Indian Journal of Nephrology About us |  Subscription |  e-Alerts  | Feedback | Login   
  Print this page Email this page   Small font sizeDefault font sizeIncrease font size
 Home | Current Issue | Archives| Ahead of print | Search |Instructions |  Editorial Board  

Users Online:1784

Official publication of the Indian Society of Nephrology
 ~  Similar in PUBMED
 ~  Search Pubmed for
 ~  Search in Google Scholar for
 ~Related articles
 ~  Article in PDF (606 KB)
 ~  Citation Manager
 ~  Access Statistics
 ~  Reader Comments
 ~  Email Alert *
 ~  Add to My List *
* Registration required (free)  

   Article Figures
   Article Tables

 Article Access Statistics
    PDF Downloaded280    
    Comments [Add]    

Recommend this journal


  Table of Contents  
Year : 2021  |  Volume : 31  |  Issue : 1  |  Page : 1-8

Enamel renal syndrome: A systematic review

1 Medicine School, Institute of Health Sciences, State University of Montes Claros, Unimontes, Minas Gerais State, Brazil
2 Department of Oral Diagnosis, School of Dentistry, State University of Campinas, FOP-UNICAMP, Piracicaba, Sao Paulo, Brazil
3 Dentistry School, State University of Montes Claros, Unimontes, Minas Gerais State, Brazil

Date of Submission16-Jan-2019
Date of Acceptance31-May-2019
Date of Web Publication27-Jan-2021

Correspondence Address:
Ms. Gabriela Oliveira Ornela
Rua Porto Seguro, 1100, Montes Claros- Minas Gerais, Postal Code: 39.401-290
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijn.IJN_27_19

Rights and Permissions


The enamel renal syndrome (ERS) is a rare autosomal recessive disease that is associated with mutations in the FAM20A gene. The syndrome is characterized by impaired amelogenesis of the hypoplastic type and nephrocalcinosis, presenting with presence of thin or absence of enamel, late dental eruption, intrapulpal calcifications, bilateral nephrocalcinosis, and normal plasma calcium level. The objective is to characterize ERS by systematically literature reviewing, highlighting the main findings of the syndrome to increase knowledge about this condition in the health professionals. The study is a systematic review of the scientific literature, whose research was developed in the PubMed database in March 2018. A total of 69 articles were found. Two authors analyzed their abstracts and selected, according to the language and main subject, 30 articles to write this study. A total of 69 patients were cited in the studies and their data were analysed. There was gender equivalence and the ages ranged from 1 to 64 years old. There is a clear hereditary relation of the syndrome, since there was consanguinity in 18 cases, indicating a percentage of 26.08% and family history in 30 cases (43.47%). Laboratory changes vary greatly from patient to patient and may even remain unchanged. The relationship between the syndrome and the mutation in the FAM20A gene can be proven from the data, since all patients with ERS screened by the mutation were positive. With the advancement of the ERS studies, some associations with the syndrome are suspected, such as the presence of gingival fibromatosis, hearing loss, and hypertrichosis. Thus, it is noticed that the syndrome does not show a predilection for gender or age and there is a strong hereditary character, marked by the consanguinity and family history of the patients. The association with the FAM20A gene is reinforced, since the mutation was identified in all patients analyzed.

Keywords: Amelogenesis imperfecta, enemal renal syndrome, nephrocalcinosis

How to cite this article:
Morais Farias ML, Ornela GO, de Andrade RS, B. Martelli DR, Dias VO, Júnior HM. Enamel renal syndrome: A systematic review. Indian J Nephrol 2021;31:1-8

How to cite this URL:
Morais Farias ML, Ornela GO, de Andrade RS, B. Martelli DR, Dias VO, Júnior HM. Enamel renal syndrome: A systematic review. Indian J Nephrol [serial online] 2021 [cited 2022 Dec 6];31:1-8. Available from:

  Introduction Top

The enamel renal syndrome (ERS) is considered a rare disease according to the Office of Rare Diseases (ORD) of the National Institutes of Health (NIH), affecting less than 200,000 people in the United States population.[1] It is an autosomal recessive disorder characterized by amelogenesis imperfecta of the hypoplastic type and nephrocalcinosis (OMIM #204690), presenting with presence of thin or absence of enamel, delayed dental eruption, intrapulpal calcifications, bilateral nephrocalcinosis, and normal plasma calcium level.[1]

