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The use of conventional intermittent hemodialysis (IHD) represents a mainstay of supportive care of patients with acute kidney injury (AKI). However, a number of fundamental questions regarding the optimal management of IHD remain unanswered after more than six decades of renal replacement therapy (RRT). This review summarizes current evidence regarding the timing of initiation of intermittent hemodialysis, the comparative outcomes (mortality and recovery of renal function), the prescription of the intensity of this therapy and discontinuation of dialysis. The way conventional IHD is performed has an impact on the outcome of sick patients with AKI. The value of regular education and training of those who provide IHD cannot be emphasized enough. However, we must be realistic in our expectations that no mode of RRT per se will substantially alter the excessive mortality of critically ill-patients with AKI.

Acute kidney injury (AKI) secondary to acute tubular necrosis (ATN) is common in critically ill patients, and causes significant morbidity and mortality. The underlying etiology of ATN can be divided into pure ischemic, pure nephrotoxic, and mixed causes. This post-hoc analysis of a prospective cohort study aimed to investigate whether the cause (pure vs. mixed) of ATN affects the short- and long-term outcome of critically-ill patients. A total of 425 critically-ill patients with AKI secondary to clinically diagnosed ATN were divided into three groups according to the cause of ATN. Of these patients, 215 had mixed ATN, 203 had pure ischemic ATN, and seven had pure nephrotoxic ATN. All patients had one episode of AKI only. No patient had pre-existing chronic kidney disease. Patients were followed throughout their hospital stay (mortality rate, recovery of renal function at discharge) and up to 7 years thereafter. The three patient groups differed in their demographic and clinical characteristics. The in-hospital mortality rates were 55% in the presumably mixed-cause ATN group, 39% in the pure ischemic group, and 29% in the pure nephrotoxic group. Complete renal recovery at discharge was documented in five out of five surviving patients with nephrotoxic ATN (100%) and in 92 out of 124 surviving patients with pure ischemic ATN (74%), but only in 29 out of 97 patients with mixed ATN (30%). None of the surviving patients was lost during the 7-year follow-up. At the end of the observation period, 60% of the survivors of pure ATN, compared with 22% of the survivors of mixed ATN, were alive. After 7 years, 6% of the living patients with pure ATN had mild-to-moderate chronic kidney disease, whereas 38% of the mixed group patients had advanced CKD or end-stage renal disease. The cause of presumed ATN has a profound impact on short- as well as long-term outcomes of critically-ill patients with AKI requiring renal replacement therapy. The challenge for intensivists is to avoid further injury to the kidneys of these patients.

Acute kidney injury plays a pivotal role in intensive care medicine and exerts crucial adverse effects on the course of the disease and overall prognosis of the critically ill patient. Intensive renal support, including initiation of earlier dialysis or maximal uremic toxin removal by higher dosage and frequency of renal replacement therapy, and individualized selection of modality were not able to decrease excessive mortality in this population. Systemic acute inflammation, mediated, at least in part, by cytokines, and not secondary uremic side effects, seems to have a major impact on nonrenal organ damage. Assessment of short-term outcome in critically ill patients who develop acute kidney injury may underestimate the true burden of disease. The overall survival at 5 years in patients discharged alive after severe acute kidney injury necessitating renal replacement therapy is only 20-30%, comparable to cancer patients. In addition, acute renal damage was identified as an independent risk factor for progression of chronic renal insufficiency. Current research focuses on strategies for the prevention of acute kidney injury and on the establishment of effective biomarkers for the early recognition and accurate diagnosis of subclinical renal damage.

Zwei Epi so den ei ner aku ten He pa ti tis C mit un ter schied li chen Ge no ty pen bei ei nem auf Peg in ter fe ron-Mo no the ra pie an spre chen den Dia ly se pa tien ten Wir be rich ten uber den Fall ei nes 63-jah ri gen Lang zeit dia ly se pa tien ten, der zwei auf ein and er fol gen de Epi so den ei ner He pa ti tis C-Vi rus-In fek tion mit un ter schied li chen Ge no ty pen er litt und in bei den Fal len er folg reich durch eine Mo no the ra pie mit pe gy lier tem IFN-a be han delt wer den konn te.

