Association of Urinary Biomarkers Noninvasively Forecasts The Extent of Renal Injury In The Early Diabetic Nephropathy Patients With Kidney Qi Deficiency Syndrome: A Retrospective Investigation 

Abstract

Background: Recently, diabetic nephropathy (DN) becomes a common health problem in China as one of the major microvascular complications of diabetes mellitus. Therefore, the incipient diagnosis and noninvasive detections in clinic by the association of urinary biomarkers are important for preventing the progress of DN. However, the clinical significance of urinary biomarkers is controversial nowadays. This study thereby aimed to further evaluate the clinical significance of the association of urinary biomarkers in noninvasively predicting the renal damaged extent of the early type 2 DN patients with kidney qi deficiency syndrome in an integrated traditional and western medical center, and preliminarily confirm the correlation between urinary tubular biomarkers and the biological bases of DN patients.Methods: Ninety-two patients in an integrated traditional and western medical center of China were categorized into 3 groups, 20 patients with normo-albuminuria, 50 patients with micro-albuminuria, and 22 patients with macro-albuminuria. In addition to urinary albumin (UAlb) and urinary albumin-to-creatinine ratio (UACR), serum creatinine, estimated glomerular filtration rate and various urinary tubular biomarkers were tested respectively. Besides, clinical characteristics and kidney asthenia syndrome distribution in all patients were observed. Results: In these 3 groups, 24-h UAlb and UACR showed stepwise and significant increases. Urinary cystatin C (UCysC), urinary N-acety1-β-D-glucosaminidase (UNAG) and urinary retinal binding protein (URBP) synchronously showed gradual increases consistent with albuminuria degree in 3 groups. Moreover, 24-h UAlb and UACR were positively correlated with UCysC, UNAG and URBP. In the 72 DN patients with albuminuria, there was a positive correlation between UNAG and URBP, and UCysC was also positively correlated with UNAG and URBP. Additionally, TCM syndrome distributional characteristics in all patients were consistent with the clinical manifestations of kidney qi deficiency syndrome. Conclusion: In this investigation, we ulteriorly demonstrated that the association within UCysC, UNAG, URBP and UAlb may be used as practical targets in noninvasively forecasting the extent of renal injury in the early type 2 DN patients with kidney qi deficiency syndrome. More importantly, we found that urinary tubular biomarkers may be one of the biological bases of DN patients with the specific traditional Chinese medicine syndrome.

Inhibiting NLRP3 signaling in aging podocytes improves their life- and health-span

“…Studies have shown an increase in NLRP3 in injured podocytes in disease. [23][24][25][26][27][28][29][30][31][32][33][34][35][36][37] This was confirmed in our experimental model of podocyte depletion induced FSGS, which showed an increase in NLRP3 staining (Supplementary Figure 3A, 3B). To determine if NLRP3 was further increased in aged mice with disease, experimental FSGS was induced in mice 24 months of age with a cytopathic anti-podocyte antibody.…”

“…In sum, these findings are consistent with an age-induced increase in NLRP3 inflammasome signaling in podocytes by middle-age. Moreover, this study shows that similar to many forms of podocyte injury, [23][24][25][26][27][28][29][30][31][32][33][34][35][36][37] aging and injury are both associated with increased NLRP3 expression.…”

“…Although the NLRP3 inflammasome was initially considered restricted to immune cells following induction by DAMPs and PAMPs [22], it has gained wider importance as being the cause of sterile inflammation in non-immune cells including podocytes [21]. NLRP3 expression is increased in podocytes and contributes to their damage in APOL-1 associated podocytopathy [23], diabetic kidney disease [24][25][26][27][28][29], lupus nephritis [30,31], several primary nephrotic syndromes [32][33][34] and complement- [35] aldosterone- [36] and angiotensin II- [37] induced injury.…”