Amelogenesis imperfecta (AI) is a hereditary group of disorders that affects the quality and quantity of enamel on deciduous and/or permanent teeth, and may affect all or only a few teeth.[2],[3] The clinical characteristics of AI vary depending on the type: in the hypoplastic, which is present in the syndrome, the teeth have a white to dark brown chalk color, occlusal surfaces, and incisal edges are generally worn, and occasionally complete loss of enamel is observed; In the hypocalcified, the enamel exhibits a consistency of cheese and can be easily removed with a sharp explorer and in the hypomaturated is characterized by the enamel with normal thickness and white opaque areas on the incisal surfaces.[4]

Nephrocalcinosis is a condition characterized by calcium deposition in renal tissue and may be predominantly cortical or, more commonly, medullary. It is found in conditions, such as primary hyperparathyroidism, distal renal tubular acidosis, spongy spinal cord kidney, hypervitaminosis D, oxalosis, and some forms of Bartter's syndrome.[3],[5],[6] Nephrocalcinosis may remain unnoticed until patients have recurrent urinary tract infections, pyelonephritis, or the passage of a stone, leading to renal failure.[7]

The ERS diagnosis is clinical, based on orodental alterations and renal findings that represent the degree of impairment of the kidneys.[8] However, as renal changes occur late, the presence of the characteristic oral phenotype, even in the absence of other manifestations, is sufficient to clinically diagnose this syndrome.[9]

Thus, the objective of the systematic review is to present and discuss the characteristics of the ERS, which is relevant due to the scarcity of studies and knowledge about the syndrome.

  Methodology Top

The present review was carried out in accordance with the Cochrane Collaboration Group protocol for systematic reviews. Our review was performed in March 2018, when we searched on PubMed database the following terms: 'Enamel Renal Syndrome' [title/abstract] OR 'Enamel Renal Gengival Syndrome' [title/abstract] OR 'Amelogenesis imperfecta and nephrocalcinosis syndrome' [title/abstract] OR 'Enamel hypoplasia and renal dysfunction' [title/abstract], including a literature search strategy, selection of papers through the inclusion and exclusion of criteria, data extraction, and quality assessment. Meta-analysis was not possible since selected studies did not observe the same variables, methods, participants, and outcomes, which prevented comparisons.

As seen in [Figure 1], in the search, 108 studies were identified and after removing the repeated results, 69 articles remained. Of these, 39 were excluded, after 2 authors analyzed their abstracts, as criteria not to approach the ERS and non-English language; thus remaining 30 studies. From each of these articles, the following data were extracted for analysis: type of study, first author, publication year, country of publication, age, sex, family history, consanguinity, presence of amelogenesis imperfect, nephrocalcinosis and gingival fibromatosis, laboratory tests results, and mutation in the FAM20A gene.
Figure 1: Flowchart of process of systematic literature search, using Cochrane and flowchart of process of systematic literature search

Click here to view

  Results Top

The results found with the research are summarized in [Table 1]. Of a total of 69 articles found after research, only 30 (43.47%) were in agreement with the methodology,[1],[7],[8],[9],[10],[11],[12],[13],[14],[15],[16],[17],[18],[19],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30],[31],[32],[33],[34] of these 27 (39,13%) were case reports,[1],[7],[8],[10],[11],[12],[13],[14],[15],[16],[17],[18],[20],[21],[23],[24],[25],[26],[27],[28],[29],[30],[31],[32],[33],[34] 1 (1.44%) was case series[22] and 2 were review of scientific literature.[9],[19] The most recent publication date was in May 2018[34] and the older was in February 1972.[11]
Table 1: Articles from the literature that evaluated with Renal Enamel Syndrome that fulfilled the inclusion criteria of this study

Click here to view

Among the case reports, we can observe that the average age was 38.3 years old. The youngest age reported was in the first year of life[25] and the highest age was at 64 years old.[21] In ten (14.4%) patients,[7],[8],[11],[14],[17],[27],[33] there was a difference between the ages of diagnosis of AI and nephrocalcinosis. In 6 (8.64%) patients,[7],[8],[14],[33] AI was first identified at 1,[8] 6,[33] 8[7],[14] and 12 years[7],[33] and in 4 patients[11],[17],[27] nephrocalcinosis was first diagnosed at 8,[27] 11,[11] and 15 years.[11],[17] When it comes to gender, there were 33 (47.82%) women[1],[6],[7],[9],[10],[11],[12],[13],[16],[17],[19],[21],[22],[23],[25],[27],[29],[31] and 36 (52.17%) men.[6],[7],[9],[10],[11],[12],[14],[15],[17],[21],[22],[24],[25],[26],[28],[29],[30],[31],[32],[33],[34]

