Incomplete Renal Tubular Acidosis in ‘Primary’ Osteoporosis
Abstract: Chronic metabolic acidosis may increase alkali mobilization from bone and thus promote the development of osteoporosis. While it is undisputed that overt metabolic acidosis is associated with metabolic bone disease, renal acidification in patients with idiopathic osteoporosis has not been...
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
1999 |
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| Umfang: |
5 |
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Springer Online Journal Archives 1860-2002 |
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| Übergeordnetes Werk: |
in: Osteoporosis international - 1990, 10(1999) vom: Apr., Seite 325-329 |
| Übergeordnetes Werk: |
volume:10 ; year:1999 ; month:04 ; pages:325-329 ; extent:5 |
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NLEJ206813325 |
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| 520 | |a Abstract: Chronic metabolic acidosis may increase alkali mobilization from bone and thus promote the development of osteoporosis. While it is undisputed that overt metabolic acidosis is associated with metabolic bone disease, renal acidification in patients with idiopathic osteoporosis has not been studied systematically. The purpose of this study was to investigate the prevalence of renal acidification defects in patients with ‘primary’ osteoporosis. Thirty-two women (including 10 premenopausal women) and 16 men who were referred to our department for investigation of osteoporosis were enrolled in this study. Patients with obvious or possible secondary osteoporosis were excluded. None of the patients had overt metabolic acidosis. In random urine samples 12 of the 48 patients had pH levels below 5.5 and were therefore considered to have normal renal acidification. The remaining 36 patients underwent further testing by a short-course oral ammonium chloride load. In this test nine of these 36 patients (7 men and 2 premenopausal women) failed to lower urinary pH below 5.5 despite the induction of systemic metabolic acidosis. In these patients, therefore, the diagnosis of incomplete distal renal tubular acidosis was made (RTA I). Patients with incomplete RTA I had significantly lower spontaneous plasma pH (7.38 ± 0.0081 vs 7.41 ± 0.004, mean ± SEM, p= 0.002), a lower serum bicarbonate concentration (21.9 ± 0.49 mmol/l vs 23.1 ± 0.24 mmol/l, p= 0.034), a lower base excess (−2.33 ± 0.42 mmol/l vs −0.55 ± 0.21 mmol/l, p= 0.001) and lower Z-scores in bone densitometry (−2.18 ± 0.27 vs −1.40 ± 0.15, p= 0.028) than patients with normal renal acidification. In conclusion, a high prevalence of incomplete RTA I (in 44% of the male patients, 20% of the premenopausal female patients and 6% of all female patients) was found in patients with osteoporosis who, without testing, would have been diagnosed as having ‘primary’ osteoporosis. The mild metabolic acidosis observed in these patients may have contributed to loss of bone mass by a compensatory mobilization of alkali and calcium from bone. Because of possible therapeutic consequences (e.g., administration of alkali salts and high doses of vitamin D) we propose that measurements of urinary pH and, if necessary, ammonium chloride testing should be included in the diagnostic investigation especially of male and of premenopausal female patients with osteoporosis. Since referral bias, although unlikely, cannot be excluded in our study, the prevalence of RTA I in unselected patients with osteoporosis needs to be determined at primary screening institutions. | ||
