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Abstract Background The explosion in availability of whole genome data provides the opportunity to build phylogenetic hypotheses based on these data as well as the ability to learn more about the genomes themselves. The biological history of genes and genomes can be investigated based on the taxomonic history provided by the phylogeny. A phylogenetic hypothesis based on complete genome data is presented for the genus Shewanella (Gammaproteobacteria: Alteromonadales: Shewanellaceae). Nineteen taxa from Shewanella (16 species and 3 additional strains of one species) as well as three outgroup species representing the genera Aeromonas (Gammaproteobacteria: Aeromonadales: Aeromonadaceae), Alteromonas (Gammaproteobacteria: Alteromonadales: Alteromonadaceae) and Colwellia (Gammaproteobacteria: Alteromonadales: Colwelliaceae) are included for a total of 22 taxa. Results Putatively homologous regions were found across unannotated genomes and tested with a phylogenetic analysis. Two genome-wide data-sets are considered, one including only those genomic regions for which all taxa are represented, which included 3,361,015 aligned nucleotide base-pairs (bp) and a second that additionally includes those regions present in only subsets of taxa, which totaled 12,456,624 aligned bp. Alignment columns in these large data-sets were then randomly sampled to create smaller data-sets. After the phylogenetic hypothesis was generated, genome annotations were projected onto the DNA sequence alignment to compare the historical hypothesis generated by the phylogeny with the functional hypothesis posited by annotation. Conclusions Individual phylogenetic analyses of the 243 locally co-linear genome regions all failed to recover the genome topology, but the smaller data-sets that were random samplings of the large concatenated alignments all produced the genome topology. It is shown that there is not a single orthologous copy of 16S rRNA across the taxon sampling included in this study and that the relationships among the multiple copies are consistent with 16S rRNA undergoing concerted evolution. Unannotated whole genome data can provide excellent raw material for generating hypotheses of historical homology, which can be tested with phylogenetic analysis and compared with hypotheses of gene function.

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., Methods: This was a prospective randomized controlled study to compare hydration status measured by clinical assessment compared to BIA using a body composition monitor (BCM). The primary outcome was defined as the decline of cardiac biomarker N-terminal pro brain natriuretic peptide (NT-proBNP) from baseline to the end of the study., Findings: About 281 chronic hemodialysis patients were assessed for eligibility, and 132 patients provided written informed consent to participate (65 BIA group, 67 clinical group). Predialytic NT-proBNP, and decline of NT-proBNP were similar in both groups. The amount of overhydration (2.18 ± 2.11 L vs. 1.29 ± 1.97 L; p 0.016) and the number of patients with severe overhydration (46.0% vs. 30.6%, p = 0.04) were significantly higher in the BIA group at the end of the study. Fluid accumulation in the interdialytic period was significantly lower in the clinical group (p = 0.013). Adverse events occurred more often in the BIA group (p = 0.032). The cumulative number of hypovolemic events was significantly higher in the BIA group (p = 0.002)., Discussion: Fluid management by BIA does not lead to a better cardiac outcome (appraised by surrogate markers) than fluid management by careful clinical assessment. Adapting the dry weight according to BIA results increases the risk of adverse events, especially hypovolemic episodes. Careful clinical fluid assessment is important for optimal care of chronic hemodialysis patients., (© 2021 The Authors. Hemodialysis International published by Wiley Periodicals LLC on behalf of International Society for Hemodialysis.)

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. Renal function and comorbidities were assessed. HRQoL and fatigue symptoms were determined by self-reporting validated test systems [Short-Form 36 (SF-36), Multidimensional Fatigue Inventory (MFI-20), Patient Health Questionnaire (PHQ)]. In total, 430 of 519 living renal donors were eligible to participate: 295 living donors (68.6%) provided informed consent (age at donation 49 ± 11 years) with a median time after donation of 77 (24-484) months. Renal function was lower compared with predonation (66 ± 15 ml/min vs. 88 ± 14 ml/min). Blood pressure remained stable (128 ± 14 mmHg vs. 129 ± 15 mmHg) with an increase of 56 donors receiving antihypertensive treatment (27.1% vs. 19%). The SF-36 physical component summary score was significantly better for both genders compared with the general population; the SF-36 mental component summary score was lower for female donors, caused by a reduced role functioning. Prevalence of fatigue was increased in female donors between the ages of 40 and 59 years. Renal function and blood pressure were as expected from previous studies. Concerning the psychosocial outcome, female donors might be at risk of impairments postdonation. Future evaluations will confirm and specify whether these results are necessary., (© 2015 Steunstichting ESOT.)

