Hypertensive patients with renal parenchymal disease had significantly higher muscle sympathetic nerve activity compared to matched controls (31 vs 18 bursts/min; P<0.01).
Case-Control
Sympathetic nerve activity is inappropriately elevated in hypertensive patients with chronic renal disease relative to their volume status, and this overactivity is not solely due to a reduced nephron mass.
Absolute Event Rate: 31% vs 18%
p-value: p=<0.01
The hypothesis that in hypertensive patients with renal parenchymal disease sympathetic activity is "inappropriately" elevated and that this overactivity is a feature of renal disease and not of a reduced number of nephrons per se is addressed. Fifty seven patients with renal disease (various causes, no diabetes, all on antihypertensive medication) were studied, age range 18 to 62, creatinine clearance 10 to 114 ml/min per 1.73 m(2). Antihypertensives were stopped, but diuretics were allowed, to prevent overhydration. Matched control subjects were also studied. The effect of changes in fluid status was examined in seven patients while on and after stopping diuretics and in eight control subjects while on low- and high-sodium diet. Seven kidney donors were studied before and after unilateral nephrectomy. Sympathetic activity was quantified as muscle sympathetic nerve activity (MSNA) in the peroneal nerve. Mean arterial pressure, MSNA, and plasma renin activity were higher in patients than in control subjects, respectively (115 +/- 12 and 88 +/- 11 mmHg, 31 +/- 15 and 18 +/- 10 bursts/min, and 500 20 to 6940 and 220 40 to 980 fmol/L per s; P < 0.01 for all items). Extracellular fluid volume (bromide distribution) did not differ. Seven patients were studied again after stopping diuretics. MSNA decreased from 34 +/- 18 to 19 +/- 18 bursts/min (P < 0.01). Eight healthy subjects were studied during low- and high-sodium diet. MSNA was 26 +/- 12 and 13 +/- 7 bursts/min (P < 0.01). The curves relating extracellular fluid volume to MSNA were parallel in the two groups but shifted to a higher level of MSNA in the patients. In the kidney donors, creatinine clearance reduced by 25%, but MSNA was identical before and after donation. It is concluded that in hypertensive patients with renal parenchymal disease, sympathetic activity is inappropriately high for the volume status and that reduction of nephron number in itself does not influence sympathetic activity.
Klein et al. (Mon,) conducted a case-control in Chronic Renal Disease and Hypertension. Renal parenchymal disease vs. Matched control subjects was evaluated on Muscle sympathetic nerve activity (MSNA) (p=<0.01). Hypertensive patients with renal parenchymal disease had significantly higher muscle sympathetic nerve activity compared to matched controls (31 vs 18 bursts/min; P<0.01).
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