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(DE-627)NLEJ206813325 DE-627 ger DE-627 rakwb eng Incomplete Renal Tubular Acidosis in ‘Primary’ Osteoporosis 1999 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: Chronic metabolic acidosis may increase alkali mobilization from bone and thus promote the development of osteoporosis. While it is undisputed that overt metabolic acidosis is associated with metabolic bone disease, renal acidification in patients with idiopathic osteoporosis has not been studied systematically. The purpose of this study was to investigate the prevalence of renal acidification defects in patients with ‘primary’ osteoporosis. Thirty-two women (including 10 premenopausal women) and 16 men who were referred to our department for investigation of osteoporosis were enrolled in this study. Patients with obvious or possible secondary osteoporosis were excluded. None of the patients had overt metabolic acidosis. In random urine samples 12 of the 48 patients had pH levels below 5.5 and were therefore considered to have normal renal acidification. The remaining 36 patients underwent further testing by a short-course oral ammonium chloride load. In this test nine of these 36 patients (7 men and 2 premenopausal women) failed to lower urinary pH below 5.5 despite the induction of systemic metabolic acidosis. In these patients, therefore, the diagnosis of incomplete distal renal tubular acidosis was made (RTA I). Patients with incomplete RTA I had significantly lower spontaneous plasma pH (7.38 ± 0.0081 vs 7.41 ± 0.004, mean ± SEM, p= 0.002), a lower serum bicarbonate concentration (21.9 ± 0.49 mmol/l vs 23.1 ± 0.24 mmol/l, p= 0.034), a lower base excess (−2.33 ± 0.42 mmol/l vs −0.55 ± 0.21 mmol/l, p= 0.001) and lower Z-scores in bone densitometry (−2.18 ± 0.27 vs −1.40 ± 0.15, p= 0.028) than patients with normal renal acidification. In conclusion, a high prevalence of incomplete RTA I (in 44% of the male patients, 20% of the premenopausal female patients and 6% of all female patients) was found in patients with osteoporosis who, without testing, would have been diagnosed as having ‘primary’ osteoporosis. The mild metabolic acidosis observed in these patients may have contributed to loss of bone mass by a compensatory mobilization of alkali and calcium from bone. Because of possible therapeutic consequences (e.g., administration of alkali salts and high doses of vitamin D) we propose that measurements of urinary pH and, if necessary, ammonium chloride testing should be included in the diagnostic investigation especially of male and of premenopausal female patients with osteoporosis. Since referral bias, although unlikely, cannot be excluded in our study, the prevalence of RTA I in unselected patients with osteoporosis needs to be determined at primary screening institutions. Springer Online Journal Archives 1860-2002 Weger, M. oth Deutschmann, H. oth Weger, W. oth Kotanko, P. oth Skrabal, F. oth in Osteoporosis international 1990 10(1999) vom: Apr., Seite 325-329 (DE-627)NLEJ188995951 (DE-600)1480645-9 1433-2965 nnns volume:10 year:1999 month:04 pages:325-329 extent:5 http://dx.doi.org/10.1007/s001980050235 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 10 1999 4 325-329 5 |
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(DE-627)NLEJ206813325 DE-627 ger DE-627 rakwb eng Incomplete Renal Tubular Acidosis in ‘Primary’ Osteoporosis 1999 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: Chronic metabolic acidosis may increase alkali mobilization from bone and thus promote the development of osteoporosis. While it is undisputed that overt metabolic acidosis is associated with metabolic bone disease, renal acidification in patients with idiopathic osteoporosis has not been studied systematically. The purpose of this study was to investigate the prevalence of renal acidification defects in patients with ‘primary’ osteoporosis. Thirty-two women (including 10 premenopausal women) and 16 men who were referred to our department for investigation of osteoporosis were enrolled in this study. Patients with obvious or possible secondary osteoporosis were excluded. None of the patients had overt metabolic acidosis. In random urine samples 12 of the 48 patients had pH levels below 5.5 and were therefore considered to have normal renal acidification. The remaining 36 patients underwent further testing by a short-course oral ammonium chloride load. In this test nine of these 36 patients (7 men and 2 premenopausal women) failed to lower urinary pH below 5.5 despite the induction of systemic metabolic acidosis. In these patients, therefore, the diagnosis of incomplete distal renal tubular acidosis was made (RTA I). Patients with incomplete RTA I had significantly lower