Skip to main content
Erschienen in: International Urology and Nephrology 4/2011

01.12.2011 | Nephrology – Review

Novel techniques and newer markers for the evaluation of “proximal tubular dysfunction”

verfasst von: Michael Ludwig, Sidharth K. Sethi

Erschienen in: International Urology and Nephrology | Ausgabe 4/2011

Einloggen, um Zugang zu erhalten

Abstract

Renal Fanconi syndromes are both clinically challenging and physiologically fascinating. The diagnosis requires a certain index of suspicion to correctly identify the clinical symptomatology and pursue the appropriate laboratory evaluations. The renal Fanconi syndrome (FS) is a defect of proximal tubular function attributable to different rare inherited diseases or acquired disorders caused by a multitude of exogenous agents. It can manifest as complete or incomplete FS, characterized by low molecular weight proteinuria, glucosuria, aminoaciduria, and loss of electrolytes, bicarbonate and lactate. Implementation of new methods and recent findings from urinary proteome pattern in patients with renal FS has led to the identification of new markers for proximal tubular dysfunction. Future combined proteomic and metabonomic studies will provide additional potential biomarkers and may help to gain novel insights in the diagnosis and differentiation of the various forms of FS. Moreover, the observation of poor renal uptake of 99 mTc-DMSA in patients with tubular proteinuria, which is not fully understood yet, may also help to elucidate the individual basis of FS in early stages. This review focuses on the new advances in the evaluation of proximal tubular dysfunction in various forms of Fanconi syndrome.
Literatur
1.
2.
Zurück zum Zitat Bökenkamp A, Ludwig M (2011) Disorders of the renal proximal tubule. Nephron Physiol 118:1–6CrossRef Bökenkamp A, Ludwig M (2011) Disorders of the renal proximal tubule. Nephron Physiol 118:1–6CrossRef
3.
Zurück zum Zitat Monnens L, Levtchenko E (2008) Evaluation of the proximal tubular function in hereditary renal Fanconi syndrome. Nephrol Dial Transplant 23:2719–2722PubMedCrossRef Monnens L, Levtchenko E (2008) Evaluation of the proximal tubular function in hereditary renal Fanconi syndrome. Nephrol Dial Transplant 23:2719–2722PubMedCrossRef
4.
Zurück zum Zitat Norden AG, Scheinman SJ, Deschodt-Lanckman MM et al (2000) Tubular proteinuria defined by a study of Dent’s (CLCN5 mutation) and other tubular diseases. Kidney Int 57:240–249PubMedCrossRef Norden AG, Scheinman SJ, Deschodt-Lanckman MM et al (2000) Tubular proteinuria defined by a study of Dent’s (CLCN5 mutation) and other tubular diseases. Kidney Int 57:240–249PubMedCrossRef
5.
Zurück zum Zitat Sethi SK, Bagga A, Gulati A et al (2008) Mutations in OCRL1 gene in Indian children with Lowe syndrome. Clin Exp Nephrol 12:358–362PubMedCrossRef Sethi SK, Bagga A, Gulati A et al (2008) Mutations in OCRL1 gene in Indian children with Lowe syndrome. Clin Exp Nephrol 12:358–362PubMedCrossRef
6.
Zurück zum Zitat Sethi SK, Ludwig M, Kabra M et al (2009) Vitamin A responsive night blindness in Dent’s disease. Pediatr Nephrol 24:1765–1770PubMedCrossRef Sethi SK, Ludwig M, Kabra M et al (2009) Vitamin A responsive night blindness in Dent’s disease. Pediatr Nephrol 24:1765–1770PubMedCrossRef
7.
Zurück zum Zitat Vilasi A, Cutillas PR, Maher AD et al (2007) Combined proteomic and metabonomic studies in three genetic forms of the renal Fanconi syndrome. Am J Physiol Renal Physiol 293:F456–F467PubMedCrossRef Vilasi A, Cutillas PR, Maher AD et al (2007) Combined proteomic and metabonomic studies in three genetic forms of the renal Fanconi syndrome. Am J Physiol Renal Physiol 293:F456–F467PubMedCrossRef
8.