Background: The Hawaiian honeycreepers are an avian adaptive radiation containing many endangered and extinct species. They display a dramatic range of phenotypic variation and are a model system for studies of evolution, conservation, disease dynamics and population genetics. Development of a genome-scale resources for this group would augment the quality of research focusing on Hawaiian honeycreepers and facilitate comparative avian genomic research., Results: We assembled the genome sequence of a Hawaii amakihi (Hemignathus virens),and identified ~3.9 million single nucleotide polymorphisms (SNPs) in the genome. Using the amakihi genome as a reference, we also identified ~156,000 SNPs in RAD tag (restriction site associated DNA) sequencing of five honeycreeper species (palila [Loxioides bailleui], Nihoa finch [Telespiza ultima], iiwi [Vestiaria coccinea], apapane [Himatione sanguinea], and amakihi). SNPs are distributed throughout the amakihi genome, and the individual sequenced shows several large regions of low heterozygosity on chromosomes 1, 5, 6, 8 and 11. SNPs from RAD tag sequencing were also found throughout the genome but were found to be more densely located on microchromosomes, apparently a result of differential distribution of the particular site recognized by restriction enzyme BseXI., Conclusions: The amakihi genome sequence will be useful for comparative avian genomics research and provides a significant resource for studies in such areas as disease ecology, evolution, and conservation genetics. The genome sequences will enable mapping of transcriptome data for honeycreepers and comparison of gene sequences between avian taxa. Researchers will be able to use the large number of SNP markers to genotype honeycreepers in regions of interest or across the whole genome. There are enough markers to enable use of methods such as genome-wide association studies (GWAS) that will allow researchers to make connections between phenotypic diversity of honeycreepers and specific genetic variants. Genome-wide markers will also help resolve phylogenetic and population genetic questions in honeycreepers.

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. To date, however, only limited evidence is available in the comparison of SLED-BD versus continuous veno-venous hemofiltration (CVVH) in intensive care unit (ICU) patients with AKI., Methods: Prospective, randomized, interventional, clinical study at a surgical intensive care unit of a university hospital. Between 1 April 2006 and 31 January 2009, 232 AKI patients who underwent renal replacement therapy (RRT) were randomized in the study. Follow-up was assessed until 30 August 2009. Patients were either assigned to 12-h SLED-BD or to 24-h predilutional CVVH. Both therapies were performed at a blood flow of 100 to 120 ml/min., Results: 115 patients were treated with SLED-BD (total number of treatments n = 817) and 117 patients with CVVH (total number of treatments n = 877).The primary outcome measure, 90-day mortality, was similar between groups (SLED: 49.6% vs. CVVH: 55.6%, P = 0.43). Hemodynamic stability did not differ between SLED-BD and CVVH, whereas patients in the SLED-BD group had significantly fewer days of mechanical ventilation (17.7 ± 19.4 vs. 20.9 ± 19.8, P = 0.047) and fewer days in the ICU (19.6 ± 20.1 vs. 23.7 ± 21.9, P = 0.04). Patients treated with SLED needed fewer blood transfusions (1,375 ± 2,573 ml vs. 1,976 ± 3,316 ml, P = 0.02) and had a substantial reduction in nursing time spent for renal replacement therapy (P < 0.001) resulting in lower costs., Conclusions: SLED-BD was associated with reduced nursing time and lower costs compared to CVVH at similar outcomes. In the light of limited health care resources, SLED-BD offers an attractive alternative for the treatment of AKI in ICU patients., Trial Registration: ClinicalTrials.gov NCT00322530.