spontaneous plasma pH (7.38 ± 0.0081 vs 7.41 ± 0.004, mean ± SEM, p= 0.002), a lower serum bicarbonate concentration (21.9 ± 0.49 mmol/l vs 23.1 ± 0.24 mmol/l, p= 0.034), a lower base excess (−2.33 ± 0.42 mmol/l vs −0.55 ± 0.21 mmol/l, p= 0.001) and lower Z-scores in bone densitometry (−2.18 ± 0.27 vs −1.40 ± 0.15, p= 0.028) than patients with normal renal acidification. In conclusion, a high prevalence of incomplete RTA I (in 44% of the male patients, 20% of the premenopausal female patients and 6% of all female patients) was found in patients with osteoporosis who, without testing, would have been diagnosed as having ‘primary’ osteoporosis. The mild metabolic acidosis observed in these patients may have contributed to loss of bone mass by a compensatory mobilization of alkali and calcium from bone. Because of possible therapeutic consequences (e.g., administration of alkali salts and high doses of vitamin D) we propose that measurements of urinary pH and, if necessary, ammonium chloride testing should be included in the diagnostic investigation especially of male and of premenopausal female patients with osteoporosis. Since referral bias, although unlikely, cannot be excluded in our study, the prevalence of RTA I in unselected patients with osteoporosis needs to be determined at primary screening institutions. Springer Online Journal Archives 1860-2002 Weger, M. oth Deutschmann, H. oth Weger, W. oth Kotanko, P. oth Skrabal, F. oth in Osteoporosis international 1990 10(1999) vom: Apr., Seite 325-329 (DE-627)NLEJ188995951 (DE-600)1480645-9 1433-2965 nnns volume:10 year:1999 month:04 pages:325-329 extent:5 http://dx.doi.org/10.1007/s001980050235 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 10 1999 4 325-329 5 |
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(DE-627)NLEJ206813325 DE-627 ger DE-627 rakwb eng Incomplete Renal Tubular Acidosis in ‘Primary’ Osteoporosis 1999 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: Chronic metabolic acidosis may increase alkali mobilization from bone and thus promote the development of osteoporosis. While it is undisputed that overt metabolic acidosis is associated with metabolic bone disease, renal acidification in patients with idiopathic osteoporosis has not been studied systematically. The purpose of this study was to investigate the prevalence of renal acidification defects in patients with ‘primary’ osteoporosis. Thirty-two women (including 10 premenopausal women) and 16 men who were referred to our department for investigation of osteoporosis were enrolled in this study. Patients with obvious or possible secondary osteoporosis were excluded. None of the patients had overt metabolic acidosis. In random urine samples 12 of the 48 patients had pH levels below 5.5 and were therefore considered to have normal renal acidification. The remaining 36 patients underwent further testing by a short-course oral ammonium chloride load. In this test nine of these 36 patients (7 men and 2 premenopausal women) failed to lower urinary pH below 5.5 despite the induction of systemic metabolic acidosis. In these patients, therefore, the diagnosis of incomplete distal renal tubular acidosis was made (RTA I). Patients with incomplete RTA I had significantly lower spontaneous plasma pH (7.38 ± 0.0081 vs 7.41 ± 0.004, mean ± SEM, p= 0.002), a lower serum bicarbonate concentration (21.9 ± 0.49 mmol/l vs 23.1 ± 0.24 mmol/l, p= 0.034), a lower base excess (−2.33 ± 0.42 mmol/l vs −0.55 ± 0.21 mmol/l, p= 0.001) and lower Z-scores in bone densitometry (−2.18 ± 0.27 vs −1.40 ± 0.15, p= 0.028) than patients with normal renal acidification. In conclusion, a high prevalence of incomplete RTA I (in 44% of the male patients, 20% of the premenopausal female patients and 6% of all female patients) was found in patients with osteoporosis who, without testing, would have been diagnosed as having ‘primary’ osteoporosis. The mild metabolic acidosis observed in these patients may have contributed to loss of bone mass by a compensatory mobilization of alkali and calcium from bone. Because of possible therapeutic consequences (e.g., administration of alkali salts and high doses of vitamin D) we propose