Zurück zum Zitat Norden AG, Gardner SC, Van’t Hoff W et al (2008) Lysosomal enzymuria is a feature of hereditary Fanconi syndrome and is related to elevated CI-mannose-6-P-receptor excretion. Nephrol Dial Transplant 23:2795–2803PubMedCrossRef Norden AG, Gardner SC, Van’t Hoff W et al (2008) Lysosomal enzymuria is a feature of hereditary Fanconi syndrome and is related to elevated CI-mannose-6-P-receptor excretion. Nephrol Dial Transplant 23:2795–2803PubMedCrossRef
9.
Zurück zum Zitat Lee BH, Lee SH, Choi HJ et al (2009) Decreased renal uptake of (99 m)Tc-DMSA in patients with tubular proteinuria. Pediatr Nephrol 24:2211–2216PubMedCrossRef Lee BH, Lee SH, Choi HJ et al (2009) Decreased renal uptake of (99 m)Tc-DMSA in patients with tubular proteinuria. Pediatr Nephrol 24:2211–2216PubMedCrossRef
10.
Zurück zum Zitat Wu J, Chen YD, Gu W (2010) Urinary proteomics as a novel tool for biomarker discovery in kidney diseases. J Zhejiang Univ-Sci B (Biomed & Biotechnol) 11:227–237CrossRef Wu J, Chen YD, Gu W (2010) Urinary proteomics as a novel tool for biomarker discovery in kidney diseases. J Zhejiang Univ-Sci B (Biomed & Biotechnol) 11:227–237CrossRef
11.
Zurück zum Zitat Caubet C, Lacroix C, Decramer S et al (2010) Advances in urinary proteome analysis and biomarker discovery in pediatric renal disease. Pediatr Nephrol 25:27–35PubMedCrossRef Caubet C, Lacroix C, Decramer S et al (2010) Advances in urinary proteome analysis and biomarker discovery in pediatric renal disease. Pediatr Nephrol 25:27–35PubMedCrossRef
12.
Zurück zum Zitat Nesterova G, Gahl W (2008) Nephropathic cystinosis: late complications of a multisystemic disease. Pediatr Nephrol 23:863–878PubMedCrossRef Nesterova G, Gahl W (2008) Nephropathic cystinosis: late complications of a multisystemic disease. Pediatr Nephrol 23:863–878PubMedCrossRef
13.
Zurück zum Zitat Wilmer MJG, de Graaf-Hess A, Blom HJ et al (2005) Elevated oxidized glutathione in cystinotic proximal tubular epithelial cells. Bichem Biophys Res Commun 337:610–614CrossRef Wilmer MJG, de Graaf-Hess A, Blom HJ et al (2005) Elevated oxidized glutathione in cystinotic proximal tubular epithelial cells. Bichem Biophys Res Commun 337:610–614CrossRef
14.
Zurück zum Zitat Drube J, Schiffer E, Mischak H et al (2009) Urinary proteome pattern in children with renal Fanconi syndrome. Nephrol Dial Transplant 24:2161–2169PubMedCrossRef Drube J, Schiffer E, Mischak H et al (2009) Urinary proteome pattern in children with renal Fanconi syndrome. Nephrol Dial Transplant 24:2161–2169PubMedCrossRef
15.
Zurück zum Zitat Nielsen R, Courtoy PJ, Jacobsen C et al (2007) Endocytosis provides a major alternative pathway for lysosomal biogenesis in kidney proximal tubular cells. Proc Natl Acad Sci USA 104:5407–5411PubMedCrossRef Nielsen R, Courtoy PJ, Jacobsen C et al (2007) Endocytosis provides a major alternative pathway for lysosomal biogenesis in kidney proximal tubular cells. Proc Natl Acad Sci USA 104:5407–5411PubMedCrossRef
16.
