An Instructor Is Reviewing the Process of Tubular Secretion Which Would the Nurse Include?
Clin Nutr Res. 2015 Jul; four(3): 137–152.
Nutritional Management of Kidney Stones (Nephrolithiasis)
Haewook Han
1Department of Nephrology, Harvard Vanguard Medical Associate, Boston, MA 02115, Usa.
Adam M. Segal
iiHarvard Vanguard Medical Associate, Clinical Teacher at Harvard Medical School, Boston, MA 02115, USA.
Julian L. Seifter
3Harvard Vanguard Medical Associates; Brigham and Women's Hospital, Boston, MA 02115, USA.
Johanna T. Dwyer
4Tufts University Friedman School of Nutrition and Schoolhouse of Medicine, Boston, MA 02111, United states of america.
Received 2015 Jul six; Revised 2015 Jul twenty; Accepted 2015 Jul twenty.
Abstract
The incidence of kidney stones is common in the United States and treatments for them are very costly. This review commodity provides information near epidemiology, mechanism, diagnosis, and pathophysiology of kidney stone formation, and methods for the evaluation of stone risks for new and follow-up patients. Acceptable evaluation and management tin forbid recurrence of stones. Kidney stone prevention should be individualized in both its medical and dietary direction, keeping in mind the specific risks involved for each type of stones. Recognition of these gamble factors and evolution of long-term direction strategies for dealing with them are the virtually effective ways to prevent recurrence of kidney stones.
Keywords: Nephrolithiasis, Calcium oxalate, Uric acid rock, Hypercalciuria, Hyperoxaluria, Risk factors for kidney stones, Prevention of kidney stone
Introduction
Nephrolithiasis, or kidney rock, is the presence of renal calculi caused past a disruption in the residue between solubility and precipitation of salts in the urinary tract and in the kidneys. The incidence is at peak among white males age 20 and 30 years old. The National Health and Diet Examination Survey (NHANES) III (1988-1994) reported that in that location was a 5% prevalence of stone germination among adults in the Us and this represented a 4% increase from the NHANES Ii (1976-1980) [one,2]. Nephrolithiasis is considered to be a disease of affluence like obesity, hypertension, and type 2 diabetes because it is so prevalent in wealthy countries [3,4]. Urologic intervention is required in as many equally 20% of patients with renal colic [5] and more than $two billion is spent on treatment each twelvemonth. The lifetime prevalence of kidney stones in the United States is 12% amidst men and vii% among women [half-dozen,7]. Kidney stones develop when urine becomes "supersaturated" with insoluble compounds containing calcium, oxalate (CaOx), and phosphate (CaP), resulting from dehydration or a genetic predisposition to over-excrete these ions in the urine. About 5-10% of Americans have this predisposition.
Kidney stone germination
When CaOx concentration is iv times to a higher place the normal solubility a crystal starts to grade. If the CaOx concentration is 7 to 11 times higher than normal solubility the nucleation begins. In low urine volume, the presence of high calcium, high oxalate the supersaturation (SS) of CaOx is increased. Citrate in the urine forms soluble complex with urinary Ca. If urine has low citrate concentration SSCaOx is promoted to course CaOx stone. If urine pH is > 6.5, proportion of divalent and trivalent ions are increased then SSCaP is favorable. The levels of urinary supersaturation of the dissimilar solutes determine the specific types of stones [eight,9,10].
Kidney stones tend to recur. Approximately 50% people who grade one stone form another within 10 years. The risk of recurrence ranges from thirty-l% at 5 years in observational studies. The control groups in recent randomized controlled trials accept a 2-five% annual recurrence rate later an incident calcium oxalate stone. Recurrence rates also depend on the stone type. When nuclei of uric acrid form, they lower the metastable limit (e.g. susceptibility to perturbation) and favor further rock precipitation. Decreased supersaturation of the urine filtrate will decrease the hazard of recurrence of kidney rock [11].
Types of Kidney Stones
Table one describes the various types of kidney stones and their prevalence. Approximately 70-80% of kidney stones are composed of calcium oxalate and calcium phosphate. Of the residual, 10% are struvite, 10% of uric acid; and less than ane% are composed of cystine or are diagnosed as drug-related stones. Calcium and uric acid stones are more common in men; women have more struvite stones. Figure 1 shows the appearance of the different types of stones.
Blazon of stones. Calorie-free microscopy of urine crystals. (A) Hexagonal cystine crystal (200X); (B) coffin-lid shaped struvite crystals (200X); (C) pyramid-shaped calcium oxalate dehydrate crystals (200X); (D) dumbbell-shaped calcium oxalate monohydrate crystal (400X); (E) rectangular uric acrid crystals (400X); and (F) rhomboidal uric acid crystals (400X). Reprinted with permission by Elsevier and reference [12].
Table 1
Type of stones
| Type | Frequency (%) | Sex | Crystals | Radiography |
|---|---|---|---|---|
| Calcium oxalate/ mix | 75 | M | Envelope | Round, radiodense, sharply outlined |
| Calcium phosphate (brushite) | v | F>M | Amorphous: Alkaline urine | Small, radiodense, sharply outlined |
| Uric acid | 5-fifteen | 1000=F | Diamond; Acid urine | Round/ staghorn, radiolucent, filling defect |
| Struvite (Mg ammonium phosphate) | ten-20 | F | Coffin lid; Infection/ urea splitter | Staghorn, laminated radiodense |
| Cystine | ane | M=F | Hexagon | Staghorn, radiodense |
Calcium stones
Nigh calcium stones are composed of calcium oxalate, either past itself or much more commonly in combination with calcium phosphate or calcium urate [9,13]. Hypercalciuria, low urine volume and hypocitraturia all predispose to the evolution of calcium stones. Hypercalciuria often occurs with diseases associated with hypercalcemia like hyperparathyroidism, malignancy, sarcoidosis and vitamin D excess [fourteen,15]. When no other cause is constitute the hypercalcuria is known as "idiopathic hypercalciuria". Idiopathic hypercalciuria is familial and is likely a polygenic trait, although there are some rare monogenic causes of hypercalciuria and kidney stones such as Dent's illness, an X-linked disorder characterized past hypercalciuria, nephrocalcinosis, and the evolution of renal failure. Alkaline metal urine is a risk factor for the development calcium phosphate stones [xi,16,17]. Another risk factor for calcium oxalate stone is hyperoxaluria, which occurs due to bowel disease (enteric hyperoxaluria) and genetic disorders of oxalate metabolism (primary hyperoxaluria) [eighteen].
