Survival of patients older than 60 years with kidneys transplanted from Spanish expanded criteria donors versus patients continued on hemodialysis.

A retrospective study was performed in patients >60 years of age who had initiated hemodialysis (HD) at our hospital between 2000 and 2005 (n = 211). Of these, 47 were placed on the kidney transplantation waiting list and 164 were excluded and continued on HD. Cadaveric transplantation was performed in 31 patients using an expanded criteria donor organ (TR), while 16 remained on the waiting list (WL). We compared the 12-month survivals of patients in the 3 groups (TR/WL/HD), namely, 97%/78%/75% (P < .045). Survival at 24, 36, 48, and 60 months for TR/HD were 89%/57%; 86%/43%; 79%/32%; and 70%/16% (P < .001). HD patients showed greater comorbidity than TR patients: Charlson index >8 was 67.9% vs 19.4%. A total of 23.7% of patients were excluded solely due to advanced age. We compared survivals among the TR patients vs those excluded only because of age using paired comorbidity (Charlson index <8): 97%/95%, 89%/58%, and 86%/44% at 12, 24, and 36 months (P < .023). We concluded that kidney transplantation with an expanded criteria donor organ in elderly patients was a procedure that provided greater survival than HD for patients excluded from transplantation, for patients on the WL who did not receive a transplant, and for patients excluded solely due to advanced age who showed comorbidity comparable to the transplant recipients. According to our data, elderly patients with low comorbidity should be considered for inclusion on the WL for transplantation.

[Preliminary results of the Spanish Society of Nephrology multicenter study of quality performance measures: hemodialysis outcomes can be improved]. / Resultados del proyecto de mejora de la calidad de la asistencia en hemodiálisis: estudio multicéntrico de indicadores de calidad de la Sociedad Española de Nefrología (SEN).

INTRODUCTION: The Spanish Society of Nephrology "Quality in Nephrology Working Group" (QNWG) was created in 2002. The aims of this group are the identification, diffusion, implementation and consolidation of a systematic, objective and comprehensive set of quality performance measures (QPMs) to help along the improvement of patient care and outcomes on hemodialysis, by means of strategies of feedback and benchmarking, and the design of quality improvement projects. The objective of this study is to present the preliminary results of a set of quality performance measures obtained in a group of Spanish hemodialysis centers, as well as to evaluate the repercussion of the application of the aforementioned thecniques on the observed results. METHODS: During 2007 a total of 28 hemodialysis units participated in the study; 2516 patients were evaluated. A specific software was designed and used to facilitate the calculation of CPMs in each unit. The clinical indicators used refered to dialysis adequacy; anemia; mineral metabolisme; nutrition; viral infections; vascular access; mortality, morbidity (number and days of hospital admissions); and renal transplant. Every three months each center received its own data and its comparison with the rest of the group. RESULTS: Except for hemoglobin levels we observed a global improvement. The percentage of centers reaching the stablished standards defined by the QNWG passed from 65% to 90,9% for Kt/V Daugirdas II (> 1,3 in > that 80% of the patients); from 71,4 % to 77,2 % for PTH (> 30 % of patients with serum PTH between 150 and 300 pg/ml); and from 42,8 % to 63,5 % for phosphate (> 75 % of patients with a serum phsphate < 5,5 mg/dl). More than 50% of centers showed an improvement in their final results as compared with their own initial results in all analyzed CPMs. Those centers that did not obtained an improvement in their results started the study with better percentages of acomplishment than those that showed a significant improvement in QPMs. (80,6+/-15,4 versus 71,8+/-16,6 respectively; p<0,001) CONCLUSIONS: We are starting to make progresses in our knowledge of clinical results in our hemodialysis units, although there is still a long way to go over. To monitor and share CPMs results within hemodialysis centers might help to improve their results as well as to reduce intecenters variability.

Impairment of renal vasodilation with l-arginine is related to more severe disease in untreated hypertensive patients.

