Risk factors for renal failure in children with non-glomerular nephropathies
Abstract The aim of the present study was to analyze the progression of chronic renal failure (CRF), the effects of modification of risk factors for disease progression, and to formulate a theoretical model of CRF progression in an unselected group of children with CRF. The study was a cross-section...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Litwin, Mieczysław [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2003 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Pediatric nephrology - Berlin : Springer, 1987, 19(2003), 2 vom: 18. Dez., Seite 178-186 |
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| Übergeordnetes Werk: |
volume:19 ; year:2003 ; number:2 ; day:18 ; month:12 ; pages:178-186 |
| Links: |
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| DOI / URN: |
10.1007/s00467-003-1329-4 |
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| Katalog-ID: |
SPR006662609 |
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| 520 | |a Abstract The aim of the present study was to analyze the progression of chronic renal failure (CRF), the effects of modification of risk factors for disease progression, and to formulate a theoretical model of CRF progression in an unselected group of children with CRF. The study was a cross-sectional, retrospective analysis of 92 patients aged 9.2±5.8 years with CRF and low-level proteinuria [glomerular filtration rate (GFR) 43±18 ml/min per 1.73 $ m^{2} $, proteinuria 0.57 g/day, range 0–3.9 g/day]. Inclusion criteria were an established diagnosis of CRF and completion of any surgical treatment. The etiology of CRF in the majority of patients was congenital uropathy. Sixty-nine patients observed for longer than 3 years were divided into two groups according to progression of CRF or improvement of GFR. Forty-three patients were on renoprotective therapy. Over a 3-year period GFR decreased in 39 children and improved in 30 children. There were no differences between the groups in the etiology of CRF. Patients with progression of CRF were older (P<0.08), grew faster (P<0.004), had higher blood pressure (P<0.01), and were more often proteinuric (P<0.03). Arterial hypertension in patients with progression of CRF was resistant to therapy and these patients needed more intensive treatment. Renoprotective therapy led to improvement of kidney function in 50% of patients, and resistance to renoprotective therapy was correlated with increased body mass and height. Patients who received renoprotective drugs showed stabilized kidney function (P<0.007) and decreased proteinuria (P<0.05) and blood pressure (P<0.02), despite higher basal values. In patients on renoprotective therapy in whom CRF progressed despite treatment, proteinuria was persistent in contrast to patients with improvement (P<0.02). The best model of CRF progression in the path diagram included systolic blood pressure and anthropometric parameters. In conclusion, in unselected patients with CRF of non-glomerular origin and nil-to-moderate proteinuria the main risk factors for CRF progression are rapid somatic growth, age, and blood pressure. Arterial hypertension and proteinuria, even of mild intensity, differ significantly between patients with progression of CRF and those with stable or improved renal function. Renoprotective therapy is related to significant slowing of CRF progression, but the risk factors for resistance to therapy include persistent proteinuria and somatic growth. | ||
| 650 | 4 | |a Chronic renal failure |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Renoprotective therapy |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Disease progression |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Proteinuria |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Hypertension |7 (dpeaa)DE-He213 | |
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10.1007/s00467-003-1329-4 doi (DE-627)SPR006662609 (SPR)s00467-003-1329-4-e DE-627 ger DE-627 rakwb eng 610 ASE 44.88 bkl 44.67 bkl Litwin, Mieczysław verfasserin aut Risk factors for renal failure in children with non-glomerular nephropathies 2003 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The aim of the present study was to analyze the progression of chronic renal failure (CRF), the effects of modification of risk factors for disease progression, and to formulate a theoretical model of CRF progression in an unselected group of children with CRF. The study was a cross-sectional, retrospective analysis of 92 patients aged 9.2±5.8 years with CRF and low-level proteinuria [glomerular filtration rate (GFR) 43±18 ml/min per 1.73 $ m^{2} $, proteinuria 0.57 g/day, range 