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Although results from observational and epidemiological studies suggested a survival benefit associated with high-flux hemodialysis, conclusive evidence from prospective randomized clinical trials has been lacking. Both the HEMO Study in the USA and the Membrane Permeability Outcome Study (MPO Study) in Europe are randomized studies investigating the effect of high- and low-flux hemodialysis on patient outcomes, even though there were some significant differences in the design of the two studies. An earlier randomized clinical trial could not show differences on patient survival between patient groups being treated with membranes of different material and permeability, but this trial was not designed specifically to examine this particular endpoint. Based on these previous experiences, the MPO Study addressed a hemodialysis patient population which was considered to be more susceptible to the intervention with high-flux dialysis. To identify these patients with an elevated risk, low serum albumin levels were chosen as an indicator; low serum albumin is associated with malnutrition, inflammation, atherosclerosis, and with increased risk of morbidity and mortality. Together with low serum albumin, patients had to be new to dialysis to be selected for the MPO Study. These particular considerations on patient selection, together with additional methodological refinements in the study design allow the conclusion that the MPO Study is valid on its own rather than being a European version of the HEMO Study., ((c) 2008 S. Karger AG, Basel.)

Optimization of methods for ruling out Bacillus anthracis leads to increased yields, faster turnaround times, and a lighter workload. We used 72 environmental non-B. anthracis bacilli to validate methods for ruling out B. anthracis. Most effective were the use of horse blood agar, motility testing after isolates had a 2-h incubation in trypticase soy broth, and screening isolates with a B. anthracis-selective agar.

The incidence of fungal peritonitis (FP) and the fungi that caused FP were evaluated in 422 patients treated with peritoneal dialysis. During an 11-year period, 804 episodes of peritonitis occurred, 46 (5.7%) of which were caused by fungi. Treatment was successful for 39 patients. Early diagnosis of FP and prompt therapy decreases morbidity and mortality.

Background: Cellular immune responses and C5b-9 seem to play an important role in the pathogenesis and progression of idiopathic membranous nephropathy (IMN). The aim of the study was to investigate the role of C5b-9 and adhesion molecules in the pathogenesis of the disease., Methods: The clinical and pathological data of 35 patients with biopsy-proven IMN were correlated with immunohistochemical findings using monoclonal antibodies against T lymphocytes, monocytes/macrophages (MM), HLA-DR antigens, C5b-9, and adhesion molecules such as alpha3beta1, LFA-1beta, and ICAM-1., Results: In the glomeruli, C5b-9 deposits showed a significant correlation with the intensity of IgG and C3 deposition. The stage of the disease had a significant negative relationship with the glomerular alpha3beta1 expression. In the tubulointerstitium (TIN), the number of HLA-DR(+) cells was highly correlated with the numbers of total T lymphocytes, MM, and LFA-1beta(+) cells, as well as with the percentage of tubules with C5b-9 deposits. The extent of ICAM-1 expression in the TIN was significantly correlated with the numbers of interstitial MM, HLA-DR(+), and LFA-1beta(+) cells, as well as with the extent of tubular C5b-9 deposition. The severity of tubular atrophy and interstitial fibrosis had a relationship with the numbers of total T lymphocytes, MM, HLA-DR(+), and LFA-1beta(+) cells and with the extent of tubular C5b-9 deposition and ICAM-1 expression in the TIN. Serum creatinine (Scr) was highly correlated with the numbers of interstitial total T lymphocytes, MM, HLA-DR(+), and LFA-1beta(+) cells. Moreover, Scr had a significant relationship with the severity of tubular atrophy and interstitial fibrosis, as well as with the extent of tubular C5b-9 deposition and ICAM-1 expression in the TIN. Proteinuria was significantly correlated with the extent of tubular alpha3beta1 expression., Conclusions: In IMN, C5b-9 formation may be secondary to IgG and C3 deposition. Proteinuria may contribute to the TIN damage by altering the expression of alpha3beta1 integrins in tubular cells. De novo ICAM-1 and C5b-9 expression within the TIN as well as the activated interstitial cells may be important factors leading to renal damage and renal function impairment.

