Results 1 to 2 of 2

Thread: [Laboratory] Serum Uric Acid

  1. #1
    PharmD Year 1 TomHsiung's Avatar
    Join Date
    Jan 2013
    Location
    Chengdu, Sichuan, China
    Posts
    594

    Default [Laboratory] Serum Uric Acid

    Reference range:
    Males > 17 yrs of age, 4.0 - 8.5 mg/dL (237 - 506 umol/L)
    Females > 17 yrs of age, 2.7 - 7.3 mg/dL (161 - 434 umol/L)

    Uric acid is the metabolic end-product of the purine bases of DNA. In humans, uric acid is not metabolized further and is eliminated unchanged by renal excretion. It is completely filtered at the renal glomerulus and is almost completely reabsorbed. Most excreted uric acid (80% to 86%) is the result of active tubular secretion at the distal end of the proximal convoluted tubule.

    As urine becomes more alkaline, more uric acid is excreted because the percentage of ionized uric acid molecules increases. Conversely, reabsorption of uric acid within the proximal tubule is enhanced and uric acid excretion is suppressed as urine becomes more acidic.

    In plasma at normal body temperature, the physicochemical saturation concentration for rate is 7 mg/dL. However, plasma can become supersaturated, with the concentration exceeding 12 mg/dL (711 umol/L). In nongouty subjects with normal renal function, urine uric acid excretion abruptly increases when the serum uric acid concentration approaches or exceeds 11 mg/dL (652 umol/L). At this concentration, urine uric acid excretion usually exceeds 1000 mg/24 hr.
    Last edited by TomHsiung; Wed 15th March '17 at 10:44pm.
    B.S. Pharm, West China School of Pharmacy, Class of 2007, Health System Pharmacist, RPh. Hematology, Infectious Disease.

  2. #2
    PharmD Year 1 TomHsiung's Avatar
    Join Date
    Jan 2013
    Location
    Chengdu, Sichuan, China
    Posts
    594

    Default Re: [Laboratory] Serum Uric Acid

    Hyperuricemia
    When serum uric acid exceeds the upper limit of the reference range, the biochemical diagnosis of hyperuricemia can be made. Hyperuricemia can result from an overproduction of purines and/or reduced renal clearance of uric acid. When specific factors affecting the normal disposition of uric acid cannot be identified, the problem is diagnosed as primary hyperuricemia. When specific factors can be identified (e.g., another disease or drug therapy), the problem is referred to as secondary hyperuricemia.

    As the serum rate concentration increases above the upper limit of the reference range, the risk of developing clinical signs and symptoms of gouty arthritis, renal stones, uric acid nephropathy, and subcutaneous tophaceous deposits increases. However, many hyperuricemic patients are asymptomatic. If a patient is hyperuricemic, it is important to determine if there are potential causes of false laboratory test elevation and contributing extrinsic factors. In general, clinical studies have not shown that impaired renal function is caused by chronic hyperuricemia (unless there are other renal risk factors and excluding acute uric acid nephropathy resulting from tumor lysis syndrome). However, long-term, very high serum uric acid levels (e.g., >=13 mg/dL [770 umol/L] in men and 10 mg/dL [593 umol/L] in women) may predispose individuals to renal dysfunction. This level of hyperuricemia is uncommon, and a conclusive link to renal insufficiency has not been established. Also, renal disease accompanying hyperuricemia is often related to uncontrolled hypertension. Correction of hyperuricemia has no measurable effect on renal function.

    Exogenous causes
    Medications are the most common exogenous causes of hyperuricemia. The two primary mechanisms whereby drugs increase serum uric acid concentrations are 1) decreased renal excretion resulting from drug-induced renal dysfunction or competition with uric acid for secretion within the kidney tubules, and 2) rapid destruction of large numbers of cells from anti-neoplastic therapy for leukemias and lymphomas.

    Diet is another exogenous cause of hyperuricemia. High-protein weight-reduction programs can greatly increase the amount of ingested purines and subsequent uric acid production. If the average daily diet contains a high proportion of meats, the excess nucleoprotein intake can lead to increased uric acid production. Fasting or starvation also can cause hkyperuricemia because of increased muscle catabolism. Furthermore, lead poisoning from paint, batteries, or "moonshine," in addition to recent alcohol ingestion, obesity, diabetes mellitus, and hypertriglyceridemia, is associated with increases in serum uric acid concentration.

    Endogenous causes
    Endogenous causes of hyperuricemia include diseases, abnormal physiological conditions that may or may not be disease related, and genetic abnormalities.

    Diseases include 1) renal diseases (e.g., renal failure); 2) disorders associated with increased destruction of nucleoproteins (e.g., leukemia, lymphoma, polycythemia, hemolytic anemia, sickle cell anemia, toxemia of pregnancy, and psoriasis); and 3) endocrine abnormalities (e.g., hypothyroidism, hypoparathyroidism, pseudohypoparathyroidism, nephrogenic diabetes insidious, and Addision disease).

    Predisposing abnormal physiological conditions include shock, hypoxia, lactic acidosis, diabetic ketoacidosis, alcoholic ketosis, and strenuous muscular exercise. In addition, males and females are at risk of developing asymptomatic hyperuricemia at puberty and menopause, respectively.

    Genetic abnormalities include Lesch-Nyhan syndrome, gout with partial absence of the enzyme hypoxanthine guanine phosphoribosyl-transferase, increased phosphoribosyl pyrophosphate P-ribose-PP synthetase, and glycogen storage disease type I.
    Last edited by TomHsiung; Wed 15th March '17 at 11:10pm.
    B.S. Pharm, West China School of Pharmacy, Class of 2007, Health System Pharmacist, RPh. Hematology, Infectious Disease.

Posting Permissions

  • You may not post new threads
  • You may not post replies
  • You may not post attachments
  • You may not edit your posts
  •