We report the case of a 63-year-old male patient on long-term hemodialysis who suffered two consecutive episodes of persistent hepatitis C virus infection with different genotypes and was successfully treated with pegylated IFN-alpha monotherapy each time.

Ein wichtiges Problem der Nierenersatztherapie ist die prinzipielle Bioinkompatibilitat: Die Materalien der Dialysebehandlung werden vom Organismus als fremd angesehen und fuhren zu komplexen Interaktionen mit negativer Auswirkung, die sowohl vom jeweiligen Verfahren als auch vom jeweiligen Patienten abhangen. Bei der extrakorporalen Nierenersatztherapie, der Hamodialyse, hangt diese Interaktion hauptsachlich von der Dialysemembran ab, bei der intrakoporalen Nierenersatztherapie, der Peritonealdialyse, von den Dialyselosungen und deren Einwirkung auf die Peritonealmembran sowie von lokalen Abwehrmechanismen. Ziel der vorliegenden Arbeit ist, die Mechanismen der Bioinkompatibilitat detailliert aufzuzeigen und Wege zu weisen, um eine grostmogliche Biokompatibilitat zu erreichen. Dazu sind viele Schritte erforderlich, von denen allerdings schon manche getan sind. Unubersehbar ist aber die Tatsache, das es diesbezuglich noch viele ungelosten Probleme gibt.

The purpose of this study was to characterize the changes in noradrenergic blood pressure regulation and the causes of this dysregulation in patients with histologically proven primary hyperparathyroidism before and after parathyroidectomy. In untreated hypertensive patients with primary hyperparathyroidism slightly higher plasma levels of norepinephrine, enhanced cardiovascular reactivity to norepinephrine (p0.05) and increased cytosolic free calcium concentration in platelets (p0.05) were found. Parathyroidectomy resulted in the correction of noradrenergic blood pressure dysregulation and in the reduction of cytosolic free calcium and led to normotension. In vitro incubation of platelets from normal subjects with heterologous plasma ultrafiltrates from either hypertensive patients with primary hyperparathyroidism or normotensive uremic patients with secondary hyperparathyroidism led to raised platelet calcium in primary hyperparathyroidism but not in secondary hyperparathyroidism, although in both conditions intact parathormone levels were elevated equally. Furthermore, when platelets of normotensive subjects were preincubated with commercially available parathormone, no effect on resting platelet cytosolic calcium was observed. Our results suggest that hypertension in primary hyperparathyroidism may be caused in part by noradrenergic blood pressure dysregulation and seems to be causally linked to the secretion of a parathyroid hypertensive factor, which increases cytosolic calcium and alters vascular tone and reactivity.

