GLORIA

GEOMAR Library Ocean Research Information Access

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Online Resource
    Online Resource
    S. Karger AG ; 2001
    In:  Nephron Experimental Nephrology Vol. 9, No. 6 ( 2001-11-7), p. 436-443
    In: Nephron Experimental Nephrology, S. Karger AG, Vol. 9, No. 6 ( 2001-11-7), p. 436-443
    Abstract: Podocyte function appears to be regulated by vasoactive factors. In vivo podocytes express parathyroid hormone-related protein (PTHrP), the N-terminal fragment of which has vasoactive properties. Since the signaling pathway(s) of PTHrP(1–36) are unknown in podocytes, differentiated cells of a conditionally immortalized mouse podocyte cell line were studied. Gene expression of PTHrP and the PTH/PTHrP receptor was investigated by RT-PCR; protein distribution of PTHrP was examined by immunofluorescence. Accumulation of cAMP was determined by an enzyme immunoassay; [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 was measured by fura-2 ratio imaging. PTHrP and PTH/PTHrP receptor mRNA was detected in differentiated podocytes. Immunoreactive PTHrP exhibited a granular distribution in the cytoplasm of differentiated podocytes. With regard to the signaling pathway(s) of PTHrP(1–36), a concentration-dependent increase of cAMP levels with an EC 〈 sub 〉 50 〈 /sub 〉 value of 4 ± 2 n 〈 i 〉 M 〈 /i 〉 was found. PTHrP(1–36) (1 µ 〈 i 〉 M 〈 /i 〉 ) increased cAMP levels 5.5 ± 1.1-fold above baseline as compared with a 25.4 ± 4.2-fold increase in response to forskolin (10 µ 〈 i 〉 M 〈 /i 〉 ). The PTH/PTHrP receptor antagonist PTHrP(7–34) significantly diminished the PTHrP(1–36)-induced cAMP increase. While superfusion of podocytes with bradykinin (100 n 〈 i 〉 M 〈 /i 〉 ) increased [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 , PTHrP(1–36) (100 n 〈 i 〉 M 〈 /i 〉 ) was without effect on [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 . However, PTHrP(1–36) attenuated the bradykinin-induced increase in [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 . Our results suggest that PTHrP is an autocrine hormone in podocytes, which selectively activates the cAMP pathway through the PTH/PTHrP receptor.
    Type of Medium: Online Resource
    ISSN: 1660-2129
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2001
    detail.hit.zdb_id: 2098337-2
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 2
    In: Kidney and Blood Pressure Research, S. Karger AG, Vol. 42, No. 1 ( 2017), p. 145-155
    Abstract: 〈 b 〉 〈 i 〉 Background/Aims: 〈 /i 〉 〈 /b 〉 Several studies sought to identify new biomarkers for chronic kidney disease (CKD). As the renal renin-angiotensin system is activated in CKD, urinary angiotensinogen or renin excretion may be suitable candidates. We tested whether urinary angiotensinogen or renin excretion is elevated in CKD and whether these parameters are associated with estimated glomerular filtration rate (eGFR). We further tested whether urinary angiotensinogen or renin excretion may convey additional information beyond that provided by albuminuria. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 We measured urinary and plasma angiotensinogen, renin, albumin and creatinine in 177 CKD patients from the 〈 i 〉 Greifswald Approach to Individualized Medicine 〈 /i 〉 project and in 283 healthy controls from the 〈 i 〉 Study of Health in Pomerania 〈 /i 〉 . The urinary excretion of specific proteins is given as protein-to-creatinine ratio. Receiver operating characteristic (ROC) curves, spearman correlation coefficients and linear regression models were calculated. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 Urinary angiotensinogen [2,511 (196-31,909) vs. 18.6 (8.3-44.0) pmol/g, * 〈 i 〉 P 〈 /i 〉 & #x3c;0.01] and renin excretion [0.311 (0.135-1.155) vs. 0.069 (0.045-0.148) pmol/g, * 〈 i 〉 P 〈 /i 〉 & #x3c;0.01] were significantly higher in CKD patients than in healthy controls. The area under the ROC curve was significantly larger when urinary angiotensinogen, renin and albumin excretion were combined than with urinary albumin excretion alone. Urinary angiotensinogen (ß-coefficient -2.405, standard error 0.117, 〈 i 〉 P 〈 /i 〉 & #x3c;0.01) and renin excretion (ß-coefficient -0.793, standard error 0.061, 〈 i 〉 P 〈 /i 〉 & #x3c;0.01) were inversely associated with eGFR. Adjustment for albuminuria, age, sex, systolic blood pressure and body mass index did not significantly affect the results. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 Urinary angiotensinogen and renin excretion are elevated in CKD patients. Both parameters are negatively associated with eGFR and these associations are independent of urinary albumin excretion. In CKD patients urinary angiotensinogen and renin excretion may convey additional information beyond that provided by albuminuria.
    Type of Medium: Online Resource
    ISSN: 1420-4096 , 1423-0143
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2017
    detail.hit.zdb_id: 1482922-8
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 3
    In: American Journal of Nephrology, S. Karger AG, Vol. 33, No. 3 ( 2011), p. 209-217
    Abstract: 〈 i 〉 Background: 〈 /i 〉 Chronic kidney disease (CKD) and low serum total testosterone (TT) concentrations are independent predictors of mortality risk in the general population, but their combined potential for improved mortality risk stratification is unknown. 〈 i 〉 Methods: 〈 /i 〉 We used data of 1,822 men from the population-based Study of Health in Pomerania followed- up for 9.9 years (median). The direct effects of kidney dysfunction (estimated glomerular filtration rate 〈 60 ml/min/ 1.73 m 〈 sup 〉 2 〈 /sup 〉 ), albuminuria (urinary albumin-creatinine ratio ≧2.5 mg/mmol) and their combination (CKD) on all-cause and cardiovascular mortality were analyzed using multivariable Cox regression models. Serum TT concentrations below the age-specific 10th percentile (by decades) were considered low and were used for further risk stratification. 〈 i 〉 Results: 〈 /i 〉 Kidney dysfunction (hazard ratio, HR, 1.40; 95% confidence interval, CI, 1.02–1.92), albuminuria (HR, 1.38; 95% CI, 1.06–1.79), and CKD (HR, 1.42; 95% CI, 1.09–1.84) were associated with increased all-cause mortality risk, while only kidney dysfunction (HR, 2.01; 95% CI, 1.21–3.34) was associated with increased cardiovascular mortality risk after multivariable adjustment. Men with kidney dysfunction and low TT concentrations were identified as high-risk individuals showing a more than 2-fold increased all-cause mortality risk (HR, 2.52; 95% CI, 1.08–5.85). Added to multivariable models, nonsignificant interaction terms suggest that kidney dysfunction and low TT are primarily additive rather than synergistic mortality risk factors. 〈 i 〉 Conclusion: 〈 /i 〉 In the case of early loss of kidney function, measured TT concentrations might help to detect high-risk individuals for potential therapeutic interventions and to improve mortality risk assessment and outcome.
    Type of Medium: Online Resource
    ISSN: 0250-8095 , 1421-9670
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2011
    detail.hit.zdb_id: 1468523-1
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...