that measurements of urinary pH and, if necessary, ammonium chloride testing should be included in the diagnostic investigation especially of male and of premenopausal female patients with osteoporosis. Since referral bias, although unlikely, cannot be excluded in our study, the prevalence of RTA I in unselected patients with osteoporosis needs to be determined at primary screening institutions. Springer Online Journal Archives 1860-2002 Weger, M. oth Deutschmann, H. oth Weger, W. oth Kotanko, P. oth Skrabal, F. oth in Osteoporosis international 1990 10(1999) vom: Apr., Seite 325-329 (DE-627)NLEJ188995951 (DE-600)1480645-9 1433-2965 nnns volume:10 year:1999 month:04 pages:325-329 extent:5 http://dx.doi.org/10.1007/s001980050235 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 10 1999 4 325-329 5 |
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(DE-627)NLEJ206813325 DE-627 ger DE-627 rakwb eng Incomplete Renal Tubular Acidosis in ‘Primary’ Osteoporosis 1999 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: Chronic metabolic acidosis may increase alkali mobilization from bone and thus promote the development of osteoporosis. While it is undisputed that overt metabolic acidosis is associated with metabolic bone disease, renal acidification in patients with idiopathic osteoporosis has not been studied systematically. The purpose of this study was to investigate the prevalence of renal acidification defects in patients with ‘primary’ osteoporosis. Thirty-two women (including 10 premenopausal women) and 16 men who were referred to our department for investigation of osteoporosis were enrolled in this study. Patients with obvious or possible secondary osteoporosis were excluded. None of the patients had overt metabolic acidosis. In random urine samples 12 of the 48 patients had pH levels below 5.5 and were therefore considered to have normal renal acidification. The remaining 36 patients underwent further testing by a short-course oral ammonium chloride load. In this test nine of these 36 patients (7 men and 2 premenopausal women) failed to lower urinary pH below 5.5 despite the induction of systemic metabolic acidosis. In these patients, therefore, the diagnosis of incomplete distal renal tubular acidosis was made (RTA I). Patients with incomplete RTA I had significantly lower spontaneous plasma pH (7.38 ± 0.0081 vs 7.41 ± 0.004, mean ± SEM, p= 0.002), a lower serum bicarbonate concentration (21.9 ± 0.49 mmol/l vs 23.1 ± 0.24 mmol/l, p= 0.034), a lower base excess (−2.33 ± 0.42 mmol/l vs −0.55 ± 0.21 mmol/l, p= 0.001) and lower Z-scores in bone densitometry (−2.18 ± 0.27 vs −1.40 ± 0.15, p= 0.028) than patients with normal renal acidification. In conclusion, a high prevalence of incomplete RTA I (in 44% of the male patients, 20% of the premenopausal female patients and 6% of all female patients) was found in patients with osteoporosis who, without testing, would have been diagnosed as having ‘primary’ osteoporosis. The mild metabolic acidosis observed in these patients may have contributed to loss of bone mass by a compensatory mobilization of alkali and calcium from bone. Because of possible therapeutic consequences (e.g., administration of alkali salts and high doses of vitamin D) we propose that measurements of urinary pH and, if necessary, ammonium chloride testing should be included in the diagnostic investigation especially of male and of premenopausal female patients with osteoporosis. Since referral bias, although unlikely, cannot be excluded in our study, the prevalence of RTA I in unselected patients with osteoporosis needs to be determined at primary screening institutions. Springer Online Journal Archives 1860-2002 Weger, M. oth Deutschmann, H. oth Weger, W. oth Kotanko, P. oth Skrabal, F. oth in Osteoporosis international 1990 10(1999) vom: Apr., Seite 325-329 (DE-627)NLEJ188995951 (DE-600)1480645-9 1433-2965 nnns volume:10 year:1999 month:04 pages:325-329 extent:5 http://dx.doi.org/10.1007/s001980050235 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 10 1999 4 325-329 5 |
