The purpose of this study was to elucidate the underlying mechanisms of blunted nocturnal blood pressure reduction in non-dipper hypertensive patients. We studied the diurnal variations in systemic hemodynamic indices and baroreflex sensitivity. In 45 subjects with essential hypertension (24 men; mean age, 49+/-1 years), intra-arterial pressure was monitored telemetrically. Non-dippers were defined as those with a nocturnal reduction of systolic blood pressure of less than 10% of daytime systolic blood pressure. Stroke volume was determined using Wesseling's pulse contour method, calibrated with indocyanine green dilution. Baroreflex sensitivity was calculated as deltapulse interval/deltasystolic blood pressure on spontaneous variations. The mean values of the hemodynamic parameters were calculated every 30 min. Twenty-six subjects were classified as non-dippers. Daytime blood pressure was not significantly different between dippers (149+/-4/87+/-3 mmHg) and non-dippers (147+/-3/82+/-2 mmHg), while the nighttime blood pressure was significantly reduced in dippers (131+/-3/77+/-2 mmHg) but not in non-dippers (145+/-3/80+/-2 mmHg). Nocturnal decreases in both cardiac index and stroke index were smaller in non-dippers (-12.0+/-1.2% and 1.5+/-1.0%) than in dippers (-17.5+/-1.4% and -2.2+/-1.1%). Baroreflex sensitivity significantly increased at nighttime both in dippers (6.5+/-0.6 to 8.0+/-0.7 ms/mmHg) and in non-dippers (5.1+/-0.3 to 6.4+/-0.4 ms/mmHg). Neither daytime nor nighttime baroreflex sensitivity was significantly different between the groups. We conclude that the hemodynamics of non-dipper essential hypertension are characterized by an inadequate nocturnal decrease in cardiac index and stroke index, suggestive of relative volume expansion or malsuppressed sympathetic activity.

The purpose of this study was to elucidate the effects of dietary sodium restriction on diurnal blood pressure (BP) variation in primary aldosteronism. We studied the diurnal variation in the systemic hemodynamic indices and in baroreflex sensitivity (BRS). In 13 subjects with aldosterone-producing adenomas (2 males; mean age, 39+/-2 years), intra-arterial pressure was monitored telemetrically on a normal salt diet (NaCl 10-12 g/day). Non-dippers were defined as those with a nocturnal reduction in systolic BP (SBP) of less than 10% of daytime SBP. Ten subjects showed a non-dipper pattern. Six of these "non-dippers" underwent repetitive hemodynamic studies on the last day of a 1-week low salt diet regimen (NaCl 2-4 g/day). Stroke volume was determined using Wesseling's pulse contour method, calibrated with indocyanine green dilution. BRS was calculated every 30 min as delta pulse interval/delta SBP on spontaneous variations. Nocturnal reduction of SBP was 4.1% on the normal salt diet. With sodium restriction, urinary sodium excretion decreased from 187+/-8 to 46+/-8 mmol/day, and body weight decreased from 57.9+/-2.1 to 56.6+/-1.9 kg. Night-time BP significantly decreased with dietary modification from 154+/-7/88+/-4 to 140+/-6/78+/-4 mmHg, whereas daytime BP was unaltered. With sodium restriction, cardiac index and stroke index decreased throughout the day. No significant difference was seen in either daytime or nighttime BRS between the two diets. We conclude that the non-dipper pattern is common in patients with an aldosterone-producing adenoma on a normal salt intake, and under such conditions, volume expansion appears to play a major role in the impairment of nocturnal BP reduction.

Renal artery stenting improves or preserves renal function in patients with bilateral renovascular disease and chronic renal insufficiency. An 80-year-old male was admitted to the hospital for elevated blood pressure accompanied by congestive heart failure. He had renal insufficiency and severe hypertension secondary to bilateral atherosclerotic renal artery stenosis. Unilateral renal artery stenting in the left kidney resulted in the recovery of renal function, whereas renal artery stenting in the right kidney was technically difficult due to a tortuous aorta. After the left unilateral stent implantation, the serum creatinine concentration decreased from 2.0 to 1.3 mg/dL, and control of his blood pressure required fewer antihypertensive drugs, namely a calcium antagonist, an angiotensin-converting enzyme inhibitor, and diuretics. Fifteen months after stenting, renal scintigraphy demonstrated improved function of the right kidney, despite severe renal artery stenosis, as well as improved function of the left kidney. Renal angioplasty or stenting should be attempted in bilateral atherosclerotic renovascular hypertension with renal insufficiency, even though it may only be successful unilaterally.

Antineutrophil cytoplasmic antibodies (ANCA) have been reported to be associated with systemic vasculitis. However, the roles of ANCA subtypes in patients with IgA nephropathy remain to be fully investigated. We describe three Japanese patients with IgA nephropathy complicated by ANCA-associated vasculitis. Two patients with IgG class ANCA developed rapidly progressive renal failure and demonstrated mesangial proliferation with extensive extracapillary proliferation and segmental glomerular necrosis. One patient with IgM class ANCA showed severe extrarenal symptoms, such as lung fibrosis and neuritis, in addition to glomerular crescent formation. All three patients received immunosuppressive therapies, including corticosteroids and cyclophosphamide. The two patients who received these treatments early showed improvement in urinary protein excretion and renal function, in accordance with a decrease in the serum titer of ANCA. However, one patient in whom serum creatinine was already elevated showed a poor response to the treatment. These results suggest that ANCA subtypes may participate in the pathogenesis of crescent formation in patients with IgA nephropathy, and that early treatment with a combination of methylprednisolone pulse therapy, oral prednisolone, and cyclophosphamide pulse therapy may be beneficial in these patients.

These results do not support the hypothesis that a plasma protease-antiprotease imbalance is a potential marker to predict the formation of saccular cerebral aneurysms. The increase in plasma elastase levels in patients with ruptured aneurysms might be attributable to leukocytosis after SAH.