Bioimpedance analysis is not superior to clinical assessment in determining hydration status: A prospective randomized-controlled trial in a Western dialysis population.

Introduction: Fluid management is an important goal of dialysis treatment. The accurate assessment of fluid status is still a challenge for clinical nephrologists. Bioimpedance analysis (BIA) has been proposed as an objective tool to assess hydration.

Psychosocial and physical outcome following kidney donation-a retrospective analysis.

Living renal donation is of benefit to the allograft recipient. Careful analysis of the donor outcome is necessary with respect to the medical condition, socioeconomic status, and health-related quality of life. All living kidney donors of the Transplant Center at Heidelberg were included.

Sustained low efficiency dialysis using a single-pass batch system in acute kidney injury - a randomized interventional trial: the REnal Replacement Therapy Study in Intensive Care Unit PatiEnts.

Introduction: Acute kidney injury (AKI) is associated with a high mortality of up to 60%. The mode of renal replacement therapy (intermittent versus continuous) has no impact on patient survival. Sustained low efficiency dialysis using a single-pass batch dialysis system (SLED-BD) has recently been introduced for the treatment of dialysis-dependent AKI.

Immunogenicity and efficacy in hemodialysis patients of an AS03(A)-adjuvanted vaccine for 2009 pandemic influenza A(H1N1): a nonrandomized trial.

Background: Hemodialysis patients have a reduced response to vaccinations because of uremia-related immune dysfunction. To increase the immunogenicity of vaccines, antigens can be formulated with adjuvants. The new tocopherol-containing adjuvant system AS03(A) has not been tested yet in patients with end-stage renal disease.

In renal transplants with delayed graft function chemokines and chemokine receptor expression predict long-term allograft function.

Background: Chronic loss of renal allograft function is associated with interstitial fibrosis and tubular atrophy (IF/TA). Independent of the underlying reason, one initial step in the development of fibrosis is chemokine-driven invasion of leukocytes from the blood vessels into the allograft. We studied the role of chemokines in kidney allografts with delayed graft function and the subsequent long-term outcome of renal function and fibrosis.

Proton pump inhibitors interfere with the immunosuppressive potency of mycophenolate mofetil.

Objectives: MMF is cleaved in the acidic milieu of the gastric compartment. However, its absorption might be impeded by proton pump inhibitors (PPIs), which suppress acid production and thus increase stomach pH. Since PPIs are widely used, it is useful to clarify whether the total drug amount of MMF is available in patients undergoing PPI treatment.

Uremia aggravates left ventricular remodeling after myocardial infarction.

Background: Renal failure is a well-established cardiovascular risk factor. We hypothesized that uremia negatively affects post-myocardial infarction (MI) remodeling and left ventricular (LV) function and examined the pathohistological correlations.

Methods: Subtotally nephrectomized rats (SNX) and controls with MI only (MIC) were examined 1, 4 and 8 weeks after MI.

Role of FTY720 on M1 and M2 macrophages, lymphocytes, and chemokines in 5/6 nephrectomized rats.

Renal injury is accompanied by the presence of infiltrating inflammatory cells in the glomerulus and tubulointerstitium. FTY720 modifies lymphocyte migration into injured tissues by lymphocyte sequestration to secondary lymphoid organs. The purpose of this study was to examine the potential of FTY720 to influence the inflammatory response in a nonimmunological model of renal failure.

Effect of insulin and glucose infusion on myocardial infarction size in uraemic rats.

The post myocardial infarction (MI) mortality rate is high in renal patients. One possible explanation is the reduced ischemia tolerance caused by uraemia. Previous investigations showed larger MI size in uraemic rats when compared with sham-operated controls.

Hypertension and antihypertensive treatment of diabetic nephropathy.

We are currently confronted with an epidemic of renal failure caused by diabetic nephropathy. It has become apparent that blood pressure is a major determinant of the risk of developing diabetic nephropathy; individuals with a genetic predisposition to hypertension are at increased risk of developing diabetes and diabetic nephropathy. Antihypertensive medication has an impact on development of diabetes; beyond blood-pressure lowering, the risk of diabetes is further reduced by blockade of the renin-angiotensin system (RAS).

Salt--a potential 'uremic toxin'?

It has been known for decades that salt (NaCl) determines extracellular volume as well as blood pressure and is one cause of hypertension. The difficulty to control the NaCl balance and thus treat sodium overload and hypertension in patients on dialysis has been recognized by Scribner in the early days of dialysis. In recent years, an impressive body of evidence has accumulated indicating that in essential hypertension, NaCl--blood pressure independently--causes target organ damage such as left ventricular hypertrophy, microalbuminuria, and increased aortic stiffness.

Role of calcium-phosphorous disorders in the progression of renal failure.

Among factors related to disturbed calcium-phosphate metabolism in chronic kidney disease, the following must be mainly considered as potential culprits in the progression of renal dysfunction: hyperphosphatemia, hyperparathyroidism, lack of active vitamin D, and possibly excess of the phosphaturic hormone FGF 23. Early experimental work suggested a parathyroid hormone (PTH)-independent beneficial role of phosphate restriction on progression in rats (animals with physiologic hyperphosphatemia), so that the generalization of the data is uncertain. Recent observational studies also found a correlation between S-phosphate and progression, but it remains uncertain whether the relationship is causal.