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(DE-627)NLEJ206813325 DE-627 ger DE-627 rakwb eng Incomplete Renal Tubular Acidosis in ‘Primary’ Osteoporosis 1999 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: Chronic metabolic acidosis may increase alkali mobilization from bone and thus promote the development of osteoporosis. While it is undisputed that overt metabolic acidosis is associated with metabolic bone disease, renal acidification in patients with idiopathic osteoporosis has not been studied systematically. The purpose of this study was to investigate the prevalence of renal acidification defects in patients with ‘primary’ osteoporosis. Thirty-two women (including 10 premenopausal women) and 16 men who were referred to our department for investigation of osteoporosis were enrolled in this study. Patients with obvious or possible secondary osteoporosis were excluded. None of the patients had overt metabolic acidosis. In random urine samples 12 of the 48 patients had pH levels below 5.5 and were therefore considered to have normal renal acidification. The remaining 36 patients underwent further testing by a short-course oral ammonium chloride load. In this test nine of these 36 patients (7 men and 2 premenopausal women) failed to lower urinary pH below 5.5 despite the induction of systemic metabolic acidosis. In these patients, therefore, the diagnosis of incomplete distal renal tubular acidosis was made (RTA I). Patients with incomplete RTA I had significantly lower spontaneous plasma pH (7.38 ± 0.0081 vs 7.41 ± 0.004, mean ± SEM, p= 0.002), a lower serum bicarbonate concentration (21.9 ± 0.49 mmol/l vs 23.1 ± 0.24 mmol/l, p= 0.034), a lower base excess (−2.33 ± 0.42 mmol/l vs −0.55 ± 0.21 mmol/l, p= 0.001) and lower Z-scores in bone densitometry (−2.18 ± 0.27 vs −1.40 ± 0.15, p= 0.028) than patients with normal renal acidification. In conclusion, a high prevalence of incomplete RTA I (in 44% of the male patients, 20% of the premenopausal female patients and 6% of all female patients) was found in patients with osteoporosis who, without testing, would have been diagnosed as having ‘primary’ osteoporosis. The mild metabolic acidosis observed in these patients may have contributed to loss of bone mass by a compensatory mobilization of alkali and calcium from bone. Because of possible therapeutic consequences (e.g., administration of alkali salts and high doses of vitamin D) we propose that measurements of urinary pH and, if necessary, ammonium chloride testing should be included in the diagnostic investigation especially of male and of premenopausal female patients with osteoporosis. Since referral bias, although unlikely, cannot be excluded in our study, the prevalence of RTA I in unselected patients with osteoporosis needs to be determined at primary screening institutions. Springer Online Journal Archives 1860-2002 Weger, M. oth Deutschmann, H. oth Weger, W. oth Kotanko, P. oth Skrabal, F. oth in Osteoporosis international 1990 10(1999) vom: Apr., Seite 325-329 (DE-627)NLEJ188995951 (DE-600)1480645-9 1433-2965 nnns volume:10 year:1999 month:04 pages:325-329 extent:5 http://dx.doi.org/10.1007/s001980050235 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 10 1999 4 325-329 5 |
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In this test nine of these 36 patients (7 men and 2 premenopausal women) failed to lower urinary pH below 5.5 despite the induction of systemic metabolic acidosis. In these patients, therefore, the diagnosis of incomplete distal renal tubular acidosis was made (RTA I). Patients with incomplete RTA I had significantly lower spontaneous plasma pH (7.38 ± 0.0081 vs 7.41 ± 0.004, mean ± SEM, p= 0.002), a lower serum bicarbonate concentration (21.9 ± 0.49 mmol/l vs 23.1 ± 0.24 mmol/l, p= 0.034), a lower base excess (−2.33 ± 0.42 mmol/l vs −0.55 ± 0.21 mmol/l, p= 0.001) and lower Z-scores in bone densitometry (−2.18 ± 0.27 vs −1.40 ± 0.15, p= 0.028) than patients with normal renal acidification. In conclusion, a high prevalence of incomplete RTA I (in 44% of the male patients, 20% of the premenopausal female patients and 6% of all female patients) was found in patients with osteoporosis who, without testing, would have been diagnosed as having ‘primary’ osteoporosis. 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Elektronische Aufsätze |