Introduction Current assessments of renal function by serum creatinine or blood urea nitrogen display poor sensitivity and specificity for indicating early changes in kidney function and do not differentiate between causes of acute kidney injury (AKI). The discovery, characterization and validation of novel biomarkers specific for structural kidney damage, such as neutrophil gelatinaseassociated lipocalin, kidney injury molecule-1, interleukin-18 and liver fatty acid binding protein enable a timely diagnosis of AKI through better reflection of real-time damage of AKI, promise discrimination of the underlying aetiology and may enable incremental risk identification for worsening AKI, need of renal replacement and death. However, case-mix, comorbidities, aetiology of the renal insult, timing of measurements and selected thresholds for diagnosis influence the performance of these novel biomarkers. Additional studies are necessary before novel biomarkers can be used in routine clinical practice. To answer the question of how to optimally utilize novel biomarkers (the right test, at the right time, on the right patient, for the right clinical setting of AKI) all promising AKI biomarkers should undergo systematic evaluation in various clinical setting of AKI in order to validate the temporal expression patterns of these biomarkers for early detection of AKI, to determine how to combine multiple biomarkers for earlier diagnosis and to discover how the temporal course relates to onset, severity and outcome of AKI. There is a vital need that large future investigations demonstrate the association between biomarkers and hard clinical outcomes independent of serum creatinine concentrations. It needs to be shown that early renoprotective treatment for AKI based on high biomarker levels actually results in an improved outcome. The aim of this review is to discuss early diagnosis of acute kidney injury in critically ill patients by novel biomarkers. Conclusion Until effective renoprotective therapies are available, there is little benefit from early diagnosis of AKI during critical illness. Introduction Acute kidney injury in the intensive care setting (ICU AKI) is a complex disorder with multiple aetiologies and risk factors, various clinical presentations and unpredictable outcomes. Various combinations of ischemic, septic and nephrotoxic effects are the main causes of hospitalacquired AKI in critically ill patients. Today, ICU AKI is often found in the setting of multiple organ failure and occurs rarely as single organ dysfunction. In general, the incidence of hospital-acquired AKI is increasing as physicians subject an increasingly aged patient population to major surgery, aggressive medical therapeutics and extended radiologic interventions. AKI is widespread and occurs in up to 18% of all hospital admissions with reports of up to 67% in critically ill patients in the ICU. ICU AKI represents a continuum of morbidity that can vary from subclinical injury, in which serum creatinine changes minimally, to severe oligoanuric kidney failure requiring renal replacement therapy (up to 4–6%)1. The diagnosis of AKI has a significant negative impact on the prognosis of critically ill patients and is associated with a poor shortand long-term outcome. Recently, it has been recognized that kidney function does not completely recover in many patients and that AKI represents an antecedent to the development to chronic kidney failure, particularly in patients with preexisting chronic kidney disease2. Even the mildest forms of AKI are independently associated with increased, early as well as late, mortality, and the risk increases in the wake of increasingly severe renal injury1. Current management of ICU AKI is restricted to supportive care. Reports on specific pharmacologic interventions to treat established AKI showed minimal effects, if any. The attributable mortality of hospital-acquired AKI, however, remains distressingly high (up to 70%), despite numerous advances in intensive care medicine and renal replacement therapy1. This review discusses targeted renoprotection used in earlier diagnosis of acute kidney injury in critically ill patients. * Corresponding author Email: h-schiffl@t-online.de 1 Department of Internal Medicine IV, University Hospital Munich, University of Munich, Munich, Germany 2 Medizinische Klinik, SRH Wald-Klinikum Gera, Gera, Germany A na es th es io lo gy , P er io pe ra tiv e & Cr iti ca l C ar e M ed ic in e

Acute kidney injury plays a pivotal role in intensive care medicine and exerts crucial adverse effects on the course of the disease and overall prognosis of the critically ill patient. Intensive renal support, including initiation of earlier dialysis or maximal uremic toxin removal by higher dosage and frequency of renal replacement therapy, and individualized selection of modality were not able to decrease excessive mortality in this population. Systemic acute inflammation, mediated, at least in part, by cytokines, and not secondary uremic side effects, seems to have a major impact on nonrenal organ damage. Assessment of short-term outcome in critically ill patients who develop acute kidney injury may underestimate the true burden of disease. The overall survival at 5 years in patients discharged alive after severe acute kidney injury necessitating renal replacement therapy is only 20-30%, comparable to cancer patients. In addition, acute renal damage was identified as an independent risk factor for progression of chronic renal insufficiency. Current research focuses on strategies for the prevention of acute kidney injury and on the establishment of effective biomarkers for the early recognition and accurate diagnosis of subclinical renal damage.

A 36-year-old patient suffered from repeated exsudative pleural effusions and renal insufficiency (serum creatinine 1.9 mg/dl) combined with glomerular erythrocyturia, proteinuria and renal hypertension.The diagnosis of the underlying etiology of the pleural effusions was difficult in spite of a thorough diagnostic work-up. Pleural tuberculosis was finally detected by an interferon gamma release assay (IGRA). Kidney biopsy revealed mesangioproliferative glomerulonephritis, immunhistology showed mesangial IgA deposits. Renal insufficiency did not progress when blood pressure control was achieved.The pleural effusions resolved permanently when antituberculous treatment was begun. Eight weeks after initiation of therapy normalization of kidney function (eGFR75 ml/min), resolution of hematuria and reduction of proteinuria were observed.This report of a partial remission of IgA nephropathy by treatment of pleural tuberculosis supports the hypothesis that there may be a causal relationship between mycobacterial infections and IgA nephropathy.