The presence of consanguinity was reported in 18 (26.08%) cases[1],[6],[14],[15],[16],[17],[19],[22],[23],[24],[26],[29],[31],[32] and in 30 (43.47%), there were positive family history for ERS.[6],[9],[10],[11],[12],[15],[17],[20],[21],[22],[23],[24],[29],[32] Among the 69 evaluated patients, all had Al.[1],[6],[7],[9],[10],[11],[12],[13],[14],[15],[16],[17],[19],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30],[31],[32],[33],[34] 62 (89.85%) presented with nephrocalcinosis,[1],[6],[7],[9],[10],[11],[12],[13],[14],[15],[16],[19],[20],[21],[22],[24],[25],[26],[27],[28],[29],[30],[31],[32],[33],[34] 46 (66.66%) had gingival fibromatosis[1],[7],[12],[13],[14],[17],[19],[31],[32],[33] and in 4 (5.79%) patients there was no appearance of this affection.[23],[26],[27],[28]

In the laboratory evaluation of patients, several types of alterations were reported, as seen in Table 1. In 35 cases (50.72%), there was no description of laboratory tests.[7],[17],[21],[23],[31],[34] Thus, the laboratory parameters were evaluated in 34 cases (49.27%):[1],[6],[7],[10],[12],[13],[14],[16],[20],[26],[27],[28],[32] in 18 (26.08%) no abnormalities were found[9],[11],[12],[15],[19],[22],[24],[25],[29],[30],[32],[33] and the main alterations identified were: hypocalciuria (11.59%),[1],[6],[10],[13],[27] elevated serum creatinine levels (7.24%),[6],[12],[20],[27] reduced phosphate excretion (5.79%)[1],[10],[13] and hypocitraturia (5.79%).[13],[26],[28],[32]

Since the discovery of the relationship between the syndrome and the gene FAM20A,[21] 51 patients were analyzed in 17 of the 28 case report studies.[7],[8],[17],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30],[31],[32],[33],[34] Among these 51 patients, 41 (80.39%) were screened by mutation in the gene and all 41 (100%) were positive.[7],[17],[21],[23],[25],[29],[31],[32] A total of 10 (19.60%) of the 51 patients analyzed after the discovery were not investigated about mutation on these gene,[22],[24],[26],[27],[28],[30],[33],[34] that is, a total of 28 (40.57%) patients were not screened by mutation in the FAM20A gene.[1],[9],[10],[11],[12],[13],[14],[15],[16],[18],[19],[20],[22],[24],[26],[27],[28],[30],[33],[34]

  Discussion Top

MacGibbon was the first to conduct a study, in 1972, that associates age of the diagnosis of imperfect amelogenesis and nephrocalcinosis. The case of a young woman diagnosed with both pathologies was described when her 26-year-old brother died of nephrocalcinosis and teeth similar to her own. In the reported cases, renal function remained stable until the patient was 16 years old, but progressive renal insufficiency led to the death of the patient.[10]

Nearly 40 years after the publication of the MacGibbon case report,[11] Jaureguiberry et al.[22] identified autosomal recessive FAM20A mutations as the cause of ERS. The study consisted in the genetic analysis of 25 patients from 16 families affected by the syndrome. As a result, all patients had biallelic mutations in FAM20A, with 20 different mutations. This gene, under normal conditions, has an inhibitory effect on mineralization, allowing it to occur only in bones and teeth. But in patients with homozygous mutation in FAM20A, an increase in the promoter activity and decrease of the inhibitory activity on the growth of oxalate crystals has been reported, so as to allow mineralization of the gingiva, kidneys, lungs, and dental follicles.[8],[9],[19],[22],[25],[27]

