Kidney Gout

What is Kidney Gout Damage?

Gout is a disease associated with impaired purine metabolism and the accumulation of an increased amount of uric acid in the body, as well as with the deposition and accumulation of urates in the tissues of the musculoskeletal system and internal organs. The disease is characterized by hyperuricemia, gouty arthritis, kidney damage involving the process of interstitium and blood vessels, urolithiasis.

In the postwar years, there has been a widespread increase in the incidence of gout. Given that kidneys with gout are affected in 30-80%, and according to some authors (A.P. Peleshchuk et al., 1983), in 100% of cases, the place of gouty nephropathy among other kidney diseases becomes clear.

The disease is associated both with some genetic defects that affect, to one degree or another, the mechanism of purine metabolism, and with the action of nutritional factors.

Hyperuricemia and gout are ambiguous concepts. Hyperuricemia is transformed into gout if conditions arise for the crystallization of urates and leukocyte infiltration of target zones. The lowest threshold for uricemia, at which there would be no risk of gout, is not defined, but high hyperuricemia is a risk factor. So, A. R. Heall et al. (1967) showed that with hyperuricemia exceeding 0.54 mmol / l, gouty arthritis was in 90% of the examined, and with uricemia 0.42-0.48 mmol / l – only in 17.3%. Based on the data obtained by numerous studies, the upper limit of the uricemia norm for men is 0.36 mmol / L, for women – 0.32 mmol / L. Gout usually begins at the age of 25-60, affects mainly men, women get sick less often, in the vast majority of cases during menopause.

Secondary gout is also distinguished for blood diseases, when taking cytostatics, radiation therapy for malignant neoplasms. Secondary gout can also occur in chronic renal failure due to the loss of the ability of the kidneys to sufficiently eliminate urates. Secondary hyperuricemia can be caused by thiazide diuretics, salicylates.

Pathogenesis during Kidney Damage with Gout

Gouty nephropathy (as well as gout in general) is primarily associated with impaired purine metabolism, the final product of which is uric acid. The latter is found in all tissues, it is difficult to dissolve in water, forms salts – urates. In plasma, uric acid is in the form of sodium urate. Non-formation is associated with the metabolism of guanine and adenine, two purine bases that make up the nucleic acid, which forms nucleoproteins with the protein. Through complex transformations, purine bases are converted to hypoxanthine and xanthine, which are converted to uric acid under the influence of xanthine oxidase. In the body, uric acid is formed from the nucleotides of food proteins, from the nucleotides of the tissues of your own body and by synthesis in the body. Uric acid is mainly excreted by the kidneys, which determines their high susceptibility, and only 20% of the total amount of uric acid decomposes in the colon, lungs and other tissues.

The term “gouty nephropathy” includes several types of kidney damage. Chronic interstitial nephritis is most commonly found. In this case, crystalline and amorphous deposits of uric acid and urates in the area of ​​the collecting ducts of the medulla of the kidneys and damage to the renal parenchyma in these places are determined.

Symptoms of Kidney Gout

The clinic does not have pronounced features. Urinary syndrome is characterized by a small (not more than 1.5 g / l), but constant proteinuria, slight hematuria and leukocyturia, which in many cases are detected only with quantitative research methods. Such changes in the urine most often make us think of chronic diffuse glomerulonephritis with isolated urinary syndrome and, if the patient has no history of joint damage (classic gouty crises or atypical forms), the diagnosis is very difficult. To some extent, the following data should serve as guidelines: male gender (age 30–50 years), normal or hypersthenic physique, and the presence of tofuses on the auricles. In all cases when the idea of ​​gouty jade arises, the decisive diagnostic criterion is the concentration of uric acid in the blood. This is very important, since it is known that nephropathy often precedes joint damage sometimes by several years (N. A. Mukhin, L. A. Balkarov, 1983), and the appointment of allopurinol in such cases can reduce urinary syndrome and prevent the development of urolithiasis and gouty arthritis.

