TERNOPIL STATE MEDICAL UNIVERSITY UKRAINE

DEPARTMENT OF INTERNAL MEDICINE (HEMATOLOGY)

A PRESENTATION ON GOUTY ARTHRITIS ASSOCIATED WITH KIDNEY

FAILURE BYDR JOSEPH UCHENNA VICTOR

GROUP 5 4TH COURSE

GOUTY ARTHRITIS

ASSOCIATED WITH

KIDNEY FAILURE

INTRODUCTIONETIOLOGYCAUSES AND SYMPTOMSDIAGNOSISDIFFERENTIAL DIAGNOSISTREATMENTCONCLUSION

INTRODUCTIONGouty arthritis refers to a form of arthritis caused by deposits of needle-like crystals of uric acid, usually strikes a single joint, most commonly the big toe (about 75% of people are affected at least once), however, it can also affect thefoot (instep/heel), ankles, knees, wrists, fingers, elbowsGouty arthritis is rare in children and young adults. Men are more likely to develop gouty arthritis than women.The main cause of development of gout is deposition of uric acid crystals in the synovial fluid and synovial lining of joints.

Gout may occur alone (primary gout) or may be associated with other medical conditions or medications (secondary gout). Gout results when crystals of uric acid form in tissues of the body. Gout is characterized by an overload of uric acid in the body and recurring attacks of joint inflammation (arthritis). Chronic gout can lead not only arthritis, but hard lumps of uric acid in and around the joints, decreased kidney function, and kidney stones. Gouty arthritis is usually an extremely painful attack with a rapid onset of joint inflammation. The inflammation is precipitated by the deposition of uric acid crystals in the lining of the joint (synovial lining) and the fluid within the joint. Intense joint inflammation occurs when white blood cells engulf the crystals of uric acid and release chemicals that promote inflammation. The resulting inflammation causes pain, heat, and redness of the joint.

CAUSES SYMPTOM RISk FACTOR FOR (Gouty Arthritis) This disease causes the inflammation, pain, redness and tenderness of the joints of big toe, ankles, knees, feet, wrists and hands. Higher levels of uric acid, obesity, exposure to lead in the environment, high intake of food containing purines, high alcohol intake and abnormal kidney function are the major risk factors for gout (gouty arthritis). People with impaired excretion of uric acid or increased production of uric acid have high risk for development of gout. Elevated uric acid levels may be associated with obesity, age, diabetes mellitus, type IV hyperlipidaemia, hypertension and coronary heart diseases. Besides this, certain conditions like joint injury, dehydration, excessive dining, fever, recent surgery and heavy alcohol intake are considered as the risk factors for gout (gouty arthritis

Patients with impaired renal function or kidney failure are more susceptible to gout. Uric acid present in normal amounts gets dissolved in the blood and easily passes through the kidneys. But due to kidney dysfunction, there is increase in uric acid levels in the blood which may result in formation of crystals of uric acid. These uric acid crystals get accumulated in the synovial fluid and lining and cause inflammation of joints.A person with medications like aspirin, levodopa and diuretics is more prone to gout as these medications can interfere with the ability of body to remove uric acid. Besides that, the medications like cyclosporine used to suppress the immune system of the body after organ transplant, can increase the risk for developing this disease.Intake of foods containing large amounts of uric acid such as red meats and internal organs like kidneys and liver, anchovies and some shellfish can lead to raised levels of uric acid and development of gout. Excessive intake of alcohol is associated with gout in young people.

Certain medical conditions like rapid weight loss, chronic kidney disease, high blood pressure, hypothyroidism, surgery and conditions like multiple myeloma, psoriasis, tumors or hemolytic anemia are also significant risk factors for gout (gouty arthritis). People with Lesch-Nyhan syndrome or Kelley-Seegmiller syndrome may have deficiency of enzyme that controls the uric acid levels. Such people have a greater risk of developing gouty arthritis.In addition to that, heredity, age and gender significantly contribute in development of gout. Usually, men are commonly affected by gout than women. Men in the middle age with high blood pressure, obesity, heavy alcohol intake and unhealthy cholesterol levels are more susceptible to this disorder.