Zurück zum Zitat Xaidara A, Karavitakis EM, Kosma K, Emma F, Dimitriou E, Michelakakis H (2010) chitotriosidase plasma activity in nephropathic cystinosis. J Inherit Metab Dis: Short report, #168, online. doi:10.1007/s10545-009-1118-8 Xaidara A, Karavitakis EM, Kosma K, Emma F, Dimitriou E, Michelakakis H (2010) chitotriosidase plasma activity in nephropathic cystinosis. J Inherit Metab Dis: Short report, #168, online. doi:10.​1007/​s10545-009-1118-8
17.
Zurück zum Zitat Bockenhauer D, Bokenkamp A, van’t Hoff W, Levtchenko E, Kist-van Holthe JE, Tasic V, Ludwig M (2008) Renal phenotype in Lowe syndrome: a selective proximal tubular dysfunction. Clin J Am Soc Nephrol 3:1430–1436PubMedCrossRef Bockenhauer D, Bokenkamp A, van’t Hoff W, Levtchenko E, Kist-van Holthe JE, Tasic V, Ludwig M (2008) Renal phenotype in Lowe syndrome: a selective proximal tubular dysfunction. Clin J Am Soc Nephrol 3:1430–1436PubMedCrossRef
18.
Zurück zum Zitat Bökenkamp A, Böckenhauer D, Cheong HI, Hoppe B, Tasic V, Unwin R, Ludwig M (2009) Dent-2 disease: a mild variant of Lowe syndrome. J Pediatr 155:94–99PubMedCrossRef Bökenkamp A, Böckenhauer D, Cheong HI, Hoppe B, Tasic V, Unwin R, Ludwig M (2009) Dent-2 disease: a mild variant of Lowe syndrome. J Pediatr 155:94–99PubMedCrossRef
19.
Zurück zum Zitat Jänne PA, Suchy SF, Bernard DJ et al (1998) Functional overlap between murine Inpp5b and OCRL1 may explain why deficiency of the murine ortholog for OCRL1 does not cause Lowe syndrome in mice. J Clin Invest 101:2042–2053PubMedCrossRef Jänne PA, Suchy SF, Bernard DJ et al (1998) Functional overlap between murine Inpp5b and OCRL1 may explain why deficiency of the murine ortholog for OCRL1 does not cause Lowe syndrome in mice. J Clin Invest 101:2042–2053PubMedCrossRef
20.
Zurück zum Zitat Bothwell SP, Farber LW, Hoagland A, Nussbaum RL (2010) Species-specific difference in expression and splice-site choice in Inpp5b, an inositol polyphosphate 5-phosphatase paralogous to the enzyme deficient in Lowe syndrome. Mammal Genome 21:458–466CrossRef Bothwell SP, Farber LW, Hoagland A, Nussbaum RL (2010) Species-specific difference in expression and splice-site choice in Inpp5b, an inositol polyphosphate 5-phosphatase paralogous to the enzyme deficient in Lowe syndrome. Mammal Genome 21:458–466CrossRef
21.
Zurück zum Zitat Bothwell SP, Chan E, Bernardini IM, Kuo YM, Gahl WA, Nussbaum RL (2011) Mouse model for Lowe syndrome/Dent disease 2 renal tubulopathy. J Am Soc Nephrol 22. doi:10.1681/ASN2010050565 Bothwell SP, Chan E, Bernardini IM, Kuo YM, Gahl WA, Nussbaum RL (2011) Mouse model for Lowe syndrome/Dent disease 2 renal tubulopathy. J Am Soc Nephrol 22. doi:10.​1681/​ASN2010050565
22.
Zurück zum Zitat Carr G, Simmons NL, Sayer JA (2006) Disruption of clc-5 leads to a redistribution of annexin A2 and promotes calcium crystal agglomeration in collecting duct epithelial cells. Cell Mol Life Sci 63:367–377PubMedCrossRef Carr G, Simmons NL, Sayer JA (2006) Disruption of clc-5 leads to a redistribution of annexin A2 and promotes calcium crystal agglomeration in collecting duct epithelial cells. Cell Mol Life Sci 63:367–377PubMedCrossRef
23.