Efficient removal of total body burden beta 2-Microglobulin (beta 2-M) in uremia is a continuing challenge, as dialysis-related amyloidosis represents a major complication of chronic renal replacement therapy. To investigate long-term beta 2-M removal we studied 3 groups of stable end-staged renal failure patients over a period of 4 years; we compared low flux (cuprophane) hemodialysis (n = 12), high flux (polysulfone) hemodialysis (n = 12) and hemofiltration using high flux polysulfone (n = 8). In contrast to the cuprophane membrane, the polysulfone membrane eliminated considerable amounts of beta 2-M. This was associated with a sustained reduction of predialysis serum beta 2-M-levels (by 20%). Compared with high flux hemodialysis, hemofiltration provided a 50% higher elimination of beta 2-M. Thus, our long-term evaluation of beta 2-M removal suggests that hemofiltration rather than hemodialysis may be the treatment of choice for delaying the incidence of dialysis-related amyloidosis.

Acute kidney injury is common in hospitalized patients and is associated with significant in-hospital morbidity and mortality. However, hospital-acquired acute kidney injury is neither a harmless complication of severe underlying diseases nor a life threatening short-term illness. Posthospital discharge follow-up of patients highlights that survivors of acute kidney injury may develop serious long-term sequelae. Long-term mortality is greater in those patients who survived acute kidney injury when compared with critically or non-critically ill patients without acute kidney injury. Among survivors of acute kidney injury at long-term follow-up approximately 12.5% may be dialysis dependent and 19-31% may have chronic kidney disease. The incidence of end-stage renal disease secondary to acute kidney injury will likely continue to increase with more elderly patients treated in Intensive Care Units, with a higher burden of extra renal and renal comorbid diseases. Nephrologists should recognize acute kidney injury as an underestimated cause of chronic kidney disease and patients who survive with incomplete recovery should be followed closely for new chronic kidney disease or progression of pre-existing chronic kidney disease. Non-recovery or re-need for dialysis are not only important determinants of long-term health status, quality of life and mortality of these patients, but add also a burden to health resources.

Recovery of renal function after acute renal injury is an important clinical determinant of patient morbidity and mortality. However, studies covering this field are scarce and nonhomogeneous.Despite success in animal models, translation of current pharmacologic strategies to limit the extent of kidney dysfunction or to hasten renal recovery from acute kidney injury (AKI) in human studies has failed. Renal replacement therapy is the mainstay of supportive care in patients with AKI. However, its performance can have untoward effects that contribute to the prolongation of the course of AKI or impede the ultimate recovery of complete renal function. Use of biocompatible membranes, daily hemodialysis, advanced intermittent hemodialysis (IHD) technology or continuous RRT (CRRT) have been coupled with shortened renal recovery after AKI. Rate of renal recovery to RRT independence is variable when judged at hospital discharge. The frequency of end-stage renal disease in survivors from AKI is highest in severe acute parenchymal renal disease and lowest in acute tubular necrosis (ATN). Renal recovery is less likely in patients with preexisting renal disease. Renal recovery at hospital discharge may underestimate the true rate of renal recovery. The overwhelming majority of patients (more than 85 %) with severe ATN precipitating on normal renal function recover and maintain complete renal function or any degree of chronic renal functional impairment within 6-12 months after AKI. Partial or nonrecovery of renal function represents an independent predictor of long-term mortality for survivors from AKI. Re-need for RRT occurs in a small portion of survivors of severe ATN (less than 5%).Severe AKI necessitating RRT should no longer simply be viewed as just an acute reversible complication of critical illness or short-term illness. Persistent reduction in renal function will exhibit independent effects on patient survival that extends well beyond discharge from the hospital.