Dietary oxalate may be of import in stone evolution; spinach, beets and rhubarb in particular, contain big amounts of oxalate and they may increment urinary oxalate excretion and predispose to the development of calcium oxalate stones. High dose vitamin C therapy can also lead to increased oxalate generation as vitamin C (ascorbic acrid) is metabolized. Oxalate reabsorption in the colon is reduced by the formation of insoluble calcium oxalate [nineteen,20,21,22,23,24].
This is very important in planning therapy because restricting dietary calcium results in less calcium existence available in the intestinal lumen to bind the oxalate. This leads to increased oxalate assimilation and therefore increased urinary oxalate excretion [21,25,26,27]. Therefore, dietary calcium should not exist restricted in malabsorption syndromes such as pocket-sized bowel affliction, following surgical small bowel resection, jejuno-ileal bypass surgery and inflammatory bowel disease (IBD) in which in that location is malabsorption of fat acids and bile salts. Abdominal calcium binds to fatty acids, causing less bounden to oxalate. Non-absorbed bile salts in the colon will also cause increased colonic permeability to oxalate. Bariatric (weight loss) surgical techniques that create a malabsorptive state are being performed more often today than ever earlier. Calcium oxalate stone formation is an increasingly common complication with the more restrictive procedures, due to the highly restrictive forms of bariatric surgery such as the Roux-en-Y gastric bypass, sleeve gastrectomies and duodental switches with biliopancreatic diversion that generate malabsorption syndromes. Diarrheal losses cause volume depletion and decreased urine volume. Bicarbonate loss in the stool tin cause a metabolic acidosis which can in turn lead to a low urinary pH and hypocitraturia (due to enhanced proximal reabsorption) which will predispose to the evolution uric acrid and calcium oxalate rock formation [28,29].
Uric acid stones
Pure uric acid calculi are radiolucent on plain radiographs only visible on ultrasonography or computerized tomography (CT). These stones tend to form in individuals with hyperuricosuria. Approximately 15-xx% of patients with uric acrid stones have a history of gout [30,31,32,33]. A diet rich in animal protein, because of its high purine content, which produces uric acid in its catabolism, may increment the risk of uric acid rock germination [32,34,35]. At a urinary pH of less than 5.v, uric acid is poorly soluble, but solubility increases at a pH greater than vi.5.
Cystine stones
These stones tend to course only in patients with cystinuria, an autosomal recessive disorder affecting ane in 15,000 adults in the USA that accounts for just one% of patients with nephrolithiasis. In cystinuria, nephrolithiasis is the just clinical manifestation and it arises as a effect of abnormal renal tubule transport which in plow leads to large amounts of urinary cystine excretion. Cystinuria occurs equally in males and females, although males are more severely affected. Stones brainstorm to class in the 1st to 4th decades of life and tend to be large, multiple and bilateral. The diagnosis tin be fabricated by finding typical hexagonal crystals in the urine [36,37]. Urinary tract infection and obstruction are common, equally is stone recurrence every ane-4 years.
Struvite stones
Struvite stones are also called triple phosphate stones, or infection stones. They form in the presence of upper urinary tract infections with urease-producing bacteria (most usually Proteus and Klebsiella). Normal urine is undersaturated with ammonium phosphate; struvite rock germination occurs just when ammonia production is increased and the urine pH is elevated, which decreases the solubility of phosphate. Bacterial urease is essential for the development of struvite stones because it leads to an elevation in ammonium, carbonate and urinary pH all at the same fourth dimension. In this setting phosphate combines with ammonium, magnesium and carbonate to form a stone composed of magnesium ammonium phosphate (struvite) and calcium carbonate-apatite.
Urease breaks downwardly urinary urea into ammonia and carbon dioxide:
The ammonia produced past this reaction then combines with water:
Resulting in increased availability of ammonium in an element of group i urine.
Struvite stones ordinarily occur in patients with recurrent urinary tract infections, especially if they have abnormal urinary tract beefcake, or require frequent float catheterization. The stones may likewise occur on infected calcium, uric acrid or cystine stones, particularly after instrumental procedures. Struvite stones are three times more common in women than men, presumably because urinary tract infections are more common in women. They are typically very large and may exist so big as to fill the renal pelvis (forming a "Staghorn calculus"). Their growth is rapid and they often grow dorsum after surgical removal because infected fragments of rock have been left backside [38,39,40].
Clinical Diagnosis of Kidney Stones
Non-obstructing kidney stones produce no symptoms or signs apart from hematuria. However, the kidney stone may cause severe pain, commonly accompanied past nausea, airsickness and hematuria (renal colic) when it passes into the ureter. Patients may also complain of urinary frequency and urgency. These signs and symptoms atomic number 82 to many emergency department visits and hospitalization. The pattern of the pain from rock depends on its location: a stone in the upper ureter leads to pain in the flank that may radiate to the upper abdomen.
When the stone is in the lower ureter, pain may radiate to the ipsilateral testicle in men or labium in women. If the stone is lodged at the ureterovesical junction, the main symptoms will exist urinary frequency or urgency. Symptoms chop-chop improve after passing the stone. On physical test, the patient is often in excruciating hurting, and is unable to attain a comfortable position. Ipsilateral costovertebral angle tenderness may also be present.
Laboratory tests may evidence a leukocytosis which may be due to a stress response or infection. Serum creatinine is often elevated if the patient is volume depleted, or if there is bilateral ureteral obstruction or unilateral obstruction in a patient with a solitary kidney. The urinalysis will have ruby-red blood cells, white blood cells and occasionally crystals. Notwithstanding, because of the oftentimes non-specific concrete examination and laboratory findings, imaging studies are disquisitional in making the diagnosis.
Initial evaluation includes obtaining a non-contrast helical CT, which can accurately visualize the size and location of the stones. A kidney, ureter and float (KUB) flick, although it is insensitive to uric acid stones since they are radiolucent and therefore are not visualized. Nevertheless, information technology can visualize calcium - containing, struvite and cystine stones in the kidney or ureter. Complete ureteral obstruction and upper urinary tract infection (UTI) are indications for stone removal by extracorporeal shock wave lithotripsy (ESWL) or surgery [9,12,xvi,31,41].
