Disorders of Renal Function

Disorders of Renal Function
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Question 1
Renal calculi occur when the urine is extremely saturated with salts and minerals such as calcium oxalate, struvite, uric acid as well as cystine. The majority of these stones have calcium. Renal calculi vary in size from small to large ones. They can remain in the location they were formed or move down the urinary tract creating symptoms all the way. Research shows that the primary factor intricate in the development of a stone may be the existence of nanobacteria that form calcium phosphate shell.
The formation of renal stones is caused by the amplified urinary supersaturation which occurs due to the following development of crystalline particles. Crystallization of urine occurs due to the process of supersaturation. There are various crystalline components of urinary tract stone. They include calcium, oxalate, cysteine, purines, calcium phosphate or bacterial related. The mechanism of development of crystalline particles in the urine is centered on the thermodynamic state of the urine chemistry. The natural development of urine chemistry leading to stone development is urine saturation, urine supersaturation, crystal nucleation, aggregation, the retaining of crystals by the urothelium and the constant progression of the stone on the retained crystals. Supersaturation occurs when the absorption of salt components rises further than the saturation level. The solution is termed to be thermodynamically unstable.

Supersaturation leads to nucleation, which is a process that is controlled by the thermodynamic free energy of the solution. The process of nucleation leads to the decrease of excess free energy to a more thermodynamically steady environment. According to Tiselius et al. (2017), nucleation is a process that results when a liquid is changed to a solid in a supersaturated solution. The process starts when stone salts are combined with a solution leading to loose clusters which may grow bigger when new components are added.nuclei are the first crystal that cannot dissolve and have a lattice pattern feature. Nuclei in urine normally appear on prevailing surfaces which is a process referred to as heterogeneous nucleation. Various crystals such as epithelial cells, red blood cells, urinary casts and others can perform as nucleating hubs in urine. When a nucleus is formed and attached, it requires lesser chemical pressures than necessary for the occurrence of the primary nucleus.
Aggregation seems to be the main mechanism for renal calculi growth. Aggregation is the process by which crystals in a solution stick together to create large particles. Crystal aggregation is considered to be the most critical step in stone formation. All theories of Calcium oxalate urolithiasis are in agreement with the fact that crystal aggregation is involved in crystal retention within kidneys. Another reason for the effective growth of renal calculi is the holding of microcrystals in the urinary tract, which could be related to a past injury. Additionally, renal tubular cell injury can encourage the crystallization of calcium by availing the substances for their heterogeneous nucleation. Renal tubular cell injury creates many membrane vesicles which are good nucleators of calcium crystals (Talati & Abbas, 2013). 
Citrate plays a critical role in the kidneys since it improves calcium absorption. It also plays an active role in preventing kidney stone formation. The electrostatic charge contained in citrate serves as a buffer between calcium and oxalate to prevent their bonding in the urinary tract. Low citrate in the urine indicates a high risk of developing kidney stones. Citrate works as an inhibitor of stone formation. It works through various mechanisms to increase its functionality. In the renal tubule, citrate combines with calcium, expanding its solubility and lessening the amount of free calcium in the urine. The calcium-citrate complex that is created prevents calcium supersaturation. It also thwarts nucleation of calcium oxalate as well as calcium phosphate partially through its contact with Tamm-Horsfall protein. Further, citrate inhibits crystal agglomeration and growth by binding crystal’s surface and averting union of calcium oxalate to renal epithelial cells. It can be used as an alkali therapy for people suffering from kidney stones. According to Talati & Abbas (2013), the excretion of citrate is associated with urinary pH, which may, in turn, influence the development of different types of stones. The giving of citrate or other alkali has proved to be effective for hypocitraturic stone formers. Even though several forms of citrate are used in helping patients, potassium citrate has shown to be the most advantageous to them. Patients who are not able to buy potassium citrate can benefit from drinking citrus juices which have large amounts of citrates. It is crucial for a patient suffering from calcium oxalate stones to take the calcium that he/she needs. Taking too little calcium can increase the level of oxalate leading to kidney stones. It is necessary to take the right amount of calcium in such patients as it can be helpful in preventing recurrence of the disease.
