either tyrosine aminotransferase or fumarylacetoacetate hydrolase. The absence of these enzymes results in abnormally high levels of tyrosine and in some cases increases in PHPPA and methionine. The elevated tyrosine leads to liver damage or to cirrhosis and liver cancer later in life.
3- Alkaptonuria
    The biochemical defect in alkaptonuria is a lack of homogentisate oxidase in the tyrosine catabolic pathway. A clinical manifestation of alkaptnuria is the darkening of urine upon standing exposed to the atmosphere. The phenomenon is due to an accumulation in the urine of homogentisic acid (HGA), which oxidizes to produce a dark polymer.
    Alkaptonuric patients have high levels of HGA gradually accumulates in connective tissue causing generalized pigmentation of these tissues (orchronosis) and arthritis-like degeneration.
4- Maple Syrup Urine Disease (MSUD)
    It is results from an absence or greatly reduced activity of the enzyme branched-chain keto acid decarboxylase, therby blocking the normal metabolismof the three essential branched-chain amino acids leucine, isoleucine, and valine. This enzyme is responsible for catalyzing the oxidative decarboxylation of all three branched-chain α-ketoacids to CO2 and their corresponding acyl-CoA thioesters. The result of this enzyme defect is an accumulation of the branched-chain amino acids and their corresponding ketoacids in the blood, urine, and CSF.
   If left untreated, the disease causes severe mental retardation, convulsions, acidosis, and hyperglycemia. In the classic form of the disease, death usually occurs during the first year.Elevation of the branched-chain amino acids, the levels can be controlled by limiting dietry protein intake.        5- Homocystinuria
    It is an intermediate amino acid in the synthesis of cysteine from methionine. It is caused due to an impaired activity of the enzyme cystathionine β-synthase, which results in elevated plasma and urine levels of the precursors homocysteine and methionine. Newborns show no abnormalities, but gradually, physical defects develop, thrombosis due to toxicity of homocysteine to the vascular endothelium, osteoporosis, dislocated lenses in the eye due to the lack of cysteine synthesis essential for collagen formation, and mental retardation.
   The enzyme cystathionine β-synthetase requires vitamin B6 as its cofactor. Genetic defects lead to two forms of the disease: a vitamin B6-responsive form, in which treatment consists of therapeutic doses of the vitamin, and a vitamin B6-unresponsive form, in which the treatment is a diet low in methionine and high in cysteine.
6- Cystinuria
     It is caused by a defect in the amino acid transport system rather than a metabolic enzyme deficiency. Normally, amino acids are freely filtered by the glomerulus and then reabsorbed in the proximal renal tubules. In cystinuria, there is a 20-30 fold increase in the urinary excretion of cysteine due to a genetic defect in the renal resorptive mechanism and precipitate in the kidney tubules and form urinary calculi. The formation of cysteine calculi can be minimized by a high fluid intake and alkalinizing the urine.
2- Clinical Correlations Of  Plasma .Proteins
1- Prealbumin
    It combines with thyroxine and triiodothyronine to serve as the transport mechanism for these thyroid hormones.It is also binds with retinol , vitamin A. Prealbumin is decreased in hepatic damage, burns, salicylate ingestion, and tissue necrosis. A low prealbumin level is also a sensitive marker of poor protein nutritional status because of its short half-life, 8 hours. Prealbumin is increased in some cases in nephritic syndrome.
2- Albumin
    Albumin is the protein present in highest concentration in the serum. It is synthesized in the liver. Albumin has two well-known functions, maintains the appropriate fluid in the tissues. The other function is its propensity to bind various substances in the blood as bilirubin, fatty acids, calcium, iron and some drugs.
    Abnormalities in serum albumin are exhibited by a decreased concentration in the serum, the absence of albumin, analbuminemia. Analbuminemia is an abnormality of genetic origin resulting from an autosomal recessive trait. A decreased concentration of serum albumin also may be caused by the following:

  • An inadequate source of amino acids, which is seen in malnutrition and muscle-wasting disease.
  • Liver disease resulting in the inability of hepatocytes to synthesize albumin.
  • Gastrointestinal loss as interstitial fluid leaks out in inflammation and disease of the intestinal mucosa.
  • Loss in the urine in renal disease. Albumin is normally excreted in very small amounts.

