CNP production in the kidney and effects of protein intake restriction in nephrotic syndrome

Alessandro Cataliotti, Mauro Giordano, Emanuela De Pascale, Gelsomina Giordano, Pietro Castellino, Michihisa Jougasaki, Lisa C. Costello, Guido Boerrigter, Toshihiro Tsuruda, Paola Belluardo, Shang Chiun Lee, Brenda Huntley, Sharon Sandberg, Lorenzo S. Malatino, John C Jr. Burnett

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

C-type natriuretic peptide (CNP) possesses well-established cardiovascular properties. Although present in the mammalian kidney, CNP production in human kidney and its modulation in human renal disease remain less defined. We investigated the presence of CNP in normal human kidney and in patients with nephrotic syndrome (NS). We also addressed whether or not a low-protein diet (LPD) alters plasma CNP and urinary CNP excretion in NS. In situ hybridization studies demonstrated CNP mRNA expression in tubular cells and glomeruli of normal human kidneys. CNP immunoreactivity was positive in proximal, distal, and medullary collecting duct tubular cells in both controls and patients with NS. The ratios of plasma CNP and urinary CNP to creatinine were significantly higher in patients with NS compared with controls. Urinary CNP, but not plasma CNP, was significantly lowered in patients with NS after an LPD. Similarly, the ratios of urinary protein to creatinine and urinary albumin to creatinine, but not urinary guanosine 3′,5′-cyclic monophosphate to creatinine, decreased significantly with an LPD. These data confirm and extend previous reports and demonstrate for the first time the presence of CNP in human kidney with NS. We also report increased plasma CNP concentration and urinary CNP excretion in NS patients and a significant reduction of CNP excretion with an LPD. Our findings demonstrate that CNP metabolism is altered in patients with NS and support the hypothesis that activation of renal CNP can be partially offset by an LPD. These results underscore that the beneficial effect of an LPD on protein excretion is paralleled by a substantial reduction in intrarenal CNP release.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Renal Physiology
Volume283
Issue number3 52-3
StatePublished - Sep 2002

Fingerprint

C-Type Natriuretic Peptide
Nephrotic Syndrome
Kidney
Protein-Restricted Diet
Proteins
Creatinine

Keywords

  • Immunohistochemistry
  • In situ hybridization
  • Low protein diet
  • Urinary C-type natriuretic peptide

ASJC Scopus subject areas

  • Physiology

Cite this

Cataliotti, A., Giordano, M., De Pascale, E., Giordano, G., Castellino, P., Jougasaki, M., ... Burnett, J. C. J. (2002). CNP production in the kidney and effects of protein intake restriction in nephrotic syndrome. American Journal of Physiology - Renal Physiology, 283(3 52-3).

CNP production in the kidney and effects of protein intake restriction in nephrotic syndrome. / Cataliotti, Alessandro; Giordano, Mauro; De Pascale, Emanuela; Giordano, Gelsomina; Castellino, Pietro; Jougasaki, Michihisa; Costello, Lisa C.; Boerrigter, Guido; Tsuruda, Toshihiro; Belluardo, Paola; Lee, Shang Chiun; Huntley, Brenda; Sandberg, Sharon; Malatino, Lorenzo S.; Burnett, John C Jr.

In: American Journal of Physiology - Renal Physiology, Vol. 283, No. 3 52-3, 09.2002.

Research output: Contribution to journalArticle

Cataliotti, A, Giordano, M, De Pascale, E, Giordano, G, Castellino, P, Jougasaki, M, Costello, LC, Boerrigter, G, Tsuruda, T, Belluardo, P, Lee, SC, Huntley, B, Sandberg, S, Malatino, LS & Burnett, JCJ 2002, 'CNP production in the kidney and effects of protein intake restriction in nephrotic syndrome', American Journal of Physiology - Renal Physiology, vol. 283, no. 3 52-3.
Cataliotti A, Giordano M, De Pascale E, Giordano G, Castellino P, Jougasaki M et al. CNP production in the kidney and effects of protein intake restriction in nephrotic syndrome. American Journal of Physiology - Renal Physiology. 2002 Sep;283(3 52-3).
Cataliotti, Alessandro ; Giordano, Mauro ; De Pascale, Emanuela ; Giordano, Gelsomina ; Castellino, Pietro ; Jougasaki, Michihisa ; Costello, Lisa C. ; Boerrigter, Guido ; Tsuruda, Toshihiro ; Belluardo, Paola ; Lee, Shang Chiun ; Huntley, Brenda ; Sandberg, Sharon ; Malatino, Lorenzo S. ; Burnett, John C Jr. / CNP production in the kidney and effects of protein intake restriction in nephrotic syndrome. In: American Journal of Physiology - Renal Physiology. 2002 ; Vol. 283, No. 3 52-3.
@article{54b8121e23d64b97839c9746cc8f9d1b,
title = "CNP production in the kidney and effects of protein intake restriction in nephrotic syndrome",
abstract = "C-type natriuretic peptide (CNP) possesses well-established cardiovascular properties. Although present in the mammalian kidney, CNP production in human kidney and its modulation in human renal disease remain less defined. We investigated the presence of CNP in normal human kidney and in patients with nephrotic syndrome (NS). We also addressed whether or not a low-protein diet (LPD) alters plasma CNP and urinary CNP excretion in NS. In situ hybridization studies demonstrated CNP mRNA expression in tubular cells and glomeruli of normal human kidneys. CNP immunoreactivity was positive in proximal, distal, and medullary collecting duct tubular cells in both controls and patients with NS. The ratios of plasma CNP and urinary CNP to creatinine were significantly higher in patients with NS compared with controls. Urinary CNP, but not plasma CNP, was significantly lowered in patients with NS after an LPD. Similarly, the ratios of urinary protein to creatinine and urinary albumin to creatinine, but not urinary guanosine 3′,5′-cyclic monophosphate to creatinine, decreased significantly with an LPD. These data confirm and extend previous reports and demonstrate for the first time the presence of CNP in human kidney with NS. We also report increased plasma CNP concentration and urinary CNP excretion in NS patients and a significant reduction of CNP excretion with an LPD. Our findings demonstrate that CNP metabolism is altered in patients with NS and support the hypothesis that activation of renal CNP can be partially offset by an LPD. These results underscore that the beneficial effect of an LPD on protein excretion is paralleled by a substantial reduction in intrarenal CNP release.",
keywords = "Immunohistochemistry, In situ hybridization, Low protein diet, Urinary C-type natriuretic peptide",
author = "Alessandro Cataliotti and Mauro Giordano and {De Pascale}, Emanuela and Gelsomina Giordano and Pietro Castellino and Michihisa Jougasaki and Costello, {Lisa C.} and Guido Boerrigter and Toshihiro Tsuruda and Paola Belluardo and Lee, {Shang Chiun} and Brenda Huntley and Sharon Sandberg and Malatino, {Lorenzo S.} and Burnett, {John C Jr.}",
year = "2002",
month = "9",
language = "English (US)",
volume = "283",
journal = "American Journal of Physiology - Renal Fluid and Electrolyte Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "3 52-3",