Haemodialysis (HD) patients with meticillin-resistant Staphylococcus aureus (MRSA) infections face high morbidity and mortality. Nasal carriage of Staphylococcus aureus is known to play an important role as an endogenous source for HD-access-related infections that contribute significantly to morbidity, mortality and cost of end-stage renal disease (ESRD) management. This prospective investigation in regular out-clinic haemodialysis patients was undertaken to estimate the prevalence of S.aureus nasal carriage, to define patient groups at risk and to evaluate the effect of elimination on outcomes among outclinic haemodialysis patients.136 HD patients without signs of overt clinical infection (48 women, 88 men, age 22-88 years) were screened at least twice for the nasal carriage for meticillin-susceptible SA (MSSA) or meticillin-resistant SA (MRSA). Nasal carriage of S. aureus was related to demographic (age, gender, duration on HD), comorbidity (diabetes, malignancy) and exposure to health care (dialysis staff, hospitalisation). Nasal carriers for MRSA received standardized mupirocin therapy and were followed up for elimination and infections for 1 year.The prevalence of nasal carriage for staphylococcus aureus was 53 % (41 % MSSA, 12 % MRSA). Compared with patients showing no colonization or with MSSA carriers, the 16 patients with nasal carriage for MRSA were older and more likely to have acquired the bacteria while hospitalised. Genotyping of MRSA isolates revealed different strains in patients and care-providers. Mupirocin eliminated MRSA in all patients, none of these patients experienced an infection caused by staphylococcus aureus, confirming the known value of MRSA elimination from other studies.Elderly patients hospitalised for surgery constitute a high risk group for nasal carriage for MRSA. Early diagnosis may help prevent clinically relevant infection. Elimination of colonization by mupirocin appears to be an attractive preventive strategy.

The residual uraemic syndrome that is inadequately cleared by diffusion is thought to contribute to the poor outcome of maintenance dialysis patients. Haemodiafiltration combines diffusion and convection in a single therapy, conferring theoretical benefits over haemodialysis. However, only few randomised comparisons have been carried out.The prospective crossover clinical evaluation of high-flux ultrapure haemodialysis and online haemodiafiltration included 76 clinically stable patients on low-flux conventional bicarbonate buffered haemodialysis. They were randomized to high-flux haemodialysis or online haemodiafiltration (24 months) and switched to the alternative treatment (24 months).Removal of urea (Kt/V) and phosphate was significantly greater for online haemodiafiltration than for haemodialysis. Both high-flux haemodialysis and haemodiafiltration were associated with sustained reductions of pretreatment beta 2 microglobulin levels, however, the decrease was greater with haemodiafiltration. Both modes of renal replacement therapy significantly improved nutritional status and the haematopoietic response to rHu EPO. Under unmatched conditions (sodium and energy balance) haemodiafiltration was associated with a lower number of hypotensive episodes and partial improvement of quality of life. The incidence of death was low in both groups and did not differ among the two modes of renal replacement therapy.Online haemodiafiltration is a safe, effective and well tolerated therapy for end-stage renal disease patients even in the long run. Whether the dismal mortality rates of unselected end-stage renal disease patients can be changed by online haemodiafiltration remains to be shown in large scale long-term trials.

Acute renal failure (ARF) is associated with poor clinical outcome, particularly in critically ill patients. Different renal replacement techniques are available for treatment of ARF, but a general consensus of standardization of treatment dose is lacking. Recent prospective investigations in critically ill patients with ARF utilizing either intermittent or continuous renal replacement therapy established a clear dose-outcome relationship. However, several surveys of current practices of renal replacement therapy dosing in acute renal failure revealed, that the majority of ICU patients with ARF received dialysis doses lower than prescribed for stable end-stage renal disease patients. Most nephrologists did not perform formal dose calculation. Future patterns of dosing renal replacement therapy should focus both on an earlier start and a higher dose to reduce the excess mortality associated with ARF in critically ill patients.

A 19-year-old patient on chronic ambulatory peritoneal dialysis experienced severe neurologic disturbances caused by uremia. Increased signal intensity was seen bilaterally in the cortical and subcortical areas of the occipital and parietal lobe on cranial magnetic resonance imaging (MRI). Insufficient peritoneal dialysis efficacy was documented and the patient was switched from peritoneal to hemodialysis. Cranial MRI indicated a marked regression of the lesions to nearly normal, confirming the diagnosis of uremic encephalopathy.