3- Globulins
a- α1-Antitrypsin
    Its main functions is to neutralize trypsin-like enzymes that can cause hydrolytic damage to structural protein. α1-Antitrypsin deficiency leads to Laurell and Eriksson diseases.
b- α1-Fetoprotein (AFP)
     It is synthesized initially by the fatal yolk sac and then by the parenchymal cells of the liver. The function of AFP is not well established. It has been proposed that the protein protects the fetus from immunolytic attack by its mother. AFP is detectable in the maternal blood during pregnancy up to the seventh or eight month because it is transmitted across the placenta. Conditions associated with an elevated AFP level include spina bifida and neural tube defects, atresia of the gastrointestinal tract, and fetal distress in general.
     Very high concentrations of AFP are found in many cases of hepatocellular carcinoma and certain gonadal tumors in adults.

c- α1-Acid Glycoprotein (Orsomuccid)
     It is composed of five carbohydrate units attached to a polypeptide chain. Increased concentration of this protein is the major cause of an increased glycoprotein level in the serum during inflammation, pregnancy, cancer, pneumonia, rheumatoid arthritis, and other conditiona associated with cell proliferation.
    It is an α2-Acid Glycoprotein and synthesized in the hepatocytes and, to a very small extent, in cells of the reticuloendothelial system. It is composed of two kinds of polypeptide chains, two α chains and one β chain.
    The function of haptoglobin is to bind free hemoglobin by its α chain. Abnormal hemoglobin as Barts and hemoglobin H have no α chains and cannot be bound. The reticuloendothelial cells remove the hepatoglobin-hemoglobin complex from circulation within minutes of its formation. Thus hepatoglobin prevents the loss of hemoglobin and its constituents iron into the urine. Serum haptoglobin concentration is increased in inflammatory conditionsas in rheumatic diseases and also in burns and nephritic syndrome.

  • Ceruloplasmin

It is a copper-containing α2-glycoprotein that has enzyme activities (i.e., copper oxidase, histaminase, and ferrous oxidase) and synthesized in the liver.
Low concentrations of ceruloplasmin at birth gradually increase to adult levels and slowly rise within age. Adult females have higher concentrations than do males, and pregnancy, inflammatory processes, malignancies, oral estrogen, and contraceptives caused an increased serum concentration.
Certain diseases or disorders are associated with low serum concentrations. In Wilson disease, an autosomal recessive inherited disease, the level may be low, 0.1 g/L, and the urinary excretion of copper is increased. The copper desposits in the skin, liver, and brain, resulting in degenerative cirrhosis and neurologic damage. Copper also desposits in the cornea, producing the characteristic Kayser-Fleischer rings. Low ceruloplasmin is also seen in malnutrition, malabsorption, and nephritic syndrome.

  • α2 –Macroglobulin

It is synthesized by hepatocytes. It can be found in lower concentrations in cerebrospinal fluid. The proteins reaches a maximum serum concentration at the age of 2 to 4 years and then decreases to abut one third of that at about 45 years.
     α2 –Macroglobulin inhibits proteases as trypsin, pepsin, and plasmin. In nephrosis, the level of serum α2 –Macroglobulin may increase as much as 10 times. The protein is also increased in diabetes and liver disease. Use of contraceptive medications and pregnancy increase the serum level by 20%.