Data remain insufficient to place the decreased response to L-arginine in hypertensive patients within a consistent pathophysiological sequence. The aim of the present study in patients with essential hypertension was to assess the relationships between the response to L-arginine and a set of relevant clinical and laboratory parameters. In this prospective, interventional study, we administered L-arginine to untreated hypertensive individuals and healthy control subjects and measured the clearance of inulin and of para-aminohippurate and a set of biochemical and clinical variables. L-Arginine infusion revealed major differences between control subjects and 1 subgroup (group B) of hypertensive individuals. Group B hypertensives (n=18) had no increase in inulin clearance and no decrease in renal vascular resistance with L-arginine; however, in another subset of hypertensive patients (group A, n=27), the insulin clearance increased and renal vascular resistance decreased similar to the control group (group C, n=11). The ambulatory blood pressure monitoring in group B showed both an increased mean diastolic pressure and a "nondipper" pattern in the nocturnal regulation of arterial pressure. These findings in group B were accompanied by significant alterations in optic fundus and left ventricle hypertrophy and increased microalbuminuria (all, P<0.05). Furthermore, group B individuals had significantly lower values of HDL cholesterol and a higher baseline atherogenic index, plasma insulin level, and glucose/insulin index. We disclose a previously undescribed relationship between end organ repercussion and decreased renal hemodynamic response to L-arginine. Our results may help to understand the mechanisms that lead to target organ damage in hypertension.

Clinical characteristics of ischaemic renal disease.

BACKGROUND: Longer life expectancy has favoured the ever more frequent development of ischaemic nephropathy characterized by the presence of atherosclerotic stenosis in both renal arteries. METHODS: This is an observational and multicentre study carried out during a 14-month follow-up period in 20 hospitals in SPAIN: Inclusion criteria were the presence of bilateral renal artery stenosis > 50% and a creatinine level of > or = 1.5 mg/dl. The diagnosis should be made by arterial digital angiography in every case. RESULTS: A total of 156 patients were included. Their mean age was 68.7+/-9 years, and 78.5% were male. The mean creatinine value of the group was 2.9+/-1.7 mg/dl. Arterial hypertension (BP) with a duration of 12+/-9 years was present in 97.4% of the cases, smoking habits in 69.8%, hypercholesterolaemia (> or = 240 mg/dl) in 62.9% and diabetes in 32.1%. Only 8% of the patients had a body mass index > or = 30 kg/m(2). Associated cardiovascular disease was very frequent: peripheral arteriopathy in 67.5% of the cases, ischaemic cardiopathy in 44.8%, cardiac insufficiency in 32.6% and stroke in 27.3%. In 94.4% of the patients, the lesion affected both renal arteries, with complete obstruction in 23% of the cases. CONCLUSIONS: Diagnostic suspicion of ischaemic nephropathy can be established in non-obese elderly males with chronic renal insufficiency, long-term BP evolution and cardiovascular disease at other levels, above all, peripheral arteriopathy.

Ischemic nephropathy: clinical characteristics and treatment.

Ischemic nephropathy is a long-term cause of hypertension and renal failure. Although its real incidence is unknown, ischemic nephropathy is growing because of the increased mean age of the population and the greater prevalence of hypertensive and diabetic populations. This review describes the clinical profile of afflicted patients. Atherosclerosis in different vascular beds is common in these patients. The evolution of ischemic nephropathy is generally progressive, although some patients present with acute renal failure, either secondary to the administration of angiotensin-converting enzyme inhibitors or caused by thrombosis of the renal arteries. Revascularizing surgery may stabilize or improve renal function, even in patients with nonfunctioning kidneys. The results obtained with intraluminal angioplasty are worse, with a high percentage of restenosis. Placement of an endoprothesis is recommended when the lesions affect the ostium or proximal third of the artery. This complex disease typically affects multiple organs, thus making individual assessment essential.

Hyperkalemia in patients infected with the human immunodeficiency virus: involvement of a systemic mechanism.