Peripheral polyneuropathies associated with monoclonal IgM gammopathy of undetermined significance often have a progressive course and optimal treatment has not been established. We report on a patient diagnosed with polyneuropathy associated with benign IgM gammopathy, who was successfully treated with antibody-based immunoadsorption only. The neurological symptoms of the patient improved continuously over six months of treatment. Controlled trials should be performed to define this indication for antibody-based immunoadsorption therapy.

Stark vereinfacht last sich den wenigen, nicht pathognomonischen Leitsymptomen das prinzipiell mogliche Spektrum wichtiger, erworbener, nephrologischer Krankheitsbilder gegenuberstellen: Glomerulonephritiden (GN), tubulointerstitielle Nierenkrankheiten (TIN), akute Niereninsuffizienz, chronische Niereninsuffizienz.

In May 1984 a 58-year-old woman presented with a broad spectrum of clinical symptoms including malaise, arthralgia, hemoptysis and dyspnea, proteinuria and hematuria and a vasculitic necrotizing rash. Bronchial biopsies revealed subglottic granulomatous lesions and renal biopsies showed necrosis, extracapillary proliferation and crest formation, confirming the diagnosis of Wegener granulomatosis. Positive c-ANCA and anti-proteinase 3 subfraction (anti-PR3) titers were first analysed in 1991. Clinical remission was achieved by standard immunosuppressive therapy and renal function was stabilised. Several minor relapses were treated with pulsed intravenous cyclophosphamide but the symptoms could not be completely controlled. Eight years after the onset of disease, a dramatic increase in anti-PR3 titers was observed (34438 U/ml, normal range10, ELISA), followed 3 months later by a clinically apparent relapse. Immunosuppressive therapy was reinstituted without clinical improvement. At this point plasmapheresis resulted in an amelioration of clinical symptoms as well as a reduction in anti-PR3 titers. Concomitant immunosuppressive therapy was administered with oral corticosteroids. Forty days later anti-PR3 titers increased, reaching 75000 U/ml twelve months later, however this time without associated clinical symptoms. During the following months the patient had a further transient deterioration of pulmonary and renal function due to secondary bacterial infection which was successfully treated with antibiotics. A nephritic sediment was not present during these episodes. Curiously, the anti-PR3 titers have remained excessively elevated for the last three years.

Hypertension complicating the therapy of renal anemia with rHU-EPO is characterized by an increase in total peripheral vascular resistance, but the mechanisms underlying arteriolar vasoconstriction remain unclear. To assess the role of altered cellular calcium metabolism, resting platelet cytosolic calcium was measured in 12 previously normotensive patients with end-stage renal disease before and after 12 weeks of EPO-therapy, after 12 weeks of combined antihypertensive pharmacotherapy of EPO-induced hypertension, and after 12 weeks of concurrent administration of EPO and indomethacin. Patients with EPO-induced hypertension showed a significant raise in platelet calcium by comparison with calcium levels prior to EPO (179 +/- 15 vs 120 +/- 8 nmol/l), and there was a positive correlation between their blood pressure and platelet calcium levels (r = 0.9, p0.001). Antihypertensive therapy of EPO-induced hypertension resulted in a reduction of blood pressure and a reduction of platelet calcium to near normal levels (128 +/- 6 nmol/l). The non-steroidal antiinflammatory drug indomethacin prevented EPO-induced hypertension and EPO-associated alterations in platelet calcium. The results of the present study suggest that EPO-induced hypertension might be related to altered cellular calcium homeostasis. If EPO therapy induces alterations in calcium metabolism not only in platelets but also in vascular smooth muscle cells, these changes in calcium influx may contribute to arteriolar vasoconstriction during EPO therapy.