  • Transferrin

It is the major protein in the β-globulin electrophoretic fraction. It is synthesized in the liver. The major functions of transferring are the transport of iron and the prevention of loss of iron through the kidney. Its binding of iron prevents iron deposition in the tissue during temporary increases in absorbed iron or free iron. Transferrin transports iron to its storage sites, where it is incorporated into another protein, apoferritin, to form ferritin. Transferrin also carries iron to cells such as bone marrow that synthesize hemoglobin and other iron-containing compounds.
Transferrin deficiencies lead to a hypochromic, mycrocytic anemia. In this type of anemia, transferring in serum is normal or increased. A decreased transferring level generally reflects an overall decrease in synthesis of protein. An increase of iron bound to trasferrin is found in a hereditary disorder of iron metabolism, hemochromatosis. This disorder is associated with bronze skin, cirrhosis, diabetes mellitus, and low plasma transferring levels.
4- Hemopexin
    The parernchymal cells of the liver synthezise hemopexin. The function of hemopexin is to remove circulating heme. When free heme is formed during the breakdown of hemoglobin, myoglobin, or catalase, it binds to hemopexin in a 1:1 ratio. The heme-hemopexin complex is carried to the liver, where the complex is destroyed. Hemopexin also removes ferri-heme and prophyrins.
    The level of hemopexin is very low at birth but reaches adult values within the first year of life. Pregnant mothers have increased plasma hemopexin levels. Increased concentrations are also found in diabetes mellitus, Duchenne muscular dystrophy, and some malignancies, especially melanomas. In hemolytic disorders, serum hemopexin concentrations decrease.
5- Complement
     Complement is a collective term for several proteins that participate in the immune reaction and serve as a link to the inflammatory response. These proteins circulate in the blood as nonfunctional precursors.
    Complement is able to enlist the participation of other humoral and cellular effector systems in the process of inflammation. It is increased in inflammatory states and decreased in malnutrition, lupus erythematosus, and disseminated intravascular coagulopathies. In most cases, the deficiencies are associated with recurrent infections.
6- Fibrinogen
    It is one of the largest proteins present in the blood plasma. It is synthesized in the liver and classified as a glycoprotein.
    The function of fibrinogen is to form a fibrin clot when activated by thrombine. Thus fibrinogen is virtually all removed in the clotting process and is not seen in serum.
    Fibrinogen is increased in plasma during the acute phase of inflammatory process. Fibrinogen levels also rise with pregnancy and the use of birth control pills. Decreased values generally reflect extensive coagulation during which the fibrinogen is consumed.
7- C-Reactive Protein (CRP)
     C-reactive protein (CRP) is a β-globulin that appears in the blood of patients with diverse inflammatory diseases but is undetectable in healty individuals. It is synthesized in the liver. CRP is elevated in acute rheumatoid arthritis, carcinomatosis, gout, and viral infections.
8- Immunoglobulins (Igُ s)
    There are five major groups of immunoglobulins in the serum. They are IgA, IgG, IgM, IgD, and IgE. They are synthesized in plasma cells. Their synthesis is stimulated by an immune response to foreign particles and microorganisms.
     IgG crosses the placenta, and the IgG present in the newborn’s serum is that synthesized by the mothers. IgM dose not cross the placenta and initially is 0.21g/L, but this increases rapidly to adult levels by about 6 months. IgA is lacking at birth, increases slowly to reach adult values at puberty, and continues to increases during the lifetime. IgD and IgE levels are undetectable at birth and increase slowly until adulthood.
     A marked increase in such a monoclonal Ig is found in the serum of patients who have plasma cell malignancy (myeloma).
     Increased IgM concentration is found in toxoplasmosis, cytomegalovirus, rubella, herpes, and syphilis and various bacterial and fungal diseases. Decreases are seen in protein-losting conditions and immunodeficiency disorders.

      Decreased IgD concentration is found in infections, liver disease, and connective tissue disorders.
9- Human Ventricular Myosin Light Chain (HVMLC)
    A specific human ventricular myosin light chain, HVMLC-1, is detectable in the serum within 30 minutes of the initial chest pain and confirms myocardial ischemia and acute angina. HVMLC-1 continues to be released in measurable quantities for more than 120 hours after chest pains. The quantities found in the serum are proportional to the severity of the cardiac damage.
3- Total Protein Abnormalities
1- Hyperproteinemia
     A total protein levels in serum is increased. It is found in dehydration when excess water is lost from the vascular system because of the size. Dehydration results from a variety of conditions, including vomiting, diarrhea, diabetic acidosis, and hypoaldosteronism. It is also may be due to excessive production of the gamma globulins.
2- Hypoproteinemia
    a- A total protein levels in serum is decreased. It may be lost by excretion in the urine in renal disease, leakage into the gastrointestinal tract in inflammation of the digestive system, and the loss of blood in open wounds or internal bleeding.
    b- It is also the result of decreased intake either because of deficiency of protein in the diet (malnutrition) or through intestinal malabsorption due to structural damage.
    c- It is also due to decreased synthesis as in liver disease or in inherited immunodeficiency disorders.
     d- Accelerated catabolism of proteins as in burns, trauma or other injuries may also the result of hypoproteinemia.
4-Clinical Correlations Of Glucose

