DOI: https://doi.org/10.54517/urr.v1i1

Open Access
Articles
Article ID: 2022
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by Aguilera-Méndez Asdrúbal, Nieto-Aguilar Renato, Serrato- Ochoa Deyanira, Manuel-Jacobo Gema Cecilia
Urin. Renal. Res. 2020 , 1(1);    48 Views, 0 PDF Downloads
Abstract Chronic noncommunicable diseases are the leading cause of death in the world. Among them, cardiovascular diseases occupy first place in mortality and the main risk factor is hypertension, which is usually asymptomatic until the harmful effects manifest themselves. There is a strong relationship between hypertension and the kidney, since on the one hand hypertension is the major risk factor for the initiation and progression of kidney disease and at the same time hypertension is the result of kidney disease itself. In this review, different aspects of arterial hypertension were analyzed in a general way, such as prevalence, classification, etiology, heritability and relationship with chronic noncommunicable diseases and the importance of the kidney in the regulation of blood pressure; as well as renal disease and its relationship with hypertension and the deleterious consequences for health.
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Article ID: 2029
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by Xiaoya Liu, Yali Ren, Na Guan, Sainan Zhu, Guosheng Yang, Yinghong Tao
Urin. Renal. Res. 2020 , 1(1);    26 Views, 0 PDF Downloads
Abstract Objective: To disclose the relationship between mitochondrial morphology, density and pro-teinuria in adriamycin nephropathy rats. Method: Thirty Sprague Dawley rats of clean grade were divided into adriamycin group and control group. In adriamycin nephropathy group, rats were given adriamycin at dosage of 0.7 mg /100 g body weight by tail vein injection. The control rats received equal volume of sa-line. At 2 weeks (control group = 3, adriamycin group = 3) , 4 weeks (control = 3, adriamycin group =6) and 6 weeks (control = 8, adriamycin group = 7) after adriamycin injection, the rats were sacrificed and kidneys were harvested for preparation of ultra-thin sections. Electron microscopy was performed, and podocyte mitochondrial morphology was observed. Sterological analysis was performed on morphology and density of mitochondria in podocytes. Results: 4 weeks after adriamycin injection, the rats developed proteinuria until 6 weeks. Mitochondria in the podocytes from control rats showed ellipsoid shape. Differ-ent shaped and sized mitochondria were observed in podocytes of the adriamycin nephropathy rats. No sig-nificant statistical difference was revealed in the mitochondrial area, circumference, form factor and aspect ratio between adriamycin and control groups. Before development of proteinuria, the mitochondrial density increased significantly at 2 weeks after adriamycin injection compared with that in control rats (0.17±0.00 vs. 0.14±0.01, t = 6.173, P < 0.01). Meanwhile, the surface density of mitochondria showed an increasing trend (0.78±0.03 vs. 0.71±0.04, t =-2.526, P = 0.065). 6 weeks after adriamycin injection, the surface density of mitochondria decreased significantly compared with that in the control rats (0.71±0.11 vs. 0.87±0.12, P = 0.02) , the density of mitochondria did not change significantly. Conclusions Dysmorphic mitochondria are involved in the development of proteinuria in adriamycin ne-phropathy. The increase of mitochondrial density is an early event in the development of proteinuria. De-crease of mitochondria surface density is involved in podocyte injury and development of adriamycin ne-phropathy rats.