Laboratory alterations are not always present and, when exist, are varied. Hypocalciuria was identified in 11.59% of the cases,[1],[7],[12],[15],[29] being common in patients with ERS, although hypercalciuria is an important cause of stones formation.[35] Hypocitraturia was found in 5.79% of the cases.[15],[28],[30],[34] This alteration predisposes the formation of renal stones or nephrocalcinosis, because the citrate acts in the formation of soluble complexes with calcium, inhibiting the formation of renal stones.[30] The reduction of phosphate excretion was also identified in 5.79% of the cases,[1],[12],[15] as a consequence of the mutation on FAM20A that changes calcium and phosphate homeostasis in the kidneys.[25]

The hereditary relationship of the syndrome can be observed because there was consanguinity in 18 cases,[1],[6],[14],[15],[16],[17],[19],[22],[23],[24],[26],[29],[31],[32] indicating a percentage of 26. 08% and family history in 30,[6],[11],[12],[13],[14],[15],[17],[19],[22],[23],[24],[25],[26],[31],[34] that is, 43.47%. Another relevant fact is the lack of relationship with gender, since it affects almost equally men and women. The relationship between the syndrome and the mutation in the FAM20A gene can be proven from the data, since all the patients with ERS analysed by the mutation were positive.

Some studies[3],[7],[8],[9],[14],[16],[17],[20],[21],[27],[30],[31],[32],[34] cited the nationality of the patients and, according to these data, there was no association of a certain geographic area with the occurrence of the syndrome. The countries of origin were: Iran,[3] Caribbean,[3] Jordania,[3] England,[7] Turkey,[8] France,[9] Macedonia,[14] Brazil,[16],[20],[30],[31],[34] Japan,[17] India,[21] Israel,[27] and Thailand.[32]

With the advancement of studies on ERS, it has been suspected to have some associations with the syndrome. Kantaputra et al. reported in 2014[26] two patients who presented, simultaneously, ERS and Al and gingival fibromatosis syndrome (AIGFS). Knowing that FAM20A gene is involved in both, the genetic study of the patients was carried out, confirming the presence of the mutation in the cases. Besides that, as several studies have cited the triad of AI, nephrocalcinosis, and gingival fibromatosis, the authors suggested that ERS and AIGFS would be the same entity with different manifestations, giving rise to the new term “Enamel-Renal-Gingival Syndrome”.[9],[27],[31]

In 2016, Pêgo et al., related two cases that presented typical features of ERS, such as hypoplastic AI, nephrocalcinosis, gingival overgrowth, and other dental abnormalities, besides the presence of FAM20A mutation. Both patients also presented hearing loss and hypertrichosis, without the presence of exposition to environmental factors and mutations frequently associated with nonsyndromic deafness in Brazil. Thus, the study suggested the association with ERS, FAM20A gene, hearing loss, and hypertrichosis as expansion of the phenotypic spectrum of the disease.[29]

With the data obtained from the discovery of the disease with Mac Gibbon until the last studies, it was possible to trace the profile of the patients with ERS and the main alterations found. There is equivalence between the genders and absence of predilection by any age group. The main laboratory findings were hypocalciuria, hypocitraturia, reduction of phosphate excretion, and elevation of serum creatinine levels. The presence of the hereditary character of the syndrome and the relationship with the FAM20A gene were also confirmed. But there is still a need for further studies to increase knowledge about the syndrome and its newly discovered phenotype expansions.

  Conclusion Top

Among the data analyzed, it is possible to emphasize an equivalence of cases in men and women, excluding a possibility of any association with gender and the presence of ERS. The FAM20A gene was a finding of great relevance for the syndrome, since all patients with clinical characteristics have homozygous or heterozygous mutations in this gene.