Zurück zum Zitat Smith AJ, Reed AAC, Loh NY, Thakker RV, Lippiat JD (2009) Characterization of Dent’s disease mutations of CLC-5 reveals a correlation between functional and cell biological consequences and protein structure. Am J Physiol Renal Physiol 296:F390–F397PubMedCrossRef Smith AJ, Reed AAC, Loh NY, Thakker RV, Lippiat JD (2009) Characterization of Dent’s disease mutations of CLC-5 reveals a correlation between functional and cell biological consequences and protein structure. Am J Physiol Renal Physiol 296:F390–F397PubMedCrossRef
24.
Zurück zum Zitat Wang Y, Bartlett MC, Loo TW, Clarke TM (2006) Specific rescue of cystic fibrosis transmembrane conductance regulator processing mutants using pharmacological chaperones. Mol Pharmacol 70:297–302PubMedCrossRef Wang Y, Bartlett MC, Loo TW, Clarke TM (2006) Specific rescue of cystic fibrosis transmembrane conductance regulator processing mutants using pharmacological chaperones. Mol Pharmacol 70:297–302PubMedCrossRef
25.
Zurück zum Zitat Cutillas PR, Norden AGW, Cramer R, Burlingame AL, Unwin RJ (2003) Detection and analysis of urinary peptides by on-line liquid chromatography and mass spectrometry: application to patients with renal Fanconi syndrome. Clin Sci 104:483–490PubMedCrossRef Cutillas PR, Norden AGW, Cramer R, Burlingame AL, Unwin RJ (2003) Detection and analysis of urinary peptides by on-line liquid chromatography and mass spectrometry: application to patients with renal Fanconi syndrome. Clin Sci 104:483–490PubMedCrossRef
26.
Zurück zum Zitat Cutillas PR, Chalkley RJ, Hansen KC et al (2004) The urinary proteome in Fanconi syndrome implies specifity in the reabsorption of proteins by renal proximal tubule cells. Am J Physiol Renal Physiol 287:F353–F364PubMedCrossRef Cutillas PR, Chalkley RJ, Hansen KC et al (2004) The urinary proteome in Fanconi syndrome implies specifity in the reabsorption of proteins by renal proximal tubule cells. Am J Physiol Renal Physiol 287:F353–F364PubMedCrossRef
27.
Zurück zum Zitat Norden AG, Lapsley M, Igarashi T et al (2002) Urinary megalin deficiency implicates abnormal tubular endocytic function in Fanconi syndrome. J Am Soc Nephrol 13:125–133PubMed Norden AG, Lapsley M, Igarashi T et al (2002) Urinary megalin deficiency implicates abnormal tubular endocytic function in Fanconi syndrome. J Am Soc Nephrol 13:125–133PubMed
28.
Zurück zum Zitat Tanuma A, Sato H, Takeda T et al (2007) Functional characterization of a novel missense CLCN5 mutation causing alterations in proximal tubular endocytotic machinery in Dent’s disease. Nephron Physiol 107:87–97CrossRef Tanuma A, Sato H, Takeda T et al (2007) Functional characterization of a novel missense CLCN5 mutation causing alterations in proximal tubular endocytotic machinery in Dent’s disease. Nephron Physiol 107:87–97CrossRef
29.
Zurück zum Zitat Cho HY, Lee BH, Choi HJ, Ha IS, Choi Y, Cheong HI (2008) Renal manifestations of Dent disease and Lowe syndrome. Pediatr Nephrol 23:243–249PubMedCrossRef Cho HY, Lee BH, Choi HJ, Ha IS, Choi Y, Cheong HI (2008) Renal manifestations of Dent disease and Lowe syndrome. Pediatr Nephrol 23:243–249PubMedCrossRef
30.