Question 2
The administration of calcium supplements may helpful for patients with calcium oxalate stones. Calcium supplements promote the binding of oxalate to calcium in the gut. This process fails oxalate to be absorbed into the bloodstream and therefore excreted. The intake of calcium in large amounts has proven to be useful in patients having calcium oxalate stones. The calcium binds with oxalate making it hard for the kidneys absorb it. This situation can help in reducing the formation of the stones and even preventing recurrence of the problem. The intake of calcium supplements, as well as meals rich in calcium, can be helpful since they contain calcium carbonate and calcium nitrate which help in bonding oxalate in the gastrointestinal tract. On the other hand, calcium nitrate assists kidneys to excrete urinary citrate and shrink the risk for calcium stones (Tirabassi & Langer, 2014).
Question 3
Hydronephrosis is a health condition that affects the kidney. It transpires when kidney surges because of a botch of usual drainage of urine from the kidney to the bladder. The swelling in most cases affects one kidney, but it can at times affect both kidneys. Hydronephrosis is not a primary disease, but a secondary condition that is caused by some other primary disease. It occurs due to the presence of a kidney stone or scarring and a blood clot that blocks urine from moving from the kidney to the bladder. The blockage of the ureter causes urine to go back up the kidney resulting in swelling. The obstruction of urine leads to urine accumulation in and dilation of the renal pelvis and calyces (Al-Salem, 2017).
Usually, urine moves out of the kidney to the bladder at very low pressure. However, when the flow of urine is blocked, urine backs up after the point of blockage eventually returning the tiny tubes of the kidney. The urine also reaches the renal pelvis causing a swelling of the kidney which in turn increases the pressure on the kidneys internal structure. The elevated pressure caused by the blockage can cause damage to the kidney resulting in the loss of its ability to perform its functions. In case both kidneys are blocked, it can result in kidney failure. The blockage can increase the pressure inside the urinary tract and therefore slow the movement of urine.
Long-term swelling of the renal pelvis and the ureter can impede the rhythmic muscular contractions that serve to move urine down the ureter from the kidney to the bladder. Scar tissue can develop and substitute normal muscular tissue in the walls of the ureter causing long-lasting damage. The nephron can be damaged due to the presence of back pressure. With the elevation of intrapelvic pressure, a large fraction of the nephron stops functioning due to perfunctory destruction or the termination of filtration. On the other hand, the remaining nephrons can continue with the function with the reduced tubular flow. The reduced rate of tubular flow could be because of lessened filtration per nephron or even or the rise of proximal fractional reabsorption or both. Filtration is a role of the kidney that is performed by the glomerulus of the nephrons. Compression of the bladder can cause the reverse pressure of urine from the bladder to the kidney by enlargement of the prostate or the effect of feces in the colon as well as the abnormal contractions of the gallbladder muscles which can result in neurological dysfunctions. Nephrons experience mechanical damage when intrapelvic pressure rise and the alterations in blood flow cause ischemic damage. Intratubular blockage from injury or dead epithelial cells from the proximal parts of the nephron can result in back pressure which can further reduce glomerular filtration.

References
Al-Salem, A. H. (2017). Hydronephrosis in Infants and Children. In An Illustrated Guide to Pediatric Urology (pp. 43-69). Springer, Cham.Talati, J., & Abbas, F. (2013). Urolithiasis: Basic science and clinical practice. London: Springer.
Tirabassi, J., & Langer, S. (2014). How much calcium supplement is recommended in a patient with osteoporosis and a history of calcium oxalate kidney stones?.Tiselius, H. G., Daudon, M., Thomas, K., & Seitz, C. (2017). Metabolic Work-up of Patients with Urolithiasis: Indications and Diagnostic Algorithm. European urology focus, 3(1), 62-71.