The different permeability of high-flux and low-flux dialysis membranes results in different removal capacity, particularly for uremic toxins of middle and large molecular weight. High-flux dialysers have been evaluated in clinical and epidemiological studies for their effect on mortality, morbidity, dialysis-related amyloidosis, nutritional status, response to erythropoietin treatment, dialysis tolerance and the preservation of residual renal function. Many of these studies, however, lack a prospective design and randomised treatment allocation, or have too few patients and too short a follow-up. Therefore, this clinical trial was designed to prospectively investigate the long-term effect of membrane permeability on clinical outcome in a larger number of patients. The primary objective is to compare the effect of membrane permeability on mortality of patients on bicarbonate hemodialysis and treated with a minimum dialysis dose. Patients included in the study should have been on hemodialysis for no longer than one month and have serum albumin 4 g/dl or lower. Patients will be randomised to either the experimental or the control group. During the four-week run-in period the treatment parameters will be established in order to achieve the required dialysis dose. During the maintenance period of three to five years regular visits are scheduled to record clinical and laboratory parameters, to measure Kt/V and to adapt the treatment parameters. Altogether a minimum of 660 patients should be enrolled within a two-year recruitment period.

Objective: The aim of this study was to identify prognostic factors in newborns with cerebral infarction., Design: Antenatal and perinatal factors and early clinical, electroencephalogram (EEG), and magnetic resonance imaging (MRI) findings were compared with neurodevelopmental outcome in 24 children with evidence of cerebral infarction on neonatal MRI., Results: Out of 24 infants, 19 had an infarction in the territory of a major cerebral vessel and 5 in the borderzone between cerebral arteries. Neuromotor outcome was normal in 17 and abnormal in 7 infants. Of these 7 infants, 5 infants showed a definite hemiplegia, whereas the other 2 showed some asymmetry of tone or function but no definite hemiplegia. None of the adverse antenatal or perinatal factors was significantly associated with abnormal outcome. Neonatal clinical examination was also not always predictive of the outcome. The extent of the lesion on MRI was a better predictor. In particular, it was the concomitant involvement of hemisphere, internal capsule and basal ganglia that was always associated with an abnormal outcome whereas the involvement of only one or two of the three tended to be associated with a normal outcome. EEG was also very helpful. Abnormal background activity either unilateral or bilateral was found in 6 infants and 5 out of 6 developed hemiplegia. In contrast, the presence of seizure activity in presence of a normal background was not related to abnormal outcome., Conclusions: Early MRI and EEG can help to identify the infants with cerebral infarction who are likely to develop hemiplegia.

Adhesion and stabilization of circulating tumor cells to endothelial cells in target blood vessels play an important role in the complex process of metastasis. We examined the cell surface receptors involved in the liver-metastatic adhesive interactions of murine RAW117 large-cell lymphoma cells to unstimulated hepatic sinusoidal endothelial cells (HSE) under physiological flow conditions. Flow cytometric analysis indicated that VCAM-1, ICAM-1 and PECAM-1 are constitutively expressed on the surfaces of both HSE and RAW117 cells. However, monoclonal antibody (mAb) blockade studies showed that ICAM-1 and PECAM-1 affected neither the attachment nor the stabilization step of the adhesion of RAW117 cells to HSE cell monolayers under flow. In contrast, RAW117 cells required a significantly lower shear stress to establish adhesion to HSE cells when VCAM-1 receptors on HSE cells were blocked with mAb. Furthermore, the presence of the anti-VCAM-1 mAb significantly decreased the extent of adhesion compared to that of the control, without affecting adherent cell stabilization times. Blocking the alpha4 integrin subunits present mainly on RAW117 cells produced similar results to those previously observed with anti-VCAM-1 mAb. Although constitutively present mainly on the surfaces of RAW117 cells, MAdCAM-1 and beta7 integrin subunit do not appear to play a role in either the arrest or stabilization of RAW117 cells on HSE cell monolayers. However, blocking the beta1 integrin subunit on the RAW117-H10 cells reduced adhesion to the same extent as anti-alpha4 and anti-VCAM-1 treatments. These observations suggest that an interaction of integrin alpha4/beta1 on RAW117 cells with liver endothelial VCAM-1 occurs during the early stages of the adhesion process and may be important in liver metastasis.