Pathophysiology of cardiovascular disease and renal failure.

This article discusses the epidemiology of cardiovascular (CV) events in end-stage and early renal disease, summarizes the profile of classic and nonclassic CV risk factors in renal patients, highlights recent evidence documenting accelerated atherogenesis in renal disease, and provides information on the central arteries and heart as target organs for CV damage in renal disease.

Hemodialysis--from early days to tomorrow.

The Nestor of chronic dialysis, Belding Scribner, was well aware of most problems which plague hemodialysis to this day, but the major problem we are confronted with today has emerged much later, i.e. excessive cardiovascular mortality.

Diabetic nephropathy: recent insights into the pathophysiology and the progression of diabetic nephropathy.

Diabetes has become the single most frequent comorbid condition in patients admitted for renal replacement therapy. This is the result of a greater prevalence of type 2 diabetes and better survival of diabetic patients. Progress has been made in pinpointing the predisposition to diabetes on metabolic abnormalities of muscle mitochondrial metabolism, but the long sought genes predisposing to diabetes and to diabetic nephropathy have not yet been identified.

Renal disease: value of functional magnetic resonance imaging with flow and perfusion measurements.

Purpose: To differentiate healthy kidneys from diseased kidneys, we propose a combined magnetic resonance (MR) examination that includes measurements of renal arterial blood flow and parenchymal perfusion.

Materials And Methods: A total of 130 kidneys (patients/healthy volunteers: 83/47) were examined using renal artery MR flow measurements and renal parenchymal perfusion measurements, as well as contrast-enhanced MR angiography. Cine phase-contrast-flow measurements were performed using an ECG-gated fast low angle shot pulse sequence; perfusion was measured with an arterial spin labeling flow-sensitive alternating inversion recovery technique.

Compelling drug indications in diabetic and nondiabetic nephropathy.

To halt progression of renal disease, the combination of several interventional strategies is recommended. The most important components comprise lowering of systolic blood pressure to approximately 120 mm Hg; providing pharmacologic blockade of the renin-angiotensin system by angiotensin-converting enzyme inhibitors or angiotensin receptor blockers; and reducing proteinuria to rates of less than 1 g/d.

Increased infarct size in uremic rats: reduced ischemia tolerance?

In patients with renal failure, myocardial infarction (MI) is more frequent and the rate of death from acute MI is very high. It has been argued that ischemia tolerance of the heart is reduced in uremia, but direct evidence for this hypothesis has not been provided. It was the purpose of this study (1) to ligate the left coronary artery and to measure the nonperfused area (risk area: total infarction plus penumbra) as well as the area of total infarction in subtotally nephrectomized (SNX) rats compared with sham-operated pair-fed control rats and (2) to examine the effects of potential confounders such as BP, sympathetic overactivity, and salt retention.

Angiotensin receptor antagonists in patients with nephropathy due to type 2 diabetes.

In the past few years diabetes has become the leading cause of end-stage renal disease in all Western countries. A correlation between blood pressure and rate of progression in diabetic nephropathy was noted very early, and increased local activity of the renin angiotensin system was identified as a major pathophysiological mechanism for proteinuria and nephrosclerosis in diabetic patients. Angiotensin converting enzyme (ACE) inhibitors have been shown to slow progression of nephropathy in type 1 diabetic patients.

Renal dysfunction as a cardiovascular risk factor.

Indices of altered renal function (eg, microalbuminuria, increased serum creatinine concentration, or decrease in estimated creatinine clearance, particularly overt proteinuria) are independent predictors of cardiovascular morbidity and mortality. These parameters should be routinely evaluated in the elderly and in high cardiovascular risk populations, particularly when hypertension is present. Hypertensive kidney damage should be prevented by early aggressive treatment of hypertensive patients with microalbuminuria.

Congestive heart failure due to systolic dysfunction: the Cinderella of cardiovascular management in dialysis patients.

Cardiac disease is common in dialysis patients. Survival is poorest in the subgroup with systolic dysfunction (pump failure). Audits show that cardiovascular management of dialysis patients in general, and treatment of congestive heart failure (CHF) specifically, is generally not in agreement with recommendations based on evidence obtained from controlled trials, admittedly in nonrenal patients.

Kidney and hypertension.

There is a unique relationship between the kidney and blood pressure (BP): on the one hand, renal dysfunction and particularly renal disease cause an increase in BP, while on the other hand, high BP accelerates loss of function of the diseased kidney. Transplantation studies, both in experimental animals and humans, documented that "blood pressure goes with the kidney," a normotensive recipient of a kidney genetically programmed for hypertension (HT) will develop HT, while conversely hypertensive patients with renal failure receiving the kidney of a normotensive donor may develop normotension. Family studies showed higher BP values and more frequent HT in first degree relatives of patients with primary glomerulonephritis or diabetic nephropathy, both type 1 and type 2.