0–3.9 g/day]. Inclusion criteria were an established diagnosis of CRF and completion of any surgical treatment. The etiology of CRF in the majority of patients was congenital uropathy. Sixty-nine patients observed for longer than 3 years were divided into two groups according to progression of CRF or improvement of GFR. Forty-three patients were on renoprotective therapy. Over a 3-year period GFR decreased in 39 children and improved in 30 children. There were no differences between the groups in the etiology of CRF. Patients with progression of CRF were older (P<0.08), grew faster (P<0.004), had higher blood pressure (P<0.01), and were more often proteinuric (P<0.03). Arterial hypertension in patients with progression of CRF was resistant to therapy and these patients needed more intensive treatment. Renoprotective therapy led to improvement of kidney function in 50% of patients, and resistance to renoprotective therapy was correlated with increased body mass and height. Patients who received renoprotective drugs showed stabilized kidney function (P<0.007) and decreased proteinuria (P<0.05) and blood pressure (P<0.02), despite higher basal values. In patients on renoprotective therapy in whom CRF progressed despite treatment, proteinuria was persistent in contrast to patients with improvement (P<0.02). The best model of CRF progression in the path diagram included systolic blood pressure and anthropometric parameters. In conclusion, in unselected patients with CRF of non-glomerular origin and nil-to-moderate proteinuria the main risk factors for CRF progression are rapid somatic growth, age, and blood pressure. Arterial hypertension and proteinuria, even of mild intensity, differ significantly between patients with progression of CRF and those with stable or improved renal function. Renoprotective therapy is related to significant slowing of CRF progression, but the risk factors for resistance to therapy include persistent proteinuria and somatic growth. Chronic renal failure (dpeaa)DE-He213 Renoprotective therapy (dpeaa)DE-He213 Disease progression (dpeaa)DE-He213 Proteinuria (dpeaa)DE-He213 Hypertension (dpeaa)DE-He213 Enthalten in Pediatric nephrology Berlin : Springer, 1987 19(2003), 2 vom: 18. Dez., Seite 178-186 (DE-627)254638872 (DE-600)1463004-7 1432-198X nnns volume:19 year:2003 number:2 day:18 month:12 pages:178-186 https://dx.doi.org/10.1007/s00467-003-1329-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.88 ASE 44.67 ASE AR 19 2003 2 18 12 178-186 |
| spelling |
10.1007/s00467-003-1329-4 doi (DE-627)SPR006662609 (SPR)s00467-003-1329-4-e DE-627 ger DE-627 rakwb eng 610 ASE 44.88 bkl 44.67 bkl Litwin, Mieczysław verfasserin aut Risk factors for renal failure in children with non-glomerular nephropathies 2003 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The aim of the present study was to analyze the progression of chronic renal failure (CRF), the effects of modification of risk factors for disease progression, and to formulate a theoretical model of CRF progression in an unselected group of children with CRF. The study was a cross-sectional, retrospective analysis of 92 patients aged 9.2±5.8 years with CRF and low-level proteinuria [glomerular filtration rate (GFR) 43±18 ml/min per 1.73 $ m^{2} $, proteinuria 0.57 g/day, range 0–3.9 g/day]. Inclusion criteria were an established diagnosis of CRF and completion of any surgical treatment. The etiology of CRF in the majority of patients was congenital uropathy. Sixty-nine patients observed for longer than 3 years were divided into two groups according to progression of CRF or improvement of GFR. Forty-three patients were on renoprotective therapy. Over a 3-year period GFR decreased in 39 children and improved in 30 children. There were no differences between the groups in the etiology of CRF. Patients with progression of CRF were older (P<0.08), grew faster (P<0.004), had higher blood pressure (P<0.01), and were more often proteinuric (P<0.03). Arterial hypertension in patients with progression of CRF was resistant to therapy and these patients needed more intensive treatment. Renoprotective therapy led to improvement of kidney function in 50% of patients, and resistance to renoprotective therapy was correlated with increased body mass and height. Patients who received renoprotective drugs showed stabilized kidney function (P<0.007) and decreased proteinuria (P<0.05) and blood pressure (P<0.02), despite higher basal values. In patients on renoprotective therapy in whom CRF progressed despite treatment, proteinuria was persistent in contrast to patients with improvement (P<0.02). The best model of CRF progression in the path diagram included systolic blood pressure