The kidneys play an important role in the body by ridding it of waste from the blood. They also participate in the regulation of blood pressure, electrolyte balance and the production of red blood cells. Many Americans suffer from kidney failure, and many more are added to the organ donation waiting list each year. and being paired with an organ is half the battle. Once kidney function begins to decline, the likelihood that other organs will also eventually shut down doubles. Currently, there are not many treatments that can significantly slow or stop the rapid decline in the health of a person with kidney failure and studies like the one done in Kidney Protection in Chronic Kidney Disease : activation of hypoxia-inducible factor against angiotensin. Blockade II may help find new ways to treat kidney disease[3]. In Renal Protection in Chronic Kidney Disease: Hypoxia-Inducible Factor Activation Versus Angiotensin II Blockade by Aihua Deng MAK, Mary Ann K. Arndt, Joseph Satriano et al., researchers focused on the use of a simulated kidney showing signs of a chronic kidney. (CKD) using the Winstar rat to show how unusual methodologies could stop the effects of CKD. One of these effects is hypoxia or a condition that develops when sufficient oxygen fails to reach the tissues. The research used two methods: cobalt chloride (CoCl2) and dimethyloxalyglycine (DMOG) to initiate hypoxia-inducing factors (HIF) and associated proteins. The researchers then combined these methodologies with angiotensin (Ang II) blockade and observed oxygen consumption and other renal hemodynamic parameters to evaluate whether or not these methods were effective in treating the sham kidney. Along with this, in this study, “hypoxia-inducing factor (HIF) proteins were evaluated by Western blot and PCR.” The study was divided into weeks, during which the researchers recorded what was observed and how these methods affected kidney function. Say no to plagiarism. Get a tailor-made essay on “Why Violent Video Games Should Not Be Banned”?Get the original essayIn conclusion, researchers found that the use of Ang II blockade treatment and HIF therapies helped bring back oxygen consumption levels and tissue function at their normal level. normal prices. II. Hypothesis The researchers in this article chose to examine this topic because "they wanted to identify HIF-related proteins to serve as indications of any beneficial effects when combining multiple methodologies such as ANG II blockade, cobalt chloride and dimethyloxalyglycine. In this article, the hypothesis was that "HIF induction, as demonstrated in renal tissue by Western blot and indexed by the expression of VEGF, HO-1, Epo and GLUT1, mediates the beneficial effects of blockade of ANG II in the IRC”. The most important part of this study/hypothesis specifically looks at the expression of certain proteins in the body to serve as a means to combat CKD and how their expression correlates with the functioning of a kidney. Researchers looked at oxygen consumption and renal blood function (RBF) as a basis for this measurement. This area of ​​research is important because kidney failure has increasing epidemic rates. Although there are some treatments and alternatives like transplants available, these treatments carry a high riskwith high failure rates or are a means of achieving this such as dialysis. There is acute rejection of organ transplantation. rates of 30 to 50 percent and dialysis patients reported feeling exhausted and unable to work [3]. Patients even suffered from debilitating bone diseases, dementia caused by aluminum poisoning, and severe fatigue from uncontrollable anemia. Along with this, early detection of kidney damage has increased through blood tests, but early preventive measures are difficult to implement for certain cultural groups like African Americans, some of whom come from low-income backgrounds and seek therefore costly medical care before reaching an ultimately fatal prognosis is unlikely. Previous studies like the one conducted on heme oxygenase-1 is upregulated in the kidney of hypertensive rats induced by angiotensin II: possible role in renoprotection, the researchers studied the kidneys of rats suffering from hypertension. The rats were given doses of Ang II blockade or noepinephrine for about a week to see how this would affect heme oxygenase-1 (HO-1). Researchers found that increased Ang II in the kidneys of hypertensive rats “provided protection against Ang II-induced injury” [2]. This study was conducted ten years before the focus article and helped future researchers use methodologies such as angiotensin II to further study kidney physiology. III.Methods Some of the material and methods that I found interesting and to expose the part of the study that was important for its overall objective was the "measurement of kidney function and calculation of oxygen consumption" . During this part of the study, male Wistar rats weighing between 225 and 250 grams were used and randomly divided into four groups. These groups were composed of a control group, a group designated as "A/I group at 1 week", a