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    Home > Active Ingredient News > Immunology News > What is the cause and effect of high uric acid and kidney damage?

    What is the cause and effect of high uric acid and kidney damage?

    • Last Update: 2021-05-09
    • Source: Internet
    • Author: User
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    Come on, let's battle together!
    At the time of 4.
    20 Nationwide attention to gout day, in order to appeal to all people to pay attention to gout, and also for further academic discussion and exchanges, the Department of Rheumatology and Immunology and Nephrology, The Second Xiangya Hospital of Central South University, focused on "hyperuricemia and kidney damage, what is the cause? "There was a fierce debate, analyzing this issue from multiple angles.

    Introduction to the debater Orthodox view: Hyperuricemia is the cause of kidney damage, Qi Tang, Attending physician, Department of Rheumatology and Immunology, Second Xiangya Hospital, Central South University, Ling Guanghui, Associate Chief Physician, Department of Rheumatology and Immunology, Second Xiangya Hospital, Central South University, Opposite view: Hyperuricemia is The fruit of kidney damage: Chen Xiaojun, Attending Physician, Department of Nephrology, Second Xiangya Hospital, Central South University, Dr.
    Chen Guochun, Deputy Chief Physician, Department of Nephrology, Second Xiangya Hospital, Central South University, Dr.
    Tang Qi: Uric acid>540μmol/L, the risk of kidney injury is 3 times that of normal people!
    Dr.
    Tang Qi holds the orthodox view that hyperuricemia is the cause of kidney damage.

    Dr.
    Tang Qi hyperuricemia is closely related to kidney damage.
    When blood uric acid is slightly elevated, the risk of renal function damage is about twice that of normal people.
    When the blood uric acid level is greater than 540 μmol/L, kidney function is damaged.
    The risk is 3 times that of a normal person.

    Hyperuricemia can cause 3 types of kidney damage, chronic uric acid nephropathy, acute uric acid nephropathy, and uric acid kidney stones.

    Later, Dr.
    Tang Qi explained the mechanism of hyperuric acid damage from the following three aspects: direct damage of urate crystals, urate crystals can be directly deposited in the tubular interstitium, causing inflammation and fibrosis in the tubular interstitium.
    Lead to degeneration and atrophy of renal tubules.

    Hyperuricemia affects the hemodynamics of the kidney.
    Hyperuricemia can cause the proliferation of vascular smooth muscle cells, inhibit the proliferation of vascular endothelial cells, and activate local cyclooxygenase 2 (COX2) and renin-angiotensin (RAS).
    ) System, induce oxidative stress, cause glomerular arterial disease, and cause renal ischemia.

    Hyperuricemia can induce immune activation and pro-inflammatory response.
    It is a triggering factor for the release of inflammatory mediators, including tumor necrosis factor-α, cell adhesion factor 1, interleukin-6, etc.
    , causing inflammatory hyperplasia and ischemia in the renal tubulointerstitium , Which eventually leads to kidney fibrosis.

    Dr.
    Tang Qi proposed that treatment of hyperuricemia can improve renal function, and divided patients with chronic kidney disease (CKD) into an allopurinol-lowering uric acid treatment group and a placebo control group.

    Follow-up for two years found that the use of uric acid-lowering drug treatment group can increase the glomerular filtration rate (eGFR) and improve kidney function, so lowering uric acid can reduce kidney damage.

    Dr.
    Chen Xiaojun: High uric acid does not necessarily cause kidney damage, and lowering uric acid does not delay the progression of renal function!
    Dr.
    Chen Xiaojun pointed out that the incidence of CKD combined with hyperuricemia is about 36%-50%, but we usually attribute the deterioration of renal function to other risk factors besides hyperuricemia.

    Dr.
    Chen Xiaojun, although urate crystals can cause kidney damage.

    However, many experts believe that hyperuricemia has no clinical significance for CKD, unless there is a situation where the increase in blood uric acid concentration is not proportional to the degree of renal insufficiency.

    For example, the blood creatinine concentration is less than or equal to 1.
    5 mg/dl, while the uric acid concentration is greater than 9 mg/dl.