The second most common type of lesion is urolithiasis, characterized by renal colic and the discharge (sometimes a large amount over many years) of calculi, which are X-ray negative. Acute anuria is very rare, associated with the precipitation of a large number of uric acid crystals in the tubules and, as a result, renal blockade. This pathology is noted in secondary gout, i.e., in patients with leukemia and other lymphoproliferative diseases on the background of massive therapy with cytostatics and the associated rapid destruction of many cells with the release of a huge amount of nucleoproteins. In addition, acute gouty inflammation of the kidneys occurs, which occurs with acute lower back pain, fever, and hematuria, which disappear after anti-gouty therapy (E. G. Pihlak, 1970; N. A. Korotkova, 1975). Interstitial gouty nephritis and urolithiasis are often complicated by pyelonephritis, the development of arterial hypertension, and in many cases lead to death from chronic renal failure.

Diagnosis of Kidney Damage in Gout

It should be carried out primarily with chronic glomerulonephritis, and in case of urate nephrolithiasis, it is necessary to clarify the anamnesis (joint crises) and determine the level of uric acid in the blood to establish its possible gouty genesis.

Treatment for Kidney Gout Disorders

Gouty nephropathy is treated as gout in general and does not include only funds whose use is aimed at eliminating acute articular crises. Treatment should be comprehensive, affect the pathogenetic factors of the disease and its various symptoms.

A diet with a sharp restriction of foods containing large amounts of purines is recommended. These include liver, kidneys, brains, meat, mushrooms, meat broths, jelly, sausages, ham, fish, beans, beans, lentils, cocoa, strong tea and coffee, chocolate. Alcohol intake is harmful, since alcohol reduces the excretion of uric acid by the kidneys.

Given that gouty nephropathy is almost always accompanied by oxalemia (A.P. Gorlenko, 1982), it is not recommended to use sorrel, spinach, celery, pepper, radish, rutabaga. Drink plenty of water (at least 2 liters per day) – alkaline mineral waters, milk, fruit and vegetable juices. Boiled meat is allowed at 60-100 g 2 times a week; without restrictions – cottage cheese, sour cream, milk, dairy products, eggs, vegetables, fruits, cereals, pasta; from seasonings and spices – vinegar, bay leaf, lemons. A. Kinev (1980) believes that a purine-poor diet is able to reduce uricemia by no more than 0.12 mmol / l, which, however, is quite sufficient for moderate hyperuricemia, and in more severe cases it can limit the use of medications.

Medicines used to treat chronic gout, and therefore gouty nephropathy, are divided into two groups: uricosuric and uricodepressor. The use of one or the other depends on the degree of uricosuria. If the kidneys excrete less than 600 mg of uric acid per day, gout is regarded mainly as renal and should be treated with uricosuric drugs, and if hyperuricemia is also determined by uricosuria (more than 600 mg per day), then gout is regarded as metabolic and drugs with uricodepressor action.

Uricosuric drugs include ethamide, anturan and their analogues, to uricosuppressive drugs – allopurinol and its analogues, to a much lesser extent – orotic acid. According to V.E. Arkhipov et al. (1980), allopurinol is effective in the treatment of all forms of gout, as it can significantly reduce uricemia and at the same time slightly increase uricosuria. It has the least number of side effects of all drugs and is suitable for long-term treatment, including support. At the beginning of treatment, an ege is prescribed at 0.3-0.6 g per day (depending on the degree of hyperuricemia), then, focusing on a decrease in uricemia (sometimes for years), give maintenance doses (0.1-0.2 g / day).

The use of any drugs that can enhance the excretion of uric acid by the kidneys (especially in large doses) requires constant monitoring of the degree of uricosuria, which should not exceed 1000 mg per day, and daily diuresis should be at least 2 liters. Otherwise, the risk of exacerbation of nephropathy is quite real, since all uricosuric preparations can displace uric acid salts from its deposits in tissues and contribute to the accumulation of free urate in plasma. In chronic renal failure and secondary gout, allopurinol is the drug of choice, its daily dose is 0.1-0.2 g.

Prevention of Kidney Gout

It is necessary to follow a diet with hereditary burden. Prevention of kidney damage in the presence of a history of articular gouty arthritis is reduced to the correct, long-term treatment aimed at normalizing the level of uric acid in the blood.

Patients with gouty nephropathy are subject to a medical examination similar to that for chronic glomerulonephritis, provided that the level of uricemia is determined I every 2-3 months to correct maintenance therapy.