2021
DOI: 10.1007/s11255-021-02844-4
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Hyperuricemia and hypertriglyceridemia indicate tubular atrophy/interstitial fibrosis in patients with IgA nephropathy and membranous nephropathy

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Cited by 16 publications
(12 citation statements)
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“…Uric acid can induce systemic and local inflammatory responses, oxidative stress, and activation of the local renin–angiotensin system, leading to endothelial dysfunction and glomerular hypertension [ 13 ], which result in the emergence of proteinuria. Hyperuricemia is an independent risk factor for renal tubular atrophy and interstitial fibrosis [ 14 , 15 ], and high baseline blood uric acid level is an independent predictor of poor renal outcome in PMN patients [ 15 ]. Therefore, it is of great significance to pay attention to the management of uric acid in clinical practice, the treatment of lowering uric acid should be given at the same time while treating the primary disease.…”
Section: Discussionmentioning
confidence: 99%
“…Uric acid can induce systemic and local inflammatory responses, oxidative stress, and activation of the local renin–angiotensin system, leading to endothelial dysfunction and glomerular hypertension [ 13 ], which result in the emergence of proteinuria. Hyperuricemia is an independent risk factor for renal tubular atrophy and interstitial fibrosis [ 14 , 15 ], and high baseline blood uric acid level is an independent predictor of poor renal outcome in PMN patients [ 15 ]. Therefore, it is of great significance to pay attention to the management of uric acid in clinical practice, the treatment of lowering uric acid should be given at the same time while treating the primary disease.…”
Section: Discussionmentioning
confidence: 99%
“…There is evidence that persistent hyperuricemia can cause renal tissue changes, such as arteriolonephrosclerosis, glomerulosclerosis and renal tubular lesions, leading to chronic kidney disease [ 4 , 5 ]. As Russo E et al reported in a retrospective study, Serum uric levels are independently associated with AD and poor prognosis in patients with IgAN [ 6 ].One of the mechanisms serum uric acid aggravates renal ischemic injury may be the activation of the renin–angiotensin system.…”
Section: Discussionmentioning
confidence: 99%
“…Consistently, in the present study, T1–T2 was a risk factor for poor prognosis of IgAN, even with relevant adjustment in the multivariable analysis models, and the frequency of T1–T2 among patients with higher levels of TA-SUA was also higher, especially in women. Recent research has established that hyperuricemia and hypertriglyceridemia, which are prevalent in patients with CKD, are independent risk factors for moderate tubular atrophy/interstitial fibrosis ( Liu et al, 2021 ), and by multivariate logistic regression analysis, only tubular atrophy/interstitial fibrosis (T1–T2) (HR = 3.969, P = 0.008) was significantly associated with hyperuricemia in IgAN ( Ruan et al, 2018 ). This suggests that we can combine the pathological characteristics and clinical follow-up data into a model for predicting the progression of IgAN.…”
Section: Discussionmentioning
confidence: 99%