Zurück zum Zitat Vezzoli G, Zerbi S, Baragetti I, Soldati L, Mora S, Dell’Antonio G, Bianchi G (1997) Nonacidotic proximal tubulopathy transmitted as autosomal dominant trait. Am J Kidney Dis 29:490–495PubMedCrossRef Vezzoli G, Zerbi S, Baragetti I, Soldati L, Mora S, Dell’Antonio G, Bianchi G (1997) Nonacidotic proximal tubulopathy transmitted as autosomal dominant trait. Am J Kidney Dis 29:490–495PubMedCrossRef
31.
32.
Zurück zum Zitat Holton JB, Walter HJ, Tyfield LA (2001) Galactosemia. In: Scriver CR, Beaudet AL, Sly WS, Valle D (eds) The metabolic and molecular basis of inherited disease, vol 8. McGraw-Hill, New York, pp 1553–1583 Holton JB, Walter HJ, Tyfield LA (2001) Galactosemia. In: Scriver CR, Beaudet AL, Sly WS, Valle D (eds) The metabolic and molecular basis of inherited disease, vol 8. McGraw-Hill, New York, pp 1553–1583
33.
Zurück zum Zitat Alonso-Fernandez JR, Carpinteiro MI, Baleato J, Fidalgo J (2010) Vertical sandwich-type continuous/evaporative TLC with fixed mobile phase volume for separating sugars of clinical relevance in paper-borne urine and blood samples in newborn screening. J Clin Lab Anal 24:106–112PubMedCrossRef Alonso-Fernandez JR, Carpinteiro MI, Baleato J, Fidalgo J (2010) Vertical sandwich-type continuous/evaporative TLC with fixed mobile phase volume for separating sugars of clinical relevance in paper-borne urine and blood samples in newborn screening. J Clin Lab Anal 24:106–112PubMedCrossRef
34.
Zurück zum Zitat Sturiale L, Barone R, Palmigiano A et al (2008) Multiplexed glycoproteomic analysis of glycosylation disorders by sequential yolk immunoglobulins immunoseparation and MALDI-TOF MS. Proteomics 8:3822–3832PubMedCrossRef Sturiale L, Barone R, Palmigiano A et al (2008) Multiplexed glycoproteomic analysis of glycosylation disorders by sequential yolk immunoglobulins immunoseparation and MALDI-TOF MS. Proteomics 8:3822–3832PubMedCrossRef
35.
Zurück zum Zitat Van Dyk E, Pretorius PJ (2005) DNA damage and repair in mammalian cells exposed to p-hydroxyphenylpyruvic acid. Biochem Biophys Res Commun 338:815–819PubMedCrossRef Van Dyk E, Pretorius PJ (2005) DNA damage and repair in mammalian cells exposed to p-hydroxyphenylpyruvic acid. Biochem Biophys Res Commun 338:815–819PubMedCrossRef
37.
Zurück zum Zitat Al-Dirbashi OY, Jacob M, Al-Ahaidib LJ et al (2006) Quantification of succinylacetone in urine of hepatorenal tyrosinemia patients by HPLC with fluorescence detection. Clin Chim Acta 365:243–248PubMedCrossRef Al-Dirbashi OY, Jacob M, Al-Ahaidib LJ et al (2006) Quantification of succinylacetone in urine of hepatorenal tyrosinemia patients by HPLC with fluorescence detection. Clin Chim Acta 365:243–248PubMedCrossRef
38.
Zurück zum Zitat Turgeon C, Magera MJ, Allard P et al (2008) Combined newborn screening for succinylacetone, amino acids, and acylcarnitines in dried blood spots. Clin Chem 54:657–664PubMedCrossRef Turgeon C, Magera MJ, Allard P et al (2008) Combined newborn screening for succinylacetone, amino acids, and acylcarnitines in dried blood spots. Clin Chem 54:657–664PubMedCrossRef
39.
Zurück zum Zitat Bouteldja N, Timson DJ (2010) The biochemical basis of hereditary fructose intolerance. J Inherit Metab Dis 33:105–112PubMedCrossRef Bouteldja N, Timson DJ (2010) The biochemical basis of hereditary fructose intolerance. J Inherit Metab Dis 33:105–112PubMedCrossRef
40.