Medical and nutrition evaluation of kidney stones
A comprehensive history should be taken by one of the health care providers, and the post-obit items should exist covered: prior kidney stones, composition of prior stones if known, dietary history including an judge of typical daily fluid intake, social history including details regarding occupation and lifestyle, and family history.
The medical history should focus on identifying diseases that increment rock risk including conditions that atomic number 82 to hypercalciuria, gout, chronic diarrhea and malabsorptive gastrointestinal disorders.
Interpretation of biochemical and urine tests
Urine
The urine sediment should be examined for crystals. A 24-hour urine collection should be performed to measure urine calcium, oxalate, uric acid, pH, book, creatinine and citrate. Some laboratories summate supersaturation values for calcium oxalate, calcium phosphate and uric acrid and these are particularly helpful [12,42,43].
The 24-hour urine drove
The all-time way to evaluate rock risk is a 24-hour urine drove and assay [8,12]. Ii 24-hour urine collections are recommended for the initial evaluation for an accurate assay and to determine variability [44]. The 24-hour urine collection should be several weeks later on any procedures (i.due east. 6-eight weeks after lithotripsy) in order to minimize the risk of result be existence influenced past infection or presence of claret due to these causes. Infection tin can change the pH and citrate levels. It is very important that patients continue with their usual nutrition and activities during the collection period. The 24-hr urine creatinine excretion can give information nigh the adequacy of the urine drove. In full general, developed males produce 18-24 mg creatinine/kg/d and females 15-20 mg/kg/d [9,12]. 24-hr urine collection is not authentic as the urinary creatinine levels will be higher than normal for over collection and lower than normal for under-collection [44].
Tabular array 2 provides a summary of the normal values for the 24-60 minutes urine drove and probable causes of abnormal values. The 24-hour urine sample should include volume, and the solutes calcium, phosphorus, oxalate, citrate, pH, and uric acid to provide an judge of supersaturation and the take a chance of stone formation. Creatinine is tested to ensure total collection and to normalize solute excretion to the more than constant amount of creatinine. Dietary factors include sulfates which are mostly from animal protein and sodium since they are related to calcium, potassium, and magnesium excretion. Urea nitrogen is used to estimate poly peptide catabolic charge per unit (PCR). The PCR is unremarkably indicative of dietary protein intake in an individual who is not in a catabolic state. The human relationship between urinary nitrogen appearance charge per unit and estimated dietary poly peptide intake is and so calculated. The value of the 24-hour urine is to evaluate dietary nutrients and fluid intakes and to provide guidance for the patient'southward management. For example, normal urinary calcium levels are <250 mg/d for men and <200 mg/d for women. High urinary calcium may exist caused by idiopathic hypercalciuria, or diet high in sodium or protein. Depression urinary calcium is often due to malabsorption or underlying bone affliction. A normal urinary oxalate level is xx-40 mg/d. High levels are due to loftier oxalate diet, increased endogenous production, loftier vitamin C consumption and irritable bowel affliction. Normal urinary citrate levels are >450 mg/d for men and >550 mg/d for women. High animal protein diets and renal tubular acidosis (RTA) can increase acid production affecting urinary pH and so that it declines citrate levels.
Table two
Normal values of 24-hour urinalysis
| Normal value | Cause of abnormal values | |
|---|---|---|
| Ca | <250 mg/d for males | ↑ Idiopathic hypercalciuria, high Na nutrition (loftier urine Na), high protein diet |
| <200 mg/d for females | ↓ with os disease | |
| Phosphorus | 0.vi-ane.2 chiliad/d | ↓ with bowel disease, malnutrition, with large corporeality of food intake |
| Mg | 30-120 mg/d | ↓ with some laxatives, malnutrition, malabsorption |
| Oxalate | 20-forty mg/d | ↑ with high oxalate diet, high vitamin C consumption |
| if > 80, abdominal (Inflammatory bowel affliction) or oxalosis | ||
| Citrate | >450 mg/d for males | ↓ RTA, hypokalemia, high fauna protein nutrition, acidosis, diarrhea |
| >550 mg/d for females | ||
| Uric acid | <0.8 1000/d for males | ↑ with high creature protein nutrition (high purine), alcoholic beverages, overproduction |
| <0.75 g/d for females | ||
| Volume | >2,000 ml/d | ↓ with low fluid intake |
| pH | 5.8-6.two | ↓ RTA, urea splitting infection, acidosis, high brute protein intake (high purine content) |
| ↑ vegetarian diet, high citrus consumption, soft drink | ||
| Na | 50-150 mEq/d (1,150-3,450 mg) | ↑ with high Na diet |
| ↓ with low volume | ||
| K | 20-100 mEq/d | <20 meq Bowel disease, diuretics, laxatives |
| Cl | 70-250 mEq/d | |
| Urea nitrogen | 6-14 m/kg/d | ↑ with high protein diet |
| PCR | 0.8-1.4 k/d | ↑ with high protein diet |
| Sulfate | xx-80 mEq/d | ↑ with high poly peptide diet |
| Ammonium | 15-60 mM/d | ↑ pH > 7 urea splitting infection |
| ↓ pH < v.5 CRI, UA stones, gout | ||
| Cr | xviii-24 mg/kg for males | ↑ with more than 24 60 minutes drove |
| fifteen-xx mg/kg for females | ↓ with nether drove |
Diet assessment
The dietitian's role in nephrolithiasis intendance is very important. The dietitian should assess nutritional take a chance factors by dietary intake assessments and provide therapeutic recommendations based on dietary risks. Dietary assessment is very important both in treating and preventing rock formation. The dietitian should evaluate dietary intakes of calcium, oxalates, sodium, poly peptide (both animal and plant), dietary supplements and fluid intake since these tin either promote or inhibit rock formation, and plan the therapeutic nutrition based on those information. Fluid intake is especially important to quantify.
There are several dietary cess methods: the 24-hour recall, nutrient record diet history and food frequency questionnaire. The dietary intakes should be reflected on the urinalysis and it is good mode to evaluate the causes of kidney stones and to foreclose recurrence. Nutrient records provide information on intake of foods, beverages, and dietary supplements over specific periods. The near appropriate diet assessment for kidney stones is the food record during a 24-hour urine collection, every bit well as ane-2 days before the collection. The food record should be analyzed to evaluate intakes of protein, sodium, potassium, calcium, phosphorus, magnesium, uric acid, oxalate and fluid. Based on the food intake and urinalysis, the clinicians tin provide the acceptable medical and nutrition treatments.
