Uric acid crystals in white blood cells in synovial fluid

Introduction There is uric acid crystals in leukocytes in joint fluid, which is one of the diagnostic criteria for gout. Hyperuricemia, also known as gout, is a group of diseases caused by dysbial metabolic disorders. Its clinical features are hyperuricemia and the resulting recurrent gouty acute arthritis, gout deposition gout. Stoney chronic arthritis and joint deformities often involve the formation of chronic interstitial nephritis and uric acid kidney stones in the kidney. The disease can be divided into two major types of primary and secondary primary causes, except for a small number of enzyme defects, most of which are not elucidated, often accompanied by hyperlipidemia, diabetes, hypertension, arteriosclerosis and coronary heart disease. Is a hereditary disease. Secondary people can be caused by a variety of causes such as kidney disease blood diseases and drugs.

Cause

The cause of uric acid nephropathy and gout nephropathy is an increase in blood and/or urinary uric acid concentration, and many factors that increase persistent uric acid concentration are:

1. Increased uric acid production

(1) Genetic factors: enzyme gene mutations, such as hypoxanthine-guanine phosphoribosyltransferase deficiency.

(2) Acquired factors: abnormal myeloid hyperplasia, sorghum intake, obesity and hypertriglyceridemia, high dietary fructose content, high alcohol content in beverages, exercise.

2. Reduced uric acid excretion

(1) Genetic factors: uric acid excretion or excretion score reduction.

(2) Acquired factors: drugs such as thiazide diuretics, salicylates, metabolites such as lactic acid, ketone bodies, angiotensin and vasopressin, plasma volume reduction, hypertension and obesity.

3. Excessive endogenous uric acid production

Uric acid is the end product of sputum metabolism. Uric acid is antimony trioxide, a nucleic acid and other terpenoids that are mainly metabolized by cells. The decomposition of enzymes in food produces uric acid. The cause of excessive endogenous uric acid production is hypoxia, guanine ribose conversion enzyme (HGPRT) activity, phosphoribosyl pyrophosphate amide transferase (PRPP) and hypoxanthine, xanthine (XO) activity High is the most important. In the absence of HGPRT, jaundice and guanine cannot produce corresponding nucleotides, and a large amount of hypoxanthine in the body is converted into uric acid. Increased PRPP synthase activity increases intracellular PRPP, a key enzyme in the conversion of hydrazine to uric acid, which ultimately increases uric acid production. XO converts hypoxanthine to xanthine and xanthine to form uric acid.

4. Uric acid excretion disorder

Uric acid has no physiological function in the body. Under physiological conditions, 2/3 to 3/4 of uric acid is excreted by the kidneys, and the rest is excreted by the intestines, and intestinal mucosal cells are secreted into the intestine. Intestinal bacteria contain uricase, which is broken down into water and ammonia, so it is not uric acid that is excreted in the feces. When the renal function is incomplete, the discharge from the intestine is slightly increased. The uric acid filtered from the glomerulus is almost completely reabsorbed by the proximal tubule. The uric acid in the urine is secreted by the renal tubule. It has been confirmed that the renal tubule secretes uric acid, and the renal tubule can be reabsorbed again. Renal excretion is an important part of regulating blood uric acid concentration. The factors that affect kidney excretion of uric acid are as follows:

(1) In the early stage of chronic renal insufficiency, there is a compensation for a healthy nephron. The increase in uric acid concentration is not significant, and is inconsistent with the decrease in glomerular filtration rate. When GFR <10 ml/min, significant hyperuricemia is produced. In patients with essential hypertension, hyperuricemia is caused by impaired treatment of sodium by proximal convoluted tubules or renal tubular uric acid excretion caused by early renal vascular disease.

(2) When the blood volume is reduced, such as limiting sodium intake, diuretic use and polyuria, the uric acid clearance rate is lowered. When the blood volume is reduced and the urine flow rate is less than 1 ml/min, uric acid accumulates in the proximal tubule S3 segment beyond the concentration of capillaries around the renal tubule, and a back-diffusion phenomenon may occur. Conversely, sodium salt load, antidiuretic hormone secretion increased blood volume, and uric acid clearance increased.

(3) Organic acids affect the excretion of uric acid by renal tubules: organic acids are excreted from the body by means of a renal tubular anion pump, which competes with uric acid at this time; or because of the accumulation of organic acids in the proximal tubules, the metabolic disorder limits uric acid Secretion. Increased organic acids are found in severe metabolic disorders such as alcoholism, strenuous exercise lactic acid accumulation, and diabetic ketoacidosis.

