Uric acid crystals

Introduction The uric acid crystals are similar to red sand fine particles under visual observation and are often deposited on the bottom of the urine container. Under the microscope, a yellow or dark reddish-colored diamond, a triangular shape, a rectangular shape, a rhomboidal crystal, and a solution soluble in sodium ammonia oxide can be seen. Uric acid is the terminal product of sputum metabolism in the body's nuclear protein. It is often excreted in the urine with uric acid or ammonium urate, calcium urate or sodium urate. Under normal circumstances, the viscera of the animal containing sorghum can be used in the urine. Increased uric acid, but in acute gout, acute fever in children, chronic interstitial nephritis, leukemia, due to massive decomposition of the nucleus, can also discharge Dali urate. High urate urine is also seen when the renal tubules are dysfunctional for reabsorption of uric acid.

Cause

1. Food: The high-quality seafood in the coastal areas with high content of glutinous glutinous rice has a high incidence. Just as in the "Thirty-sixth of the Chinese-Tibetan Scriptures", "the meat scorpion, the diet is not good, the cream is thick and thick, that is, the so-called "food product", and the accumulation is long, the water transport is dysfunctional and sipping, to its accumulation. It is elevated in uric acid in the vein; gouty arthritis is left in the joint, and urinary stones appear in the kidney. If it is not stained for a long time, it can cause renal failure.

2. Alcohol: All kinds of white wine, as well as beer and wine, contain a lot of cockroaches. Long-term or heavy drinking will increase the blood uric acid. Compared with the food product, it is more harmful, because the lactic acid produced by ethanol metabolism temporarily suppresses the excretion of uric acid by the renal tubule, thereby causing a greater increase in serum uric acid level. In Chinese medicine, it is believed that wine is a product that helps to get wet and damp. A lot of drinking causes excessive moisture and dampness. For a long time, it turns into damp heat, or stays in the limbs, or stagnates in the internal organs. For example, the "Zhongshangjing" has a cloud: "There are disadvantages of Zhulin urinating, all of which are unreasonable by the five filths, six sorrows, three squats, glory and loss, hot drinks, drunkenness into the house, exhausted spirits, labor and gas blood."

Uric acid is the end product of sputum metabolism and is present in blood and interstitial fluids, which are primarily in the form of sodium urate at pH 7.4. 2/3 of human uric acid is filtered through the glomerulus, excreted in the form of urate from the kidney, and the remaining 1/3 is decomposed into urea by intestinal bacteria, or further oxidized by uricase into a more soluble allantoin. . Abnormal metabolism of sputum leads to excessive production of uric acid and reduced excretion, and sputum causes hyperuricemia (greater than 330 mol? L??-1?). The pathological and clinical manifestations of uric acid and its salts in uric acid nephropathy deposited in the kidney. Excessive production of uric acid, in addition to the excessive production of terpenoids, the synthesis of terpenoids in the body through hypoxanthine transformation, there are still due to malignant tumors after chemical and radiotherapy, tissue nucleic acid decomposition and excessive intake of sorghum Food, increased exogenous sputum and excessive uric acid and hyperuricemia. The daily diet contains 600-1000 mg of strontium. Urinary acid excretion disorder is also one of the causes of hyperuricemia. In addition to glomerular filtration, uric acid is also involved in the reabsorption and secretion of uric acid, so in addition to idiopathic hyperuricemia, various kidneys Renal dysfunction caused by the disease causes damage to the function of filtering or secreting uric acid to form blood uric acid.

an examination

Related inspection

Urine routine uric acid serum uric acid kidney ultrasonography renal dynamic imaging

1. Extrarenal manifestations: arthritis, tophi, gout nodules, hyperlipidemia, hypertension and heart failure.

2. Renal damage: edema, proteinuria, hypertension, nocturia; kidney stones are manifested as low back pain, hematuria or frequent urination, urgency, dysuria and fever. There are two kinds of kidney damage in uric acid nephropathy: 1 forming urinary calculi; 2 causing renal parenchymal damage caused by uric acid. These two kinds of kidney damage can coexist at the same time, and their clinical manifestations are as follows:

(1) Chronic hyperuricemia: more common in men than middle-aged. Mostly accompanied by gouty arthritis or tophi; renal damage early manifested as mild proteinuria, a small amount of red blood cells and urinary concentrating function decline; late high blood pressure, renal dysfunction, a small number of uremia. Kidney activity can be seen in the medulla with radial needle-shaped uric acid crystals and chronic inflammation of the renal interstitial.

(2) acute uric acid nephropathy: acute onset, more common in bone marrow proliferative diseases and malignant tumors after radiotherapy and chemotherapy. The clinical manifestations are oliguria or even no urine, and a sharp deterioration of renal function (ie acute renal failure). A large amount of uric acid crystals and red blood cells can be seen in the urine. If left untreated, the condition continues to worsen and the patient eventually dies of kidney failure.

(3) uric acid stones: more asymptomatic, hematuria can occur, with or without renal colic, stones are translucent, abdominal plain film can not show, often through intravenous pyelography can be found. The urinary component is uric acid or a salt thereof.

Differential diagnosis

(1) Chronic hyperuricemia nephropathy (ie gout kidney):

1 gout performance: a history of long-term gout arthritis and gout nodules.

2 kidney performance: early back acid, polyuria and nocturia, may have mild to moderate proteinuria, hematuria and leukocyte urine, high blood pressure, renal dysfunction may occur later.

3 laboratory examination: red blood cells, white blood cells and uric acid crystals can be seen in the urine, the urine specific gravity is low, and blood uric acid is increased. Renal function: urinary enrichment decreased, and glomerular filtration rate decreased. X-ray examination: The X-ray of the affected joint showed a round or irregularly pierced translucent area of the bone. Renal biopsy: visible renal medulla has radial needle-shaped uric acid crystals and chronic inflammation of the renal interstitial.

(2) uric acid kidney stones:

1 more asymptomatic at the beginning, about 70% after the occurrence of hematuria, with or without urinary stones and renal colic, although most of the uric acid stones are small, but individual patients can also be large and prone to obstructive nephropathy and urinary tract infection.

2 laboratory examination: red blood cells and uric acid crystals can be seen in the urine, and white blood cells increase in the secondary infection. X-ray: urinary X-ray examination, the stones are light-transmissive and usually not developed. Qualitative analysis of urinary stones: The crystal component is uric acid or a salt thereof.

(3) acute hyperuricemia nephropathy:

1 acute illness, more common after bone marrow proliferative diseases or malignant tumors after radiotherapy, chemotherapy.

2 clinical features of oliguria, and even no urine and rapid development of azotemia. A large amount of uric acid crystals and red blood cells can be seen in the urine. If the treatment is not timely, the condition may worsen and die of kidney failure.

3 laboratory examination: blood uric acid increased significantly, can be as high as 1190mol / L ~ 2975mol / L, urea nitrogen, creatinine increased, increased blood potassium, blood carbon dioxide binding or pH value decreased.

How to diagnose and differentially diagnose uric acid nephropathy, middle-aged male patients with kidney disease, with joint disease and urolithiasis, should be suspected of this disease. Acidic urine, elevated blood uric acid, and urinary uric acid can be diagnosed.

The disease should be differentiated from hyperuricemia secondary to kidney disease. The main points of identification are as follows:

1 uric acid nephropathy serum uric acid increased significantly compared with urea nitrogen and creatinine, but uric acid / serum creatinine > 2.5.

2 gout nephropathy arthritis is obvious, primary glomerular disease rarely occurs in arthritis even with hyperuricemia.

3 uric acid nephropathy has a long history, usually with impaired renal tubular function, and glomerular dysfunction, and slow renal function decline. Renal biopsy can be diagnosed with bismuth uric acid crystals.

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