BACKGROUND AND OBJECTIVE OF STUDY: Continuous ambulatory peritoneal dialysis (CAPD) still plays a minor role in Germany compared with haemodialysis (HD) in the management of terminal renal failure. An investigation was undertaken to compare mortality rate, change of dialysing method as well as number and duration of hospital stays of patient undergoing CAPD or HD at a nephrological centre.All 166 patients in terminal renal failure (except those with a malignancy) admitted between January 1987 and December 1992 were included (63 women and 103 men, aged 19-84 years). The choice between the two dialysis methods was made by the patients after detailed information had been given. Taking into account basic disease and any secondary illness as well as age and sex, survival time, any change of dialysing method and hospitalisation details were prospectively analysed for the two dialysing methods.After 4 years there were no significant differences in mortality rate between the two methods (HD 37%, CAPD 29%). The Cox model revealed no influence of various parameters on the mortality rate of the two methods. However, cumulative patients survival was significantly decreased by arterio-sclerotic disease (P0.05; probability of survival after 4 years was 53% and 73%, respectively, for HD and 57% and 77% for CAPD). Similarly, ageor = 60 years at onset of dialysis significantly lowered probability of survival (after 4 years of dialysis, 53% vs 70% for HD, 45% vs 80% for CAPD: P0.05). But there were no significant differences between the two methods with respect to these two factors. After 4 years, "method survival" was more common with HD (94%) than CAPD (64%), P0.05). In particular diabetics had a significantly lower "method survival" after 4 years than non-diabetics (29% vs 74%). There was no significant difference between the two methods regarding number and duration of hospital stays.These data show that, in a nephrological centre with long experience in both methods of dialysis, CAPD is an equal alternative to HD.

Abnormal salt metabolism plays a central role in the pathogenesis of hypertension caused by early-stage renal disease. The mechanisms by which alterations in salt balance and the vasoconstrictor state are related are unclear. We studied the effects of three different salt diets (3, 6-9 and 12 g sodium chloride) on cellular ion homeostasis in platelets in 20 patients with renal hypertension. Compared to normal subjects, patients with renal hypertension had raised cytosolic sodium and calcium concentrations. The platelet sodium pump activity was significantly depressed and calcium ATPase activity increased. These abnormalities of cellular ion metabolism were aggravated by salt overload. On the other hand, dietary salt restriction tended to normalise these parameters. The data presented indicate that a circulating inhibitor of the sodium pump plays a central role in the pathogenesis of salt-induced renal hypertension and that the final common pathway of hypertension secondary to early-stage parenchymal renal disease is an elevation of resting cytosolic calcium followed by an elevation of peripheral vascular resistance.

Since intermittent hemodialysis was first used systemically during the Korean war, the mortality of acute renal failure (ARF) in critically ill patients has remained high (or 50%). The lack of improvement may be a result of better resuscitation techniques and intensive care management that allow more severely ill patients to survive long enough to develop ARF. The concept that those patients with ARF die with, but not of, renal failure was challenged recently by the results of three prospective randomized trials. Each tested the hypothesis that the course of ARF and the fate of critically ill patients may be affected adversely by bioincompatibility reactions due to the dialysis membrane used (activation of complement and neutrophils). Schiffl and colleagues were the first to publish a full report on the results of their investigation comparing bioincompatible cuprophane (CUP) and biocompatible acrylonitrile AN 69 (Hospal, Lyon, France) membranes in 52 patients with ARF following cardiovascular surgery. The AN 69 group had a lower death rate (38% vs. 65%, p = 0.052), a lower proportion of patients dying from Gram-negative sepsis (40% vs. 71%, p = 0.0162), and an improved recovery of renal function. A similar trial comparing the use of CUP with biocompatible polymethyl-methacrylate (PMMA) was performed in 72 patients with medical categories of ARF. Again, the use of a biocompatible membrane resulted in an improved survival rate (57% vs. 37%, p = 0.11) and better recovery of renal function (62% vs. 37%, p = 0.04). Of the 20 patients in each group who initially had nonoliguric ARF, the survival rates were 80% with PMMA and 40% with CUP (p = 0.01). The preliminary results of another multicenter study including 121 patients dialyzed with either bioincompatible cellulosic membranes or PMMA or polysulfone membranes seem to confirm these findings. The management of critically ill patients is sophisticated and expensive. The use of biocompatible membranes adds little to the overall costs and appears to be justified.

In spite of considerable technical advances and improved treatment strategies, the outcome of complicated acute renal failure remains depressively poor. Two main factors contribute to this apparent lack of improvement: 1) the increased number of patients carrying risk factors, and 2) the larger proportion of cases, which are complicated by multiple organ failure which require intensive care, but have a smaller chance for survival [1–3].