Hypercalciuria


Article Author:
Stephen Leslie


Article Editor:
Hussain Sajjad


Editors In Chief:
David Wood
Andrew Wilt
Hajira Basit


Managing Editors:
Avais Raja
Orawan Chaigasame
Khalid Alsayouri
Kyle Blair
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Abbey Smiley
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beenish Sohail
Hajira Basit
Phillip Hynes
Sandeep Sekhon


Updated:
9/28/2019 6:00:45 PM

Introduction

Hypercalciuria is generally considered to be the most common identifiable metabolic risk factor for calcium nephrolithiasis. It also contributes to osteopenia and osteoporosis. Its significance is primarily due to these two clinical entities: nephrolithiasis and bone resorption. On average, hypercalciuric calcium stone formers have decreased bone mineral density than matched controls which are neither stone formers nor hypercalciuric. Even among kidney stone patients, those with hypercalciuria will have average bone calcium density measurements 5% to 15% lower than their normocalciuric peers.[1]

The definition of hypercalciuria can be a bit confusing. Traditionally, it has been defined as daily urinary calcium excretion of greater than 275 mg in men and greater than 250 mg in women. This definition ignores concentration, age, renal function, and weight considerations as well as the obvious question of whether a different normal excretion amount is reasonable based solely on gender.[1]

Hypercalciuria also can be defined as a daily urinary excretion of more than 4 mg calcium/kg body weight. This definition is somewhat more useful in the pediatric age group if the child is over two years old; but in adults, it tends to allow higher urinary calcium excretions in heavier and obese individuals compared to lighter patients. One solution is to use 24-hour urinary calcium concentration (less than 200 mg calcium/liter urine is normal" but less than 125 mg calcium/liter is optimal). [2] 

Another clinically useful definition, especially in pediatrics, is the random or spot urinary calcium/creatinine ratio (less than 0.2 mg calcium/creatinine mg is normal while less than 0.18 mg calcium/creatinine mg is optimal). Its benefit is that it does not necessarily need a 24-hour urine collection with every visit just to track hypercalciuria. [3]

Which definition to use depends on the clinical situation and the availability of reliable 24-hour urine collection data. For optimal results, one approach is to look at all of the definitions and concentrate treatment on optimizing the worst of them. This "optimization" approach focuses less on what is normal and more on what an optimal level would be for a calcium stone forming patient. This type of optimization also can be used for other urinary chemical risk factors besides hypercalciuria.[1]

Young children and infants tend to have higher urinary calcium excretion and lower urinary creatinine levels, so the suggested normal limits for calcium/creatinine ratios differ by age as follows:[1][4]]

  • Up to six months of age: less than 0.8
  • Six to twelve months of age: less than 0.6
  • 24 months and older: less than 0.2 

Etiology

The traditional way of looking at hypercalciuria includes absorptive which has increased intestinal calcium absorption, renal calcium leak which is an inherent kidney problem, resorptive as in hyperparathyroidism, and renal phosphate leak hypercalciuria. Not every patient will fall nicely into one of these categories, and a simpler classification requiring much less testing is now available based on clinical response.[26]

Other causes of hypercalciuria include milk-alkali syndrome (excessive oral calcium ingestion), sarcoidosis, glucocorticoid excess, Paget disease, paraneoplastic syndrome, multiple myeloma, metastatic tumors involving bone, Addison disease, and Hypervitaminosis D. Hypercalciuria without any obvious cause, which is the majority of cases, is called idiopathic.[5]

Animal studies have suggested that in some subjects, there appears to be an increased sensitivity to Vitamin D. This may be due to an increased number of 1,25 Vitamin D receptors in those individuals.  These changes have not been reliably identified in humans; just in animal studies.[6]

High salt (sodium) intake has also been suggested as a possible cause of hypercalciuria.  An increased sodium load leads to higher urinary excretion of sodium which decreases tubular calcium reabsorption resulting in hypercalciuria.  While high salt intake may be a contributing factor, it is rarely the sole cause of significant hypercalciuria.[2]

A high animal protein diet will produce an acid load that causes a release of calcium from the bone and inhibition of renal tubular calcium reabsorption resulting in hypercalciuria. Again, this does not appear to be the sole causes of significant hypercalciuria.[7]

In children 2-12 years of age, the calcium/citrate ratio has been found to be useful clinically.  A cutoff of 0.25 has been suggested meanting that those with a calcium/citrate ratio >0.25 are more likely to develop stones.[1][4]][1]

Epidemiology

Hypercalciuria occurs in 5% to 10% of the adult population and is found in about one-third of all calcium stone formers. Close relatives of hypercalciuric patients tend to have an increased rate of hypercalciuria themselves.  Up to 40% of the first and second-degree relatives of hypercalciuric recurrent stone formers will also have hypercalciuria.[8]

There are more than 30 million kidney stone patients and 1.2 million new kidney stone cases every year in the United States with one-third of them demonstrating hypercalciuria when tested. 