group designated as "ANG II A/I blocking group at 1 week", a group designated as “group A/I at 1 week”. I cobalt chloride group”, and a group designated as “group A/I DMOG over 1 week”. Cobalt chloride and DMOG were injected into rats over a series of eight days. Kidney function and oxygen consumption were measured by placing the rats under anesthesia with Inactin and placing them on a temperature-controlled table of 37 degrees Celsius. “After cannulation of the trachea, left jugular vein, left femoral artery, and bladder, left renal blood flow (RBF, ml/min) was monitored with a perivascular ultrasonic transit time flow probe. . After the rats were stabilized for 60 minutes, the researchers recorded their systemic blood pressure and RBF. Blood samples were collected using a color spectrophotometer. “The oxygen content (O2ct) was calculated by the formula: O2ct (ml/ml blood) (1.39 tHb O2Hb% Po2 0.003) ⁄ 100. The total oxygen consumption of the left kidney (QO2) was calculated as RBF multiplied by arterial minus renal venous O2ct. » This fits into the experimental design because it initially tests the functioning of the kidneys and other organs of the body after protein treatments to see how effective these treatments are for rats. These results later help to support or refute the hypothesis, because if the oxygen consumption values ​​increase, the hypothesis can be accepted, but otherwise it is rejected. IV. Results **I thought I was supposed to include part of the article with the results verbatim, not shown in the Word document explanation but in the rubric it says to include the graph and itslegend, that's what I did but I did it. I'm not saying that's where it comes from. The part of the results section that I chose to analyze in detail was the results associated with measuring kidney function and calculating oxygen consumption. This part of the results was titled “Improvement of renal hemodynamics by cobalt treatment and ANG II blockade, illustrated in Figure 1”. Normal A/I kidneys showed significant decreases in RBF and GFR (Fig. 1). This reduction in GFR and RBF was not due to the reduction in renal mass in kidney A/I since GFR and RBF were significantly increased by ANG II. blocking as well as by the incorporation of cobalt chloride treatment. Compared with the normal kidney, total renal oxygen consumption (QO2) did not change. The elevation in QO2/TNa was indicative in that there was a decrease in “renal metabolic efficiency” [1]. “This renal metabolic inefficiency was caused by increased oxygen demand in the untreated A/I kidney, as ANG II blockade and cobalt treatment significantly increased GFR to normal levels while QO2 was reduced. remained unchanged, improving QO2/TNa to normal values.” In the article, "it was concluded that all these renal effects produced by cobalt treatment are due to activation of HIF pathways." To confirm this finding, researchers used another HIF-1 inducer, DMOG, in A/I rats, which produced renal protective effects similar to those of cobalt treatments and as renal function improved. improved and overall renal oxygen consumption decreased. V. Analysis The aim of this study was "to identify HIF-related proteins that serve as indicators to determine whether the beneficial effects of combined ANG II blockade result from the expression of these proteins." Along with this, the hypothesis of this article stated that "HIF induction, as demonstrated in renal tissue by Western blot and indexed by the expression of VEGF, HO-1, Epo and GLUT1, mediates the beneficial effects of ANG II blockade in MRC. They are related because the purpose of the article is essentially to determine whether the prediction made by the researchers in the hypothesis is correct or not. The experimental design of this study and the hypothesis are linked because the study is divided into sections: renal function and oxygen consumption, murine cortical tubular cell culture, HIF immunoprecipitation, immunoblot analysis, quantitative RT-PCR, proliferation cell by 5-bromodeoxyuridine. , and statistical analysis are all parts of the design that integrate the different proteins to test their effects on rats and that data is collected. The results and conclusion are linked because the results present a summary of the data while the conclusion explains why these results are important to the overall study. For example, the expression of other HIF-induced targets has also been studied at either protein level by Western blotting. or the mRNA level of certain molecules by real-time PCR. As shown in Figure 6, VEGF protein was constitutively expressed in normal kidneys, tended to increase in untreated A/I kidneys, further increased in ANG II blocked kidneys, and demonstrated maximal expression in kidneys Cobalt treated A/I. HO-1 protein (Fig. 7) was undetectable in normal kidneys, induced in the untreated group, suppressed in the ANG II-inhibited group, and strongly induced in the cobalt-treated group. When GLUT1 was examined, the pattern was similar to that seen with VEGF, in which it was slightly elevated in A/I kidneys and further increased in blocked kidneys.