Risk Factors for Kidney Stones
Major adventure factors
Risk factors for rock formation may be hereditary or disease related, such every bit idiopathic hypercalciuria, hyperoxalosis Paring's illness, medullary kidney disease, polycystic kidney affliction, hyperparathyroidism, irritable bowel disease (IBD), renal tubular acidosis or sarcoidosis. Patients with a family history of nephrolithiasis have a 2.five times greater adventure of stone germination [42]. Other risk factors include environs and diet (Table three).
Table 3
Run a risk factors of kidney stone
| Hereditary and other affliction related | Environs | ||
|---|---|---|---|
| Genetic | Idiopathic hypercalciuria Cystinuria: Dent's disease Hyperoxalosis | Climate | Heat H2o loss, sweating |
| Kidney disease related | Medullary sponge kidney Horseshoe PKD (10% develop stones) Metabolic causes: hypercalcemia, hyperparathyroidism, DM and obesity | Dietary | Na Oxalate Protein (animal) Acid/ element of group i ash nutrition Fluid Potassium and citrate Fluid Vitamins (C, D) Ca supplement Depression Ca diet High protein weight loss nutrition |
| Systemic disease | GI, Inflammatory bowel diseases (Ox and UA stones) | ||
| Hyperparathyroidism | CaP stone | ||
| Renal tubular acidosis (RTA) | Hypercalcemic states, Ca phosphate | ||
| Sarcoid | Hypercalciuria, CaOx stone | ||
Table four shows the conditions that favor stone formation. Urinary crystalloids tin form nucleus on the existing surface and supersaturate urine. Low urinary magnesium causes decrease circuitous formation with urinary oxalate assuasive free oxalate to be more than available in the urine. Low urinary citrate also increases stone formation considering citrate forms a complex with calcium so gratis calcium is more than bachelor for stone formation. High concentrations of uric acids in the urine will promote the nuclei to starting time stone formation. If the patient is dehydrated, he or she volition accept low urine output and therefore the urine can be supersaturated. Urine pH is very important for the germination of some types of stones. For case, low urine pH is favorable to germination of CaOx and uric acid stones while a high urine pH promotes CaP rock formation.
Table 4
Weather condition favoring development of diverse kidney stones
| Factors | Functions |
|---|---|
| Increased urinary crystalloids | Form nucleus on existing surface |
| Supersaturated urine | |
| Decreased inhibitors | Magnesium (complexes with oxalate) |
| Citrate (complexes with calcium) | |
| Nephrocalcin, uropontin | |
| Tamm Horsfall | |
| Increased promoters | Uric acid |
| Dehydration | Low urine book, supersaturated urine |
| Urine pH | Element of group i → Ca phosphate |
| Acidic → Uric acid, cysteine | |
| Diet | High protein/sodium/Ca → hypercalciuria, uricosuria, oxaluria |
| High oxalate → oxaluria | |
| Medication | Furosemide: decrease urinary volume |
| Na bicarbonate: increase urinary Ca |
Dietary causes may as well generate increased risks of diverse stones. High sodium intake increases urinary calcium excretion. High oxalate diets, large dose of vitamin C supplements (>ane,000 mg/d) will increase urinary oxalate level. Loftier protein diets (> 2.0 g/kg/d) tin increase urinary calcium, subtract urine pH and as well increase urinary uric acrid level [14]. Therefore high protein diets tin increase CaOx, and uric acid stone risks. Diuretics, such as furosemide can induce dehydration which can increase gamble of supersaturation of solutes.
Environmental conditions such as heat may increase not-renal evaporative peel losses and past doing so they reduce urine book and increase stone risk [24,45,46,47,48,49,50,51]. The most challenging aspect of encouraging patients to increment their fluid intakes is that they cannot wait for the normal thirst mechanism to urge them to potable considering the hypothalamic- pituitary sensors/ neurons pb to increased antidiuretic hormone levels; therefore, the urine becomes more full-bodied earlier the thirst mechanism is triggered and the urine becomes more dilute. I patient education method used is to remind people to drinkable fluid later each void.
Urine volume: a disquisitional factor
Urine must be supersaturated with solutes to class a crystal, the offset step to grade a stone. Low fluid intake will lead to depression urine output. When urine volume is depression, the urine tin theoretically be easily supersaturated with various solutes, such every bit calcium, oxalate, phosphorus, and uric acid. However, there are several inhibitors normally present in the urine to prevent crystallization of these solutes [52,53,54,55]. Only if the supersaturation is very high does the crystallization start. The nearly directly way for patients to decrease risks of supersaturation is to increment the urine volume with oral fluids to above 2.five L/d of urine volume [56].
Hypercalciuria
Figure 2 shows a model of how idiopathic hypercalciuria occurs. Normal urine calcium excretion is less than 200-250 mg/d. If urine calcium excretion is higher than this, stone risk increases. To evaluate the stone take a chance, it is necessary to measure serum calcium, urinary calcium, oxalate, urine urea nitrogen (UUN), citrate, magnesium, creatinine, and volume (Table 5). In idiopathic hypercalciuria, the serum calcium level is normal but urinary calcium is high because of increased absorption of calcium from the gastrointestinal tract. The increased assimilation of calcium increases the ionized calcium level, decreases parathyroid hormone (PTH) secretion and decreases renal tubular reabsorption of calcium. The increased intestinal calcium assimilation can be treated with ane, 25-dihydroxy vitamin D3. There is too prove of reduced proximal tubular reabsorption of sodium and calcium in patients with idiopathic hypercalciuria, which leads to a negative calcium residuum [57]. The combination of a depression sodium diet and thiazide diuretics may lower urinary calcium excretion by increasing reabsorption of calcium.
Model of idiopathic hypercalciuria.
