Renal Disorders; Urolithiasis

Renal Disorders; Urolithiasis

Urolithiasis

Urolithiasis is a condition primarily characterized by calculi (stones) inside the urinary tract of an individual. The formation of stones in the urinary tract occurs when there is an increased concentration of substances such as calcium oxalate, uric acid and calcium phosphate in an individual’s urine. The increased level of the named substances in the urine is supersaturation (López & Quereda, 2012). Supersaturation status in any person depends on the ionic strength, the amount of the designated elements and the pH of the urine. This paper will describe in detail the manner in which the condition occurs and further discuss other components relevant to the state from the cases study of Fred.

Similarly, an individual can develop urolithiasis when he or she has a deficiency of the substances that usually inhibit crystallization in the body. Such elements include citrate, Nephrol acing, magnesium, and troponin.  Also, the fluid volume status is another vital defining factor that plays a role in one developing kidney stones; patients who are dehydrated are more likely to develop kidney stones than hydrated patients (Knoll & Pearle, 2013). The stones are in any part of the bladder or the kidney. The stones are variant in size ranging from small sized ones called gravel or sand to the bladder stones that could be the size of an orange.

Certain factors increase the risk of stones forming in the kidneys; these factors include urinary stasis, infection, and extended periods of immobility that slow down the renal drainage and alter the metabolism of calcium.  Moreover, elevated concentrations of calcium in the blood and the urine promote precipitation of calcium and subsequently formation of stones in the kidney. Studies have revealed that up to 75% of all renal stones are calcium based.  Multiple conditions cause high levels of calcium in the blood (hypercalcemia) and elevated levels of calcium in the urine (hypercalciuria). First, hyperparathyroidism, renal tubular acidosis, cancers and granulomatous diseases such as tuberculosis and sarcoidosis; the latter may result in an increase in vitamin D production by the granulomatous diseases. Similarly, individuals who take in a lot of vitamin D consistently, people who take a lot of alkali and milk are at risk of high blood and urine calcium levels (Talati, Tiselius, Albala, & YE, 2012). To wrap it up, patients diagnosed with myeloproliferative conditions such as polycythemia Vera, leukemia, multiple myelomas; such diseases produce an abnormal proliferation of blood cells from the bone marrow.

For individuals who have calculi that contain struvite, uric acid, or cystine, a detailed physical examination and a thorough metabolic laboratory workup are indicated because of the associated disturbances that contribute to the formation of the stone. Stones from uric acid (from approximately 6% to 10% of all stones) can be seen in patients with myeloproliferative conditions or gout. Stones that develop from struvite found in about 15% of all urinary stones. Struvite stones form in urine that is persistently alkaline and rich in ammonia; this is caused by bacteria that split urea such as pseudomonas, proteus, klebsiella, and mycoplasma or Staphylococcus species (Talati, Tiselius, Albala, & YE, 2012). The risk factors for struvite stones also known as infection stones are foreign bodies, neurogenic bladders, and UTIs that are recurrent

Cystine stones on the other hand account for 1% to 2% of all kidney stones. Cystine stones only occur in patients with a rare genetic defect in the absorption of cystine by the kidneys. Cystine is an amino acid that is the primary structural component of proteins.  Formation of urinary stones could also occur in patients with inflammatory bowel disease; patients who have had a bowel resection or an ileostomy are also likely to get urinary stones because they absorb more oxalate than the average patient (Talati, Tiselius, Albala, & YE, 2012). Furthermore, there are some types of medication that when taken by patients increase their likelihood of getting urinary stones. Medications such as acetazolamide, antacids, laxatives, a high dose of aspirin and vitamin D can cause kidney stones.  Despite there being many possible causes of renal stones, for many patients, no cause may be pinned down.

Citrate is a type of weak acid that is found in the body; it is formed after the Krebs’s cycle but can be similarly taken into the body through the diet of an individual; studies have revealed that a low concentration of citrate in urine has been associated with patients diagnosed with renal stones (Talati, Tiselius, Albala, & YE, 2012).  Citrate has a protective role in kidney stones formation that is linked to many processes. Citrate reduces the likelihood of people developing kidney stones because it reduces the supersaturation of urine by calcium salts. Citrate achieves this by first forming soluble complexes with ions of calcium. Secondly, it inhibits crystal aggregation and growth in the kidney making t difficult for kidney stones to form. Also, citrate makes some macromolecules such as Tamm-Horsfall protein found in urine more active (Knoll & Pearle, 2013). Such molecules inhibit the aggregation of calcium oxalate.

Moreover, citrate has been able to reduce the expression of urinary osteopontin. Idiopathic kidney stone formation, as well as renal calculi with other causes, can, therefore, be treated with administration of alkaline citrate. Therapy with magnesium citrate or potassium citrate is a standard prescription; these drugs increase the amount of urinary citrate subsequently lowering the rate of stone formation. Further studies on the same reveal that induces an increment of protective urine analytes such as citrate, pH, and potassium (Knoll & Pearle, 2013).

