Stone Formation in the Kidney/ Role of Citrate in the Kidneys
Kidney stones are calcified or solidified molecules taking place in the upper urinary tract and the kidney. Kidney stones are usually composed of calcium as oxalate, phosphate, or carbonate. Stone formation in the kidney happens when the amount of mineral salts in the urine becomes saturated, during which the mineral will automatically crystallize (Rao et al., 2011). Stone formation is further facilitated by increasing amount of calcium in urine and dehydration. High levels of calcium in urine can indicate kidney disorder, prolonged incapacitation, hyperthyroidism or overactive thyroid, excessive intake of milk or aluminum and vitamin D. Stone formation in the kidney is a complicated mechanism that involves crystal retention; crystal buildup or growth; nucleation; saturation; and stone formation alongside complexors, inhibitors, and promoters in urine (Kopple et al., 2012).
The concentration of solutes, such as oxalate and calcium, in the urine that affects stone formation is too high that they must lead to formation of crystals in the urine of most people, yet this is apparently untrue. This occurrence is known as 'supersaturation' (Rao et al., 2011, 62). Nevertheless, inhibitors, or urinary substances, prohibit the formation of crystals. Citrate is the most widely known inhibitor, which chelates urinary calcium cations, reducing the presence of calcium to latch onto phosphate or oxalate anions. Citrate is the primary organic anion in the urine and an important substance for renal metabolism (Grossman & Porth, 2014). Because citrate is a major internal inhibitor of stone formation in the kidney, alterations in the secretion of citrate are clinically serious. Alterations in clinical derangements (e.g. acid-base homeostasis) affecting the transit of citrate into renal metabolism and renal tubule result in alterations in urinary citrate composition (Pak, 2012).
Citrate spontaneously inhibits calcium oxalate sedimentation administered clinically to slow down calcium oxalate crystal accumulation, which can damage renal cells. A positive impact on renal function and metabolic stone-forming mechanism was discovered in patients administered with citrate, linked to a significant reduction in the saturation of calcium oxalate. Current studies show that citrate could also fulfill a protective function in moderating oxalate-induced renal tubular epithelial cell damage (Pak, 2012). All these features and components of citrate contribute to the prevention of stone formation in the kidneys.
Calcium Supplements for Calcium Oxalate Stones
In the past, individuals at risk of or already suffering from calcium oxalate stones were advised to stay away from calcium supplements and calcium-rich foods. Yet, new scientific findings have proven that high levels of calcium intake in fact contribute to the prevention of stone formation because digestible calcium latches onto oxalates thus preventing the absorption of oxalates from the intestine and excretion by the kidney to create stones (Talati et al., 2012). It appears that calcium supplements create a protective mechanism, but when taken without food it only increases the possibility of stone formation because calcium is not able to bind with the oxalates.
Even though numerous physicians still advise their patients diagnosed with kidney stones to steer clear of calcium supplements, this instruction is largely obsolete. A compelling set of empirical findings has surfaced invalidating the widespread practice of limiting or preventing the intake of calcium supplements in patients with kidney stones (Pizzorno & Murray, 2012). Some studies have reported that the intake of calcium supplement decreases the excretion of oxalates. One research looked at urinary oxalate excretion after administering oxalic acid and calcium supplements. Calcium citrate malate and calcium carbonate were administered daily. The study found out that the intake of calcium supplements substantially diminished the absorption and excretion of oxalates (McDougal et al., 2015). Basically, these studies showed that the intake of calcium supplements on a daily basis could be a successful protective mechanism against calcium oxalate stones.
However, there are still concerns regarding the capability of calcium supplementation to heighten the possibility of developing calcium oxalate stones. Those with calcium stones, renal hypercalciuria, sarcoidosis, or primary hyperthyroidism must not get into calcium supplementation (McDougal et al., 2015). They could be at a higher risk for the development or intensification of long-term calcium stone formation. Other patients could undergo a urine sample analysis for calcium to identify or evaluate their susceptibility before they engage in calcium supplementation (Pizzorno & Murray, 2012).