Table 5
Summary of evaluation of stone disease
| First stone | Recurrent stone and follow up |
|---|---|
| Bones medical evaluation Ii 24-h urine analysis (no intervention prior to analyze stone run a risk): Ca, phosphorus, Mg, Oxalate, Citrate, uric acrid, volume, creatinine, pH, urea nitrogen, Na, K Blood tests: Serum Na, K, CO2, BUN, Cr, Ca, phosphorus, uric acid and PTH Usual dietary intake Dietary/ fluid intake history Diet and medical treatment | One 24-hour urine analysis: Ca, Phos, Mg, Oxalate, Citrate, uric acid, volume, creatinine, pH, urea nitrogen, Na, K Blood tests: Serum Na, K, CO2, BUN, Cr, Ca, phosphorus, uric acid and PTH Dietary and medical treatment ** If patient has recurrent stone after 2 years of last stone formation, two 24-h urinalysis is advisable. |
Hyperoxaluria
The well-nigh common type of stones are CaOx (75%) and a high urinary excretion of oxalate is a hazard factor for them. Dietary sources of oxalate include spinach, rhubarb, beets and some berries. Oxalate is also created from endogenous metabolism of glycine, hydroxyproline and ascorbic acid. A low oxalate nutrition is recommended for the prevention of CaOx stones; however, a recent study showed that dietary oxalate had little upshot on urinary oxalate excretion although vitamin C intake was highly correlated with urinary oxalate excretion [58].
Increased urinary oxalate excretion has also been noted in patients with diabetes [57,59]. Patients with IBD take a high prevalence of CaOx stones with hypocalciuria due probably to their negative calcium rest. Negative calcium residual tin can also crusade secondary hyperparathyroidism to maintain normal calcium levels in blood, and a calcium supplement may be constructive for preventing CaOx stone risk by decreasing the hyperparathyroidism. The timing of calcium supplements is important and patients should accept supplements at the meal time to bind oxalate from dietary sources. Individuals who have had restrictive bariatric surgery have a high risk of hyperoxaluria due to malabsorption and increased reabsorption of oxalate, which may increase hyperoxaluria [29,threescore]. Recent studies by Jiang et al. advise that enteric colonization with Oxalobacter formigenes, which uses oxalate as a principal energy source, reduces the hazard of CaOx stone recurrence among individuals whose intakes of calcium were low [61]. In contrast, at that place is insufficient bear witness to support the apply of probiotics to reduce stone adventure at this time [62].
Hypocitraturia
The urine is unremarkably supersaturated with solutes, especially CaOx; however, the level tends to exist less than the 10 times the level of concentration to form the CaOx crystals due to the presence of citrate in the urine. Citrate in the urine binds with urinary calcium to class a soluble compound and this increases the urine pH. CaOx stone formation is favored by a low urine pH; therefore, citrate can aid forbid CaOx rock formation. The most common form of citrate prescribed is potassium citrate. The normal value of urinary citrate for males is >450 mg/d and for females >550 mg/d. Renal tubular acidosis and chronic diarrhea tin also cause decreased citrate in the urine. Even so calcium, oxalate and urine pH should be checked before initiation of citrate handling [63]. If urine pH increases later with citrate treatment, the risk of CaP stone formation rises. In patients who have IBD with high urinary oxalate, and depression urinary sodium levels because of malabsorption and gastrointestinal loss of sodium, sodium citrate is more benign than potassium citrate, and it should be used. However, sodium citrate can increase urinary calcium excretion and therefore it may increase the risk of CaOx stones.
pH
Urine pH is an important factor in the germination of kidney stones. A depression urine pH can promote CaOx and uric acid stones, and a high urine pH tin can increase the take a chance of CaP stones. Urine pH is affected by the acid and element of group i ash from the nutrition, and earlier the advent of effective urinary acidifying and alkalinizing agents, it was necessary to rely on diet to alter urinary pH, although this could rarely be accomplished finer. The practice has been largely outdated by the appearance of amend acidifying and alkalinizing agents. The mineral common salt that predominates in foods determines whether the residue or 'ash' is acidic or alkaline. The minerals producing alkaline ash are sodium, potassium, magnesium, and calcium. Acid-forming minerals are sulfur, chlorine, and phosphorus. High fauna poly peptide diets which accept high purine content and sulfur containing amino acids can reduce urine pH and will pb to an increased adventure of uric acid stones. An alkaline ash diet which is high in citrate, mostly from fruits and vegetables, can increase urine pH and citrate excretion. Today alkali therapy is preferable because an alkaline ash diet is difficult to follow for most patients although an alkaline ash urine is preferable for the certain blazon of stone risk. However, for other stones, the reverse may be true. A high pH without alkali therapy may increase the risk of struvite stones from a UTI.
Uric acrid
The prevalence of uric acid stones is about 5% of total kidney stone affliction. The main determinant of uric acrid stones is urine pH. A low urine pH has more insoluble uric acids concentration; therefore, the risk of uric acid rock is higher. Measurements of urinary calcium, uric acid, and post-prandial urine pH are used to assess the uric acid stone. The average adult consumes about two mg of purine/kg/d, which produces 200-300 mg of uric acid daily. Endogenous product of uric acrid is about 300 mg/d. In some studies, uric acid excretion is 5.6 mg/kg/d [32] and total excretion of uric acid is less than 800 mg/d. Dietary consumption of purine varies daily among individuals. Kessler et al. conducted a cross-sessional study past using bicarbonate-rich mineral water and various types of juices on uric acrid stone germination and found that blackness electric current juice decreased uric acid stone risk the most, past increasing the urine pH [64,65]. Ingestion of alcohol tin can also touch on urinary uric acid excretion, and excesses should be avoided. If patients have gout, allopurinol is normally prescribed forth with low purine diet to reduce claret uric acrid and uricosuria [32,34].
Dietary run a risk factors
Several dietary factors can increase risk of the stone formation, including sodium, poly peptide, potassium, calcium, magnesium and other nutrients. These constituents can be modified depending on the types of different stone risks. Foods that produce acid-ash after being metabolized in the trunk can affect the lowering of urinary pH whereas alkaline-ash foods can increase urinary pH. The specific diets are based on urine pH, urinary uric acid and types of stones (Table 6).