Post menopausal women with osteoporosis and no history of kidney stones have a 20% chance of having hypercalciuria.

In children, both the incidence and prevalence of urolithiasis is increasing, particularly over the last 10 to 15 years. Hypercalciuria and hypocitraturia are the most commonly found metabolic problems identified in pediatric stone formers. The most common stone composition in children is calcium oxalate and calcium phosphate, but there is no apparent association between nephrolithiasis and obesity in the pediatric age group while there is such a linkage in adult stone formers. There also appears to be a higher incidence of hypercalciuria (and hyperuricosuria) in children with significant vesicoureteral reflux compared to controls.[1][4]]

Pathophysiology

Absorptive hypercalciuria is the most common type of excessive urinary calcium excretion. It is found in about 50% of all calcium stone forming patients. Increased gastrointestinal calcium absorption increases serum calcium levels while lowering serum Vitamin D and parathyroid hormone levels. Only about 20% of ingested calcium is absorbed, normally taking place in the duodenum. A Vitamin D dependent version of absorptive hypercalciuria can be identified by high serum Vitamin D levels. [1]

Renal Phosphate Leak Hypercalciuria is perhaps the most interesting from a pathophysiological point of view. A renal defect causes excessive urinary phosphate excretion which leads to hypophosphatemia. This induces higher Vitamin D activation in the kidney which increases intestinal phosphate absorption to correct the low serum phosphate. Unfortunately, the extra Vitamin D also increases intestinal calcium absorption. The extra calcium absorbed is eventually excreted in the urine resulting in hypercalciuria. This type of hypercalciuria is Vitamin D dependent and is relatively unresponsive to thiazides. The diagnosis is made by the findings of low or low-normal serum phosphate, hypercalciuria, high urinary phosphate, and high serum Vitamin D3 levels with normal serum calcium and PTH levels.[1]

Renal Calcium Leak is found in about 5% to 10% of hypercalciuric stone formers. It is caused by a renal defect that causes an obligatory loss of calcium in the urine regardless of serum calcium levels or dietary calcium intake. This is usually accompanied by hypocalcemia and an increase in serum parathyroid hormone (PTH) levels. The calcium/creatinine ratio tends to be high in this condition (usually greater than 0.20), and there is an association with Medullary Sponge Kidney. [1]

Resorptive hypercalciuria accounts for only about 3% to 5% of all hypercalciuric patients and is almost always due to hyperparathyroidism. Sustained, inappropriate, and excessive serum parathyroid hormone causes a release of calcium from the bone leading to osteopenia and hypercalcemia. Eventually, the hypercalcemia overcomes the normal parathyroid hormone effect of decreasing urinary calcium excretion, and the result is hypercalciuria (e.g., similar to spilling sugar in the urine in diabetics). This explains why hypercalciuria from hypercalcemia is less for any given elevated serum calcium level in patients with hyperparathyroidism than in other patients who are hypercalcemic. [1]

Pregnancy increases hypercalciuria during all three trimesters, but this does not appear to increase the risk of new stone disease as there is also an increase in kidney stone inhibitors. 

Cortical bone is more affected by hypercalciuria than cortical bone. Interestingly, bone mineral density is inversely related with hypercalciuria in nephrolithiasis patients but not in patients without nephrolithiasis.[9]

In children, there is an apparent connection between recurrent abdominal pain and hypercalciuria. A recent study has connected hypercalciuric pediatric kidney stone patients with an increase in their urinary excretion of lipid metabolism/transport-related proteins. This suggests that abnormalities in lipid metabolism may be responsible or connected in some way to pediatric hypercalciuria and nephrolithiasis.[1][4]]

History and Physical

There is no specific clinical finding of hypercalciuria itself, but it should be suspected in cases of calcium nephrolithiasis, nephrocalcinosis, hypercalcemia, hyperparathyroidism and osteopenia/osteoporosis. Hypercalciuria also can cause hematuria even without any detectable stone formation, particularly in children. The cause is thought to be from focal and microscopic tissue damage from tiny calcium crystals and focal stones that are too small to be diagnosed with standard techniques. Urinary testing makes the definitive diagnosis.