and anthropometric parameters. In conclusion, in unselected patients with CRF of non-glomerular origin and nil-to-moderate proteinuria the main risk factors for CRF progression are rapid somatic growth, age, and blood pressure. Arterial hypertension and proteinuria, even of mild intensity, differ significantly between patients with progression of CRF and those with stable or improved renal function. Renoprotective therapy is related to significant slowing of CRF progression, but the risk factors for resistance to therapy include persistent proteinuria and somatic growth. Chronic renal failure (dpeaa)DE-He213 Renoprotective therapy (dpeaa)DE-He213 Disease progression (dpeaa)DE-He213 Proteinuria (dpeaa)DE-He213 Hypertension (dpeaa)DE-He213 Enthalten in Pediatric nephrology Berlin : Springer, 1987 19(2003), 2 vom: 18. Dez., Seite 178-186 (DE-627)254638872 (DE-600)1463004-7 1432-198X nnns volume:19 year:2003 number:2 day:18 month:12 pages:178-186 https://dx.doi.org/10.1007/s00467-003-1329-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.88 ASE 44.67 ASE AR 19 2003 2 18 12 178-186 |
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10.1007/s00467-003-1329-4 doi (DE-627)SPR006662609 (SPR)s00467-003-1329-4-e DE-627 ger DE-627 rakwb eng 610 ASE 44.88 bkl 44.67 bkl Litwin, Mieczysław verfasserin aut Risk factors for renal failure in children with non-glomerular nephropathies 2003 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The aim of the present study was to analyze the progression of chronic renal failure (CRF), the effects of modification of risk factors for disease progression, and to formulate a theoretical model of CRF progression in an unselected group of children with CRF. The study was a cross-sectional, retrospective analysis of 92 patients aged 9.2±5.8 years with CRF and low-level proteinuria [glomerular filtration rate (GFR) 43±18 ml/min per 1.73 $ m^{2} $, proteinuria 0.57 g/day, range 0–3.9 g/day]. Inclusion criteria were an established diagnosis of CRF and completion of any surgical treatment. The etiology of CRF in the majority of patients was congenital uropathy. Sixty-nine patients observed for longer than 3 years were divided into two groups according to progression of CRF or improvement of GFR. Forty-three patients were on renoprotective therapy. Over a 3-year period GFR decreased in 39 children and improved in 30 children. There were no differences between the groups in the etiology of CRF. Patients with progression of CRF were older (P<0.08), grew faster (P<0.004), had higher blood pressure (P<0.01), and were more often proteinuric (P<0.03). Arterial hypertension in patients with progression of CRF was resistant to therapy and these patients needed more intensive treatment. Renoprotective therapy led to improvement of kidney function in 50% of patients, and resistance to renoprotective therapy was correlated with increased body mass and height. Patients who received renoprotective drugs showed stabilized kidney function (P<0.007) and decreased proteinuria (P<0.05) and blood pressure (P<0.02), despite higher basal values. In patients on renoprotective therapy in whom CRF progressed despite treatment, proteinuria was persistent in contrast to patients with improvement (P<0.02). The best model of CRF progression in the path diagram included systolic blood pressure and anthropometric parameters. In conclusion, in unselected patients with CRF of non-glomerular origin and nil-to-moderate proteinuria the main risk factors for CRF progression are rapid somatic growth, age, and blood pressure. Arterial hypertension and proteinuria, even of mild intensity, differ significantly between patients with progression of CRF and those with stable or improved renal function. Renoprotective therapy is related to significant slowing of CRF progression, but the risk factors for resistance to therapy include persistent proteinuria and somatic growth. Chronic renal failure (dpeaa)DE-He213 Renoprotective therapy (dpeaa)DE-He213 Disease progression (dpeaa)DE-He213 Proteinuria (dpeaa)DE-He213 Hypertension (dpeaa)DE-He213 Enthalten in Pediatric nephrology Berlin : Springer, 1987 19(2003), 2 vom: 18. Dez., Seite 178-186 (DE-627)254638872 (DE-600)1463004-7 1432-198X nnns volume:19 year:2003 number:2 day:18 month:12 pages:178-186 https://dx.doi.org/10.1007/s00467-003-1329-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.88 ASE 44.67 ASE AR 19 2003 2 18 12 178-186 |
