The kidneys play an important role in the body by clearing it of waste products from the blood. They are also involved in the regulation of blood pressure, electrolyte balance and red blood cell production. Many Americans suffer from kidney failure, and each year many more are added to the organ donation waiting list. and becoming paired with an organ is half the battle. Once kidney function begins to decline, the likelihood that other organs will eventually stop functioning also doubles. Currently, there are not many treatments to significantly slow or halt the rapid decline in health of a person dealing with kidney failure, and studies like the one conducted in Renal Protection in Chronic Kidney Disease: Activation of Hypoxia Inducible Factor vs. Angiotensin II blockade may help find new ways to treat kidney disease[3]. In the book 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 with signs of chronic kidney disease (CKD) using the Winstar rat to show how unusual methodologies could stop the effects of CKD. One such effect is hypoxia, or a condition that develops when sufficient oxygen is unable to reach the tissues. Researches used two methods: cobalt chloride (CoCl2) and dimethyloxaliglycine (DMOG) to initiate hypoxia inducing factors (HIFs) and associated proteins. The researchers subsequently combined these methodologies with angiotensin (Ang II) blockade and observed oxygen consumption and other renal hemodynamic aspects to evaluate whether or not these methods were effective in treating the simulated kidney. Along with this, in this study, “hypoxia inducing factor (HIF) proteins were evaluated using Western blotting and PCR.” The study was split week by week where researchers recorded what was observed and how these methods affected the functioning of the kidneys. Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an original essay In conclusion, the researchers found that the use of Ang II blockade treatment and HIF therapies was successful in returning oxygen consumption levels and functioning in the tissues to normal levels. normal rates. II. Hypothesis The researchers of this article chose to examine this topic because they "wanted to identify HIF-related proteins that would serve as indications of possible beneficial effects when combining multiple methodologies such as ANG II blockade, cobalt chloride, and dimethyloxaliglycine". In this article, the hypothesis was that “HIF induction, as demonstrated in renal tissue by Western blot and indexed by expression of VEGF, HO-1, Epo, and GLUT1, mediates the beneficial effects of ANG II blockade in CKD”. The most important part of this study/hypothesis specifically concerns the expression of certain proteins in the body that serve as a means to fight chronic kidney disease and how their expression correlates with the functioning of a kidney. The researchers considered oxygen consumption and renal blood function (RBF) as the basis for this measurement. This area of ​​research is important because kidney failure has increasing epidemic rates while some treatments and alternatives such as transplants are available, are these treatments high risk with high failure rates or are a means to an end such asdialysis. There is an acute organ transplant rejection rate of 30–50%, and dialysis patients have reported feeling exhausted and unable to work [3]. Patients also suffered from disabling bone disease, dementia caused by aluminum intoxication, and severe fatigue due to uncontrollable anemia. Beyond that, screening for early detection of kidney damage has increased with blood tests, but early preventative measures are difficult to obtain for some cultural groups such as African Americans, who some come from low-income backgrounds, so seeking expensive is unlikely to a fatal prognosis is reached. Previous studies such as the one conducted in Heme oxygenase-1 is upregulated in the kidney of angiotensin II-induced hypertensive rats: Possible role in renoprotection, researchers studied the kidneys of rats with hypertension. The rats were given doses of Ang II blockade or noepinephrine for about a week to see how it would affect heme oxygenase-1 (HO-1). The researchers found that increased Ang II in the kidneys of rats with hypertension “provided protection against Ang II-induced injury” [2]. This study was conducted ten years before the article in question and helped future researchers use methodologies such as angiotensin II to further study the physiology of the kidneys. III.Methods A part of the materials and methods that I found interesting and that I found interesting to expose the part of the study that was important for its overall purpose was the "measurement of renal 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 placed into four groups. These groups consisted of a control group, a group designated as the “1-week A/I group,” a group designated as the “1-week ANG II A/I block group,” a group designated as the “A/I 1-week group.” 1 week “I cobalt chloride group” and a group designated as “1 week DMOG A/I group”. Cobalt chloride and DMOG were injected into rats over a series of eight days. Kidney function and consumption of oxygen 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 urinary bladder, blood flow. left kidney (RBF, ml/min) was monitored with a perivascular ultrasound transit time flow probe. Once the rats 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 with 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 for arterial minus renal venous O2ct. “ This fits the experimental design because it initially tests the functioning of the kidneys and other organs in the body after protein treatments to see how effective these treatments are on rats. These results later help support or refute the hypothesis because if the values ​​of the oxygen consumption increases then the hypothesis can be accepted but otherwise the hypothesis is rejected IV. Results **I thought I should include a part of the article with the results word for word, not indicated in the explanation of the document but in the column, it states to include the graph and its caption, that's what I did but I didn't make it clear that that's where it came from. The part of the results section I chose to analyze indetailed were the results associated with the measurement of renal function and the calculation of oxygen consumption. This part of the results was called “Improvement of renal hemodynamics by cobalt treatment and ANG II blockade, shown in figure 1”. Normal A/I kidneys showed significant decreases in both RBF and GFR (Fig. 1). This reduction in GFR and RBF was not due to reduced renal mass in the A/I kidney as both GFR and RBF were significantly increased by ANG II blockade as well as by incorporation of cobalt chloride therapy. Compared to normal renal total oxygen consumption (QO2) of the kidney did not change. The increase in QO2/TNa was indicative as 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 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 the activation of HIF pathways." To confirm this conclusion, the researchers used another HIF-1 inducer, DMOG, in A/ rats. I, which produced renal protective effects similar to those of cobalt treatments and with the improvement of renal function and the decrease in overall renal oxygen consumption. V.Analysis The purpose of this study was to “identify the related proteins to HIF that serve as indicators of whether the beneficial effects of combined ANG II blockade result from the expression of these proteins." Along with this, the hypothesis contained in this article stated that “the induction of HIF, 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 chronic renal failure. They are linked because the purpose of the article is essentially to determine whether the prediction made by 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, immunoblotting analysis, quantitative RT-PCR, cell proliferation by 5 -bromodeoxyuridine and statistical analysis are all parts of the project that incorporate the different proteins to test their effects on rats and the data is collected. The findings and conclusion are linked because the findings present a summary of the data while the conclusion explains why these findings 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 blot or mRNA level for certain molecules by real-time PCR. As shown in Fig. 6, VEGF protein was constitutively expressed in the normal kidney, tended to increase in untreated A/I kidneys, further increased in ANG II-blocked kidneys, and demonstrated highest expression in cobalt-treated A/I kidneys. HO-1 protein (Fig. 7) was undetectable in normal kidneys, was 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, whereby it was modestly elevated in A/I kidneys and further increased in cobalt-blocked and ANG II kidneys (Fig. 8). The main findings of this study are that activation of the HIF pathway and blockade of ANG II improved renal hemodynamics. HO-1 was shown to be substantially increased