Factors Determining Blood Glucose Level
      Under normal conditions of nutritional intake and balance, the blood glucose concentration of the adult is usually between 80 and 100 mg/dl. After a meal high in carbohydrate content, it may raise to 130 to 160 mg/dl.
      Hypoglycemia is defined as a fasting glucose level less than 80 mg/l due to numerous factors. Hypoglycemia can occurs as a response to fasting for 12 to 14 hours or because of some stimulus called reactive hypoglycemia. Hyperglycemia is that fasting glucose level above 100 mg/dl. Glucose is normally filtered by the kidney tubules, if the blood glucose concentration rise above the range 160 to 180 mg/dl, glucose appears in the urine, it is the renal threshold for glucose as in diabetes mellitus, glucosuria.
     It is the only hormone that produces decrease in blood glucose levels. It increases the uptake of glucose by muscle and fat cells by increasing the cellular membrane permeability to glucose. It also increases the uptake of glucose by liver, promoting glycogenesis and lipogenesis, formation of fat from carbohydrates. Insulin also inhibits the hepatic output of glucose into the general circulation.
     It is produced by the beta cells of the islets of Langerhans in the pancreas. Insulin is synthesized from a precursor called proinsulin which is broken within the pancreatic beta cells into equimolar amounts of insulin and C-peptide. If the patient has elevated serum levels of insulin due to hyperinsulinism, excessive secretion of insulin from the pancreas, the serum C-peptide level also will be elevated.
2- Glucagon
     It is secreted from the alpha cells of the pancreas. It stimulates (1) the breakdown of liver glycogen, (2) liver glyconeogenesis, and (3) hepatic lipolysis, thus the blood glucose levels rise.
3- Epinephrine
     It is secreted by the adrenal medulla. By activating the enzyme adenylate cyclase, epinephrine increases the synthesis of cyclic 3́5́-AMP in a number of body tissues. It leads to the activation of phosphorylase in hepatic cells and thus to increased breakdown of glycogen and elevation of blood glucose levels.
4- Growth Hormone and Adrenocorticotropic Hormone (ACTH)
     It inhibits glucose uptake and increases hepatic glucose output because of its antagonistic action on insulin. It also inhibits lipogenesis from carbohydrates and causes free fatty acids to be released from fat tissues. It is secreted from the anterior pituitary.
     ACTC action is similar to that of growth hormone. It is secreted from the anterior pituitary.
5- Glucocorticoids
    The secretion of these hormones from the adrenal cortex inhibits glucose metabolism in peripheral tissues. They elevate blood glucose and increase formation of liver glycogen. They are antagonistic to insulin action and may cause a state of secondary diabetes mellitus.