The authors would like to thank The Minas Gerais State Research Foundation-FAPEMIG, Minas Gerais, Brazil and the National Council for Scientific and Technological Development - CNPq, Brazil.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Vani SVK, Varsha M, Sankar Y. Enamel renal syndrome: A rare case report. J Indian Soc Pedod Prev Dent 2012;30.2:169-72.  Back to cited text no. 1
Hunter L, Addy LD, Knox J, Drage N. Is amelogenesis imperfect an indication for renal examination? Int J Paediatr Dent 2007;17:62-5.  Back to cited text no. 2
Wang SK, Aref P, Hu Y, Milkovich RN, Simmer JP, El-Khateeb M, et al. FAM20A mutations can cause enamel-renal syndrome (ERS). PLoS Genet 2013;9:e1003302.  Back to cited text no. 3
Crawford PJ, Aldred M, Bloch-Zupan A. Amelogenesis imperfecta. Orphanet J Rare Dis 2007;2:17-23.  Back to cited text no. 4
Pereira PC, Miranda DM, Oliveira EA, Silva AC. Molecular pathophysiology of renal tubular acidosis. Curr Cenomics 2009;10:51-9.  Back to cited text no. 5
Berkow R, Fletcher AJ, Beers MH. Cenitourinary disorders. In: The Merck Manual of Diagnosis and Therapy. 16th ed. Des Plaines, Hl: Merck and Co Inc.; 1992;5:1732-43.  Back to cited text no. 6
Dellow EL, Harley KE, Unwin RJ, Wrong O, Winter GB, Parkins BJ. Amelogenesis imperfecta, nephrocalcinosis, and hypocalciuria syndromein two siblings from a large family with consanguineous parents. Nephrol Dial Transplant 1998;13:3193-6.  Back to cited text no. 7
Kantaputra PN, Bongkochwilawan C, Kaewgahya M, Ohazama A, Kayserili H, Erdem AP, et al. Enamel–renal–gingival syndrome, hypodontia, and a novel FAM20A mutation. Am J Med Genet 2014;164:2124-8.  Back to cited text no. 8
de la Dure-Molla M, Quentric M, Yamaguti PM, Acevedo AC, Mighell AJ, Vikkula M, et al. Pathognomonic oral profile of enamel renal syndrome (ERS) caused by recessive FAM20A mutations. Orphanet J Rare Dis 2014;9:1-13.  Back to cited text no. 9
Mauprivez C, Nguyen JF, de la Dure-Molla M, Naveau A. Prosthetic rehabilitation of a patient with rare and severe enamel renal syndrome. Int J Prosthodont 2018;31:31-4.  Back to cited text no. 10
MacGibbon D. Generalized enamel hypoplasia and renal dysfunction. Aust Dent J 1972;17:61-3.  Back to cited text no. 11
Lubinsky M, Angle C, Marsh PW, Witkop CJ. Syndrome of amelogenesis imperfecta, nephrocalcinosis, impaired renal concentration, and possible abnormality of calcium metabolism. Am J Med Genet 1985;20:233-43.  Back to cited text no. 12
Phakey P, Palamara J, Hall RK, McCredieu DA. Ultrastructural study of tooth enamel with amelogenesis imperfecta in Al-nephrocalcinosis syndrome. Connect Tissue Res 1995;32:253-9.  Back to cited text no. 13
Hall RK, Phakey P, Palamara J, McCredie DA. Amelogenesis imperfecta and nephrocalcinosis syndrome. Case studies of clinical features and ultrastructure of tooth enamel in two siblings. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1995;79:583-92.  Back to cited text no. 14
Normand de la Tranchade I, Bonarek H, Marteau JM, Boileau MJ, Nancy J. Amelogenesis imperfecta and nephrocalcinosis: A new case of this rare syndrome. J Clin Pediatr Dent 2003;27:171-5.  Back to cited text no. 15
Paula LM, Melo NS, Guerra ENS, Mestrinho DH, Acevedo AC. Case report of a rare syndrome associating amelogenesis imperfecta and nephrocalcinosis in a consanguineous family. Arch Oral Biol 2005;50:237-42.  Back to cited text no. 16
Suda N, Kitahara Y, Ohyama K. A case of amelogenesis imperfecta, cleft lip and palate and polycystic kidney disease. Orthod Craniofac Res 2006;9:52-6.  Back to cited text no. 17
Fu XJ, Nozu K, Goji K, Ikeda K, Kamioka I, Fujita T, et al. Enamel-renal syndrome associated with hypokalaemic metabolic alkalosis and impaired renal concentration: A novel syndrome? Nephrol Dial Transplant 2006;21:2959-62.  Back to cited text no. 18