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10.1007/s00467-003-1329-4 doi (DE-627)SPR006662609 (SPR)s00467-003-1329-4-e DE-627 ger DE-627 rakwb eng 610 ASE 44.88 bkl 44.67 bkl Litwin, Mieczysław verfasserin aut Risk factors for renal failure in children with non-glomerular nephropathies 2003 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The aim of the present study was to analyze the progression of chronic renal failure (CRF), the effects of modification of risk factors for disease progression, and to formulate a theoretical model of CRF progression in an unselected group of children with CRF. The study was a cross-sectional, retrospective analysis of 92 patients aged 9.2±5.8 years with CRF and low-level proteinuria [glomerular filtration rate (GFR) 43±18 ml/min per 1.73 $ m^{2} $, proteinuria 0.57 g/day, range 0–3.9 g/day]. Inclusion criteria were an established diagnosis of CRF and completion of any surgical treatment. The etiology of CRF in the majority of patients was congenital uropathy. Sixty-nine patients observed for longer than 3 years were divided into two groups according to progression of CRF or improvement of GFR. Forty-three patients were on renoprotective therapy. Over a 3-year period GFR decreased in 39 children and improved in 30 children. There were no differences between the groups in the etiology of CRF. Patients with progression of CRF were older (P<0.08), grew faster (P<0.004), had higher blood pressure (P<0.01), and were more often proteinuric (P<0.03). Arterial hypertension in patients with progression of CRF was resistant to therapy and these patients needed more intensive treatment. Renoprotective therapy led to improvement of kidney function in 50% of patients, and resistance to renoprotective therapy was correlated with increased body mass and height. Patients who received renoprotective drugs showed stabilized kidney function (P<0.007) and decreased proteinuria (P<0.05) and blood pressure (P<0.02), despite higher basal values. In patients on renoprotective therapy in whom CRF progressed despite treatment, proteinuria was persistent in contrast to patients with improvement (P<0.02). The best model of CRF progression in the path diagram included systolic blood pressure and anthropometric parameters. In conclusion, in unselected patients with CRF of non-glomerular origin and nil-to-moderate proteinuria the main risk factors for CRF progression are rapid somatic growth, age, and blood pressure. Arterial hypertension and proteinuria, even of mild intensity, differ significantly between patients with progression of CRF and those with stable or improved renal function. Renoprotective therapy is related to significant slowing of CRF progression, but the risk factors for resistance to therapy include persistent proteinuria and somatic growth. Chronic renal failure (dpeaa)DE-He213 Renoprotective therapy (dpeaa)DE-He213 Disease progression (dpeaa)DE-He213 Proteinuria (dpeaa)DE-He213 Hypertension (dpeaa)DE-He213 Enthalten in Pediatric nephrology Berlin : Springer, 1987 19(2003), 2 vom: 18. Dez., Seite 178-186 (DE-627)254638872 (DE-600)1463004-7 1432-198X nnns volume:19 year:2003 number:2 day:18 month:12 pages:178-186 https://dx.doi.org/10.1007/s00467-003-1329-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.88 ASE 44.67 ASE AR 19 2003 2 18 12 178-186 |
| allfieldsSound |
10.1007/s00467-003-1329-4 doi (DE-627)SPR006662609 (SPR)s00467-003-1329-4-e DE-627 ger DE-627 rakwb eng 610 ASE 44.88 bkl 44.67 bkl Litwin, Mieczysław verfasserin aut Risk factors for renal failure in children with non-glomerular nephropathies 2003 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The aim of the present study was to analyze the progression of chronic renal failure (CRF), the effects of modification of risk factors for disease progression, and to formulate a theoretical model of CRF progression in an unselected group of children with CRF. The study was a cross-sectional, retrospective analysis of 92 patients aged 9.2±5.8 years with CRF and low-level proteinuria [glomerular filtration rate (GFR) 43±18 ml/min per 1.73 $ m^{2} $, proteinuria 0.57 g/day, range 0–3.9 g/day]. Inclusion criteria were an established diagnosis of CRF and completion of any surgical treatment. The etiology of CRF in the majority of patients was congenital uropathy. Sixty-nine patients observed for longer than 3 years were divided into two groups according to progression of CRF or improvement of GFR. Forty-three patients were on renoprotective therapy. Over a 3-year period GFR decreased in 39 children and improved in 30 children. There were no differences between the groups in the etiology of CRF. Patients with progression of CRF were older (P<0.08), grew faster (P<0.004), had higher blood pressure (P<0.01), and were more often proteinuric (P<0.03). Arterial hypertension in patients with progression of CRF was resistant to therapy and these patients needed more intensive treatment. Renoprotective therapy led to