Zurück zum Zitat Pronicka E, Adamowicz M, Kowalik A et al (2007) Elevated carbohydrate-deficient transferring (CDT) and its normalization on dietary treatment as a useful biochemical test for hereditary fructose intolerance and galactosemia. Pediatr Res 62:101–105PubMedCrossRef Pronicka E, Adamowicz M, Kowalik A et al (2007) Elevated carbohydrate-deficient transferring (CDT) and its normalization on dietary treatment as a useful biochemical test for hereditary fructose intolerance and galactosemia. Pediatr Res 62:101–105PubMedCrossRef
41.
Zurück zum Zitat Quintana E, Sturiale L, Montero R et al. (2009) Secondary disorders of glycosylation in inborn errors of fructose metabolism. J Inherit Metab Dis: Short report, #187, online. doi:10.1007/s10545-009-1219-4 Quintana E, Sturiale L, Montero R et al. (2009) Secondary disorders of glycosylation in inborn errors of fructose metabolism. J Inherit Metab Dis: Short report, #187, online. doi:10.​1007/​s10545-009-1219-4
42.
Zurück zum Zitat Adamowicz M, Ploski R, Rokicki D et al (2007) Transferrin hypoglycosylation in hereditary fructose intolerance: using the clues and avoiding the pitfalls. J Inherit Metab Dis 30:407PubMedCrossRef Adamowicz M, Ploski R, Rokicki D et al (2007) Transferrin hypoglycosylation in hereditary fructose intolerance: using the clues and avoiding the pitfalls. J Inherit Metab Dis 30:407PubMedCrossRef
43.
Zurück zum Zitat Santer R, Steinmann B (2002) Schaub J (2002) Fanconi-Bickel syndrome—a congenital defect of facilitative glucose transport. Curr Mol Med 2:213–227PubMedCrossRef Santer R, Steinmann B (2002) Schaub J (2002) Fanconi-Bickel syndrome—a congenital defect of facilitative glucose transport. Curr Mol Med 2:213–227PubMedCrossRef
44.
Zurück zum Zitat Furlan F, Santer R, Vismara E, Santus F, Sersale G, Menni F, Parini R (2006) Bilateral nuclear cataracts as the first neonatal sign of Fanconi-Bickel syndrome. J Inherit Metab Dis 29:685PubMedCrossRef Furlan F, Santer R, Vismara E, Santus F, Sersale G, Menni F, Parini R (2006) Bilateral nuclear cataracts as the first neonatal sign of Fanconi-Bickel syndrome. J Inherit Metab Dis 29:685PubMedCrossRef
45.
Zurück zum Zitat Santer R, Schneppenheim R, Dombrowski A, Götze H, Steinmann B, Schaub J (1997) Mutations in GLUT2, the gene for the liver-type glucose transporter, in patients with Fanconi-Bickel syndrome. Nat Genet 17:324–326PubMedCrossRef Santer R, Schneppenheim R, Dombrowski A, Götze H, Steinmann B, Schaub J (1997) Mutations in GLUT2, the gene for the liver-type glucose transporter, in patients with Fanconi-Bickel syndrome. Nat Genet 17:324–326PubMedCrossRef
46.
Zurück zum Zitat De Bie P, Muller P, Wijmenga C, Klomp LW (2007) Molecular pathogenesis of Wilson and Menkes disease: correlation of mutations with molecular defects and disease phenotypes. J Med Genet 44:673–688PubMedCrossRef De Bie P, Muller P, Wijmenga C, Klomp LW (2007) Molecular pathogenesis of Wilson and Menkes disease: correlation of mutations with molecular defects and disease phenotypes. J Med Genet 44:673–688PubMedCrossRef
47.
Zurück zum Zitat Roberts EA, Sarkar B (2008) Liver as a key organ in the supply, storage, and excretion of copper. Am J Clin Nutr 88(suppl):851S–854SPubMed Roberts EA, Sarkar B (2008) Liver as a key organ in the supply, storage, and excretion of copper. Am J Clin Nutr 88(suppl):851S–854SPubMed
48.