Kirzioglu Z, Ulu KG, Sezer MT, Yüksel S. The relationship of amelogenesis imperfecta and nephrocalcinosis syndrome. Med Oral Patol Oral Cir Bucal 2009;14:e579-82.  Back to cited text no. 19
Martelli Júnior H, dos Santos Neto PE, de Aquino SN, Santos CCO, Borges SP, Oliveira EA, et al. Amelogenesis imperfecta and nephrocalcinosis syndrome: A case report and review of the literature. Nephron Physiol 2011;118:62-5.  Back to cited text no. 20
Elizabeth J, Lakshmi Priya E, Umadevi KM, Ranganathan K. Amelogenesis imperfecta with renal disease – A report of two cases. J Oral Pathol Med 2007;36:625-8.  Back to cited text no. 21
Jaureguiberry G, De la Dure-Molla M, Parry D, Quentric M, Himmerkus N, Koike T, et al. Nephrocalcinosis (enamel renal syndrome) caused by autosomal recessive FAM20A mutations. Nephron Physiol 2012;122:1-6.  Back to cited text no. 22
Rajathi JM, Austin RD, Mathew P. McGibbon Syndrome: A report of three siblings. Indian J Dent Res 2013;24:511-4.  Back to cited text no. 23
[PUBMED]  [Full text]  
Wang SK, Reid BM, Dugan SL, Roggenbuck JA, Read L, Aref P, et al. FAM20A mutations associated with enamel renal syndrome. J Dent Res 2014;93:42-8.  Back to cited text no. 24
Chaitanya V, Sangeetha B, Sandeep P, Varalaxmi B, Sridhar AV, Aparna G, et al. Amelogenesis imperfecta and nephrocalcinosis syndrome. Indian J Nephrol 2014;24:260-1.  Back to cited text no. 25
[PUBMED]  [Full text]  
Kantaputra PN, Kaewgahya M, Khemaleelakul U, Dejkhamron P, Sutthimethakorn S, Thongboonkerd V, et al. Enamel-renal-gingival syndrome and FAM20A mutations. Am J Med Genet A 2014;164A:1-9.  Back to cited text no. 26
Ashkenazi M, Rafe Z, Sarnat H, Levin L. Nephrocalcinosis associated with continuous enamel hypoplasia and severe alveolar bone loss: A case report and literature review. Pediatr Dent 2014;36:250-3.  Back to cited text no. 27
Patel A, Jagtap C, Bhat C, Shah R. Bilateral nephrocalcinosis and amelogenesis imperfecta: A case report. Contemp Clin Dent 2015;6:262-5.  Back to cited text no. 28
[PUBMED]  [Full text]  
Bhesania D, Arora A, Kapoor S. Enamel renal syndrome with associated amelogenesis imperfecta, nephrolithiasis, and hypocitraturia: A case report. Imaging Sci Dent 2015;45:181-5.  Back to cited text no. 29
Pêgo SPB, Coletta RD, Dumitriu S, Iancu D, Albanyan S, Kleta R. Enamel-renal syndrome in 2 patients with a mutation in FAM20 A and atypical hypertrichosis and hearing loss phenotypes. Oral Surg Oral Med Oral Pathol Oral Radiol 2016;123:229-34.  Back to cited text no. 30
Costa DC, Dourado MR, Figueiredo de Carvalho MF, Santos CR, da Cruz Batista MA, Mesquita AT. Enamel renal syndrome: A case history report. Int J Prosthodont 2017;30:22-4.  Back to cited text no. 31
Kantaputra PN, Bongkochwilawan C, Lubinsky M, Pata S, Kaewgahya M, Tong HJ, et al. Periodontal disease and FAM20A mutations. J Hum Genet 2017;62:679-86.  Back to cited text no. 32
Koruyucu M, Seymen F, Gencay G, Gencay K, Tuna EB, Shin TJ, et al. Nephrocalcinosis in amelogenesis imperfecta caused by the FAM20A mutation. Nephron 2018;139:189-96.  Back to cited text no. 33
Torres LHS, de-Azevedo-Vaz SL, Barroso DRC, Silva DN, Velloso TRG, de Barros LAP. Enamel-renal-syndrome: Case report. Spec Care Dentist 2018;38:172-5.  Back to cited text no. 34
Oliveira B, Kleta R, Bockenhauer D, Walsh SB. Genetic, pathophysiological, and clinical aspects of nephrocalcinosis. Am J Physiol Renal Physiol 2016;311:F1243-52.  Back to cited text no. 35


  [Figure 1]

  [Table 1]


Print this article  Email this article


Indian Journal of Nephrology
Published by Wolters Kluwer - Medknow
Online since 20th Sept '07