Долзарблиги. Адабиётларда келтирилган маълумотларга кўра подагра касаллиги билан оғриган беморларда буйракларнинг зарарланиши катта кўрсаткичларда, яъни 30% дан 70% гача учрайди. Замонавий адабиётларда “подагрик нефропатия” деган тушунча ажратилган, бу эса подагра касаллигида учрайдиган барча буйрак патологиялари билан характерланади. Сийдик билан микропротеинларнинг ажралиши буйраклар зарарланишидан дарак беради. Материаллар ва усуллар. Сурункали подагрик артрити бўлган 103 нафар бемор текширилди. Иммунофермент усули ёрдамида сийдикда микропротеинлар топилиши натижасида подагрик нефропатия субклиник кечаётганлиги аниқланди. Шунга кўра беморлар 2 гуруҳга ажратилди: I (n = 58) - субклиник подагрик нефропатия билан бўлган беморлар (56,3%), II (n = 45) – назорат гуруҳи, буйраклари зарарланмаган беморлар (43,7%). Тадқиқот натижалари ва муҳокама. Маълум бўлишича, семизлик, артериал гипертензия, қандли диабети бўлган подагра билан оғриган беморларда микроальбуминурия ва микроглобулинурия миқдорининг юқори даражада ошиши кузатилади. Шунингдек, сийдикдаги микроальбуминлар, микроглобулинлар қондаги сийдик кислота, триглицеридлар миқдори билан бевосита боғлиқ. Хулоса. Шундай қилиб, тадқиқот ўтказиш давомида, подагрик нефропатияни чақириши мумкин бўлган омиллар қўйидагилар эканлиги аниқланди: семизлик, артериал гипертензия, қандли диабет, гиперурикемия, гипертриглицеридемиялар. Шуни таъкидлаш керакки, подагрик нефропатияга олиб келувчи омилларни бартараф қилиш ва уларни назорат қилиш натижасида касаллик олди олиниши мумкин.
Background. According to the literature, the frequency of kidney damage in patients with gout varies in rather large limits from 30 % to 70 %. Today scientists distinguish the concept known as "gouty nephropathy", which characterizes all renal pathology that occurs due to gout. Pathogenesis of gouty nephropathy is associated with hyperproduction of uric acid and imbalance between tubular secretion and urat reabsorption processes. But there is no clear opinion that hyperuricemia is a marker of renal dysfunction or risk factor. This contradictory opinion is due to the fact that it is difficult to estimate the early stages of gouty nephropathy. This process undergoes a long time subclinically and is diagnosed only at later stages of the disease. The first harbinger of kidney damage is increasing of microproteins in urine - microproteinuria. Materials and methods. 103 patients with chronic gouty arthritis were examined. All patients were male, without history of kidney dysfunction. Determination of microproteins in urine with help of an ELISA method allowed to suspect subclinical course of gouty nephropathy. Therefore, patients were divided into 2 groups: I (n = 58) - patients with subclinical gouty nephropathy (56.3 %), II (n = 45) - control group, patients without kidney damage (43.7 %). All calculations were carried out on a personal computer using “statistica”. Also, Spearman's correlation coefficients are established. Results and discussion. It was found that the presence of obesity, hypertension, diabetes mellitus with a high level of reliability is associated with an increased level of urine microalbumins and microglobulins. Also, close relationships between urine microalbumins, microglobulins and triglycerides, uric acid levels in blood and urine have been determined. Conclusion. Thus, during the research it was established that the factors that are likely to contribute to the onset of gouty nephropathy include: the presence of obesity, hypertension, diabetes mellitus, hyperuricemia, hypertriglyceridemia. It should be noted that all the most likely predictors are modifying and close attention to them and control will be allowed to reduce the incidence of gouty nephropathy.
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1 | Smiyan S.I. |
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