Etiologic and pathogenetic factors of dysmethabolic nephropathies in children

March 13, 2018
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Resume

Recently the growth of prevalence of dysmethabolic nephropathy in the structure of kidney morbidity in children is observed. Dysmethabolic nephropathy takes 27–64% among all structure of kidney diseases of children. Data of the literature about the most common factors of pathogenesis of methabolic nephropathy in children were analized. Available scientific sources dedicated to the mechanisms of development of the dysmethabolic nephropathy, studied by the methods of overview and system analyses. The results of the modern studies with description of the inherited and biochemical factors as substantial for origin of the nephropathy, were analyzed, as well as the features in pathogenesis of oxaluria, uraturia and cystinic nephropathy. On the basis of the studied sources it is possible to assert that there is no specific model which can explain pathological changes in different parts of kidney structure depending on direction of action of unfavorable factor. For the exposure of association between interleukin content and the state of mineral methabolism in dysmethabolic nephropathy the further study of patterns obtained on the basis of clinical, laboratory, statistical and epidemiological studies are necessary.

N.R. Aib

Key words: dysmethbolic nephropathy in kids, oxaluria, uraturia, phosphaturia, interleukins.

Published: 14.03.2018

References:

  • Dlin V.V., Osmanov I.M. (2013) Dismetabolicheskaya nefropatiya s oksalatno-kaltsievoy kristalluriey. Effekt. farmakoter., 42: 8–16.
  • Maidannyk V.H., Burlaka Ye.A., Bahdasarova I.V. ta in. (2013) Klitynna hipoksiia yak mekhanizm poshkodzhennia nyrok pry khronichnomu piielonefryti u ditei. Sovr. pedyatr., 3(51): 132–135.
  • Pyrih L.A., Ivanov D.D., Taran O.I. ta in. (2014) Nefrolohiia: Natsional. pidruch. Zaslavskyi O.Iu., Donetsk, 292 s.
  • Stepanova N. (2016) Hiperoksaluriia: mekhanizmy formuvannia ta naslidky (www.ukrjnd.com.ua/files/file/archive/n51/Stepanova.pdf).
  • Stoeva T.V. (2011) Profilaktika pri nefropatiyah u detey. A.V. Zubarenko, L.G. Kravchenko (red.). Profil. pediatr., Odessa, Chornomoria, s. 139–200.
  • Taran O.I. (2013) Uratna nefropatiia ta osnovni pidkhody do yii likuvannia. Pochky, 2(04) (http://www.mif-ua.com/archive/article/36059).
  • Almardini R.I., Alfarah M.G., Salaita G.M. (2014) The clinical pattern of primary hyperoxaluria in pediatric patient at Queen Rania Abdulla Children Hospital. Arab. J. Nephrol. Transplant., 7(2): 119–123.
  • Anderson C.E., Gilbert R.D., Elia M. (2015) Basal metabolic rate in children with chronic kidney disease and healthy control children. Pediatr. Nephrol., 30(11): 1995–2001.
  • Balestracci A., MeniBattaglia L., Toledo I. et al. (2014) Idiopathic hypercalciuria in children with urinary tract infection. Arch. Argent. Pediatr., 112(5): 428–433.
  • Belostotsky R., Seboun E., Idelson G.H. et al. (2010) Mutationsin DHDPSL are responsible for primary hyperoxaluria type III. Am. J. Hum. Genet., 87(3): 392–399.
  • Bevill M., Kattula A., Cooper C.S. et al. (2017) The Modern Metabolic Stone Evaluation in Children. Urology, 101: 15–20.
  • Ceban E., Banov P., Galescu A., Tanase D. (2017) The cellular and humoral immunity assay in patients with complicated urolithiasis. J. Med. Life, 10(1): 80–84.
  • Christov M., Jüppner H. (2013) Insights from genetic disorders of phosphate homeostasis. Semin. Nephrol., 33(2): 143–157.
  • Dwyer M.E., Krambeck A.E., Bergstralh E.J. et al. (2012) Temporal trends in incidence of kidney stones among children: a 25-year population based study. J. Urol., 188(1): 247–252.