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incomplete renal tubular acidosis in ‘primary’ osteoporosis |
| title_auth |
Incomplete Renal Tubular Acidosis in ‘Primary’ Osteoporosis |
| abstract |
Abstract: Chronic metabolic acidosis may increase alkali mobilization from bone and thus promote the development of osteoporosis. While it is undisputed that overt metabolic acidosis is associated with metabolic bone disease, renal acidification in patients with idiopathic osteoporosis has not been studied systematically. The purpose of this study was to investigate the prevalence of renal acidification defects in patients with ‘primary’ osteoporosis. Thirty-two women (including 10 premenopausal women) and 16 men who were referred to our department for investigation of osteoporosis were enrolled in this study. Patients with obvious or possible secondary osteoporosis were excluded. None of the patients had overt metabolic acidosis. In random urine samples 12 of the 48 patients had pH levels below 5.5 and were therefore considered to have normal renal acidification. The remaining 36 patients underwent further testing by a short-course oral ammonium chloride load. In this test nine of these 36 patients (7 men and 2 premenopausal women) failed to lower urinary pH below 5.5 despite the induction of systemic metabolic acidosis. In these patients, therefore, the diagnosis of incomplete distal renal tubular acidosis was made (RTA I). Patients with incomplete RTA I had significantly lower spontaneous plasma pH (7.38 ± 0.0081 vs 7.41 ± 0.004, mean ± SEM, p= 0.002), a lower serum bicarbonate concentration (21.9 ± 0.49 mmol/l vs 23.1 ± 0.24 mmol/l, p= 0.034), a lower base excess (−2.33 ± 0.42 mmol/l vs −0.55 ± 0.21 mmol/l, p= 0.001) and lower Z-scores in bone densitometry (−2.18 ± 0.27 vs −1.40 ± 0.15, p= 0.028) than patients with normal renal acidification. In conclusion, a high prevalence of incomplete RTA I (in 44% of the male patients, 20% of the premenopausal female patients and 6% of all female patients) was found in patients with osteoporosis who, without testing, would have been diagnosed as having ‘primary’ osteoporosis. The mild metabolic acidosis observed in these patients may have contributed to loss of bone mass by a compensatory mobilization of alkali and calcium from bone. Because of possible therapeutic consequences (e.g., administration of alkali salts and high doses of vitamin D) we propose that measurements of urinary pH and, if necessary, ammonium chloride testing should be included in the diagnostic investigation especially of male and of premenopausal female patients with osteoporosis. Since referral bias, although unlikely, cannot be excluded in our study, the prevalence of RTA I in unselected patients with osteoporosis needs to be determined at primary screening institutions. |
| abstractGer |
Abstract: Chronic metabolic acidosis may increase alkali mobilization from bone and thus promote the development of osteoporosis. While it is undisputed that overt metabolic acidosis is associated with metabolic bone disease, renal acidification in patients with idiopathic osteoporosis has not been studied systematically. The purpose of this study was to investigate the prevalence of renal acidification defects in patients with ‘primary’ osteoporosis. Thirty-two women (including 10 premenopausal women) and 16 men who were referred to our department for investigation of osteoporosis were enrolled in this study. Patients with obvious or possible secondary osteoporosis were excluded. None of the patients had overt metabolic acidosis. In random urine samples 12 of the 48 patients had pH levels below 5.5 and were therefore considered to have normal renal acidification. The remaining 36 patients underwent further testing by a short-course oral ammonium chloride load. In this test nine of these 36 patients (7 men and 2 premenopausal women) failed to lower urinary pH below 5.5 despite the induction of systemic metabolic acidosis. In these patients, therefore, the diagnosis of incomplete distal renal tubular acidosis was made (RTA I). Patients with incomplete