Patients with end-stage renal disease have a high mortality, with the majority of deaths due to vascular disease. The prevalence of vascular risk factors and vascular disease in predialysis chronic renal failure (CRF) is poorly characterized. The aim of the present study was to determine the prevalence of vascular risk factors and clinically overt vascular disease in an Australian cohort of patients with predialysis CRF. We performed a retrospective chart review of outpatients with CRF and noted demographic data, the cause of renal failure, the presence or otherwise of vascular risk factors and vascular disease and calculated glomerular filtration rate. The prevalence of overt vascular disease and modifiable vascular risk factors was calculated. One hundred and eighty patients completed the study. Eighty-nine per cent of patients had hypertension, 68% had dyslipidaemia, 32% were diabetic and 38% were previous smokers. The subgroup with diabetic nephropathy had significantly more risk factors (P < 0.001) than other groups. Twenty-seven per cent of the group had cardiovascular disease, 22% had cerebrovascular disease, 23% had peripheral vascular disease and 9% had renal artery stenosis. Patients with ischaemic nephropathy had significantly more vascular disease than other groups (P < 0.001). Patients with overt vascular disease were older, had a higher number of risk factors and a higher calcium phosphate product than those without vascular disease. In conclusion, the present study suggests a high prevalence of vascular risk factors and vascular disease in predialysis CRF. Early detection provides an opportunity for early intervention and may help reduce the development of vascular disease, and the associated mortality, once these patients progress to dialysis.
SUMMARY: Some studies have suggested a disturbing incidence of chronic renal failure (CRF) and renal papillary necrosis (RPN) following regular non‐steroidal anti‐inflammatory drug (NSAID) use. This study was undertaken to assess the prevalence of renal insufficiency in rheumatology patients taking regular NSAIDs and a control group of age‐matched subjects who had other chronic illnesses but were not taking regular NSAIDs. Sixty‐nine patients with rheumatological disorders and significant NSAID use but no known renal abnormalities were compared with 69 age‐matched subjects with non‐renal chronic disease who were not taking NSAIDs. Each patient completed a questionnaire regarding NSAIDs and analgesic use, and then had their blood pressure measured along with urinalysis, urine microscopy, serum electrolytes and creatinine and calculated creatinine clearance using the Cockroft‐Gault formula. If clinically indicated, patients had further renal imaging to detect structural renal damage. By definition of the study design, rheumatology patients took significantly more NSAIDs than control subjects (P < 0.0001). Twelve patients (19%) in the rheumatology group had renal impairment compared with 10 (17%) in the control group (P= 0.67). Seven patients (10%) in the rheumatology group had microscopic haematuria with or without proteinuria, which was not statistically different to that in the control group (3%, P= 0.09), but isolated microscopic haematuria was detected more commonly in the rheumatology group (11 vs2%, P= 0.03). No patient in either group had clinically apparent RPN, which appeared to be an uncommon complication of chronic NSAID use in rheumatology patients. Chronic renal insufficiency is present in approximately one in five rheumatology patients taking long‐term NSAIDs, but this prevalence is no greater than in patients with other chronic illnesses who do not take long‐term NSAIDs.
1. The aim of the present study was to examine the acute effects of cortisol infusion on plasma nitrate/nitrite (NO) activity and forearm vascular responsiveness to acetylcholine. 2. We performed two randomized, placebo-controlled, cross-over studies. Study A examined the effects of intravenous hydrocortisone (200 mg over a 3 h period) on blood pressure (BP) and plasma NO activity in six healthy male volunteers. Study B examined the effects of intra-arterial hydrocortisone on cholinergic vasodilator responsiveness in six healthy male volunteers. Vasodilator responsiveness was measured by bilateral strain gauge plethysmography. 3. In study A, there was no significant change in BP during the hydrocortisone infusion. Comparing values obtained following 180 min infusion of hydrocortisone and control, there were significant increases in plasma cortisol (3441 +/- 342 vs 209 +/- 29 nmol/L, respectively; P < 0.001) and glucose (5.7 +/- 0.2 vs 4.6 +/- 0.2 mmol/L, respectively; P < 0.05) and a reduction in plasma renin concentration (PRC) (8.1 +/- 1.2 vs 11.0 +/- 1.8 pg/mL, respectively; P < 0.05) following hydrocortisone infusion. However, there were no significant changes in either plasma NO or in the endogenous NO synthase inhibitors asymmetrical and symmetrical dimethylarginine. 4. In study B, there was no significant change in BP or in cholinergic vasodilator responsiveness during the hydrocortisone infusion. 5. Short-term cortisol infusions do not alter biochemical or physiological markers of NO activity. If cortisol-induced hypertension is mediated by suppression of NO activity in humans, it seems likely that these changes take more than 3 h to become detectable.
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