Natriuretic response to volume expansion in polycystic kidney disease

Vicente Torres, D. M. Wilson, K. P. Offord, John C Jr. Burnett, J. C. Romero

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Hypertension is an early manifestation of autosomal dominant polycystic kidney disease (ADPKD). Whether polycystic kidneys have an intrinsic abnormality that leads to sodium retention, volume expansion, and hypertension is uncertain. We studied the natriuretic response to a 4-hour infusion of physiologic saline at a rate of 6.5 ml/kg per hour in 10 patients with ADPKD who had normal renal function and 10 gender- and age-matched control subjects. Baseline 24-hour urinary excretions of sodium and potassium were similar in both groups. The baseline filtration fraction was significantly higher in the patients with ADPKD than in the control subjects. During the infusion of saline, no significant changes in blood pressure, clearance of inulin, or clearance of p-aminohippuric acid were detected. The increase in fractional excretion of sodium over baseline was significantly higher in the patients with ADPKD than in the control subjects. The pressure-natriuresis regression line was significantly shifted to the right in patients with ADPKD who had hypertension. The fractional excretion of potassium was significantly lower in patients with ADPKD than in control subjects. No significant differences in plasma renin activity, aldosterone, or atrial natriuretic factor were detected between the two groups. These observations suggest the presence of subtle abnormalities in the management of renal sodium that might contribute to the development and maintenance of hypertension in patients with ADPKD.

Original languageEnglish (US)
Pages (from-to)509-515
Number of pages7
JournalMayo Clinic Proceedings
Volume64
Issue number5
StatePublished - 1989

Fingerprint

Autosomal Dominant Polycystic Kidney
Polycystic Kidney Diseases
Sodium
Hypertension
Potassium
p-Aminohippuric Acid
Kidney
Natriuresis
Inulin
Patient Rights
Atrial Natriuretic Factor
Aldosterone
Renin
Maintenance
Blood Pressure
Pressure

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Natriuretic response to volume expansion in polycystic kidney disease. / Torres, Vicente; Wilson, D. M.; Offord, K. P.; Burnett, John C Jr.; Romero, J. C.

In: Mayo Clinic Proceedings, Vol. 64, No. 5, 1989, p. 509-515.

Research output: Contribution to journalArticle

Torres, V, Wilson, DM, Offord, KP, Burnett, JCJ & Romero, JC 1989, 'Natriuretic response to volume expansion in polycystic kidney disease', Mayo Clinic Proceedings, vol. 64, no. 5, pp. 509-515.
Torres, Vicente ; Wilson, D. M. ; Offord, K. P. ; Burnett, John C Jr. ; Romero, J. C. / Natriuretic response to volume expansion in polycystic kidney disease. In: Mayo Clinic Proceedings. 1989 ; Vol. 64, No. 5. pp. 509-515.
@article{8435cabaa3074e2686d37dc388c9a1cf,
title = "Natriuretic response to volume expansion in polycystic kidney disease",
abstract = "Hypertension is an early manifestation of autosomal dominant polycystic kidney disease (ADPKD). Whether polycystic kidneys have an intrinsic abnormality that leads to sodium retention, volume expansion, and hypertension is uncertain. We studied the natriuretic response to a 4-hour infusion of physiologic saline at a rate of 6.5 ml/kg per hour in 10 patients with ADPKD who had normal renal function and 10 gender- and age-matched control subjects. Baseline 24-hour urinary excretions of sodium and potassium were similar in both groups. The baseline filtration fraction was significantly higher in the patients with ADPKD than in the control subjects. During the infusion of saline, no significant changes in blood pressure, clearance of inulin, or clearance of p-aminohippuric acid were detected. The increase in fractional excretion of sodium over baseline was significantly higher in the patients with ADPKD than in the control subjects. The pressure-natriuresis regression line was significantly shifted to the right in patients with ADPKD who had hypertension. The fractional excretion of potassium was significantly lower in patients with ADPKD than in control subjects. No significant differences in plasma renin activity, aldosterone, or atrial natriuretic factor were detected between the two groups. These observations suggest the presence of subtle abnormalities in the management of renal sodium that might contribute to the development and maintenance of hypertension in patients with ADPKD.",
author = "Vicente Torres and Wilson, {D. M.} and Offord, {K. P.} and Burnett, {John C Jr.} and Romero, {J. C.}",
year = "1989",
language = "English (US)",
volume = "64",
pages = "509--515",
journal = "Mayo Clinic Proceedings",
issn = "0025-6196",
publisher = "Elsevier Science",
number = "5",

}

TY - JOUR

T1 - Natriuretic response to volume expansion in polycystic kidney disease

AU - Torres, Vicente

AU - Wilson, D. M.

AU - Offord, K. P.

AU - Burnett, John C Jr.

AU - Romero, J. C.

PY - 1989

Y1 - 1989

N2 - Hypertension is an early manifestation of autosomal dominant polycystic kidney disease (ADPKD). Whether polycystic kidneys have an intrinsic abnormality that leads to sodium retention, volume expansion, and hypertension is uncertain. We studied the natriuretic response to a 4-hour infusion of physiologic saline at a rate of 6.5 ml/kg per hour in 10 patients with ADPKD who had normal renal function and 10 gender- and age-matched control subjects. Baseline 24-hour urinary excretions of sodium and potassium were similar in both groups. The baseline filtration fraction was significantly higher in the patients with ADPKD than in the control subjects. During the infusion of saline, no significant changes in blood pressure, clearance of inulin, or clearance of p-aminohippuric acid were detected. The increase in fractional excretion of sodium over baseline was significantly higher in the patients with ADPKD than in the control subjects. The pressure-natriuresis regression line was significantly shifted to the right in patients with ADPKD who had hypertension. The fractional excretion of potassium was significantly lower in patients with ADPKD than in control subjects. No significant differences in plasma renin activity, aldosterone, or atrial natriuretic factor were detected between the two groups. These observations suggest the presence of subtle abnormalities in the management of renal sodium that might contribute to the development and maintenance of hypertension in patients with ADPKD.

AB - Hypertension is an early manifestation of autosomal dominant polycystic kidney disease (ADPKD). Whether polycystic kidneys have an intrinsic abnormality that leads to sodium retention, volume expansion, and hypertension is uncertain. We studied the natriuretic response to a 4-hour infusion of physiologic saline at a rate of 6.5 ml/kg per hour in 10 patients with ADPKD who had normal renal function and 10 gender- and age-matched control subjects. Baseline 24-hour urinary excretions of sodium and potassium were similar in both groups. The baseline filtration fraction was significantly higher in the patients with ADPKD than in the control subjects. During the infusion of saline, no significant changes in blood pressure, clearance of inulin, or clearance of p-aminohippuric acid were detected. The increase in fractional excretion of sodium over baseline was significantly higher in the patients with ADPKD than in the control subjects. The pressure-natriuresis regression line was significantly shifted to the right in patients with ADPKD who had hypertension. The fractional excretion of potassium was significantly lower in patients with ADPKD than in control subjects. No significant differences in plasma renin activity, aldosterone, or atrial natriuretic factor were detected between the two groups. These observations suggest the presence of subtle abnormalities in the management of renal sodium that might contribute to the development and maintenance of hypertension in patients with ADPKD.

UR - http://www.scopus.com/inward/record.url?scp=0024320916&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024320916&partnerID=8YFLogxK

M3 - Article

C2 - 2725063

AN - SCOPUS:0024320916

VL - 64

SP - 509

EP - 515

JO - Mayo Clinic Proceedings

JF - Mayo Clinic Proceedings

SN - 0025-6196

IS - 5

ER -