6- Thyroid Hormones
     They are T3, triiodothyronine and T4, thyroxine which are secreted from the thyroid gland. They increase absorption of glucose from the gastrointestinal tract and stimulate glycogenolysis. They may accelerate the degradation of insulin. The action of these two hormones is hyperglycemic. A person diagnosed as having hyperthyroidism may have symptoms of mild diabetes.
Diabetes Mellitus
     Diabetes mellitus may be defined as a genetically heterogeneous group of disorders manifested by insulin deficiency and loss of carbohydrate tolerance. Two general classifications of idiopathic diabetes mellitus have been identified: (type1) insulin-dependent diabetes mellitus (IDDM) and (type2) non-insulin-dependent diabetes mellitus (NIDDM). In the past, IDDM was termed juvenile diabetes. NIDDM was classified as maturity-onest diabetes.
     IDDM may begin with a 1 or 2 week progressive polyuria and polydipsia, weight loss, irritability, respiratory infection, and a carving for sweet beverages. If undiagnosed, the person will develop nausea, vomiting, dehydration, stuper, coma and, finally death. Treatment with insulin is required for IDDM.
      NIDDM is a milder disease and the diagnosis may occur by finding hyperglycemia, glucose intolerance, or glucosuria. NIDDM can usually be treated with weight reduction, dietary restrictions, or oral hypoglycemic medications.
       In uncontrolled diabetes mellitus, the excessive hydrogen ions liberated from the ketoacids must be buffered by the bicarbonate-carbonic acid buffering system, resulting in the formation of water and carbon dioxide.
5-Liver Function
Excretory and secretory function
    Bile is composed of bile acids or salts, bile pigments, cholesterol;, and other substances extracted from the blood. Total bile production averages about 3L per day, although only 1L is excreted.
    Bilirubin is transported to the liver in the blood stream bound to proteins, cheiflr albumin. It is then separated from the albumin and taken up by the hepatic cells. The conjugation of bilirubin takes place in the endoplasmic reticulum of the hepatocyte. Conjugated bilirubin is secreted from the hepatic ceels into the bile canaliculi and then passes along with the rest of the bile into larger bile ducts and into the intestines.
    A total of 200 to 300 mg of bilirubin is produced daily in the healthy adult. A normally functioning liver is required to eliminate this amount of bilirubin from the body in the feces and a small amount of the colorless product uroblinigen is excreted in the urine. Under theses normal conditions, a low concentration of bilirubin is found in the serum, 0.2-1.0 mg/dL. A small percentage of this total bilirubin exists in normal serum as the conjugated form, 0.2 mg/dL.
Disorders Of The Liver