BACKGROUND: The appearance of hyperkalemia has been described in human immunodeficiency virus (HIV)-positive patients treated with drugs with amiloride-like properties. Recent in vitro data suggest that individuals infected with HIV have alterations in transcellular K+ transport. METHODS: With the objective of examining the presence of alterations in transmembrane K+ equilibrium in HIV-positive patients, we designed a prospective, interventional study involving 10 HIV-positive individuals and 10 healthy controls, all with normal renal function. An infusion of L-arginine (6%, intravenously, in four 30-min periods at 50, 100, 200, and 300 ml/hr) was administered, and plasma and urine electrolytes, creatinine, pH and osmolality, total and fractional sodium and potassium excretion, transtubular potassium gradient, plasma insulin, renin, aldosterone, and cortisol were measured. RESULTS: A primary disturbance consisting of a significant rise in plasma [K+] induced by L-arginine was detected in only the HIV patients but not in the controls (P < 0.001 between groups). A K+ redistribution origin of the hyperkalemia was supported by its rapid development (within 60 min) and the lack of significant differences between HIV-positive individuals and controls in the amount of K+ excreted in the urine. The fact that the HIV-positive individuals had an inhibited aldosterone response to the increase in plasma K+ suggested a putative mechanism for the deranged K+ response. CONCLUSIONS: These results reveal that HIV-infected individuals have a significant abnormality in systemic K+ equilibrium. This abnormality, which leads to the development of hyperkalemia after the L-arginine challenge, may be related, in part, to a failure in the aldosterone response to hyperkalemia. These results provide a new basis for understanding the pathogenesis of hyperkalemia in HIV individuals, and demonstrate that the risk of HIV-associated hyperkalemia exists even in the absence of amiloride-mimicking drugs or overt hyporeninemic hypoaldosteronism.

Induction of microalbuminuria by l-arginine infusion in healthy individuals: an insight into the mechanisms of proteinuria.

Despite evidence from individuals with diabetes mellitus or reduced renal mass, the actual relationship between protein- or amino acid-induced changes in renal function and urinary albumin excretion (UAE) is largely unknown in subjects without renal disease. In humans, infusions of l-arginine have been used recently in vascular and renal pathophysiological studies. The present study was undertaken to analyze the mechanisms involved in a particular effect; namely, the behavior of UAE during amino acid loading. A prospective interventional protocol was performed on 10 healthy adults by means of an intravenous infusion of l-arginine. The main results show that l-arginine induced a significant increase in UAE from 13.1 +/- 3.8 before to 53.3 +/- 11.1 microgram/min after the infusion (P < 0.005). This increment was simultaneous to an increase in glomerular filtration rate (GFR) and renal plasma flow (RPF). Furthermore, l-arginine markedly increased the urinary excretion of beta2-microglobulin. UAE correlated significantly with GFR (r = 0. 738; P = 0.014) and RPF (r = 0.942; P < 0.0001), but not with urinary beta2-microglobulin (r = 0.05; P = not significant). Furthermore, marked differences (P = 0.001) were found between the percentage of increase in UAE (306.8% +/- 163.2%) with respect to either albumin filtered load (FLAlb; 57.9% +/- 16.3%) and beta2-microglobulin excretion (1,088.5% +/- 424.6%). No changes were found in vehicle-infused individuals. In conclusion, the present study shows, in controlled conditions, that l-arginine infusion induces a relevant increase in UAE in healthy individuals that significantly exceeds that expected from the increase in GFR alone. The intense and simultaneous increment in beta2-microglobulin excretion strongly suggests that the effect of l-arginine on UAE is, in a relevant part, mediated through a blockade in the tubular protein reabsorption pathways. However, the profound differences observed in the changes induced by l-arginine on UAE and beta2-microglobulin excretion and the differences in the correlation of UAE and beta2-microglobulin with respect to GFR suggest that substantial diversity exists in the mechanisms by which l-arginine affects the renal management of albumin and beta2-microglobulin. These findings are relevant for understanding the renal response to l-arginine and protein/amino acid loads.

Ischaemic renal injury.

Ischaemic renal injury is becoming one of the main causes of end-stage renal failure. The appearance of new diagnostic methods, as well as the evidence that surgery or percutaneous transluminal angioplasty techniques are capable of inducing a significant degree of recovery in a subset of patients, are encouraging events. The identification of the precise cellular pathogenetic mechanisms of ischaemic injury is an area for future research.

Aging abolishes the renal response to L-arginine infusion in essential hypertension.

A defect in the endothelium-dependent vasorelaxation could contribute to the development of arterial hypertension through the facilitation of renal vasoconstriction and sodium retention. In this study, we tested the hypothesis that aging impairs kidney function in essential hypertension through a derangement of nitric oxide-dependent renal mechanisms. To this end, we compared the renal response to an intravenous infusion of the precursor of nitric oxide synthesis, L-arginine, in young and aged essential hypertensives. In young hypertensives, L-arginine induced a significant increase in renal plasma flow, glomerular filtration rate, natriuresis and kaliuresis, without changes in filtration fraction. These effects were not observed in aged hypertensives. Neither PRA nor PA were affected by L-arginine infusion in any group. These results indicate that aging produces a derangement of endothelial function in essential hypertension.

