Why does she have bacteria and white blood cell casts in her urine?
In this case, Ms, Cornwall has focal bacterial infection of her calyces, medulla and renal pelvis. The presence of these bacterial and their invasion within the mentioned parts causes a body response to defend against the invasion. This occurs though a trigger of the inflammatory mediators and other body defense mechanism in this case the white blood cells. With the white blood cells now dominating the region of infection, there occurs a systematic abscess formation and necrosis within the medulla (Alexander et al., 2012). At this point, the next step that could occur is the scar tissue formation which is an indication of the healing [process. However, in Ms. Cornwall’s case, the inflammation leads to the formation of puss and the white blood cells fight against the invading bacteria. Their dominance leads to the death of bacteria as well as some of the white blood cell which are shed off together with the bacteria and stored in the inflamed region as puss. The urine from the glomeruli will in some way have to pass through the regions that have been affected and more specifically, the region where the inflammation and puss formation is present. This implies that there is a mix of the inflammatory exudates and the urine from the glomeluri with much of the concentration being in the regions that are extensively infected (Hu, Shi, Zhang, Quiñones, Griffith, Kuro-o & Moe, 2011). Thus, as the urine passes, it washes away the white blood cells in the infected region of the tract which therefore causes the formation of purulent urine since the white blood cells will be shed off as part of the puss
Differences between prerenal acute renal failure, intrarenal acute renal failure, and postrenal acute renal failure
Prerenal acute renal failure is essentially the description of the condition that causes a decreased functionality of the renal system with significant elevations in the blood urea nitrogen as well as plasma creatinine. In most cases, this condition is caused by the situation where the flow of blood into the kidney is impaired in one way or another. In this event, the blood that reaches the afferent arteriole of the renal system is low. This is further coupled by the low pressure of the blood within the same arteriole with the end result being the formation of low rate of glomerular filtration and the subsequent occurrence of renal ischemia. It causes conditions such as hypotension, hemorrhage, myocardial infarction characterized by insufficient cardiac output as well as left ventricular failure (Gansevoort et al., 2013).
On the other hand, intrarenal acute failure is caused by the situation where there occurs an impairment of the flow of blood into the renal systems or the kidney. It usually progresses from a possible direct damage of the kidney which may be through an inflammatory damage or the ischemia. It is associated with conditions such as disseminated intravascular coagulation, malignant hypertension, glomerulonephritis, acute tubular necrosis as well as renal vasculitis which refer to the inflammation of the vascular tubes (Alexander et al., 2012). In the case of post-renal acute renal failure, the common cause is the occurrence of an impaired system of outflow from the kidney. This in essence means that the passage of urine will experience an obstruction which will cause the urine to ‘return’ or ‘back-up’ into the renal pelvis, ultimately, causing a serious alteration of the pressures within the kidney. It is associated with conditions such as obstruction of the bladder outlet, kidney stones and the presence of enlarged prostate (Gansevoort et al., 2013).
References
Alexander, R. T., Hemmelgarn, B. R., Wiebe, N., Bello, A., Morgan, C., Samuel, S., & Tonelli, M. (2012). Kidney stones and kidney function loss: a cohort study.
Gansevoort, R. T., Correa-Rotter, R., Hemmelgarn, B. R., Jafar, T. H., Heerspink, H. J. L., Mann, J. F., & Wen, C. P. (2013). Chronic kidney disease and cardiovascular risk: epidemiology, mechanisms, and prevention.The Lancet, 382(9889), 339-352.
Hu, M. C., Shi, M., Zhang, J., Quiñones, H., Griffith, C., Kuro-o, M., & Moe, O. W. (2011). Klotho deficiency causes vascular calcification in chronic kidney disease. Journal of the American Society of Nephrology, 22(1), 124-136.