  1. Jundice

    Jundice  refers to the yellowish discoloration of the skin and sclerae resulting from hyperbilirubinemia. Although the upper limit of mormal for total serum bilirubin is 1 mg/dL, jaundice is not clinically appearent until the bilirubin level exceeds 2 to 3 mg/dL. In black or Oriental patients, yellowing of the sclerae may be the only clinical evidence of jaundice.
    Except in infants, hyperbilirubinemia is generally well tolerated and dose not produce serious clinical side effects. Hyperbilirubinemia levels in infants exceeding 15-20 mg/dL.
    While the majority of cases of jaundice are associated with liver disorders, hyperbilirubinemia may also result from erythrocyte destruction, or hemolysis, in patients with normal liver function.
2- Cirrhosis
     Cirrhosis is derived from the Greek word that means "yellow", refers to the irreversible scarring process by which normal liver architecture is transformed into abnormal nodular architecture.
     Other causes of cirrhosis include hemochromatosis, postnecrotic cirrhosis, and primary biliary cirrhosis. Portal hypertension results when the blood flow through the portal vein is obstructed by the cirrhotic liver. The synthetic ability of the liver is reduced, causing hypoalbuminemia and deficiency of the clotting factors, which may lead to hemorrhage.
3- Tumors of the Liver
     Primary malignant tumors of the liver, known as hepatocellular carcinoma, hepatocarcinoma or hepatoma, are an important cause of cancer mortality. Most cases of hepatocellular carcinoma can be related to previous infection with a hepatitis virus. Generally, the only hope for cure relies in surgical resection, which is not usually possible. Patients with malignancies of the liver usually have a survival measured in months.
4- Reyeُs Syndrome
     It is a disorder of unknown cause involving the liver. It is a form of hepatic destruction that usually occurs following recovery form a vital infection such as varicella or influenza. Shortly after the infection, the patient develops neurologic abnormalities, which may include seizures or coma. Liver functions are always abnormal, but the bilirubin level is not usually elevated. Without treatment, rapid clinical deterioration leading to death may occur.
5- Drug- and Alcohol-Related Disorders
     Many drugs or chemicals are toxic to the liver. Of all hepatic toxins, the most important is ethanol. In small amounts, alcohol may cause mild, inapparent injury. Heavier consumption leads to more serious damage, and prolonged heavy use may lead to cirrhosis.
      Certain drugs, including tranquilizers such as phenothiazines, certain antibiotics, antineoplastic agents, and anti-inflammatory drugs, may cause liver injury.
       One of the most common drugs associated with serious hepatic injury is acetaminophen. This drug, when taken in massive overdose, produce fatal hepatic necrosis.
Enzymes in Liver Disease
      Any injury to the liver that results in cytolysis and necrosis causes the liberation of various enzymes. The measurement of these hepatic enzymes in the serum is used to assess the extent of liver damage and to differentiate hepatocellular from obstructive disease.
     The most common enzymes assayed in hepatobiliary disease include alkaline phosphatase and the aminotransferases.
1- Alkaline Phosphatase (ALP)
     It is found in a number of tissues but is used most often in the clinical diagnosis of bone and liver disease. Slight to moderate increases in alkaline phosphatase activity occur in many patient with hepatocellular disorders as hepatitis and cirrhosis, and transient increases may occur in all types of liver disease. The most striking elevations occur in extrahepatic biliary obstruction, as a stone in the common bile duct, or intrahepatic cholestasis, as drug cholestasis or primary biliary cirrhosis. This enzme may be the only abnormality or routine liver function tests. Since bone is a source of the enzyme, Pagetُs disease, bony metastases, and other disease associated with increased osteoplastic activity may produce high levels of alkaline phosphatase in the absence of liver disease. The enzyme is found in placenta, and pregnant women also have elevated levels.
2- Aminotransferases (Transaminases)
     Aspartate aminotransferase (AST), or glutamate oxaloacetic transaminase (GOT), and alanine aminotransferase (ALT), or glutamate pyruvate transaminase (GPT), are two enzymes used to assess hepatocellular damage. AST is found in all tissues, especially in the heart, liver, and skeletal muscle. ALT is present in the liver and in the kidney and in skeletal muscle.
3- 5́-Nucleotidase
     It is elevated in liver disease and in primary bone disease. It is used clinically to determine an elevation of the alkaline phosphatase.It is synthesizes in the liver.
6- γ-Glutamyl Transpeptidase (GGT)
     It is found in high concentrations in the kidney and the liver and is elevated in the serum of most all patients with hepatobiliary disorders. It is not specific for any type of liver disease but is the first abnormal liver function test demonstrated in the serum of heavy drinkers.
7- Ornithine Carbamyl Transferase (OCT)  
     It is a urea cycle enzyme present only in liver and intestinal tissue. Elevated levels of this enzyme occurs primary in liver disease but are not specific for any type of liver disease.
8- Leucine Aminopeptidase
     It is widely distributed in human tissues and is found in the pancreas, gastric mucosa, liver, spleen, large intestine, brain, small intestine, and kidney. The serum activity of leucine aminopeptidase can not be used to differentiate hepatocelleular from obstructive jaundice.
9- Lactate Dehydrogenase (LD)
     It is present in all organs and released into the serum from a variety of tissue injuries. Moderate elevations of total serum LD levels are common in acute viral hepatitis and in cirrhosis. High serum levels may be found in metastatic carcinoma of the liver.