Table 6
Acid-ash and element of group i-ash foods
| Acid-ash foods | Alkali metal ash foods | ||
|---|---|---|---|
| Meat | Meat, fish, fowl, shellfish, egg | ||
| Dairy and other poly peptide | All types of cheese Peanut butter Peanuts | Dairy | Milk and milk products Butter milk |
| Fat | Bacon, nuts (Brazil, filberts, walnuts) | Fat | Nuts (almonds, chestnuts, coconuts) |
| Starch | All types esp. whole wheat Crackers, cereal, macaroni, spaghetti, noodle, rice | ||
| Vegetables | Corn, lentils | Vegetables | All types except corn and lentils Beets, beet greens, Swiss chard, dandelion greens, kale, mustard greens, spinach, turnip greens |
| Fruits | Cranberries, plums, prunes | Fruits | All types except cranberries, plum and prunes |
| Desserts | Obviously cakes, cookies | Sweets | Molasses |
Sodium
Dietary sodium restriction alone decreases urinary calcium excretion [54,67]. Proximal tubular calcium reabsorption is increased on a depression sodium diet (2,000-3,000 mg/d) and this in turn decreases the SSCaOx. In add-on of thiazide diuretics, calcium reabsorption is enhanced and further decreases hypercalciuria. However, addition of thiazide tin can lead to volume depletion; although ion substitution and volume status volition come up to the steady state in a few days. If the patient continues to consume a high sodium diet, sodium volition reach the distal nephron and increase the excretion of calcium and potassium along with citrate, resulting in a modify in the urinary pH that volition somewhen increase the risk of stone formation. Therefore, after analyzing the 24-hour urine, stone risk is high, prescribing a depression sodium diet will aid avoid inappropriate thiazide utilise for patients with CaOx stones. Patients with IBD usually take low urinary sodium levels and low urinary citrate, and so use of sodium citrate instead of potassium is beneficial to improve fluid status from gastrointestinal losses and increment urine volume.
Potassium
Potassium is abundant in near fruits and vegetables. However, if the patient has low urinary citrate and low urine pH, potassium citrate is commonly used forth with such a nutrition to further improve hypocitruria. Monitoring 24-hour urinary excretion of potassium is important to evaluate compliance to diet and medications. Taylor et al. analyzed the 24-hour urine with the Nutrition Approaches to Stop Hypertension (DASH) diet and found that diets conforming more closely to Dash had decreased chance of rock formation [68,69]. Because high DASH score foods are high in potassium, magnesium, and phosphorus, these may increase urine pH, resulting in a subtract in SSCaOx and uric acid in the urine as well every bit increased urine volume and citrate [68,69]. If patients accept chronic kidney disease and accept angiotensin converting enzyme inhibitors (ACEI) equally antihypertensive medications, serum potassium level should be monitored closely.
Poly peptide
There are few markers of 24-hour urine to evaluate dietary protein intake, product and excretion. Urea nitrogen appearance (UNA) and PCR are measurements of daily poly peptide intake that are calculated per kg torso weight. In normal healthy steady state, intake of protein can be equivalent to protein catabolism; therefore, PCR determines the nitrogen remainder from 24-60 minutes urine urea concentration:
PCR=[6.25({24-h urea N} +{0.031x weight})]/ weight
Patients who have acute, or chronic infection are usually malnourished and feel catabolism, and have more nitrogen in the urine. Therefore, this formula should not be used to evaluate protein intake. For patients without active stress of illness, the PCR tin guide protein recommendations for patients to prevent further stone risks.
The ammonium (NH4) level should be depression in patients who are prescribed alkali therapy or who present with RTA. Monitoring citrate, an indicator of urine acerbity, tin can place these problems. Patients who have brine therapy especially with depression citrate levels have depression urinary ammonium levels with higher pHs and therefore the risk of uric acids or CaOx can be substantially decreased.
High ammonium and sulfate are indicators of a high protein diet, especially ane which is high in animate being protein [30,lxx]. A loftier protein diet (>two.0 g/kg/d) tin reduce urine pH; therefore, a moderate to depression protein diet should be advised (0.viii-i.4 g/kg/d). Currently most common and pop weight loss diets promote consumption of big amounts of poly peptide but such a reducing diet is not recommended for the patients who have a history of kidney stones. This high protein nutrition regimen increases hypercalciuria, lowers pH of urine and increases uric acrid levels, which increase kidney stone gamble [14]. Massey et al. conducted a written report to monitor the effect of stone risk in beef vs. plant poly peptide and concluded that a moderate corporeality of protein intake of either type had the same effects in reducing CaOx rock adventure [71]. The amount of protein seemed to exist a more important factor in that report. Recently, an epidemiological report showed that animal protein intake was not independently associated with the incidence of nephrolithiasis amongst a large cohort of postmenopausal women [72]. However, the evaluation of stone take a chance varies by individuals and is complicated. Therefore, the recommendation of a usual poly peptide intake remains until the scientific evidence to change this recommendation is provided.
Calcium
Approximately twenty% of dietary calcium is captivated under normal conditions. There is substantial evidence that a college calcium diet is associated with lower kidney stone formation, because the higher calcium intake will bind oxalate in the gut if information technology is consumed with meals thereby reducing oxalate absorption. Patients who consumed a diet with a normal calcium intake (i.e., one,200 mg/d) plus a depression animal protein intake had a 51% lower incidence of recurrent stones than patients who consumed depression (400 mg/d) calcium diets [xx]. Although data to date on taking calcium supplements does not evidence that they are theoretically effective in reducing rock gamble, taking a calcium supplement with meals is beneficial considering calcium can bind with the dietary oxalate and thus it is non captivated.
Magnesium
Magnesium forms a complex with oxalate and decreases SSCaOx in the urine, which can reduce the run a risk of stone formation [68,69]. The Nuance diet, which is high in magnesium, showed a subtract in stone gamble by increasing pH and lowering SSCaOx [13,68,69,73]. Magnesium can besides demark with oxalate in the gastrointestinal tract to reduce oxalate absorption; however, a magnesium supplement is not recommended especially patients with chronic kidney disease because magnesium is accumulated in the claret in advanced kidney disease. Decreased urinary magnesium may be a sign of malabsorption, malnutrition, small bowel disease or laxative abuse. Hypomagnesemia is not a risk cistron for stone formation.
Vitamin C
Vitamin C is metabolized to dehydroascorbic acid and then converted to oxalate which is so excreted in the urine; therefore, a loftier vitamin C intake can exist a adventure for stone germination by increasing endogenous oxalate. A recent observational study showed that consumption of more than 1,000 mg/d vitamin C was associated with a twoscore% higher risk of stone formation in men than in those who consumed the Dietary Reference Intake (DRI) for vitamin C [74].
Other dietary factors
Citrate consumption can increase urine pH, and besides increases citrate concentration in the urine. Citrate also decreases SSCaOx due to its capacity to form a complex with calcium ions and inhibit crystallization of CaOx [63]. Notwithstanding, citrate may increase the hazard of CaP stones. A clinical trial conducted by Koff et al. used potassium citrate and lemonade for 21 rock patients, and showed that potassium citrate increased urine pH with increased urinary citrate level but lemonade did non take an result on urinary pH or citrate levels except for increasing urine volume [75].