In general, the biggest likelihood of stone formation would take place in the initial months of taking calcium supplements when levels of urinary calcium and free calcium absorption are at their peak. Calcium citrate could decrease the possibility of kidney stone formation in at-risk patients. Moderate intake of calcium supplements, administered as prescribed, is quite safe in patients without any history of hypercalciuria and nephrolithiasis and has a normal or average serum calcium (Talati et al., 2012). The consequences of a long-term intake of calcium supplements in a sizeable number of people are still unidentified.
Hydronephrosis/ Back-Pressure in the Kidney
Hydronephrosis is a restrained swelling of renal pelvis, attended by the loss of renal pelvis brought about by a persistent fragmentary or irregular total blockage to urinary flow. In other words, hydronephrosis is the breaking of renal sinus echoes (Anderson, 2013). It is caused by a disruptive pathology within the urinary tract, as well as by excessive dilation of the urinary bladder for a long duration of time. The condition occurs when there is a dilation of all the calyces alongside swelling of the renal pelvis. Hydronephrosis and hydroureter stem from chronic and worsening back pressure on the kidney calyces and ureter (Quaia, 2011). Basically, hydronephrosis is the swelling of the kidney and the pelvis caused by back pressure in the ureter. This condition is largely brought about by blockage of the ureter. Hydronephrosis is a severe illness because, once the tension in the pelvis sharply increases, back-pressure on the kidney can damage the nephrons or disrupt tubular function (Anderson, 2013).
Progressive and chronic hydronephrosis can bring about long-term nephron damage; and, heighten the risk of stone formation, infection, and renal failure. Urinary blockage or back-pressure in the kidney results in nephron destruction when pressure accumulates in the kidney tissue (Vincent, 2013). The pressure on the tubular filtrate also intensifies in the nephron as drainage infiltration or discharge mechanisms through the collecting zone are damaged. Because of such increased back pressure, glomerular filtration diminishes or breaks off. Necrosis, or cell injury, of the impaired kidney can take place (Pennell, 2014). Pennell (2014) explains that electrolytes-- phosphorus, potassium, and sodium-- and nitrogen wastes-- uric acid and urea are absorbed or maintained, and the balance between acid and base becomes defective.
Conclusions
Based on the discussion, patients, like Fred, with possible renal stones should be evaluated for distress and pain, including related symptoms, like abdominal bloating, diarrhea, vomiting, and nausea. The location and seriousness of pain must be identified, alongside any diffusion of pain. Nurses must assess and observe symptoms and indications of urinary tract infection (UTI), such as fever and chills, and obstructions or blockages, such as persistent discharge of small amounts of urine. The urine should then be examined for blood and filtered for stones. Nursing professionals should also properly inform or educate patients, like Fred, and their families so that they would know how to correctly address renal disorders once it occurs.
References
Anderson, J. (2013). Hydronephrosis. St. Louis, Missouri: Elsevier.
Grossman, S. & Porth, C. (2014). Porth's pathophysiology: concepts of altered health states. Philadelphia, PA: Lippincott Williams & Wilkins.
Kopple, J. et al. (2012). Nutritional management of renal disease. UK: Academic Press.
McDougal, W. et al. (2015). Campbell-Walsh urology. St. Louis, Missouri: Elsevier Health Sciences.
Pak, C. (2012). Renal stone disease: pathogenesis, prevention, and tratment. New York: Springer Science & Business Media.
Pennell, V. (2014). A handbook of urology for students and practitioners. Cambridge, UK: Cambridge University Press.
Pizzorno, J. & Murray, M. (2012). Textbook of natural medicine. St. Louis, Missouri: Elsevier Health Sciences.
Quaia, E. (2011). Radiological imaging of the kidney. New York: Springer Science & Business Media.
Rao, N. et al. (2011). Urinary tract stone disease. New York: Springer Science & Business Media.
Talati, J. et al. (2012). Urolithiasis: basic science and clinical practice. New York: Springer Science & Business Media.
Vincent, J. (2013). Annual update in intensive care and emergency medicine 2013. New York: Springer Science & Business Media, 2013.