Lipoprotein(a) and vascular access survival in patients on chronic hemodialysis.

Lipoprotein(a) [Lp(a)] is an independent risk factor for atherosclerotic and cardiovascular complications in the general population and in hemodialysis patients. Increased Lp(a) levels have been also described as a possible predictor of vascular access occlusion in patients on chronic hemodialysis. We have studied prospectively the relationship between vascular access survival and Lp(a) levels in 40 hemodialysis patients. The Lp(a) plasma concentrations were measured by enzyme-linked immunosorbent assay in all patients in April 1993. Throughout the following year, evolution and survival of their vascular accesses were analyzed. Failure of vascular access was established when there were complications requiring surgical repair or transluminal angioplasty. Fourteen patients showed failure of vascular access, and the cumulative survival of vascular accesses after 1 year of follow-up was 63.8%. The Lp(a) levels were higher in patients with failure of vascular access than in the others (35.2 +/- 31 vs. 22.4 +/- 25 md/dl), but this difference did not reach statistical significance (p = 0.064). The vascular access survival in patients with Lp(a) levels > 75th percentile (52.5 mg/dl) was significantly lower than in the remaining patients (40 vs. 72%; p = 0.045). This difference increased when we analyzed the patients with Lp(a) levels > 90th percentile (76 md/dl; 25 vs. 68%; p = 0.002). Our results suggest that patients with the highest levels of Lp(a) are at risk of developing complications in their vascular accesses, and they also have lower vascular access survival.

Randomly allocated study of the effects of standard therapy versus ACE inhibition on micro-albuminuria in essential hypertension.

OBJECTIVE: To compare the effects of standard therapy (diuretic, beta-blocker or both) with those of angiotensin converting enzyme (ACE) inhibition with quinapril on renal function and urinary albumin excretion in patients with essential hypertension. METHODS: A 1-year, placebo-controlled, randomly allocated study was conducted in a group of 40 patients with essential hypertension. Before beginning the active treatment phase, all patients were given a matched placebo for quinapril for at least 14 days. At baseline and after 1, 3, 6 and 12 months of treatment, blood pressure, heart rate, body weight, renal plasma flow, glomerular filtration rate, plasma renin activity, plasma aldosterone and urinary albumin excretion were measured. RESULTS: Both the standard therapy and quinapril produced similar decreases in blood pressure, but only quinapril produced a significant decrease in micro-albuminuria, from 68.5 +/- 16.7 to 47.2 +/- 14.9 mg/24 h (P < 0.05). The renal plasma flow remained constant in both study groups while the glomerular filtration rate and filtration fraction decreased significantly (P < 0.05) in the quinapril group. CONCLUSIONS: The results of this study indicate that long-term therapy for essential hypertension with ACE inhibition has a more favorable effect on micro-albuminuria than standard therapy for an equal level of blood pressure control.

Calcium antagonists and renal protection.

AIM: To review the renal benefits of calcium antagonists. METHODS: Review of published studies. RESULTS: Both experimental and clinical studies have indicated that, apart from being highly potent antihypertensive agents, calcium antagonists may also provide tissue protection and preservation. In three well defined clinical situations, the use of calcium antagonists has proved to be of value. First, in acute renal failure we and others have shown that the administration of dihydropyridine or diltiazem can, by preventing an intracellular calcium overload, avoid the renal damage induced by the use of a radiographic contrast agent. Second, in chronic renal failure, the administration of a calcium antagonist has been shown to be safe and at least similar in efficacy to other commonly used antihypertensive drug classes. Third, in renal transplant patients, calcium antagonists have been shown to prevent both acute and chronic cyclosporin nephrotoxicity. Calcium antagonists have a clear advantage in the case of acute toxicity because they allow faster renal function recovery and a shorter hospitalization time. The mechanisms by which this class reduces cyclosporin toxicity may be related to a reduction in the calcium influx into cells during ischaemic and reperfusion periods, which would reduce the generation of oxygen-free radicals and perhaps reduce thromboxane production. CONCLUSIONS: Calcium antagonists have potential renal protective effects that favour their use in many clinical situations where renal function is impaired.