    Later, Dr.
    Chen Xiaojun proved his argument through the following studies: Some animal studies and clinical studies also support that hyperuricemia is the result of CKD.
    In the study of mice models of hyperuricemia and chronic uric acid crystal nephropathy with granulomatous nephritis, It can be observed that unless uric acid forms crystals in the kidney, asymptomatic hyperuricemia will not affect the progression of CKD, while uric acid crystal granuloma develops later in chronic uric acid crystal nephropathy, which is triggered by M1-like giant Interstitial inflammation and fibrosis associated with phages promote the progression of CKD.

    Research published in the New England Journal of Medicine in 2020 suggests that reducing uric acid levels through allopurinol cannot delay the decline in eGFR.

    Another randomized controlled trial (RCT) study included patients with high blood uric acid levels in CKD3-4.
    These patients had uric acid levels as high as 8.
    2 mg/dl.
    The result of the study was that lowering blood uric acid levels did not delay the decline in renal function.

    In summary, if most CKD patients are only asymptomatic hyperuricemia without the formation of uric acid crystals, they may not promote kidney damage, and for early and mid-term CKD patients, lowering uric acid cannot delay the progression of eGFR.

    Simple hyperuricemia has limited damage to the kidneys, and it is more the result of kidney damage.

    After Dr.
    Chen Xiaojun refuted the key argument of the square, Dr.
    Chen Xiaojun believed that a prerequisite was needed for this topic, such as whether the patient had symptomatic hyperuricemia or asymptomatic hyperuricemia?
    If the patient has damage to other organs, such as gout, it may have formed crystals, which can cause acute kidney damage or kidney stones.

    Asymptomatic hyperuricemia has little effect on the kidneys, but hyperuricemia can cause high blood pressure, atherosclerosis and insulin resistance, thereby increasing the risk of kidney disease.

    Dr.
    Tang Qi Dr.
    Tang Qi believes that whether the use of uric acid-lowering drugs can improve the renal function of CKD patients is still inconclusive.
    However, for patients with normal kidneys, hyperuricemia can damage the kidneys.
    Controlling uric acid at an ideal level can improve the kidney function.
    Long-term recovery of renal function.

    Studies have shown that the kidney damage caused by hyperuricemia has nothing to do with the onset of arthralgia.
    The kidney damage caused by hyperuricemia is related to the level of uric acid.
    Every 60μmol/L increase in blood uric acid level increases the chance of kidney damage by 70%.
    Therefore, blood uric acid itself is related to kidney damage.

    Then comes the most exciting part of the debate game-free debate, scan the QR code below to watch ~ At the end of the debate, Deputy Chief Physician Ling Guanghui and Deputy Chief Physician Chen Guochun of the Department of Nephrology, Xiangya Second Hospital of Central South University, both published Viewed: The two debaters, deputy chief physician Ling Guanghui, quoted many studies to state their views, and the debate was very exciting.

    Gout is a disease that is diagnosed and treated by multiple departments.
    Although there are academic controversies at present, it is expected that in the future, nephrology, rheumatology and immunology, endocrinology, etc.
    can carry out large-scale research to provide clinical diagnosis and treatment with more data on the Chinese population.

    Deputy Chief Physician Chen Guochun speaks of the causal relationship between the two in a narrow sense.
    Hyperuricemia may cause urate crystals to be deposited in the renal tubules, which can cause related kidney damage; and conversely, the progression of CKD leads to a decrease in glomerular filtration rate.
    Decreased excretion of uric acid can cause hyperuricemia; however, recent clinical and basic research results emphasize the pathogenesis of persistent inflammation between hyperuricemia and kidney damage: primary hyperuricemia can lead to inflammation of the body Even if there are no gout-related complications, it may cause chronic damage to multiple organs, including the kidneys.
    Conversely, a large number of studies have confirmed that CKD can cause systemic micro-inflammatory reactions in the early stage.

    In this case, even if there is no significant decline in renal function, the chronic micro-inflammatory state will affect the anabolic pathway of uric acid, thereby inducing the occurrence of hyperuricemia.

    Therefore, the wonderful debates of the two young doctors actually call for us to increase our understanding of hyperuricemia and CKD from the perspectives of early prevention, early detection, and early intervention, and both emphasized that systemic inflammation includes the above two types.
    The key pathogenic mechanisms of most chronic diseases, including common diseases, require further education and publicity to increase the importance of medical workers and the general public.

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