Evaluation

In clinical practice, a 24-hour urinary calcium level of 250 mg is a useful initial threshold for determining hypercalciuria. In pediatrics, a ratio of more than 4 mg calcium/kg body weight, a random calcium/creatinine ratio of more than 0.18, or a 24-hour urinary calcium concentration of more than 200 mg/liter may be more useful. In practice, it often is used to identify whichever method gives the most abnormal reading and try to "optimize" it. [1]

Spot urinary chemistry has shown poor sensitivity and specificity for hypercalciuria which is why the 24 hour urine test is so critical in making the diagnosis. [2] 

Hyperparathyroidism should be suspected in all adult hypercalciuric patients with elevated or borderline elevated serum calcium levels.  It can be diagnosed simply by checking a parathyroid hormone level in those individuals.[10]

Vitamin D Levels can help detect Renal Phosphate Leak (where Vitamin D is elevated along with high urinary but low serum phosphate levels). High Vitamin D Levels and possible Renal Phosphate Leak should be suspected in patients who do not respond to adequate thiazide therapy.[11]

Treatment / Management

If serum calcium levels are normal (which rules out hyperparathyroidism), dietary calcium is moderated if excessive but is not overly restricted to avoid increased oxalate absorption and bone demineralization. A diet that is low in animal protein and salt (sodium) is recommended. Then, a repeat 24-hour urine test can be done to determine the response. [10]  If hypercalciuria persists, then medication (such as thiazides) likely will be needed. If thiazides fail, even after adjusting the dose and moderating sodium intake (which negates the hypocalciuric effect of the thiazides), then the patient could have renal phosphate leak hypercalciuria which does not typically respond to thiazide-type medications. [2]  

Thiazides can induce a positive calcium balance and reduce urinary calcium by up to 50%. Hydrochlorothiazide and chlorthalidone are used most often, but indapamide also can be used. The advantage of chlorthalidone and indapamide is their longer half-life as hydrochlorothiazide would need to be given twice a day. Thiazides will not be effective unless dietary salt intake is limited. For every gram of daily dietary salt decrease, 24 hour urinary calcium would be expected to drop by 5.46 mg. [2][12]

Thiazides will also tend to reduce serum potassium, increase uric acid levels, and lower urinary citrate excretion. For that reason, it often is useful to add potassium citrate to these patients when they start on thiazide therapy. [1]

When thiazides fail even at adequate dosages in patients with reasonable sodium restriction, it could be due to a Vitamin D-dependent form of hypercalciuria such as Renal Phosphate Leak. This variant can be treated with orthophosphates, which generally lower serum Vitamin D, or with ketoconazole which blocks cytochrome P450 3A4 resulting in a 30% to 40% reduction in circulating Vitamin D3 levels. [1]

Orthophosphate therapy not only increases serum phosphate levels, which naturally lower Vitamin D3 activation, but also increases renal calcium reabsorption and urinary stone inhibitors like pyrophosphate. They also may act as gastrointestinal calcium binders to help reduce absorption. Orthophosphates can reduce urinary calcium excretion by up to 50% and may be given together with thiazides when necessary. However, they are most useful in cases where thiazides have failed or cannot be used as well as for renal phosphate leak hypercalciuria.  [13] [2] 

Amiloride, a potassium-sparing diuretic, is not a thiazide but when added to thiazides may further increase calcium reabsorption as well as minimizing potassium loss. (Amiloride is not usually recommended with potassium citrate due to the potential for hyperkalemia.) Triamterene is not recommended in stone formers as it can form triamterene calculi. [12]

Potassium citrate therapy will not only increase urinary citrate levels, but it may also increase renal calcium reabsorption reducing hypercalciuria. [14]

In children, treatment of hypercalciuria is primarily dietary, at least initially. Calcium intake should not be restricted unless it exceeds the usual recommended amount. Vitamin D supplementation should be avoided, and dietary animal protein intake should be limited to within the usually recommended limits. A 3 to 6 month trial of dietary measures alone is reasonable before resorting to thiazide medications. [4]][14]