improvement of kidney function in 50% of patients, and resistance to renoprotective therapy was correlated with increased body mass and height. Patients who received renoprotective drugs showed stabilized kidney function (P<0.007) and decreased proteinuria (P<0.05) and blood pressure (P<0.02), despite higher basal values. In patients on renoprotective therapy in whom CRF progressed despite treatment, proteinuria was persistent in contrast to patients with improvement (P<0.02). The best model of CRF progression in the path diagram included systolic blood pressure and anthropometric parameters. In conclusion, in unselected patients with CRF of non-glomerular origin and nil-to-moderate proteinuria the main risk factors for CRF progression are rapid somatic growth, age, and blood pressure. Arterial hypertension and proteinuria, even of mild intensity, differ significantly between patients with progression of CRF and those with stable or improved renal function. Renoprotective therapy is related to significant slowing of CRF progression, but the risk factors for resistance to therapy include persistent proteinuria and somatic growth. Chronic renal failure (dpeaa)DE-He213 Renoprotective therapy (dpeaa)DE-He213 Disease progression (dpeaa)DE-He213 Proteinuria (dpeaa)DE-He213 Hypertension (dpeaa)DE-He213 Enthalten in Pediatric nephrology Berlin : Springer, 1987 19(2003), 2 vom: 18. Dez., Seite 178-186 (DE-627)254638872 (DE-600)1463004-7 1432-198X nnns volume:19 year:2003 number:2 day:18 month:12 pages:178-186 https://dx.doi.org/10.1007/s00467-003-1329-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.88 ASE 44.67 ASE AR 19 2003 2 18 12 178-186 |
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English |
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Enthalten in Pediatric nephrology 19(2003), 2 vom: 18. Dez., Seite 178-186 volume:19 year:2003 number:2 day:18 month:12 pages:178-186 |
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Enthalten in Pediatric nephrology 19(2003), 2 vom: 18. Dez., Seite 178-186 volume:19 year:2003 number:2 day:18 month:12 pages:178-186 |
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Chronic renal failure Renoprotective therapy Disease progression Proteinuria Hypertension |
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Pediatric nephrology |
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Litwin, Mieczysław @@aut@@ |
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2003-12-18T00:00:00Z |
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The study was a cross-sectional, retrospective analysis of 92 patients aged 9.2±5.8 years with CRF and low-level proteinuria [glomerular filtration rate (GFR) 43±18 ml/min per 1.73 $ m^{2} $, proteinuria 0.57 g/day, range 0–3.9 g/day]. Inclusion criteria were an established diagnosis of CRF and completion of any surgical treatment. The etiology of CRF in the majority of patients was congenital uropathy. Sixty-nine patients observed for longer than 3 years were divided into two groups according to progression of CRF or improvement of GFR. Forty-three patients were on renoprotective therapy. Over a 3-year period GFR decreased in 39 children and improved in 30 children. There were no differences between the groups in the etiology of CRF. Patients with progression of CRF were older (P<0.08), grew faster (P<0.004), had higher blood pressure (P<0.01), and were more often proteinuric (P<0.03). Arterial hypertension in patients with progression of CRF was resistant to therapy and these patients needed more intensive treatment. Renoprotective therapy led to improvement of kidney function in 50% of patients, and resistance to renoprotective therapy was correlated with increased body mass and height. Patients who received renoprotective drugs showed stabilized kidney function (P<0.007) and decreased proteinuria (P<0.05) and blood pressure (P<0.02), despite higher basal values. In patients on renoprotective therapy in whom CRF progressed despite treatment, proteinuria was persistent in contrast to patients with improvement (P<0.02). The best model of CRF progression in the path diagram included systolic blood pressure and anthropometric parameters. In conclusion, in unselected patients with CRF of non-glomerular origin and nil-to-moderate proteinuria the main risk factors for CRF progression are rapid somatic growth, age, and blood pressure. Arterial hypertension and proteinuria, even of mild intensity, differ significantly between patients with progression of CRF and those with stable or improved renal function. Renoprotective therapy is related to significant slowing of CRF progression, but the risk factors for resistance to therapy include persistent proteinuria and somatic growth.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Chronic renal failure</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Renoprotective therapy</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Disease progression</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Proteinuria</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Hypertension</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Pediatric nephrology</subfield><subfield code="d">Berlin : Springer, 1987</subfield><subfield code="g">19(2003), 2 vom: 18. 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Litwin, Mieczysław |
