Role of angiotensin II in the hypertension induced by renal artery stenosis

Identical degrees of renal artery stenosis were induced in 5 dogs on two separate occasions; once during continuous inhibition of angiotensin I converting enzyme with enalapril, and once with the dogs untreated. Arterial pressure rose about 25 mm Hg during 3 days of stenosis in untreated dogs, due to increased total peripheral resistance. When the dogs were treated with enalapril, blood pressure had risen 14.5 ± 3.4 mm Hg 24 hours after stenosis due to a 35% increase in cardiac output while total peripheral resistance fell by 16%. By the third day, blood pressure had returned to pre-stenosis levels, cardiac output was close to normal and total peripheral resistance had increased. The stenosis on the renal artery increased the resistance to blood flow of the kidneys in both untreated and enalapril treated dogs. This increase in kidney resistance in the untreated dogs accounted for about 30% of the change in total peripheral resistance. In the enalapril treated dogs, the increased kidney resistance helped offset the vasodilatation in the rest of the vasculature. These results suggest that angiotensin II mediated vasoconstriction of nonrenal vascular beds was responsible for about ⅔ of the hypertension following renal artery stenosis, and the resistance of the stenosis responsible for about ⅓.

Renal responses to angiotensin II in conscious dogs : effects of aspirin and indomethacin

1. Angiotensin II was infused into the renal artery of unanaesthetized dogs at 0.4 and 2.0 ng/kg per min for 40 min each.

2. Indomethacin (3 mg/kg, and 1 mg/kg per h infusion i.v.) accentuated the angiotensin II-induced falls in glomerular filtration rate, renal blood flow and urine flow rate. Indomethacin did not alter the effects of angiotensin II on Na+ or K+ excretions.

3. Aspirin (35 mg/kg p.o. 2.5 h and 0.5 h prior to experiment) did not significantly change the renal effects of angiotensin II.

4. Both aspirin and indomethacin accentuated renal vasoconstriction during briefer (5 min) angiotensin II infusion.

5. Thus indomethacin and aspirin had markedly different effects on the actions of angiotensin II in the kidney. This suggests that at least one of these drugs has actions which affect angiotensin II-mediated vasoconstriction other than via cyclooxygenase inhibition.

The Renal Treatment Satisfaction Questionnaire (RTSQ): a measure of satisfaction with treatment for chronic kidney failure.

BACKGROUND: Quality and effectiveness of care can be enhanced through the use of condition-specific measures of satisfaction with treatment. The aim of the present study was to design and develop a measure of satisfaction with treatment for patients with chronic kidney failure (CKF) for use in routine clinical care and clinical trials. The Renal Treatment Satisfaction Questionnaire (RTSQ) was designed to be suitable for people using any of the various treatment modalities for CKF. Items measure satisfaction with aspects of treatment, including convenience, flexibility, freedom, and satisfaction to continue with present form of treatment.

METHODS: A 12-item RTSQ was investigated at a UK hospital-based renal unit, using data from 140 outpatients undergoing renal replacement therapy (hemodialysis, n = 35; continuous ambulatory peritoneal dialysis, n = 57; transplantation, n = 46).

RESULTS: An 11-item scale was developed from the original 12-item version, with a single factor accounting for 59% of the variance and item loadings greater than 0.58. Scale reliability was excellent (alpha = 0.93) in the full sample and proved robust to analysis in separate treatment subgroups. As expected, RTSQ scores differed significantly ( P < 0.0001) between the transplantation and other treatment groups. Those who had received a transplant expressed greater overall satisfaction, with specific advantages of transplantation shown by all individual items, including convenience, time, lifestyle, freedom, and satisfaction to continue current treatment.

CONCLUSION: The RTSQ provides a brief reliable measure of satisfaction with treatment for patients with CKF that is suitable for use in routine clinical care and clinical trials.

Renal artery stenosis and hypertension : whom and how to screen and treat

Renovascular disease is an underlying cause in a significant proportion of patients who have refractory hypertension. Aggressive medical therapy to lower cardiovascular risk is the first priority in these patients. Endovascular treatment is required in only a few carefully selected cases

RAN-Vic : renal access nurses of Victoria unite.

The Renal Access Nurse has recently become an integral member of the renal health care team in Australia. Research has shown that the introduction of a Renal Access Nurse into dialysis units enhances the referral process for new access, improves survival rates, and success of access creation. Australia has been relatively slow in the introduction of the role of the Renal Access Nurse. The USA, UK and Europe have been utilising Renal Access Nurses in renal units for many years and their roles are firmly entrenched.

The first Renal Access Nurse was introduced in Victoria in 2003, increasing to 7 in 2007. It was evident in 2006 that a networking system for Renal Access Nurses was needed in Victoria, so RAN-Vic was born.

RAN-Vic consists of 6 Renal Access Nurses from the major hubs in Melbourne and Geelong, thus covering a large part of the Victorian dialysis community through satellite units throughout the state.

The group meet quarterly, with the main goals being to network, share ideas, support each other with challenges arising from the new role, benchmark, undertake quality initiatives and education of renal nursing staff. By doing this, we hope to improve outcomes for patients, improve work practices pertaining to renal access, and further redefine the new role.