Pearls and Other Issues

Treatment Summary for Idiopathic Hypercalciuria

First try dietary modifications, such as avoiding excessive dietary calcium intake and lowering dietary animal protein and salt.[1]  If this is not successful, initiate thiazide therapy and maintain a low salt diet. If this is also ineffective, start orthophosphate therapy. Additional medications that can help control hypercalciuria include amiloride and potassium citrate.[1] 

Dent Disease

Dent disease is a rare, X-linked hereditary disorder that primarily affects the proximal renal tubules resulting in hypercalciuria and proteinuria starting in childhood. It may progress from there, leading to osteomalacia, short stature, nephrocalcinosis, nephrolithiasis, hypophosphatemia and eventually renal failure. Up to 80% of affected males will develop end-stage renal failure by age 50. Vitamin D levels (1,25 (OH)2 Vit. D) are elevated or in the high normal range while parathyroid hormone levels are low. There are only about 250 families known to carry this disorder, so the incidence is quite low.[15]

Treatment is based on controlling hypercalciuria and preserving renal function. While this can be done with thiazide diuretics, the hypercalciuria almost always responds to dietary therapy. ACE inhibitors and citrate supplements are used in children with the disorder to help preserve renal function, but their effectiveness is unclear.[15]

Enhancing Healthcare Team Outcomes

Hypercalciuria can be difficult to identify and manage.  Diagnosis usually begins with primary care, the nurse practitioner, nephrology or urology.  It can take time to identify the type of hypercalciuria and its optimal treatment. A high index of suspicion should be maintained by all members of the health care team treating the patient.

The outcomes depend on the cause. For benign causes, the outcomes are excellent but if the cause is a malignancy, the outcomes are guarded. an interprofessional team of a specialty trained urology nurse and clinical for follow up and monitoring will provide the best results. [Level V]


Interested in Participating?

We are looking for contributors to author, edit, and peer review our vast library of review articles and multiple choice questions. In as little as 2-3 hours you can make a significant contribution to your specialty. In return for a small amount of your time, you will receive free access to all content and you will be published as an author or editor in eBooks, apps, online CME/CE activities, and an online Learning Management System for students, teachers, and program directors that allows access to review materials in over 500 specialties.

Improve Content - Become an Author or Editor

This is an academic project designed to provide inexpensive peer-reviewed Apps, eBooks, and very soon an online CME/CE system to help students identify weaknesses and improve knowledge. We would like you to consider being an author or editor. Please click here to learn more. Thank you for you for your interest, the StatPearls Publishing Editorial Team.

Hypercalciuria - Questions

Take a quiz of the questions on this article.