Zurück zum Zitat Roelofsen H, Balgobind R, Vonk RJ (2004) Proteomic analyzes of copper metabolism in an in vitro model of Wilson disease using surface enhanced laser desorption/ionization-time of flight-mass spectrometry. J Cell Biochem 93:732–740PubMedCrossRef Roelofsen H, Balgobind R, Vonk RJ (2004) Proteomic analyzes of copper metabolism in an in vitro model of Wilson disease using surface enhanced laser desorption/ionization-time of flight-mass spectrometry. J Cell Biochem 93:732–740PubMedCrossRef
49.
Zurück zum Zitat Huster D, Purnat TD, Burkhead JL et al (2007) High copper selectively alters lipid metabolism and cell cycle machinery in the mouse model of Wilson disease. J Biol Chem 282:8343–8355PubMedCrossRef Huster D, Purnat TD, Burkhead JL et al (2007) High copper selectively alters lipid metabolism and cell cycle machinery in the mouse model of Wilson disease. J Biol Chem 282:8343–8355PubMedCrossRef
50.
Zurück zum Zitat Ralle M, Huster D, Vogt S et al (2010) Wilson disease at a single cell level. Intracellular copper trafficking activates compartment-specific responses in hepatocytes. J Biol Chem 285:30875–30883PubMedCrossRef Ralle M, Huster D, Vogt S et al (2010) Wilson disease at a single cell level. Intracellular copper trafficking activates compartment-specific responses in hepatocytes. J Biol Chem 285:30875–30883PubMedCrossRef
51.
Zurück zum Zitat Skinner R, Pearson ADJ, Price L, Coulthard MG, Craft AW (1990) Nephrotoxicity after ifosfamide. Arch Dis Child 65:732–738PubMedCrossRef Skinner R, Pearson ADJ, Price L, Coulthard MG, Craft AW (1990) Nephrotoxicity after ifosfamide. Arch Dis Child 65:732–738PubMedCrossRef
52.
Zurück zum Zitat Yaseen Z, Michoudet C, Baverel G, Dubourg L (2008) Mechanisms of the ifosfamide induced inhibition of endocytosis in the rat proximal kidney tubule. Arch Toxicol 82:607–614PubMedCrossRef Yaseen Z, Michoudet C, Baverel G, Dubourg L (2008) Mechanisms of the ifosfamide induced inhibition of endocytosis in the rat proximal kidney tubule. Arch Toxicol 82:607–614PubMedCrossRef
53.
Zurück zum Zitat Foxall PJ, Singer JM, Hartley JM et al (1997) Urinary proton magnetic resonance studies of early ifosfamide-induced nephrotoxicity and encephalopathy. Clin Cancer Res 3:1507–1518PubMed Foxall PJ, Singer JM, Hartley JM et al (1997) Urinary proton magnetic resonance studies of early ifosfamide-induced nephrotoxicity and encephalopathy. Clin Cancer Res 3:1507–1518PubMed
54.
Zurück zum Zitat Ciarimboli G, Holle SK, Vollenbröcker B et al. (2010) New clues for nephrotoxicity induced by ifosfamide: preferential uptake via the human organic cation transporter 2. Mol Pharm. doi:10.1021/mp100329u Ciarimboli G, Holle SK, Vollenbröcker B et al. (2010) New clues for nephrotoxicity induced by ifosfamide: preferential uptake via the human organic cation transporter 2. Mol Pharm. doi:10.​1021/​mp100329u
55.
Zurück zum Zitat Suzuki S, Suzuki J, Kume K et al (1999) Poor renal accumulation of 99 mTc-DMSA in idiopathic tubular proteinuria. Nephron 81:49–54PubMedCrossRef Suzuki S, Suzuki J, Kume K et al (1999) Poor renal accumulation of 99 mTc-DMSA in idiopathic tubular proteinuria. Nephron 81:49–54PubMedCrossRef
56.
