Long-term effects of radiofrequency-based renal denervation on blood pressure and renal function by degree of renal dysfunction

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Renal artery stenting may improve blood pressure (BP) and renal function in resistant hypertension patients; however, benefit may differ depending on the degree of renal dysfunction. The authors analyzed 67 consecutive patients receiving stenting for obstructive renal artery disease between 2002 and 2005. Patients were categorized as normal or mildly impaired according to estimated glomerular filtration rate (eGFR) (> or =60 mL/min/1.73 m(2)), moderately impaired (eGFR 30 to 59 mL/min/1.73 m(2)), and severely impaired (eGFR <30 mL/min/1.73 m(2)). In patients with eGFR > or =60, systolic BP did not significantly improve from baseline. However, in patients with an eGFR between 30 and 59 mL/min/1.73 m(2), systolic BP decreased by 12 mm Hg at 6 months (P=.02) and 14 mm Hg at 12 months (P=.01). Greater benefit was observed in patients with eGFR <30 mL/min/1.73 m(2), with a 16 mm Hg (P=.10) and 21 mm Hg (P=.02) decrease at 6 and 12 months, respectively. Renal function was stable across all groups. Renal artery stenting reduced BP and produced greatest benefit in patients with baseline impaired renal function.

The International Scoring System (ISS) for Multiple Myeloma Remains a Robust Prognostic Tool Independently of Patients' Renal Function

Renal artery stent revascularization with embolic protection in patients with ischemic nephropathy

A New Era of Renal Denervation Trials for Patients With Hypertension?

The use of ACE inhibitors in patients with myocardial infarction (MI) has been the subject of several studies conducted during recent years. These studies have demonstrated the capacity of these agents to improve both survival and morbidity of patients with MI. However, the use of ACE inhibitors in patients with MI has been shown to reduce blood pressure (BP) and so could jeopardise the ischaemic myocardium. A significant reduction in systemic BP has been demonstrated by all the studies of ACE inhibitors in patients with MI, but no relationship has been found between the occurrence of hypotension and a worse clinical outcome. An increased risk of death has been observed exclusively in association with severe and sudden hypotension, the occurrence of which can be largely prevented by the administration of the ACE inhibitor according to an increasing dose-titration scheme. Conversely, a certain degree of long term BP reduction could result in some beneficial effect in patients with MI and contribute to the lower incidence of re-infarction observed in patients with acute MI undergoing long term treatment with captopril. Since the renin-angiotensin system is strictly related to kidney function, its blockade by an ACE inhibitor could result in some degree of renal dysfunction, particularly in patients with MI and impaired ventricular function. The available results from large-scale studies suggest that abnormalities in kidney function (namely an increase in serum creatinine) are observed in 0.9 to 2.4% of patients with MI who, nevertheless, experience some benefit from treatment with ACE inhibitors. Interestingly, the administration of ACE inhibitors does not seem to further compromise severely impaired renal function, and may also represent a useful tool for the treatment of patients with renal dysfunction associated with MI. The use of ACE inhibitors in patients with MI is associated with a satisfactory clinical and laboratory safety profile. The occurrence of significant adverse effects seems to be very low and mainly attributable to a rather modest prevalence of cough (2.4 to 6.8%). Discontinuation of treatment because of biochemical and haematological abnormalities has been observed in less than 1% of treated patients. Thus, the beneficial effects of ACE inhibitor treatment seem to outweigh safety concerns, thereby reinforcing the role of ACE inhibition as a suitable therapeutic strategy in the treatment of patients with MI.

Renal Impairment Is Not An Independent Adverse Prognostic Factor In Multiple Myeloma Patients Who Are Treated Upfront with Novel Agent-Based Regimens

Renal denervation in hypertension patients: Proceedings from an expert consensus roundtable cosponsored by SCAI and NKF.

37-Year-Old Woman With Bilateral Lower Extremity Edema, Proteinuria, and Microscopic Hematuria

Administration of lithium in the diet to new-born rats induces chronic renal failure associated with hypertension, proteinuria and irreversible tubulo-interstitial morphological changes. In the present study we induced chronic renal failure by administration of lithium for 16 weeks to new-born rats, and examined the spontaneous course of this nephropathy and the effects of antihypertensive treatment with either perindopril (12 mg/kg diet) or hydrochlorothiazide (500-1000 mg/kg diet) during a 24 weeks follow up period without lithium. In the placebo group, progression to terminal uraemia occurred in all rats with severe renal failure (initial Purea > 15 mM) (10 of 18). Rats with mild-moderate renal failure (Purea 9-15 mM) showed no deterioration in renal function despite persistent systolic hypertension and irreversible structural renal changes. Perindopril normalized the blood pressure in all rats but did not prevent the progression to terminal uraemia (8 to 18). Hydrochlorothiazide partially controlled the hypertension and accellerated the progression of uraemia without increasing the mortality (7 of 17). Irrespective of treatments, the predominant quantitative structural changes (e.g. decreased volume of proximal tubular cells) showed significant correlations with the degree of renal dysfunction, but not with systolic blood pressure in the surviving rats. It is concluded that progression of lithium-induced nephropathy to terminal uraemia occurs when the nephrotoxic insult results in a more than 50% reduction of the glomerular filtration rate, judged from Purea levels. The failure of effective antihypertensive treatment with an angiotension-converting enzyme inhibitor to modify the progression suggests that in this model, systemic or glomerular hypertension may not be an important pathophysiological factor. The structural and functional deterioration observed in Li-uraemic rats during treatment with hydrochlorothiazide remains unexplained.