}

TY - JOUR

T1 - CNP production in the kidney and effects of protein intake restriction in nephrotic syndrome

AU - Cataliotti, Alessandro

AU - Giordano, Mauro

AU - De Pascale, Emanuela

AU - Giordano, Gelsomina

AU - Castellino, Pietro

AU - Jougasaki, Michihisa

AU - Costello, Lisa C.

AU - Boerrigter, Guido

AU - Tsuruda, Toshihiro

AU - Belluardo, Paola

AU - Lee, Shang Chiun

AU - Huntley, Brenda

AU - Sandberg, Sharon

AU - Malatino, Lorenzo S.

AU - Burnett, John C Jr.

PY - 2002/9

Y1 - 2002/9

N2 - C-type natriuretic peptide (CNP) possesses well-established cardiovascular properties. Although present in the mammalian kidney, CNP production in human kidney and its modulation in human renal disease remain less defined. We investigated the presence of CNP in normal human kidney and in patients with nephrotic syndrome (NS). We also addressed whether or not a low-protein diet (LPD) alters plasma CNP and urinary CNP excretion in NS. In situ hybridization studies demonstrated CNP mRNA expression in tubular cells and glomeruli of normal human kidneys. CNP immunoreactivity was positive in proximal, distal, and medullary collecting duct tubular cells in both controls and patients with NS. The ratios of plasma CNP and urinary CNP to creatinine were significantly higher in patients with NS compared with controls. Urinary CNP, but not plasma CNP, was significantly lowered in patients with NS after an LPD. Similarly, the ratios of urinary protein to creatinine and urinary albumin to creatinine, but not urinary guanosine 3′,5′-cyclic monophosphate to creatinine, decreased significantly with an LPD. These data confirm and extend previous reports and demonstrate for the first time the presence of CNP in human kidney with NS. We also report increased plasma CNP concentration and urinary CNP excretion in NS patients and a significant reduction of CNP excretion with an LPD. Our findings demonstrate that CNP metabolism is altered in patients with NS and support the hypothesis that activation of renal CNP can be partially offset by an LPD. These results underscore that the beneficial effect of an LPD on protein excretion is paralleled by a substantial reduction in intrarenal CNP release.

AB - C-type natriuretic peptide (CNP) possesses well-established cardiovascular properties. Although present in the mammalian kidney, CNP production in human kidney and its modulation in human renal disease remain less defined. We investigated the presence of CNP in normal human kidney and in patients with nephrotic syndrome (NS). We also addressed whether or not a low-protein diet (LPD) alters plasma CNP and urinary CNP excretion in NS. In situ hybridization studies demonstrated CNP mRNA expression in tubular cells and glomeruli of normal human kidneys. CNP immunoreactivity was positive in proximal, distal, and medullary collecting duct tubular cells in both controls and patients with NS. The ratios of plasma CNP and urinary CNP to creatinine were significantly higher in patients with NS compared with controls. Urinary CNP, but not plasma CNP, was significantly lowered in patients with NS after an LPD. Similarly, the ratios of urinary protein to creatinine and urinary albumin to creatinine, but not urinary guanosine 3′,5′-cyclic monophosphate to creatinine, decreased significantly with an LPD. These data confirm and extend previous reports and demonstrate for the first time the presence of CNP in human kidney with NS. We also report increased plasma CNP concentration and urinary CNP excretion in NS patients and a significant reduction of CNP excretion with an LPD. Our findings demonstrate that CNP metabolism is altered in patients with NS and support the hypothesis that activation of renal CNP can be partially offset by an LPD. These results underscore that the beneficial effect of an LPD on protein excretion is paralleled by a substantial reduction in intrarenal CNP release.

KW - Immunohistochemistry

KW - In situ hybridization

KW - Low protein diet

KW - Urinary C-type natriuretic peptide

UR - http://www.scopus.com/inward/record.url?scp=17344377159&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=17344377159&partnerID=8YFLogxK

M3 - Article

C2 - 12167597

AN - SCOPUS:17344377159

VL - 283

JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

SN - 1931-857X

IS - 3 52-3

ER -