  • Fanos V., Noto A., Caboni P. et al. (2014) Urine metabolomic profiling in neonatal nephrology. Clin. Biochem., 47(9): 708–710.
  • Figueres M.L., Linglart A., Bienaime F. et al. (2015) Kidney function and influence of sunlight exposure in patients with impaired 24-hydroxylation of vitamin D due to CYP24A1 mutations. Am. J. Kidney Dis., 65(11): 122–126.
  • Gambaro G., Croppi E., Coe F. at al. (2016) Metabolic diagnosis and medical prevention of calcium nephrolithiasis and its systemic manifestations: a consensus statement. J. Nephrol., 29(6): 715–734.
  • Gómez J., Gil-Peña H., Santos F. et al. (2016) Primary distal renal tubular acidosis: novel findings in patients studied by next-generation sequencing. Pediatr. Res., 79(3): 496–501.
  • Harambat J., Kunzmann K., Azukaitis K. et al. (2017) Metabolic acidosis is common and associates with disease progression in children with chronic kidney disease — 4C Study Consortium. Kidney Int., 17: 30330–30337.
  • Hernandez J.D., Ellison J.S., Lendvay T.S. (2015) Management of Pediatric Nephrolithiasis. Current Trends, Evaluation, and treatment. JAMA Pediatr., 169(10): 964–970.
  • Ingulli E.G., Mak R.H. (2014) Growth in children with chronic kidney disease: role of nutrition, growth hormone, dialysis, and steroids. Curr. Opin. Pediatr., 26(2): 187–192.
  • Konkoľová J., Chandoga J., Kováčik J. et al. (2017) Severe child form of primary hyperoxaluria type 2 — a case report revealing consequence of GRHPR deficiency on metabolism. BMC Med. Genet., 18(1): 59.
  • Kuwahara E., Murakami Y., Okamura T. et al. (2017) Increased childhood BMI is associated with young adult serum uric acid levels: a linkage study from Japan. Pediatr. Res., 81(2): 293–298.
  • Lee S.T., Cho H. (2016) Metabolic features and renal outcomes of urolithiasis in children. Ren. Fail., 38(6): 927–932.
  • Mulay S.R., Evan A., Anders H.-J. (2014) Nephrol Molecular mechanisms of crystal-related kidney inflammation and injury. Implications for cholesterol embolism, crystalline nephropathies and kidney stone disease. Dial. Transplant., 29(3): 507–514.
  • Mulay S.R., Kulkarni O.L., Rupanagudi K.V. et al. (2013) Calcium oxalate crystals induce renal inflammation by NLRP3-mediated IL-1β Clin. Invest., 123(1): 236–246.
  • Pietrement C., Allain-Launay E., Bacchetta J. et al. (2016) Diagnosis and management of chronic kidney disease in children: Guidelines of the French Society of Pediatric Nephrology. Arch. Pediatr., 23(11): 1191–1200.
  • Rodieux F., Wilbaux M., van den Anker J.N., Pfister M. (2015) Effect of kidney function on drug kinetics and dosing in neonates, infants, and children. Clin. Pharmacokinet., 54: 1183–1204.
  • Sayer J.A. (2017) Progress in understanding the genetics of calcium-containing nephrolithiasis. J. Am. Soc. Nephrol., 28(3): 748–759.
  • Taguchi K., Okada A., Hamamoto S. et al. (2016) M1/M2-macrophage phenotypes regulate renal calcium oxalate crystal development. Sci. Rep., 6: 35167.
  • Xiao X., Dong Z., Ye X. et al. (2016) Association between OPN genetic variations and nephrolithiasis risk. Biomed. Rep., 5(3): 321–326.
  • Yaseen A., Tresa V., Lanewala A.A. et al. (2017) Acute kidney injury in idiopathic nephrotic syndrome of childhood is a major risk factor for the development of chronic kidney disease. Ren. Fail., 39(1): 323–327.
  • Zhang B., Sun Y., Li Y. et al. (2015) Association analysis between genetic variants in interleukin genes among different populations with hyperuricemia in Xinjiang Autonomous Region. J. Clin. Exp. Pathol., 8(10): 13432–13440.