Phytates are nowadays in whole grains and legumes and they can inhibit CaOx stone formation. Some studies have shown an inverse correlation with phytate intake and the chance of kidney rock germination in women [74,76,77,78].
Treatment of Kidney Stones
Management in the acute setting
Urgent surgical intervention is indicated in a patient with an obstructed, infected urinary tract, worsening renal function, intractable pain or vomiting or obstruction of a solitary or transplanted kidney. Analgesia is essential and parenteral Non-Steroid Anti-Inflammatory Drugs (NSAIDs: Ketorolac) are as effective as narcotics. NSAIDS are less likely to cause nausea, but should be avoided if the patient has impaired renal office. Pain is due to renal capsule dilatation, and so intractable pain may require decompression of the obstruction. Book expansion with intravenous fluids is important in correcting the book depletion that may have occurred from decreased intake and/ or airsickness and it may as well increase the likelihood of stone passage by increasing urine production.
If urgent intervention is not required, the treating doc needs to decide if the rock tin be passed spontaneously. The likelihood of spontaneous passage decreases as the size of the stone increases and stones >5-6 mm are not likely to pass spontaneously.
Patients who are having repeated stone attacks should exist instructed to strain their urine and to submit the rock for composition analysis. Repeated imaging (plain abdominal radiography (KUB) for radiopaque stones and CT for radiolucent stones) is warranted to ostend stone passage. If follow-upwards imaging reveals no movement subsequently a month, urologic intervention is generally warranted [79].
Surgical treatment
Larger and more proximal ureteral stones are less likely to pass spontaneously and usually crave urologic evaluation. If the rock does not pass rapidly, the patient can be sent home with oral analgesia and instructions to return for fever or uncontrollable pain. Well-nigh urologists wait a few days before intervening unless in that location is a possible infection, low likelihood of spontaneous passage or unrelenting pain. Infection in the setting of obstacle is a surgical emergency and mandates emergency drainage.
Extracorporeal shock wave lithotripsy (ESWL) is a non-surgical process using shock waves to fragment stones into small pieces which pass spontaneously several days or weeks later. Obese patients may not exist effectively treated with ESWL. Cystine stones are very hard and are ofttimes not effectively treated with ESWL (Figure 3).
Extracorporeal shock wave lithotripsy (ESWL).
Flexible ureteroscopic stone removal, although invasive, is associated with a better chance of becoming rock free with a single procedure. It does have college complication rates of ureteral injury or structure, though has become increasingly popular, considering of the variety of devices that are available for rock removal including small diameter flexible ureteroscopes, ureteral access sheaths, holmium laser lithotripsy and stone baskets.
Percutaneous nephrostolithotomy is more invasive, simply may be necessary for large stones or stones that cannot exist removed cystoscopically. It is rare that a patient requires open ureterolithotomy or nephrolithotomy.
Medical and dietary treatment - preventive therapy
A recurrent rock sometime should undergo an evaluation for a treatable metabolic cause of kidney stones. This is guided by the results of the 24-hour urine collection.
Table seven summarizes the dietary managements of kidney stones. Fluid intake is an essential component of treatment and should be adjusted and then that urine output is greater than two.5 L/day. Depression urine citrate tin can exist corrected using potassium citrate. Table viii provides some full general guidelines for treatment.
Table 7
Management of all types of kidney stones
| Abnormality | Evaluate | Management |
|---|---|---|
| Hypercalciuria | Urine Na and urea nitrogen | Na, protein restriction, Thiazide, not low Ca diet |
| Hypercalcemia | PTH, ionized Ca, vitamin D, malignancy, thyroid, bone illness etc | Parathyroidectomy, care for underlying disorder |
| Hyperoxaluria | Dietary oxalate, low dietary Ca, vitamin D, sweeteners, ileal illness, gastric bypass, ethylene glycol, enzyme deficiencies | Restrict oxalate, supplement magnesium, Ca, pyridoxine, cholestyramine |
| Hypocitraturia | Urinary citrate, serum potassium (1000), creatinine, malabsorption, RTA, acetazolamide | Alkali (potassium citrate), sodium citrate if book deplete |
| Hyperuricosuria | Dietary purines | Purine brake, allopurinol, brine |
| Acid urine (pH) | Exclude chronic diarrhea, gout, ileostomy | Alkali (Potassium citrate) |
| Depression urine book | 24 60 minutes urine volume | At to the lowest degree 2.5 liters fluid intake |
Table 8
Dietary recommendation to prevent kidney stones
| Nutrients | Recommendation |
|---|---|
| Ca | 800-ane,200 mg/d |
| Oxalate | twoscore-l mg/d |
| Na | 2,000-3,000 mg/d |
| Protein | 0.8-1.four chiliad/kg/d |
| Fluid | >ii.5 L/d |
| Vitamin D | Depression dose if vitamin D insufficiency or deficiency (ane,000 IU/d) |
| Vitamin C | Dietary Reference Intake |
Treating calcium stones
Dietary sodium brake is important every bit it is associated with a reduction in urine calcium excretion. Thiazide diuretics lead to increased serum calcium levels and reduced urine calcium levels and are therefore used in therapy for patients with hypercalciuria. Oxalate reabsorption in the colon is reduced by the formation of insoluble calcium oxalate. This is very of import in therapy because restricting dietary calcium results in less calcium being available in the intestinal lumen to bind oxalate. This leads to increased oxalate assimilation and therefore increased urinary oxalate excretion [25]. Tabular array ix shows the listing of high oxalate foods.