(4) Diuretics, anti-tuberculosis drugs, aspirin, catecholamines, etc. can affect the excretion of uric acid: diuretic drugs reduce renal tubular secretion of uric acid or increase its reabsorption, it is still unclear. Antituberculosis drugs such as ethambutol and pyrazinamide inhibit the secretion of uric acid from the renal tubules. A small dose of aspirin inhibits the secretion of uric acid from the renal tubules. When the dose is increased to 2 to 3 g, it can inhibit the reabsorption of uric acid by the renal tubules and remove the uric acid. Catecholamine affects renal blood flow and reduces the effects of uric acid.

(5) Lead can inhibit the secretion of uric acid by renal tubules: chronic lead poisoning, uric acid clearance rate decreased compared with creatinine clearance rate is obvious.

an examination

Related inspection

Joint cavity fluid examination

1. General laboratory test

(1) uric acid test: blood uric acid level increased, male is higher than 416mol / L, female is higher than 357mol / L. Urinary uric acid level is affected by many factors, and its clinical significance is not significant, but it has certain significance in identifying excessive uric acid production or reducing excretion: lower than 600mg/24 hours after 5 days of low-grade diet or 1000mg/24 hours or less of normal diet is uric acid cut back. At the same time should pay attention to serum creatinine, blood lipids and blood sugar.

(2) Renal function test: urine PH value.

2. Special inspection

(1) Synovial fluid: When an acute attack occurs, the synovial fluid is examined, and the sodium acicular sodium urate crystals in the white blood cells are visualized under an optical and polarized light microscope. The increase in neutrophils is usually (5 to 75) × 10 ⁹ /L, and even as high as 1000 × 10 ⁹ /L.

(2) Synovial biopsy of the joint: Confirmation of the presence of urate crystals.

3. X-ray inspection

(1) Early stage: visible soft tissue swelling, after repeated episodes, the edge of the articular cartilage may gradually appear, the articular surface is irregular, the joint space is narrow, the tophi is deposited, and the bone is worn and cut, like insect eclipse.

(2) Abdominal plain film test: There are no urinary stones.

4. Double kidney B ultrasound

Showing kidney stones, the simple uric acid stone X-ray is not developed.

Differential diagnosis

1. Primary glomerulopathy, the following points help to differentiate the diagnosis:

(1) Serum uric acid rise in uric acid nephropathy is significantly higher than urea nitrogen and creatinine, and blood uric acid/creatinine is >2.5 (in mg/dl).

(2) gout nephropathy arthritis is obvious, frequent attacks, even if there is hyperuricemia in primary glomerulopathy, arthritis rarely occurs, which may be due to its small response to uric acid.

(3) The history of uric acid nephropathy is long, usually only the renal tubular function is impaired; while the glomerular function is less damaged, and the renal function is slow.

(4) Gout stone only appears in primary gout.

(5) Renal biopsy tissue can be seen under polarized light microscopy uric acid crystal can establish the diagnosis of uric acid nephropathy. However, because the urate deposition is mainly in the deep part of the renal tissue, the puncture of the kidney tissue is often insufficient in depth and it is difficult to obtain the diseased tissue.

2. Chronic renal insufficiency, even if there is hyperuricemia in this disease, the possibility of uric acid crystal deposition is very small, so there is no cortical-medullary gradient, and the sodium concentration in the medulla is decreased.

3. Other diseases that cause renal failure and hyperuricemia, such as acute renal failure caused by striated muscle sclerosing, acute pancreatitis, severe dehydration-induced pre-renal azotemia, lead poisoning, polycystic kidney disease, Analgesic nephropathy, obstructive nephropathy caused by bilateral hydronephrosis, familial nephropathy and medullary cyst disease, etc., can cause renal failure and uric acid increased significantly, these lesions are renal damage caused by tubulointerstitial, Should pay attention to the identification of uric acid nephropathy.

(1) There is uric acid crystals in leukocytes in joint fluid.

(2) Gout nodule needle aspiration or biopsy has sodium urate crystal.

(3) Those with more than 6 of the following 12 items can also be diagnosed (98% accuracy): more than one episode of acute arthritis. Single arthritis attack. The inflammation peaked within 1 day. The joints are congested and swollen. The first metatarsophalangeal joint is painful or swollen. Unilateral first metatarsophalangeal joint swelling and pain. Unilateral tibial joint lesions. Suspicious tophi. Serum uric acid levels are elevated. Asymmetric single joint pain. X-ray showed subcortical cystic changes without bone infiltration. During the onset of joint inflammation, the bacterial culture of the joint fluid was negative.

(4) typical single arthritis, followed by an asymptomatic intermittent period; after colchicine treatment, synovitis can be quickly relieved. Hyperuricemia exists at the same time. Any one of the above four items can be diagnosed.

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