Overview of the Kidney Function Mechanisms

Case summary

Ms. Cornwall is admitted with pyelonephritis. She has chills, and her temperature is 101°F. She is complaining of flank pain, frequency, and dysuria. Her urine has white blood cell casts and shows growth of Escherichia coli (E. coli).

The Cause of Bacteria and White Blood Cell Casts in Ms. Cornwall’s Urine

Ms. Cornwall’s urine contains bacteria and white blood cells because she has a kidney infection. Pyelonephritis, which is the irritation of the renal tissue, occurs when bacteria that cause a urinal tract infection escape and progress to the upper urinary tract (to the kidneys through the urethra) (McCance & Huether, 2014). E. coli is the most common cause of acute pyelonephritis because of its capacity to hold and invade the urinary tract. There is a tenderness of the lining of renal structures. Pustules may form in the kidneys leading to the destruction of nephron tubules.

Differences between Prerenal Acute Renal Failure, Intrarenal Acute Renal Failure, and Postrenal Acute Renal Failure

Acute renal failure is typified by the unexpected decline in kidney function, which is expressed by elevated serum creatinine levels that may be accompanied by a decrease in urine production (Rahman, Shad & Smith, 2012). The scale of damage varies from mild to advanced and may necessitate renal replacement rehabilitation. The indicative assessment is used to categorize acute kidney failure as prerenal, intrarenal (intrinsic renal), or postrenal.

Prerenal acute kidney failure implies that the obstruction is before the kidneys and impedes the flow of blood to the kidneys. Any disorder that reduces the flow of blood to the kidneys may lead to renal impairment and failure. An example of such a condition is extremely low arterial blood pressure following myocardial infarction.

Intrarenal acute renal failure indicates that the complication is within the kidneys. Its causes are classified depending on the affected kidney component and may be tubular, glomerular, interstitial, or vascular. For example, glomerulonephritis may cause intrarenal acute renal failure.

Postrenal acute renal failure occurs when there is a complication in the rest of the urinary tract leading to inadequate drainage of urine. Blockage of urine flow may be brought about by kidney stones or prostatic hypertrophy (Scanlon & Sanders, 2007). Therefore, the treatment of renal failure entails rectifying the exact cause. When the damage cannot be corrected, an individual is said to have chronic renal failure.

Pathophysiological Processes Related to the Three Disease Processes

Myocardial infarction lowers blood pressure hence reduces the volume of blood entering the afferent arteriole. As a result, there is a decreased glomerulus filtration rate. There is real hypoperfusion within a short time leading to the increase in blood urea nitrogen and plasma creatinine concentrations. In the initial hours, defensive autoregulatory machinery, through the action of angiotensin II, causes the distention of the afferent arteriole and narrowing of the efferent arteriole (McCance & Huether, 2014). However, the reduced filtration pressure ultimately leads to reduced GFR. If the blood volume and oxygen supply are not reinstated, cell injury and acute tubular necrosis may occur.

The main feature of glomerulonephritis is irremediable, gradual glomerular and tubulointerstitial fibrosis, which eventually causes a decline in the glomerular filtration rate and retention of uremic poisons. The initial damage reduces the mass of the nephron, which lowers the GFR thereby resulting in hypertrophy and hyperfiltration of the persisting nephrons. Additionally, intraglomerular hypertension may result in a bid to elevate the GFR of the remaining nephrons thus abating the functional outcomes of nephron loss. However, these changes are in the long run harmful because they bring about glomerulosclerosis and additional nephron loss.

Kidney stones, which are also called renal lithiasis, are solid deposits formed in the kidneys due to mineral deposits, particularly calcium. Nearly all cases of kidney stones are deposits of calcium oxalate while a few instances are caused by calcium phosphate. These deposits may be formed due to low volumes of urine, excessive calcium in urine, anomalies in urine pH, and hyperoxaluria among others. These stones block the passage of urine hence causing damage to kidneys.

References

McCance, K. L. & Huether, S. E. (2014). Pathophysiology: The biology basis for disease in adults and children (7th ed.). St. Louis, Missouri: Elsevier Health Sciences.

Rahman, M., Shad, F., & Smith, M. C. (2012). Acute kidney injury: a guide to diagnosis and management. American Family Physician, 86(7), 631-639.

Scanlon, V. C. & Sanders, T. (2007). Essentials of anatomy and physiology (5th ed.). Philadelphia: F. A. Davis.