Take Quiz
A 17-year-old male presents with the intermittent complaint of "burning" when he urinates. Urinalysis shows trace blood on his urine dip test and presence of calcium crystals, but there is no evidence of urinary infection. A 24-hour urinary calcium level was noted to be more than 250 mg/L. Lab reports revealed a serum calcium level of 12.0 mg/dL. Idiopathic hypercalciuria is best treated with which of the following?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 17-year-old boy presents with the intermittent complaint of "burning" when he urinates. Urinalysis shows trace blood on his urine dip test, presence of calcium crystals, and a urinary calcium/creatinine ratio of more than 0.2, but there is no evidence of urinary infection. Ultrasound pelvis revealed hyperechoic foci with acoustic shadowing in the urinary bladder. Lab reports revealed a serum calcium level of 11.2 mg/dL and a serum phosphate level of 4.0 mg/dL. What is the initial best step in the management of this disease?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 17-year-old boy presents with complaints of intermittent burning micturition and infrequent bone pains. Urinalysis shows trace blood on his urine dip test and presence of calcium crystals. Ultrasound pelvis revealed hyperechoic foci with acoustic shadowing in the urinary bladder. Lab reports revealed a serum calcium level of 11.3 mg/dL and a serum phosphate level of 4.0 mg/dL. 24-hour urinary calcium level revealed a value of 403 mg/L. A DEXA-scan to determine the bone density was advised. What is the significance of average bone density reading in such patients compared to that of normocalciuric stone formers?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 45-year-old male presents to a clinic with complaints of burning micturition and hematuria for one month. He has a past medical history of hypertension for which he is taking a combination drug containing lisinopril and hydrochlorothiazide. He also reports a long history of bone pains for which he takes nonsteroidal anti-inflammatory drugs (NSAIDs), infrequently. The general physical examination is unremarkable. Urinalysis reveals hematuria and the presence of calcium phosphate crystals, but there was no evidence of urinary infection. X-ray abdomen and ultrasound-KUB (kidneys, ureters, and bladder) did not show any evidence of nephrolithiasis. Blood workup showed serum calcium level of 8.6 mg/dL, serum phosphate level of 2.0 mg/dL, vitamin D3 25-hydroxyvitamin D level of 200 ng/dL, and a normal parathyroid hormone (PTH) level. Based on the given lab reports, a 24-hour urinary calcium test was advised, which revealed a calcium level of more than 200 mg/L and a high phosphate content as well. What is the most likely cause of hypercalciuria?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 65-year-old male presents to a clinic with complaints of burning micturition and hematuria for one month. He also reports a long history of bone pains for which he takes nonsteroidal anti-inflammatory drugs (NSAIDs), infrequently. The general physical examination is unremarkable. Urinalysis reveals hematuria and the presence of calcium phosphate crystals, but there was no evidence of urinary infection. Ultrasound-KUB (kidneys, ureters, and bladder) did not show any evidence of nephrolithiasis. Blood workup showed serum calcium level of 8.9 mg/dL, serum phosphate level of 2.1 mg/dL, vitamin D3 25-hydroxyvitamin D level of 189 ng/dL, and a normal parathyroid hormone (PTH) level. Based on the given lab reports, a urinary calcium/creatinine ratio was determined to be greater than 0.2. The clinician prescribed him hydrochlorothiazide, but there was no change in urinary calcium level. A clinical trial of which one of the following therapy would confirm the diagnosis?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 3-year-old male child was brought to a clinic with complaints of inability to walk since one year of age. However, he had achieved all the other developmental milestones at the appropriate age. On physical examination, he has all the classical features of rickets. He was started on calcitriol and elemental calcium but no avail. The mother also reported that her father died of a rare genetic disorder at the age of 50 years. Lab reports revealed a hemoglobin of 12.4 mg/dL, the serum calcium level of 8.6 mg/dL, serum phosphate level of 1.8 mg/dL, and a normal parathyroid hormone (PTH) level. Urinalysis revealed the presence of calcium phosphate crystals. Random urinary calcium/creatinine ratios were repeatedly noted to be more than 0.2. Based on the given lab and clinical findings, an ultrasound abdomen was advised, which demonstrated multiple hyperechogenic foci in both kidneys. Which other disorder is typically associated with this disease and what is the mainstay of therapy in this patient?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 65-year-old male presents with complaints of bone pains and hematuria for one month. Urinalysis revealed the presence of red blood cells casts and calcium crystals. The physical examination was unremarkable. Blood workup revealed a serum calcium level of 12.1 mg/dL, parathyroid hormone (PTH) level of 154 pg/mL, and 25-hydroxyvitamin D level of 19.2 ng/mL. X-ray of hands showed subperiosteal bone resorption of digits, and chest x-ray demonstrated distal clavicular resorption. 24-hour urinary calcium levels were noted to be 504 mg/L. Which of the following type of hypercalciuria is associated with this disease?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up