Zurück zum Zitat Frishberg Y, Dinour D, Belostotsky R et al (2009) Dent’s disease manifesting as focal glomerulosclerosis: is it the tip of the iceberg? Pediatr Nehrol 24:2369–2373CrossRef Frishberg Y, Dinour D, Belostotsky R et al (2009) Dent’s disease manifesting as focal glomerulosclerosis: is it the tip of the iceberg? Pediatr Nehrol 24:2369–2373CrossRef
57.
Zurück zum Zitat Kim SE, Cho JT, Lee DS et al (1995) Poor renal uptake of Tc-99 m DMSA and Tc-99 m MDP in a patient with Fanconi syndrome and near normal glomerular filtration rate. Clin Nucl Med 20:215–219PubMedCrossRef Kim SE, Cho JT, Lee DS et al (1995) Poor renal uptake of Tc-99 m DMSA and Tc-99 m MDP in a patient with Fanconi syndrome and near normal glomerular filtration rate. Clin Nucl Med 20:215–219PubMedCrossRef
58.
Zurück zum Zitat Hecht H, Ohlsson J, Starck SA (1996) Poor renal uptake of 99mtechnetium-dimercaptosuccinic acid and near-normal 99mtechnetium-mercaptoacetyltriglycine renogram in nephronophthisis. Pediatr Nephrol 10:167–170PubMed Hecht H, Ohlsson J, Starck SA (1996) Poor renal uptake of 99mtechnetium-dimercaptosuccinic acid and near-normal 99mtechnetium-mercaptoacetyltriglycine renogram in nephronophthisis. Pediatr Nephrol 10:167–170PubMed
59.
Zurück zum Zitat Caglar M, Topaloğlu R (2002) Reduced Tc-99m DMSA uptake in a patient with renal tubular acidosis: effect of acid-base imbalance. Ann Nucl Med 16:499–501PubMedCrossRef Caglar M, Topaloğlu R (2002) Reduced Tc-99m DMSA uptake in a patient with renal tubular acidosis: effect of acid-base imbalance. Ann Nucl Med 16:499–501PubMedCrossRef
60.
Zurück zum Zitat Tasic V, Lozanovski VJ, Korneti P, Ristoska-Bojkovska N, Sabolic-Avramovska V, Gucev Z, Ludwig M (2011) Clinical and laboratory features of Macedonian children with OCRL mutations. Pediatr Nephrol (in press) Tasic V, Lozanovski VJ, Korneti P, Ristoska-Bojkovska N, Sabolic-Avramovska V, Gucev Z, Ludwig M (2011) Clinical and laboratory features of Macedonian children with OCRL mutations. Pediatr Nephrol (in press)
61.
Zurück zum Zitat van Luÿk WH, Ensing GJ, Piers DA (1983) Low renal uptake of 99mTc-DMSA in patients with proximal tubular dysfunction. Eur J Nucl Med 8:404–405PubMedCrossRef van Luÿk WH, Ensing GJ, Piers DA (1983) Low renal uptake of 99mTc-DMSA in patients with proximal tubular dysfunction. Eur J Nucl Med 8:404–405PubMedCrossRef
62.
Zurück zum Zitat de Lange MJ, Piers DA, Kosterink JG et al (1989) Renal handling of technetium-99m DMSA: evidence for glomerular filtration and peritubular uptake. J Nucl Med 30:1219–1223PubMed de Lange MJ, Piers DA, Kosterink JG et al (1989) Renal handling of technetium-99m DMSA: evidence for glomerular filtration and peritubular uptake. J Nucl Med 30:1219–1223PubMed
Metadaten
Titel
Novel techniques and newer markers for the evaluation of “proximal tubular dysfunction”
verfasst von
Michael Ludwig
Sidharth K. Sethi
Publikationsdatum
01.12.2011
Verlag
Springer Netherlands
Erschienen in
International Urology and Nephrology / Ausgabe 4/2011
Print ISSN: 0301-1623
Elektronische ISSN: 1573-2584
DOI
https://doi.org/10.1007/s11255-011-9914-0

Weitere Artikel der Ausgabe 4/2011

International Urology and Nephrology 4/2011 Zur Ausgabe

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.