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., Study Design: Nonrandomized trial., Setting & Participants: 291 hemodialysis patients from 3 dialysis units co-operating with the Department of Nephrology at the University Hospital Heidelberg, Germany: 169 patients were vaccinated using either 1 (64 patients) or 2 doses (105 patients); 123 patients refused the vaccination and served as controls., Intervention: Intramuscular immunization with 3.75 μg of an inactivated split-virion A/California/7/2009 H1N1v pandemic vaccine adjuvanted with AS03(A) in a single- or double-dose regimen., Outcomes: A pandemic influenza A immunoglobulin G (IgG) enzyme-linked immunosorbent assay (ELISA) response >11 AU (arbitrary units) was defined as a positive response., Measurements: Quantitative antibody testing using the pandemic influenza A IgG ELISA. Antibody titers were tested 3 months after vaccination and compared with nonimmunized dialysis patients., Results: After vaccination against 2009 pandemic influenza A(H1N1), 41 of 64 (64.1%) patients with 1 vaccination and 93 of 105 (88.6%) with 2 vaccinations showed a protective immune response compared with 43 of 123 (34.9%) unvaccinated patients (P < 0.001). Logistic regression analysis confirmed vaccination dose as an independent factor for response to pandemic H1N1 vaccination. No episode of pandemic H1N1 illness occurred in any group within the study period of 6 months after vaccination. No serious adverse events occurred, and local symptoms ranged from mild to moderate in 143 of 169 (84.6%) patients., Limitations: Nonrandomized assignment; use of nontreated patients as controls; no comparison to nonadjuvanted vaccines; dose variation in the intervention group., Conclusions: Pandemic H1N1 vaccine adjuvanted with AS03(A) is immunogenic, effective, and safe in hemodialysis patients., (Copyright © 2011 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)

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., Methods: We examined repetitive biopsies of 30 patients without signs of acute rejection but with initially delayed graft function for IF/TA. In addition, we examined the expression of chemokine receptor (CCR)-1 and CCR2 on invaded leukocytes and macrophages and the corresponding ligands regulated upon activation, normal t-cell expressed, and secreted (RANTES) and monocyte chemotactic protein-1 on residential kidney cells., Results: The initial expression of CCR1 positive invading cells and RANTES in glomerular cells correlated with the allograft function 12 months after transplantation and at last follow-up. The expression was independent of donor characteristics such as age, gender, infectious state, cause of death, or use of vasopressive agents. Furthermore, it did not correlate with the duration of cold ischemia time. Among the patients with the most progressive loss of allograft function follow-up biopsy specimen did not reveal any signs of rejection but showed increased CCR1 and RANTES expression in the interstitium suggesting ongoing inflammation and fibrosis., Conclusion: An early expression of RANTES in renal allografts with delayed graft function with consecutive invasion of CCR1 positive cells seems to promote ongoing IF/TA and to worse renal allograft outcome.

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. MI size, ejection fraction (EF), cardiac fibrosis, vascular density and cardiomyocyte density were studied., Results: The extension of MI was 0.08 +/- 0.02 in SNX versus 0.06 +/- 0.02 in MIC rats (p < 0.031). Prior to MI, EF was comparable in SNX and MIC (74 +/- 3 vs. 72 +/- 2%, n.s.). Despite a relatively small infarct size EF in SNX decreased to 58 +/- 4% 1 week after infarction and progressively worsened to 51 +/- 4% after 8 weeks. In MIC animals EF only slightly decreased 1 week after MI (70 +/- 3%) and remained unchanged at follow-up. In SNX animals LV end-diastolic diameter continuously increased following MI throughout the study period indicating accelerated remodeling. Furthermore, accelerated myocardial fibrosis was already notable 1 week after MI in SNX animals and the volume density of capillaries and cardiomyocytes was significantly lower in SNX rats., Conclusion: MI in experimental uremia is associated with progressive impairment of LV function, LV dilatation and accelerated myocardial fibrosis., (Copyright 2010 S. Karger AG, Basel.)

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. Sham-operated and 5/6 nephrectomized (SNX) Sprague-Dawley rats received two different doses of FTY720 or vehicle orally for 14 wk. Treatment with FTY720 reduced glomerular and tubulointerstitial damage in SNX rats but failed to stabilize creatinine clearance. The increase in gene expression of chemokine receptors CCR1, CCR2, and CCR5 in kidneys of vehicle-treated SNX rats was significantly attenuated by high-dose FTY720. Treatment with high-dose FTY720 tended to normalize RANTES and MCP-1 renal gene expression. FTY720 affected not only glomerular and tubulointerstitial lymphocytes, but M1 and M2 phenotype macrophages were also reduced. FTY720 significantly reduced key mediators of renal inflammation and fibrosis. FTY720 also decreased immunoregulation of M2 macrophages, which are beneficial for tissue remodeling and repair.