Prehypertension Is Associated With Insulin Resistance State and Not With an Initial Renal Function Impairment: A Metabolic Syndrome in Active Subjects in Spain (MESYAS) Registry Substudy

Alterations in glomerular hemodynamics may play an important role in the progression of renal dysfunction. Accordingly, treating not only systemic hypertension, but also glomerular hypertension is important for conservation of renal function in patients with renal disease. However, glomerular capillary pressure does not necessarily change in parallel with systemic blood pressure due to unique mechanisms that control the resistance of glomerular afferent and efferent arterioles. While myogenic response and tubuloglomerular feedback play an important role in controlling afferent arteriolar resistance, angiotensin II is a major determinant of efferent arteriolar tone. Calcium antagonists block almost all mechanisms that constrict the afferent arteriole, rendering glomerular capillary pressure dependent on systemic pressure. On the other hand, angiotensin-converting enzyme inhibitors dilate efferent arterioles, thereby lowering glomerular capillary pressure. Such differences should be taken into account when selecting adequate drugs for the treatment of hypertension with various degrees of renal dysfunction.

Posttransplantation chronic renal damage in nonrenal transplant recipients

Objective : Assessment and comparison of pregnancy outcomes in women with renal disease and women with high risk pregnacies due to medical illness without renal disease. Design : A prospective, matched controlled study. Setting : The High Risk Obstetrical Clinics of Magee Women's Hospital, a primary and referral center where approximately 9,500 deliveries occur per year. Patients : Two groups of pregnant women, all identified in the first trimester. The study group included 43 pregnancies in 40 women with renal disease as defined by : 1) known renal disease antedating pregnancy, 2) prepregnant proteinuria ≥150 mg/24 hours, or 3) first trimester serum creatinine ≥0.8 mg/dl or proteinuria ≥300 mg/24 hours. The 43 controls included women with medical problems other than renal disease that placed them at high obstetrical risk. Control women were matched to study women for parity, advanced maternal age, race, and insulin-dependent diabetes mellitus. Measurements : For all patients, blood pressure was recorded once at approximately 10, 20, and 30 weeks gestation. For study patients, serum creatinine, 24-hour urinary protein, and creatinine clearance were obtained at least once in each trimester. Pregnancy outcomes were recorded as favorable if gestation was ≥36 weeks and without evidence of intrauterine growth retardation. Adverse pregnancy outcomes included prematurity, intrauterine growth retardation, intrauterine fetal death, spontaneous abortion, or neonatal death. Results : Forty-two percent of study and control patients were diabetic. First trimester renal function was normal (creatinine <0.8 mg/dl) in 12 study patients, mildly impaired in 24 (creatinine 0.8-1.4 mg/dl) and moderately impaired in 5 (creatinine ≥1,4 mg/dl). Compared with controls, first and third trimester hypertension was more prevalent in the study patients (p = 0.003, p = 0.012) ; overall mean blood pressure was also higher in study patients (92 ± 11 mmHg vs 85 ± 8 mmHg, p = 0.002). The mean gestational age was shorter in the study patients (33.4 ± 6.9 weeks vs 37.2 ± 4 weeks, p = 0.001). Overall pregnancy loss was more common in the study patients (14/43 vs 3/43, p = 0.003) with spontaneous abortion contributing half of those pregnancy losses (7/14). Hypertension in any trimester was associated with adverse pregnancy outcome in study but not control patients. In the subset of study patients, adverse fetal outcome was directly associated with degree of renal dysfunction and proteinuria. Conclusions : Pregnancy outcome in women with renal disease was significantly worse than in the control group and showed no improvement over retrospective reports from the 1970's and 1980's. Specifically, fetal deaths were more common in women with renal disease and were predicted by proteinuria and the degree of renal dysfunction. The uncommonly low number of spontaneous abortions in the control group may have contributed to the worse fetal outcome in the study patients compared with controls. Women with diabetes mellitus and hypertension are at particularly high risk for relatively poor pregnancy outcome. These higher risks should be discussed when counseling women with renal disease who contemplate pregnancy.

Low Birth Weight and Kidney Function: Is There a Relationship and Is it Determined by the Intrauterine Environment?