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- Title
Association of plasma somatostatin with disease severity and progression in patients with autosomal dominant polycystic kidney disease.
- Authors
Messchendorp, A. Lianne; Spithoven, Edwin M.; Casteleijn, Niek F.; Dam, Wendy A.; van den Born, Jacob; Tonnis, Wouter F.; Gaillard, Carlo A. J. M.; Meijer, Esther; DIPAK Consortium
- Abstract
<bold>Background: </bold>Somatostatin (SST) inhibits intracellular cyclic adenosine monophosphate (cAMP) production and thus may modify cyst formation in autosomal dominant polycystic kidney disease (ADPKD). We investigated whether endogenous plasma SST concentration is associated with disease severity and progression in patients with ADPKD, and whether plasma SST concentrations change during treatment with a vasopressin V2 receptor antagonist or SST analogue.<bold>Methods: </bold>In this observational study, fasting concentrations of SST were measured in 127 ADPKD patients (diagnosed upon the revised Ravine criteria) by ELISA. cAMP was measured in 24 h urine by Radio Immuno Assay. Kidney function was measured (mGFR) as 125I-iothalamate clearance, and total kidney volume was measured by MRI volumetry and adjusted for height (htTKV). Disease progression was expressed as annual change in mGFR and htTKV. Additionally, baseline versus follow-up SST concentrations were compared in ADPKD patients during vasopressin V2 receptor antagonist (tolvaptan) (n = 27) or SST analogue (lanreotide) treatment (n = 25).<bold>Results: </bold>In 127 ADPKD patients, 41 ± 11 years, 44% female, eGFR 73 ± 32 ml/min/1.73m2, mGFR 75 ± 32 ml/min/1.73m2 and htTKV 826 (521-1297) ml/m, SST concentration was 48.5 (34.3-77.8) pg/ml. At baseline, SST was associated with urinary cAMP, mGFR and htTKV (p = 0.02, p = 0.004 and p = 0.02, respectively), but these associations lost significance after adjustment for age and sex or protein intake (p = 0.09, p = 0.06 and p = 0.15 respectively). Baseline SST was not associated with annual change in mGFR, or htTKV during follow-up (st. β = - 0.02, p = 0.87 and st. β = - 0.07, p = 0.54 respectively). During treatment with tolvaptan SST levels remained stable 38.2 (23.8-70.7) pg/mL vs. 39.8 (31.2-58.5) pg/mL, p = 0.85), whereas SST levels decreased significantly during treatment with lanreotide (42.5 (33.2-55.0) pg/ml vs. 29.3 (24.8-37.6), p = 0.008).<bold>Conclusions: </bold>Fasting plasma SST concentration is not associated with disease severity or progression in patients with ADPKD. Treatment with lanreotide caused a decrease in SST concentration. These data suggest that plasma SST cannot be used as a biomarker to assess prognosis in ADPKD, but leave the possibility open that change in SST concentration during lanreotide treatment may reflect therapy efficacy.
- Subjects
SOMATOSTATIN; DISEASE progression; POLYCYSTIC kidney disease; PEPTIDE hormones; CYCLIC adenylic acid; VASOPRESSIN; SCIENTIFIC observation; ANTINEOPLASTIC agents; ANTHROPOMETRY; FASTING; GLOMERULAR filtration rate; KIDNEYS; MAGNETIC resonance imaging; PEPTIDES; SEVERITY of illness index; CHEMICAL inhibitors
- Publication
BMC Nephrology, 2018, Vol 19, Issue 1, pN.PAG
- ISSN
1471-2369
- Publication type
journal article
- DOI
10.1186/s12882-018-1176-y