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Articles
Article ID: 2030
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by Weimin Li
Urin. Renal. Res. 2020 , 1(1);    27 Views, 0 PDF Downloads
Abstract Objective: To observe the protective mechanism of protein kinase B (Akt)-mediated phosphoserine binding domain and leucine zipper motif 1APPL1) on renal fibrosis in mice with renal ischemia reperfusion injury. Methods : A total of 24 male C57BL/6 mice were selected to randomly divide into 2 groups: Normal mice-sham operation group (WT-C group) and normal mice-renal ischemia reperfusion group (WT-I/R group). Forty-eight mice with APPL1 gene knockout mice were divided into 4 groups randomly:APPL1 gene knockout/sham surgery group (AK-C group), APPL1 gene knockout/renal ischemia reperfusion group (AK-I/R group), APPL1 gene knockout+Akt inhibitor treatment group (AK-L group), and APPL1 gene knockout+saline treatment group (AK-S group). Except the two control groups of WT-C ad AK-C, the renal ischemia reperfusion injury (IRI) model was prepared in the other groups. After the successful preparation of the model of bilateral renal ischemia reperfusion injury in mice, the AK-L group was intraperitoneally injected with LY294002 mg/kg, once every 24 hours till day 7, and the same dose of normal saline was injected in the AK-S group. At 24h after reperfusion, 6 mice were randomly selected from each group and detected for the concentration of serum BUN and Scr to score renal tubular injury and determine APPL1 expression and Akt phosphorylation levels in the renal tissues. At 14 days after reperfusion, 6 mice in each group were randomly sacrificed to obtain kidney tissues. The degree of renal fibrosis was evaluated; expression of collagen 1, fibronectin, α- smooth muscle actin and APLL1 and Akt phosphorylation levels in renal tissue were determined. Results: At 24h after reperfusion, comparisons of serum BUN and Scr concentrations and renal tubular injury scores showed no statistically significant difference between the WT-C group and AK-C group (P>0.05). Compared with the WT-C and AK-C groups, the levels of them in the WT-I/R group, the AK-I/R group, and the AK-S group increased ( P <0.05), and the levels in the AK-L group were the highest ( P <0.05). At 14 days after reperfusion, the expression of collagen 1, fibronectin and alpha smooth muscle actin in renal tissues and the degree of renal fibrosis showed no significant difference between WT-C group and AK-C group (P>0.05).  Compared with the WT-C and AK-C groups, the levels of expression of fibrosis-related indices were increased in the WT-I/R group, the AK-I/R group, and the AK-S group ( P <0.05), with the highest level in the AK-L group ( P <0.05).  At 24h and 14 d after reperfusion, APPL1 expression and Akt phosphorylation level in renal tissues in the WT-I/R group were up-regulated compared with those in the WT-C group ( P <0.05). At 24h after reperfusion, compared with the AK-C group, Akt phosphorylation level increased in the AK-I/R group and the AK-S group ( P <0.05). Compared with the AK-I/R group, Akt phosphorylation level decreased in the AK-L group ( P <0.05). Conclusions APPL1 mediated by Akt has protective effect on chronic renal fibrosis in mice with renal ischemia reperfusion injury.
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Articles
Article ID: 2032
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by Chunmao Zheng, An-fa Wang
Urin. Renal. Res. 2020 , 1(1);    22 Views, 0 PDF Downloads
Abstract Objective: To optimize the antibiotic drug regimens to patients with renal dysfun-ction based on endogenous creatinine clearance(CLcr) and to comment on its rationality. Methods: Rationality and optimizability of the antimicrobial regimens in a medical record were disscussed via the renal function based on CLcr. The original regimens which were considered to be optimized were adjusted via the renal function based on CLcr, When these adjusted regimens achieved the preset threshold of the PK/PD target index which was used to predict the efficacy of regimens, they were considered to be feasible. Results: In the elected medical record, it was found that the dosage of the original regimens was too high or the interval of administration was too short, which indicated that the original regimens could be optimized. The optimized regimens, obtained by adjustment on the original regimens via the renal function based on CLcr and according to the preset threshold of the PK/PD target index, were theoretically not only effective but also more secure. Conclusion: Based on the renal function status reflected by CLcr, the optimization and commenting of antimicrobial drug administration plan and its rationality are helpful for the development of safe, effective and reasonable individualized treatment plan for patients with renal insufficiency complicated with infection; it can serve as the theoretical guidance in clinical practice.
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Articles
Article ID: 2034
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by Abarca Zúñiga Vivian, Álvarez Rodríguez Nicole
Urin. Renal. Res. 2020 , 1(1);    56 Views, 0 PDF Downloads
Abstract Nephrotic syndrome is a glomerulopathy caused by renal diseases that increase the permeability of the glomerular filtration barrier; minimal change disease is the cause most associated with the development of nephrotic syndrome in pediatrics. The clinical manifestations that characterize this syndrome are: proteinuria in nephrotic range, hypoalbuminemia, edema in areas of decline and alterations in the lipid profile. The diagnosis is made by clinical findings and other studies including urinalysis, urinary proteins as initial tests, serum albumin levels and sometimes alterations in the lipid profile, in few cases renal biopsy is required to confirm the diagnosis. Most patients respond to first line medical treatment with disease remission and symptomatology control.
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Editorial
Article ID: 2036
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by Johnson Jade
Urin. Renal. Res. 2020 , 1(1);    27 Views, 0 PDF Downloads
Abstract The urinary system, or renal system, consists of the kidneys, ureters, bladder, and urethra. It is the body's drainage system for the eventual removal of urine. The urinary system is to eliminate waste from the body, control levels of electrolytes and metabolites, regulate blood volume and blood pressure, and regulate blood pH.
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