As said earlier, 80% of the kidney stones that occur are calcium based. Important to note is the fact that 80% of those calcium based kidney stones are calcium oxalate stones. Such calcium oxalate stones can be prevented in patients through pharmacologic and dietary means. Dietary calcium inhibits absorption of oxalate from the intestines. Patients who take calcium carbonate in their diet reduce their oxaluria (Knoll & Pearle, 2013). Calcium supplements are therefore taken to lower the risk of the patient developing calcium oxalate nephrolithiasis.

Hydronephrosis can be described the distension of the renal pelvis and calyces that are caused by the obstruction to the outflow of urine distal to the pelvis.  Hydronephrosis can result from an anatomic or functional blockage that interrupts the flow of urine to the urethral meatus from the kidney. The increase in the pressure within the ureter leads to substantial changes in the Glomerular filtration, renal blood flow, and tubular function. The rate of Glomerular filtration reduces hours after the acute obstruction by the kidney stone. The decline in the GFR can stay for longer periods even after the obstruction is gone (Iravani, Tay, Bay, & Ng, 2014). Moreover, the ability of the renal tubules to transport potassium, sodium, protons and to cause dilution of the urine is reduced severely

Elevated pressure in the ureter similarly results in perilymphatic as well as pyelovenous backflow. The gross changes in the urinary tract are dependent on the degree, duration, and level of obstruction of the stone. Hydronephrosis is accompanied by swelling of the ureter that is known as hydrotreater. The swelling is essentially from the buildup of urine that has been formed in the kidneys. Because the path of urine is now blocked by a stone that has been established the urine can no longer pass and is trapped behind the stone. Because the urinary tract is blocked urine cannot escape (Okumus, 2013). What follows is the swelling of the kidney. It is rare for any rupture to occur on the distended wall unless the individual is involved in a traumatic accident like a motor vehicle accident.

Obstruction of the general flow of urine causes it to back up leading to elevated pressure in the kidney.  Should the obstructing stone be in the bladder or the urethra the back pressure created affects both the kidneys but should the stone be small and be located in one of the ureters then the back pressure will only damage one of the kidneys. Intermittent or partial blockage can occur due to a renal stone that has formed in the renal pelvis and later moved into the ureter and blocked it too. When urine accumulates in the pelvis, it causes distension of the pelvis and its calyces (Okumus, 2013). As time goes by, the kidney undergoes atrophy.  As one of the kidneys is gradually destroyed, the other kidney enlarges gradually in what is termed as compensatory hypertrophy. The result is a bilateral renal failure. The swollen pelvis will gradually thin out and develop distended spaces within them.

The patients are likely to complain of an ache in their affected flank and in their backs too.  If the patients develop an infection, they will have chills, dysuria, tenderness, fever and pyuria. Pyuria and hematuria may be present. Pooling of urine in the kidneys or the ureter provides a nidus for infection arising. If both the kidneys are affected, the patient is likely to present with symptoms of chronic renal failure (Okumus, 2013).

In conclusion, it is important to note that, urolithiasis is condition primarily characterized by calculi (stones) inside the urinary tract of an individual. The formation of stones in the urinary tract occurs when there is an increased concentration of substances such as calcium oxalate, uric acid and calcium phosphate in an individual’s urine. The increased level of the named substances in the urine is termed as supersaturation. Supersaturation status in any person depends on the ionic strength, the amount of the designated elements and the pH of the urine. This paper has described the pathophysiology of the condition. It is caused by some factors such as hyperparathyroidism, renal tubular acidosis, cancers and granulomatous diseases such as tuberculosis and sarcoidosis; the latter may result in an increase in vitamin D production by the granulomatous diseases. Similarly, individuals who take in a lot of vitamin D consistently, people who take a lot of alkali and milk are at risk of high blood and urine calcium levels. All these increase the amount of calcium in the blood and urine. Finally, the paper discussed Hydronephrosis that is distension of the kidneys and ureter due to back pressure build up.

 

 

References

Damasio, P., Amaro, C., Padovani, C., Leitão, V., Yamamoto, H., & Amaro, J. (2014). Influence of clinical therapy and nutritional counseling on the recurrence of urolithiasis. Acta Cirurgica Brasileira29(6), 400-404. http://dx.doi.org/10.1590/s0102-86502014000600009

Iravani, O., Tay, E., Bay, B., & Ng, Y. (2014). Unilateral ureteric stone associated with gross hydronephrosis and kidney shrinkage: a cadaveric report. Anatomy & Cell Biology47(4), 267. http://dx.doi.org/10.5115/acb.2014.47.4.267

Knoll, T. & Pearle, M. (2013). Clinical management of urolithiasis. Berlin: Springer.

López, F. & Quereda, C. (2011). Melamine toxicity: one more culprit in calcium kidney lithiasis. Kidney International80(7), 694-696. http://dx.doi.org/10.1038/ki.2011.174

Okumus, M. (2013). Correlation of volume, position of stone, and hydronephrosis with microhematuria in patients with solitary urolithiasis. Medical Science Monitor19, 295-299. http://dx.doi.org/10.12659/msm.889077

Talati, J., Tiselius, H., Albala, D., & YE, Z. (2012). Urolithiasis. Dordrecht: Springer.

 

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