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Litwin, Mieczysław ddc 610 bkl 44.88 bkl 44.67 misc Chronic renal failure misc Renoprotective therapy misc Disease progression misc Proteinuria misc Hypertension Risk factors for renal failure in children with non-glomerular nephropathies |
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610 ASE 44.88 bkl 44.67 bkl Risk factors for renal failure in children with non-glomerular nephropathies Chronic renal failure (dpeaa)DE-He213 Renoprotective therapy (dpeaa)DE-He213 Disease progression (dpeaa)DE-He213 Proteinuria (dpeaa)DE-He213 Hypertension (dpeaa)DE-He213 |
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ddc 610 bkl 44.88 bkl 44.67 misc Chronic renal failure misc Renoprotective therapy misc Disease progression misc Proteinuria misc Hypertension |
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Litwin, Mieczysław |
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10.1007/s00467-003-1329-4 |
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risk factors for renal failure in children with non-glomerular nephropathies |
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Risk factors for renal failure in children with non-glomerular nephropathies |
| abstract |
Abstract The aim of the present study was to analyze the progression of chronic renal failure (CRF), the effects of modification of risk factors for disease progression, and to formulate a theoretical model of CRF progression in an unselected group of children with CRF. The study was a cross-sectional, retrospective analysis of 92 patients aged 9.2±5.8 years with CRF and low-level proteinuria [glomerular filtration rate (GFR) 43±18 ml/min per 1.73 $ m^{2} $, proteinuria 0.57 g/day, range 0–3.9 g/day]. Inclusion criteria were an established diagnosis of CRF and completion of any surgical treatment. The etiology of CRF in the majority of patients was congenital uropathy. Sixty-nine patients observed for longer than 3 years were divided into two groups according to progression of CRF or improvement of GFR. Forty-three patients were on renoprotective therapy. Over a 3-year period GFR decreased in 39 children and improved in 30 children. There were no differences between the groups in the etiology of CRF. Patients with progression of CRF were older (P<0.08), grew faster (P<0.004), had higher blood pressure (P<0.01), and were more often proteinuric (P<0.03). Arterial hypertension in patients with progression of CRF was resistant to therapy and these patients needed more intensive treatment. Renoprotective therapy led to improvement of kidney function in 50% of patients, and resistance to renoprotective therapy was correlated with increased body mass and height. Patients who received renoprotective drugs showed stabilized kidney function (P<0.007) and decreased proteinuria (P<0.05) and blood pressure (P<0.02), despite higher basal values. In patients on renoprotective therapy in whom CRF progressed despite treatment, proteinuria was persistent in contrast to patients with improvement (P<0.02). The best model of CRF progression in the path diagram included systolic blood pressure and anthropometric parameters. In conclusion, in unselected patients with CRF of non-glomerular origin and nil-to-moderate proteinuria the main risk factors for CRF progression are rapid somatic growth, age, and blood pressure. Arterial hypertension and proteinuria, even of mild intensity, differ significantly between patients with progression of CRF and those with stable or improved renal function. Renoprotective therapy is related to significant slowing of CRF progression, but the risk factors for resistance to therapy include persistent proteinuria and somatic growth. |
| abstractGer |