6- Clinical Correlations of the Kidney
      Disorders or diseases that damage the renal glomeruli may exhibit normal tubular function. With time, disease progression involves the renal tubules as well.
1- Acute Glomerulonephritis
        Pathologic lesions involve large, inflamed g;omeruli with a decreased capillary lumen, hematuria and proteinuria. A decreased Glomerular Filtrate Rate GFR, anemia, elevated BUN and serum creatinie, oliguria, Na+ and water retention and sometimes congestive heart failure CHF.
        It is related to recent infection by group Aβ-hemolytic streptococci. Circulating immune complexes trigger a strong inflammatory response in the glomerular basement membrane, resulting in a direct injury to the glomerulus itself.
2- Chronic Glomerulonephritis
         It is caused from renal disease or from an idiopathic cause, may lead to glomerular scarirng and the eventual loss of operational nephroms. Slight proteinuria and hematuria are observed. Gradual development of uremia may sometimes the first sign of this process.
3- Nephrotic Syndrome
     An abnormally increased permeability of the glomerular basement membrane, massavie proteinuria, >2-3.5 g/day and even up to 20 g/day, resultant hypoalbuminuria, edema due to the movement of body fluids out of the vascular and into the intestinal spaces, hyperlipidemia and lipiduria.
4- Tubular Diseases
     Tubular defects occur to a certain extent in the progression of all renal diseases as the Glomerular Filtrate Rate (GFR) falls. Decreased excretion and reabsorption of certain substances and or reduced urinary concentrating capability. Clinically, the most important defect is the primary tubular disorder affecting acid-base balance: renal tubular acidosis.
      Acute inflammation of the tubules may occur as a result of radiation toxicity, methicillin hypersensitivity reactions, renal transplant rejection, and viral-fungal-bacterial infections. In theses cases, decrease in GFR, urinary concentrating ability, and metabolic acid excretion; the presence of leukocyte casts in the urine; inappropriate control of Na+ balance.
5- Urinary Tract Infection/ Obstruction
a- Infection
     The site of infection may be either in the kidneys themselves or in the urinary bladder. In general, a microbiologic colony count of greater than 105 colonies /ml is considered diagnostic for infection in either locale.,Bacteruria, hematuria and pyuria are all frequently encountered abnormal laboratory results in these cases. In particular, the presence of white blood cell (leukocyte) casts in the urine is considered diagnostic for pyelonephritis.
b- Obstruction
     Renal obstructions cause disease in one of two ways. They may be either gradually raise the intratubular preesure until nephrons necrose and chronic renal failure ensuses, or they may predispose the urinary tract to repeated infections.
      Obstractions may be located in either the proximal or distal urinary tract. Causes of obstractions include neoplasias such as prostate / bladder carcinoma or lymph node tumors constricting uterus, acquired diseases as uretheral strictures or renal calculi, and congenital deformities of the lower urinary tract. The clinical symptoms of obstructive disease are: decreased urinary concentrating capability seen first, succeeded by diminished metabolic acid excretion, decreased GFR, and reduced renal blood flow.
6- Renal Calculi
     Renal calculi termed kidney stones, are formed by the combination of a variety of crystallized substances as calcium osalate, magnesium ammonium phosphate, calcium phosphate, uric acid and cystine. It is currently believed that recurrence of calculi in susceptible individuals is due to complex mixture of causes. Reduced urine flow rate and saturation of the urine with large amounts of essentially insoluble substances. Clinical symptoms are similar to those encountered in other obstructive processes: hematuria, urinary tract infections, and "renal colic".
7- Renal Failure
a- Acute Renal Failure
     It is defined as a sudden, sharp decline in renal operation due to an acute toxic or hypoxic insult to the kidneys. The GFR is reduced to less than 10 ml / minute. In primary renal failure, the defect invloves the kidney itself. The most common cause is acute tubular necrosis; other etiologies include vascular obstruction/ inflammations and glomerulonephritis.
     The most commonly observed symptoms of acute renal failure are oliguria and anuria, < 400 ml/ day. The diminished ability to excrete electrolytes and water results in a marked increase in extracellular fluid volume, leading to peripheral edema, and hypertension. If more water is retained than Na+, hyponatremia may develop, central nervous system effects are seen, coma, and death. The hyperkalemia also may become severe enough to cause dangerous cardiac arrhythmias. In addition, variable amounts of erythrocytic casts, hematuria, proteinuria, and metabolic acidosis are seen.
b- Chronic Renal Failure
     It is a clinical syndrome that occurs when there is a gradual decline in renal operation over time. Chronic renal failure is classified into four progressive stages. The first stage is marked by a period of silent deterioration in renal status, kidney function decreases, but BUN and creatinine values stay within normal limits. The second stage is characterized by development of a slight renal insufficiency, a 50% reduction in normal functioning before the BUN and creatinine values increasing above reference ranges. The third stage is typified by impending renal failure, anemia begins to develop, and systemic acidosis commences. The fourth and last stage commences with the onest of the classic symptoms of the uremic syndrome.

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