RAN-Vic is the first of its kind in Australia, providing care for renal access for the dialysis population throughout Victoria. We recommend for all states in Australia to consider forming a Renal Access Group to help improve renal access outcomes.

Vascular access surveillance : the role of the access nurse in the renal dialysis unit.

Introduction
In January 2006, the Renal Dialysis Unit at Geelong Hospital appointed a Vascular Access Nurse. A Transonic Flow Qc HDO2 Ultrasound Dilution Monitor was purchased to monitor access flow and recirculation in arteriovenous fistulae in an attempt to predict AVF stenoses requiring early surgical correction.

Methods
A bi-monthly monitoring program tested all facility-based patients. 82 patients were assessed for access flow and recirculation between February and December 2006.

Results
18 (22%) had poor AVF function; 13 with access flows <500ml/minute on initial testing and 5 with an access flow decreasing >25% over a four month period. Of the 18 patients shown to have poor access flow, 2 died within one month of measurement while 5 were too frail to attempt corrective surgery. The remaining 11 proceeded to ultrasound or fistulography. A >50% stenosis was detected in all 11 cases. Of these, 4 had successful vein patch surgery and one had PTFE grafting, each with marked improvement in access flow. One had failed vein patch surgery requiring creation of a femoral AVF, one patient required cvc insertion to await AVF creation, and one had failed stenting requiring a permanent cvc. 3 died before planned surgery.

Conclusion
5 of the 82 patients that had access flow assessment, and needed further evaluation, proceeded to successful pre-emptive surgical intervention. We believe the Transonic is a useful adjunct to routine clinical AVF surveillance, in providing early evidence of AVF failure that can be avoided by pre-emptive surgery.

Evidence that renal arginine transport is impaired in spontaneously hypertensive rats

Low renal nitric oxide (NO) bioavailability contributes to the development and maintenance of chronic hypertension. We investigated whether impaired L-arginine transport contributes to low renal NO bioavailability in hypertension. Responses of renal medullary perfusion and NO concentration to renal arterial infusions of the L-arginine transport inhibitor L-lysine (10 μmol·kg⁻¹·min⁻¹; 30 min) and subsequent superimposition of L-arginine (100 μmol·kg⁻¹·min⁻¹; 30 min), the NO synthase inhibitor N^G-nitro-L-arginine (2.4 mg/kg; iv bolus), and the NO donor sodium nitroprusside (0.24 μg·kg⁻¹·min⁻¹) were examined in Sprague-Dawley rats (SD) and spontaneously hypertensive rats (SHR). Renal medullary perfusion and NO concentration were measured by laser-Doppler flowmetry and polarographically, respectively, 5.5 mm below the kidney surface. Renal medullary NO concentration was less in SHR (53 ± 3 nM) compared with SD rats (108 ± 12 nM; P = 0.004). L-Lysine tended to reduce medullary perfusion (−15 ± 7%; P = 0.07) and reduced medullary NO concentration (−9 ± 3%; P = 0.03) while subsequent superimposition of L-arginine reversed these effects of L-lysine in SD rats. In SHR, L-lysine and subsequent superimposition of L-arginine did not significantly alter medullary perfusion or NO concentration. Collectively, these data suggest that renal L-arginine transport is impaired in SHR. Renal L-[³H]arginine transport was less in SHR compared with SD rats (P = 0.01). Accordingly, we conclude that impaired arginine transport contributes to low renal NO bioavailability observed in the SHR kidney.

Rapid onset of renal sympathetic nerve activation in rabbits fed a high-fat diet

Hypertension and elevated sympathetic drive result from consumption of a high-calorie diet and deposition of abdominal fat, but the etiology and temporal characteristics are unknown. Rabbits instrumented for telemetric recording of arterial pressure and renal sympathetic nerve activity (RSNA) were fed a high-fat diet for 3 weeks then control diet for 1 week or control diet for 4 weeks. Baroreflexes and responses to air-jet stress and hypoxia were determined weekly. After 1 week of high-fat diet, caloric intake increased by 62%, accompanied by elevated body weight, blood glucose, plasma insulin, and leptin (8%, 14%, 134%, and 252%, respectively). Mean arterial pressure, heart rate, and RSNA also increased after 1 week (6%, 11%, and 57%, respectively). Whereas mean arterial pressure and body weight continued to rise over 3 weeks of high-fat diet, heart rate and RSNA did not change further. The RSNA baroreflex was attenuated from the first week of the diet. Excitatory responses to air-jet stress diminished over 3 weeks of high-fat diet, but responses to hypoxia were invariant. Resumption of a normal diet returned glucose, insulin, leptin, and heart rate to control levels, but body weight, mean arterial pressure, and RSNA remained elevated. In conclusion, elevated sympathetic drive and impaired baroreflex function, which occur within 1 week of consumption of a high-fat, high-calorie diet, appear integral to the rapid development of obesity-related hypertension. Increased plasma leptin and insulin may contribute to the initiation of hypertension but are not required for maintenance of mean arterial pressure, which likely lies in alterations in the response of neurons in the hypothalamus.