Abstract The aim of the present study was to analyze the progression of chronic renal failure (CRF), the effects of modification of risk factors for disease progression, and to formulate a theoretical model of CRF progression in an unselected group of children with CRF. The study was a cross-sectional, retrospective analysis of 92 patients aged 9.2±5.8 years with CRF and low-level proteinuria [glomerular filtration rate (GFR) 43±18 ml/min per 1.73 $ m^{2} $, proteinuria 0.57 g/day, range 0–3.9 g/day]. Inclusion criteria were an established diagnosis of CRF and completion of any surgical treatment. The etiology of CRF in the majority of patients was congenital uropathy. Sixty-nine patients observed for longer than 3 years were divided into two groups according to progression of CRF or improvement of GFR. Forty-three patients were on renoprotective therapy. Over a 3-year period GFR decreased in 39 children and improved in 30 children. There were no differences between the groups in the etiology of CRF. Patients with progression of CRF were older (P<0.08), grew faster (P<0.004), had higher blood pressure (P<0.01), and were more often proteinuric (P<0.03). Arterial hypertension in patients with progression of CRF was resistant to therapy and these patients needed more intensive treatment. Renoprotective therapy led to improvement of kidney function in 50% of patients, and resistance to renoprotective therapy was correlated with increased body mass and height. Patients who received renoprotective drugs showed stabilized kidney function (P<0.007) and decreased proteinuria (P<0.05) and blood pressure (P<0.02), despite higher basal values. In patients on renoprotective therapy in whom CRF progressed despite treatment, proteinuria was persistent in contrast to patients with improvement (P<0.02). The best model of CRF progression in the path diagram included systolic blood pressure and anthropometric parameters. In conclusion, in unselected patients with CRF of non-glomerular origin and nil-to-moderate proteinuria the main risk factors for CRF progression are rapid somatic growth, age, and blood pressure. Arterial hypertension and proteinuria, even of mild intensity, differ significantly between patients with progression of CRF and those with stable or improved renal function. Renoprotective therapy is related to significant slowing of CRF progression, but the risk factors for resistance to therapy include persistent proteinuria and somatic growth. |
| abstract_unstemmed |
Abstract The aim of the present study was to analyze the progression of chronic renal failure (CRF), the effects of modification of risk factors for disease progression, and to formulate a theoretical model of CRF progression in an unselected group of children with CRF. The study was a cross-sectional, retrospective analysis of 92 patients aged 9.2±5.8 years with CRF and low-level proteinuria [glomerular filtration rate (GFR) 43±18 ml/min per 1.73 $ m^{2} $, proteinuria 0.57 g/day, range 0–3.9 g/day]. Inclusion criteria were an established diagnosis of CRF and completion of any surgical treatment. The etiology of CRF in the majority of patients was congenital uropathy. Sixty-nine patients observed for longer than 3 years were divided into two groups according to progression of CRF or improvement of GFR. Forty-three patients were on renoprotective therapy. Over a 3-year period GFR decreased in 39 children and improved in 30 children. There were no differences between the groups in the etiology of CRF. Patients with progression of CRF were older (P<0.08), grew faster (P<0.004), had higher blood pressure (P<0.01), and were more often proteinuric (P<0.03). Arterial hypertension in patients with progression of CRF was resistant to therapy and these patients needed more intensive treatment. Renoprotective therapy led to improvement of kidney function in 50% of patients, and resistance to renoprotective therapy was correlated with increased body mass and height. Patients who received renoprotective drugs showed stabilized kidney function (P<0.007) and decreased proteinuria (P<0.05) and blood pressure (P<0.02), despite higher basal values. In patients on renoprotective therapy in whom CRF progressed despite treatment, proteinuria was persistent in contrast to patients with improvement (P<0.02). The best model of CRF progression in the path diagram included systolic blood pressure and anthropometric parameters. In conclusion, in unselected patients with CRF of non-glomerular origin and nil-to-moderate proteinuria the main risk factors for CRF progression are rapid somatic growth, age, and blood pressure. Arterial hypertension and proteinuria, even of mild intensity, differ significantly between patients with progression of CRF and those with stable or improved renal function. Renoprotective therapy is related to significant slowing of CRF progression, but the risk factors for resistance to therapy include persistent proteinuria and somatic growth. |
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| score |
7.3998566 |