Table 9
Oxalate content of foods
| Foods (iii.5 oz or 100 g) | Oxalate (mg) | Foods (3.5 oz or 100 g) | Oxalate (mg) | Foods (three.5 oz or 100 g) | Oxalate (mg) |
|---|---|---|---|---|---|
| Flours & Mills | Seed containing vegetables | Leafy vegetables | |||
| Barley flour | 56 | Cucumber, raw | 20 | Amaranth leaves, raw | 1,090 |
| Buckwheat flour | 269 | Eggplant, raw | 190 | Beet leaves, raw | 610 |
| Corn repast | 54 | Eggplant, greenish, long, raw | 55 | Brussels sprouts, raw | 360 |
| Rice flour, brown | 37 | Okra, raw | l | Cabbage, green raw | 100 |
| Rye flour, night | 51 | Pepper, raw | 40 | Chicory, raw | 210 |
| Semolina flour | 48 | Snap beans, raw | 360 | Chinese cabbage, raw | half-dozen |
| Soy flour | 183 | Squash, raw | 20 | Chinese, kale, raw | 23 |
| Wheat flour, white unbleached | 40 | Tomato, raw | 50 | Chives, raw | ane,480 |
| Wheat flour, whole | 67 | Yard long beans, green, raw | 38 | Collards, raw | 450 |
| Wheat Germ | 269 | Coriander, raw | 10 | ||
| Endive, raw | 110 | ||||
| Kale, raw | 20 | ||||
| Fruits | Legumes (Beans & Peas) | Leek | 89 | ||
| Bitter melon, raw | 71 | Anasazi beans, boiled | 80 | Lettuce, raw | 330 |
| Papaya raw | 5 | Azuki beans, boiled | 25 | Parsley, raw | i,700 |
| Light-green goose berries | 88 | Blackness beans, boiled | 72 | Purslane, raw | i,310 |
| Black berries | nineteen | Cowpeas (blackeye peas), boiled | 4 | Spinach, raw | 970 |
| Blueberries, strawberries, blood-red | fifteen | Gabanzo beans, boiled | ix | Turnip greens, raw | l |
| raspberries | Great northern beans, boiled | 75 | Watercress, raw | 310 | |
| Blackness raspberries | 55 | Kidney beans, reddish cooked | xvi | ||
| Hold grapes | 25 | Lentils, boiled | 8 | Tuber & Root vegetables | |
| Currents | nineteen | Lima beans, large, boiled | eight | Beetroot, boiled | 675 |
| Lemon skin | 83 | Navy beans, boiled | 57 | Carrot, raw | 500 |
| Lime peel | 110 | Peas, green, divide, boiled | 6 | Cassava root, raw | 1,260 |
| Rhubarb | 800 | Peas, raw | fifty | Parsnip, raw | 40 |
| Peas, yellow, split, boiled | 5 | Potato, raw | l | ||
| Pinkish beans, boiled | 75 | Radish, raw | 480 | ||
| Pinto beans, boiled | 27 | Rutabaga, raw | 30 | ||
| Scarlet beans, boiled | 35 | Sweetness potato, raw | 240 | ||
| Soybeans, boiled | 56 | Turnip, raw | 210 | ||
| Nuts | White beans, small boiled | 78 | Other vegetables | ||
| Almonds, roasted | 469 | Corn, sweet, raw | 10 | ||
| Cashews, roasted | 262 | Garlic, raw | 360 | ||
| Hazelnuts, raw | 222 | Onion, raw | 50 | ||
| Macadamia nuts, raw | 42 | ||||
| Peanuts, raw | 142 | Miscellaneous foods | |||
| Pecans, raw | 64 | Black pepper | 419 | ||
| Pine nuts, raw | 198 | Chocolate | 117 | ||
| Pine nuts, roasted | 140 | Stem & Stalk vegetables | Cocoa powder | 623 | |
| Pistachio nuts, roasted | 49 | Asparagus, raw | 130 | Indian tea (i C) | 72 |
| Soy nuts (1 oz) | 392 | Broccoli, raw | 190 | Soy protein | 496 |
| Walnuts, raw | 74 | Cauliflower, raw | 150 | Soy yogurt | 113 |
| Celery, raw | 190 | Soybean cracker | 207 | ||
| Tofu | 275 |
The high oxalate foods are considered to exist healthy, with high fiber and nutrient dense in vitamins and minerals. Patients who take diabetes, hypertension and loftier blood cholesterol are often instructed to consume loftier oxalate foods such equally fruits and vegetables. When patients develop kidney stones, they are instructed to change the diet to lower oxalate contents and therefore almost patients are confused. The clinical dietitian should be able to advise the patients individualized diet to prevent kidney stone but to keep healthy diet.
Treating uric acid stones
As uric acrid is more soluble in an alkaline urine, urine alkalinization is an important part of the treatment of uric acid stones. Patients should decrease their intake of brute proteins which helps decrease uric acrid generation. Allopurinol, a xanthine oxidase inhibitor, is used to subtract the formation of uric acid.
Low purine diet is recommended if patient has elevated blood uric acid level [32,34]. A high poly peptide nutrition (>two.0 yard/kg) can cause a decrease in urine pH which can increase chance of uric acrid stone therefore moderate amount of poly peptide (0.eight-1.4 yard/kg/twenty-four hours) is recommended.
Treating cystine stones
At that place are no specific diet recommendations for cysteine stones except increasing fluid intake. Cystine solubility can exist increased by alkalinization of the urine, although solubility only increases when the pH reaches 7-7.5. Thiol containing drugs like Penicillamine and Tiopronin may be given to patients who are unable to comply with increased fluid intake and urinary alkalinization or neglect despite it. These drugs increase the solubility of cystine. Tiopronin is better tolerated than penicillamine which is associated with multiple side effects including rash, fever, serum sickness, epidermolysis and membranous nephropathy. Captopril is used because of its sulfhydryl group forms a thiol-cysteine disulfide bond that is more than soluble than cysteine. However its efficacy is unclear. Low animal protein nutrition tin lower the stone risk by lowering methionine which is precursor of cystine [84].
Treating Struvite stones
The preferred treatment of struvite stones is surgical removal considering they are large. Antibody therapy is of import and may slow stone growth. It is of import to culture stone material to help straight antibiotic therapy. Even so low sodium diet can help prevention of struvite rock [84].
Determination
Kidney stones are common and recur frequently. Calcium oxalate stones are the virtually common. Urine supersaturation is increased with low urine volume and with increased urinary excretion of calcium, oxalate, phosphate, cysteine or uric acid. Citrate is the most common inhibitor of crystal germination and urinary pH is very important for preventing or treating different types of stones. There are many rock take a chance factors among which diet is very of import 1. Urgent stone removal and treatments are washed past urology using surgery or ESWL. Medical and dietary treatments are most important means to foreclose recurrence of stone. Consumption of ample fluids is essential, and dietetic advice is helpful.
Footnotes
Conflict of interest: The authors have declared no conflict of interest.
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4525130/