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. To explore a possible link between uraemic insulin resistance syndrome and MI size in uraemia, we studied an intervention model with administration of insulin and glucose during acute MI in subtotally nephrectomized (SNX) rats and sham-operated controls. In 16 SNX rats and 16 sham-operated controls, the left coronary artery was ligated for 60 min, followed by reperfusion for 90 min. To visualize the perfused myocardium, lissamine-green ink was injected. The nonperfused area (lissamine exclusion) and the area of total infarction (TTC stain) were assessed in sections of the left ventricle (LV) using image analysis. While eight SNX rats and eight sham-operated controls were treated with a placebo during the procedure, the other animals received an insulin bolus of 85 mU/kg and then a continuous insulin infusion of 8 mU/kg per minute. Blood glucose levels were clamped to baseline levels with an infusion of 25% glucose. Insulin receptor substrates (IRS-1 and IRS-2) and glucose transporter (GLUT 4) were studied by western blot in another seven SNX and seven sham-operated controls without further intervention. The infarcted area, given as a proportion of the nonperfused risk area, was not different in sham-operated controls treated with a hyperinsulinaemic clamp versus untreated (0.55 +/- 0.07 vs. 0.51 +/- 0.13, p = 0.477). The eight SNX animals treated with the hyperinsulinaemic clamp utilized significantly less glucose to stabilize baseline glucose levels when compared with the sham-operated controls (5,637 vs. 3,207 microl Glc 25%, p = 0.007). The infarcted area was significantly lower in SNX rats treated with the hyperinsulinaemic clamp compared to non-treated SNX animals (0.56 +/- 0.06 vs. 0.79 +/- 0.09, p < 0.001). SNX rats with the insulin clamp had the same infarcted area size as sham-operated controls (0.56 +/- 0.06 vs. 0.51 +/- 0.13, p = 0.357). Western blotting did not show any change in the expression of GLUT 4 and IRS-1/IRS-2 in SNX animals when compared with sham-operated controls. The size of MI in uraemic rats is significantly reduced by a glucose/insulin infusion. The results suggest an insulin resistance in uraemic rats with similar benefits of glucose/insulin application during acute MI, as found in diabetic individuals. Further analysis did not reveal a down regulation in GLUT 4 and IRS-1/IRS-2.

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). In experimental studies, blockade of the RAS in the pre-diabetic stage ameliorates the severity of subsequent diabetic nephropathy. Guidelines recommend a target blood pressure of 130/80 mmHg for diabetic patients without proteinuria and some guidelines recommend a target of less than 125/175 mmHg for diabetic patients with proteinuria. Above a systolic blood pressure of approximately 110 mmHg, the risk of progression of diabetic nephropathy increases progressively with increasing blood pressure. Blood-pressure lowering and blockade of the RAS delays or prevents onset of microalbuminuria, slows worsening of microalbuminuria and attenuates progression of diabetic nephropathy, even in advanced stages. In addition to blood pressure, proteinuria is a treatment target and should be reduced to below 1 g/24 h.

Acute renal failure in critically ill patients in the intensive care unit is associated with high morbidity and mortality which is independent of the underlying etiology. Despite improvements in intensive care medicine and renal replacement therapy, patients with acute renal failure have much higher morbidity and mortality rates than patients without acute renal failure in the intensive care unit. In this overview, we summarize the literature on the incidence and mortality of patients with acute renal failure in the intensive care unit. Furthermore, we discuss timing of the initiation of renal replacement therapy, patient outcome with different renal replacement therapies and the adequate dialysis dose to be delivered.

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. It has further been recognized that NaCl increases oxidative stress and, again blood pressure independently, amplifies tissue injury induced by aldosterone. In renal damage models, progression is dramatically accelerated by high NaCl intake. Sodium as a potential culprit in progression to target organ damage in terminal renal failure has not been well investigated so far. However, it is possible, and indeed likely, that sodium plays an adverse role in the genesis of target organ damage in terminal renal failure., (Copyright 2006 S. Karger AG, Basel.)