Hypercalciuria - References

References

Association between Circulating Vitamin D Level and Urolithiasis: A Systematic Review and Meta-Analysis., Hu H,Zhang J,Lu Y,Zhang Z,Qin B,Gao H,Wang Y,Zhu J,Wang Q,Zhu Y,Xun Y,Wang S,, Nutrients, 2017 Mar 18     [PubMed]
Pharmacology for renal calculi., Blair B,Fabrizio M,, Expert opinion on pharmacotherapy, 2000 Mar     [PubMed]
Idiopathic hypercalciuria: Can we prevent stones and protect bones?, Ryan LE,Ing SW,, Cleveland Clinic journal of medicine, 2018 Jan     [PubMed]
Pak CY,Sakhaee K,Moe OW,Poindexter J,Adams-Huet B,Pearle MS,Zerwekh JE,Preminger GM,Wills MR,Breslau NA,Bartter FC,Brater DC,Heller HJ,Odvina CV,Wabner CL,Fordtran JS,Oh M,Garg A,Harvey JA,Alpern RJ,Snyder WH,Peters PC, Defining hypercalciuria in nephrolithiasis. Kidney international. 2011 Oct;     [PubMed]
Vieira MS,Francisco PC,Hallal ALLC,Penido MGMG,Bresolin NL, Association between dietary pattern and metabolic disorders in children and adolescents with urolithiasis. Jornal de pediatria. 2019 Feb 5;     [PubMed]
Penniston KL,Nakada SY, Updates in the Metabolic Management of Calcium Stones. Current urology reports. 2018 Apr 16;     [PubMed]
Pozdzik A,Maalouf N,Letavernier E,Brocheriou I,Body JJ,Vervaet B,Van Haute C,Noels J,Gadisseur R,Castiglione V,Cotton F,Gambaro G,Daudon M,Sakhaee K, Meeting report of the     [PubMed]
Martínez García M,Trincado Aznar P,Pérez Fernández L,Azcona Monreal I,López Alaminos ME,Acha Pérez J,Albero Gamboa R, A comparison of induced effects on urinary calcium by thiazides and different dietary salt doses: Implications in clinical practice. Nefrologia : publicacion oficial de la Sociedad Espanola Nefrologia. 2019 Jan - Feb;     [PubMed]
Quiñones-Vázquez S,Liriano-Ricabal MDR,Santana-Porbén S,Salabarría-González JR, Calcium-creatinine ratio in a morning urine sample for the estimation of hypercalciuria associated with non-glomerular hematuria observed in children and adolescents. Boletin medico del Hospital Infantil de Mexico. 2018;     [PubMed]
Prezioso D,Strazzullo P,Lotti T,Bianchi G,Borghi L,Caione P,Carini M,Caudarella R,Ferraro M,Gambaro G,Gelosa M,Guttilla A,Illiano E,Martino M,Meschi T,Messa P,Miano R,Napodano G,Nouvenne A,Rendina D,Rocco F,Rosa M,Sanseverino R,Salerno A,Spatafora S,Tasca A,Ticinesi A,Travaglini F,Trinchieri A,Vespasiani G,Zattoni F, Dietary treatment of urinary risk factors for renal stone formation. A review of CLU Working Group. Archivio italiano di urologia, andrologia : organo ufficiale [di] Societa italiana di ecografia urologica e nefrologica. 2015 Jul 7;     [PubMed]
Ehlayel AM,Copelovitch L, Update on Dent Disease. Pediatric clinics of North America. 2019 Feb;     [PubMed]
Minisola S,Gianotti L,Bhadada S,Silverberg SJ, Classical complications of primary hyperparathyroidism. Best practice     [PubMed]
Negri AL,Spivacow R,Del Valle E,Fradinger E,Marino A,Zanchetta JR, Renal phosphate leak in patients with idiopathic hypercalciuria and calcium nephrolithiasis. Urological research. 2003 Dec;     [PubMed]
Alon US, The Effects of Diuretics on Mineral and Bone Metabolism. Pediatric endocrinology reviews : PER. 2018 Mar;     [PubMed]
Doizi S,Poindexter JR,Pearle MS,Blanco F,Moe OW,Sakhaee K,Maalouf NM, Impact of Potassium Citrate vs Citric Acid on Urinary Stone Risk in Calcium Phosphate Stone Formers. The Journal of urology. 2018 Dec;     [PubMed]

Disclaimer

The intent of StatPearls is to provide practice questions and explanations to assist you in identifying and resolving knowledge deficits. These questions and explanations are not intended to be a source of the knowledge base of all of medicine, nor is it intended to be a board or certification review of Pediatrics-Medical Student. The authors or editors do not warrant the information is complete or accurate. The reader is encouraged to verify each answer and explanation in several references. All drug indications and dosages should be verified before administration.

StatPearls offers the most comprehensive database of free multiple-choice questions with explanations and short review chapters ever developed. This system helps physicians, medical students, dentists, nurses, pharmacists, and allied health professionals identify education deficits and learn new concepts. StatPearls is not a board or certification review system for Pediatrics-Medical Student, it is a learning system that you can use to help improve your knowledge base of medicine for life-long learning. StatPearls will help you identify your weaknesses so that when you are ready to study for a board or certification exam in Pediatrics-Medical Student, you will already be prepared.

Our content is updated continuously through a multi-step peer review process that will help you be prepared and review for a thorough knowledge of Pediatrics-Medical Student. When it is time for the Pediatrics-Medical Student board and certification exam, you will already be ready. Besides online study quizzes, we also publish our peer-reviewed content in eBooks and mobile Apps. We also offer inexpensive CME/CE, so our content can be used to attain education credits while you study Pediatrics-Medical Student.