RTA I had significantly lower spontaneous plasma pH (7.38 ± 0.0081 vs 7.41 ± 0.004, mean ± SEM, p= 0.002), a lower serum bicarbonate concentration (21.9 ± 0.49 mmol/l vs 23.1 ± 0.24 mmol/l, p= 0.034), a lower base excess (−2.33 ± 0.42 mmol/l vs −0.55 ± 0.21 mmol/l, p= 0.001) and lower Z-scores in bone densitometry (−2.18 ± 0.27 vs −1.40 ± 0.15, p= 0.028) than patients with normal renal acidification. In conclusion, a high prevalence of incomplete RTA I (in 44% of the male patients, 20% of the premenopausal female patients and 6% of all female patients) was found in patients with osteoporosis who, without testing, would have been diagnosed as having ‘primary’ osteoporosis. The mild metabolic acidosis observed in these patients may have contributed to loss of bone mass by a compensatory mobilization of alkali and calcium from bone. Because of possible therapeutic consequences (e.g., administration of alkali salts and high doses of vitamin D) we propose that measurements of urinary pH and, if necessary, ammonium chloride testing should be included in the diagnostic investigation especially of male and of premenopausal female patients with osteoporosis. Since referral bias, although unlikely, cannot be excluded in our study, the prevalence of RTA I in unselected patients with osteoporosis needs to be determined at primary screening institutions. |
| abstract_unstemmed |
Abstract: Chronic metabolic acidosis may increase alkali mobilization from bone and thus promote the development of osteoporosis. While it is undisputed that overt metabolic acidosis is associated with metabolic bone disease, renal acidification in patients with idiopathic osteoporosis has not been studied systematically. The purpose of this study was to investigate the prevalence of renal acidification defects in patients with ‘primary’ osteoporosis. Thirty-two women (including 10 premenopausal women) and 16 men who were referred to our department for investigation of osteoporosis were enrolled in this study. Patients with obvious or possible secondary osteoporosis were excluded. None of the patients had overt metabolic acidosis. In random urine samples 12 of the 48 patients had pH levels below 5.5 and were therefore considered to have normal renal acidification. The remaining 36 patients underwent further testing by a short-course oral ammonium chloride load. In this test nine of these 36 patients (7 men and 2 premenopausal women) failed to lower urinary pH below 5.5 despite the induction of systemic metabolic acidosis. In these patients, therefore, the diagnosis of incomplete distal renal tubular acidosis was made (RTA I). Patients with incomplete RTA I had significantly lower spontaneous plasma pH (7.38 ± 0.0081 vs 7.41 ± 0.004, mean ± SEM, p= 0.002), a lower serum bicarbonate concentration (21.9 ± 0.49 mmol/l vs 23.1 ± 0.24 mmol/l, p= 0.034), a lower base excess (−2.33 ± 0.42 mmol/l vs −0.55 ± 0.21 mmol/l, p= 0.001) and lower Z-scores in bone densitometry (−2.18 ± 0.27 vs −1.40 ± 0.15, p= 0.028) than patients with normal renal acidification. In conclusion, a high prevalence of incomplete RTA I (in 44% of the male patients, 20% of the premenopausal female patients and 6% of all female patients) was found in patients with osteoporosis who, without testing, would have been diagnosed as having ‘primary’ osteoporosis. The mild metabolic acidosis observed in these patients may have contributed to loss of bone mass by a compensatory mobilization of alkali and calcium from bone. Because of possible therapeutic consequences (e.g., administration of alkali salts and high doses of vitamin D) we propose that measurements of urinary pH and, if necessary, ammonium chloride testing should be included in the diagnostic investigation especially of male and of premenopausal female patients with osteoporosis. Since referral bias, although unlikely, cannot be excluded in our study, the prevalence of RTA I in unselected patients with osteoporosis needs to be determined at primary screening institutions. |
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Incomplete Renal Tubular Acidosis in ‘Primary’ Osteoporosis |
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