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. There is very little direct experimental or clinical evidence for a role of PTH in accelerating progression, although the PTH1 receptor is expressed in podocytes and PTH affects podocyte function (i.e., Kf). It is undoubtedly a candidate that requires more sophisticated investigation. Recently, it has been shown that progression is significantly attenuated by calcimimetics (and equally by parathyroidectomy), but it is currently impossible to exclude a confounding effect of lower blood pressure values. The most solid evidence for an impact on progression exists for active vitamin D. In the past, it was widely assumed that vitamin D was "nephrotoxic." In retrospect, nephrotoxicity was the result of hypercalcemia. Recent evidence is overwhelming that 1,25(OH)2D3 and its analogues attenuate progression in noninflammatory and inflammatory models of chronic kidney disease. The main target cells identified so far are podocytes and mesangial cells. It is currently unknown whether the novel phosphaturic hormones have an impact on progression.

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.

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. Of great concern are experimental studies documenting that maternal hyperglycemia causes nephron underdosing in the offspring. Relevant to pathogenesis and treatment of diabetic nephropathy are, among others, recent insights that hyperglycemia sensitizes target organs to blood pressure-induced damage, and that local renin-angiotensin systems play an important role in genesis and progression of diabetic nephropathy.

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. Contrast-enhanced MR angiography was performed with a fast 3D gradient echo sequence in a single breath hold. For evaluation, kidneys were divided into groups based on nephrologic diagnosis of the patient. Recursive partitioning and Wilcoxon rank-sum tests were used to separate the different groups., Results: Significant differences in mean renal artery flow and parenchymal perfusion were found in kidneys with renal artery stenosis as well as parenchymal disease as compared with healthy kidneys. Using a classification tree derived from the recursive partitioning, a specificity of 99% and sensitivity of 69% with a positive/negative predictive value of 97%/84% was achieved for the separation of healthy kidneys from kidneys with vascular, parenchymal or combined disease. The overall accuracy was 88%., Conclusion: The combination of cine PC flow measurements and MR perfusion measurements offers a comprehensive assessment of both renovascular and renoparenchymal disease and provide a noninvasive approach to differentiate between these kidneys and normal kidneys.

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.

History: A 22 year old patient had noted progressive flank pain without recognizable urinary abnormalities for five days., Investigations: A urologist had noted increased serum creatine (2.1 mg/dl), hypertension (180/100 mmHg) and microhematuria. A post-renal cause was excluded by excretory urography. An interview revealed that the patient had consumed cocaine on weekends since age 19; the acute episode was preceded by a rave party with consumption of a total of 3 g of street quality cocaine., Diagnosis and Treatment: Because of microhematuria with a suggestive nephritic urinary sediment, the patient underwent renal biopsy. It showed acute tubular necrosis and interstitial edema, but no signs of glomerulonephritis and negative immunohistology. The patient received antihypertensive treatment. This led to rapid reversal of elevated serum creatinine and microhematuria was noted, but hypertension persisted. Currently the patient receives ACE inhibitors., Conclusion: Similar to what is seen in the US, cocaine use has to be considered in the differential diagnosis of acute renal failure with hypertension.

With current immunosuppression elevated blood pressure is found in almost 90% of renal graft recipients. Major causes of this finding are impairment of renal function, secondary to chronic allograft nephropathy or (less frequently) recurrence of primary renal disease, the use of calcineurin inhibitors as immunosuppresants, uncontrolled renin secretion by the shrunken kidneys of the recipient, stenos- ing lesions of the transplant artery (or the upstream arteries of the recipient), polycytemia and (genetic predisposition to) hypertension of the graft donor. Even minor degrees of blood pressure elevation have a significant impact on survival of the recipient and on graft survival, presumably by amplifying vascular injury to the graft. In this respect, elevation of systolic blood pressure and an abnormal circadian blood pressure profile are of particular relevance. In contrast to previous opinion, ACE inhibitors are indicated in the treatment, but, given the causal role of sodium retention in graft vasoconstriction, diuretics and calcium channel blockers remain main stays of antihypertensive treatment in the renal allograft recipient.

The examination of renal function in the daily practice may give important information on the risk status of a given patient. For example, the diagnosis of microalbuminuria carries high predictive value for a future cardiovascular risk of patients with hypertension, diabetes, congestive heart failure, as well as myocardial infarction. The findings of the Hypertension and Diabetes Screening and Awareness Study (HYDRA) indicate that screening for microalbuminuria is performed not often enough in patients with diabetes or hypertension, respectively, and a positive screening finding often does not trigger necessary consequences as for additional diagnosis or therapy.