[Does any relationship exist between metabolic disturbances and some markers of renal damage in patients with untreated essential hypertension?]

Pol Arch Med Wewn. 2000 Sep;104(3):563-7.
[Article in Polish]

Abstract

The essential arterial hypertension is the second (after diabetes mellitus) cause of chronic renal failure which means a great social and economic burden to the society. It is well known that hypertension is a metabolic syndrome resulting in tissue injury. We tried to investigate the possible influence of some metabolic disturbances on renal function in nontreated essential hypertension. We have compared 25 patients with nontreated essential hypertension (11 women, 14 men) with 14 healthy volunteers (7 women, 7 men) matched for age. The patients' group was characterized by significantly higher urine excretion of NAG (N-acetyl-beta-D-glucosaminidase) (2.75 +/- 1.69 vs 1.82 +/- 1.46 p < 0.05) and a tendency to significantly higher urine fractional sodium excretion without significant difference in albumin excretion. These findings suggest that the tubular damage is present. We noticed the negative linear correlation between mean arterial pressure and (MAP) and NAG urine excretion in the group of hypertensive patients which may reflect the renal ischemia in tubulo-interstitial pathology. Our data suggests that in nontreated arterial hypertension the renal blood flow disturbances are the important cause of the deterioration of tubular function (which are earlier to glomerular damage).

Publication types

  • Clinical Trial
  • Controlled Clinical Trial
  • English Abstract

MeSH terms

  • Acetylglucosaminidase / urine
  • Adult
  • Albuminuria / diagnosis
  • Albuminuria / etiology
  • Biomarkers / urine
  • Female
  • Humans
  • Hypertension / complications*
  • Hypertension / drug therapy
  • Hypertension / urine*
  • Kidney / blood supply
  • Kidney Diseases / etiology*
  • Kidney Diseases / prevention & control
  • Kidney Diseases / urine
  • Male
  • Sodium / urine

Substances

  • Biomarkers
  • Sodium
  • Acetylglucosaminidase