DIAGNOSIS Joint aspiration: This is the most important diagnostic test. It is the ultimate method of being certain of a diagnosis of gouty arthritis, as opposed to other causes such as an infection in the joint. Blood tests:Your doctor may obtain a blood sample to look at your cell counts, uric acid levels, kidney function, etc. Radiographs:X-rays are primarily used to assess underlying joint damage, especially in those who have had multiple episodes of gouty arthritis.

DIFFERENTIAL DIAGNOSISDiagnostic ConsiderationsThe history and physical examination alone cannot reliably determine the cause of new-onset acute monoarticular arthritis. Septic arthritis, gout, and pseudogout can present in very similar ways.Certain clinical presentations are so characteristic of gout that attempts have been made to accurately diagnose or exclude gout without joint aspiration. Male sexPrevious arthritis attackOnset within 1 dayJoint rednessFirst metatarsophalangeal joint involvementHypertension or one or more cardiovascular diseasesA serum uric acid level of more than 5.88 mg/dL

Arthritis as a Manifestation of Systemic DiseaseBursitisCellulitisChondrocalcinosisHyperparathyroidismNephrolithiasisParonychiaRheumatoid ArthritisSeptic ArthritisTenosynovitis

TREATMENT Nonsteroidal anti-inflammatory drugs (NSAIDs) Examples include indomethacin(Indocin), ibuprofen (Advil), andnaproxen (Aleve). Newer drugs such ascelecoxib (Celebrex) can also be used. Aspirin should not be used for this condition.High doses of anti-inflammatory medications are needed to control the inflammation and can be tapered off within a couple of weeks.

Colchicine (Colcry)This medication is given in two different ways, either to treat the acute attack of arthritis or to prevent recurring attacksTo treat the hot, swollen joint, colchicine is given rapidly (generally, two tablets at once followed by another tablet an hour later).To help prevent an attack from coming back, colchicine can be given once or twice a day. While the chronic use of colchicine can reduce the attacks of gout, it does not prevent the accumulation of uric acid that can lead to joint damage even without attacks of hot, swollen joints.Tell your doctor if you have any problems with your kidney or liver function.

CorticosteroidsCorticosteroids such as prednisone (Meticorten, Sterapred, Sterapred DS) are generally given when your doctor feels this is a safer approach than using NSAIDs.When given by mouth, high-dose corticosteroids are used initially and tapered off within a couple of weeks. It is important to take these medications as prescribed to avoid problems.Some complications with the short-term use of corticosteroids include altered mood, elevated blood pressure, and problems with control of glucose in patients with diabetesCorticosteroids can also be injected into the swollen joint. Resting the joint temporarily, after it is injected with steroids, can be helpful.Occasionally, corticosteroids or a related compound, corticotropin(ACTH), can also be injected into the muscle or given intravenously.

CONCLUSION In this study a high prevalence of CKD was observed among gout patients. Serum uric acid goal attainment was low among patients treated with allopurinol, and poorest among those with CKD. The

findings suggest that poor outcomes among gout patients with CKD are partly due to clinicians' reluctance to prescribe higher doses of

allopurinol to patients with impaired renal function. The benefits and risks of allopurinol treatment must be weighed carefully in patients

with CKD, and alternate treatment approaches are needed to improve the prognosis of these patients. Future research should address at

least three additional issues: (1) the role of non-oxypurinol metabolites of allopurinol in efficacy and toxicity, (2) more

sophisticated pharmacogenomics-based studies of allopurinol dosing in the presence of CKD, and (3) development of urate-lowering drugs

that are not renally cleared. Additionally, our results suggest a need to raise awareness among physicians regarding the importance of

titrating therapy to reach uric acid goals.