To define possibly affected members of 69 families and to identify the factors influencing the progression of autosomal dominant polycystic kidney disease (ADPKD), 276 subjects at risk of having inherited the mutant gene underwent ultrasonographic scanning (US), using an ultrasound real-time scanner. At a mean age of 26 +/- 12 years (range 4-71), 85/276 individuals (31%) presented ultrasound evidence of the disease (at least two cysts in one kidney and one cyst in the other) (US: positive), while only 19/85 (22%) had one or more manifestations of ADPKD prior to diagnosis. The prevalence of the disease in subjects at risk aged < 30 years was 53/154 (34%), while hepatic cysts were also detected in 7/85 ADPKD probands (8%) (five females) at a mean age of 40 +/- 6 years (range 30-45) and their frequency correlated with the number of pregnancies. History was proved to be important in suspecting the disease since symptoms were more common in US positive as compared to negative subjects (22% vs 6%, p < 0.001). On the other hand, physical examination and routine laboratory data at presentation revealed abnormal signs mainly in US positive individuals aged 30-39 years. Forty ADPKD families met the criterion for genetic study (at least two members affected) but in three of them (7.5%), no linkage to DNA-markers for the short arm of chromosome 16 was detected ("unlinked" or ADPKD2). DNA-analysis in the rest 37 "linked" (ADPKD1) families identified the gene-carrier state in 18/123 (15%) US negative subjects at risk, at a mean age of 13 +/- 7 years (range 3-25). There were significantly more US positive subjects aged > or = 30 years in ADPKD2 as compared to ADPKD1 families (83% vs 35%, p < 0.05) suggesting that the progression of the disease is slower in the former families. During a 5-year follow-up, 6/18 gene-carriers (33%) had already developed distinct renal cysts on US, at a mean age of 20 +/- 9 years (range 8-29). On the contrary, none of the ADPKD1 non-carriers and the US negative ADPKD2 subjects had shown any ultrasound findings of cystic renal disease at that period.

Tubulointerstitial lesions represent not only a constant component of the pathology of a "classical" glomerular disease such as idiopathic membranous nephropathy but also the most important prognostic indicator and a new "target" for its treatment. Proper "quantification" of the cellular events occurring within the interstitium may enable us to accurately assess the amount of disease activity and identify patients who might benefit from treatment.

When hemolytic uremic syndrome (HUS) is occasionally inherited in an autosomal recessive mode, this occurs mainly in infants and children. We describe four families in which two adult siblings were affected with HUS in each kindred. HUS first occurred between the ages of 19 to 36 years, and the intervals between the onset of HUS in each sibling pair ranged from 6 months to 6 years. None of the patients had a typical prodrome of bloody diarrhea, and one had a recurrence of HUS before transplantation. All eight patients developed renal failure requiring dialysis and transplantation, and seven patients received kidney transplants. Donor kidneys were from parents, siblings, and cadavers. The initial renal transplants were performed from 6 months to 6 years after the onset of the syndrome. HUS recurred in six of the seven patients 2 weeks to 6.5 years after transplantation regardless of the interval between the onset of HUS and transplantation, the origin of the allograft, or the use of cyclosporin A. The only marker for autosomal recessive HUS is the occurrence of the syndrome in a second sibling several months to many years after its occurrence in the proband. In patients with the autosomal recessive form of HUS, the risk for a recurrence in an allograft is high regardless of the source of the kidney.

The cell populations infiltrating the kidneys and the LFA-1 expression were studied in renal biopsy specimens from patients with proteinuric (n = 15, group 1) and non-proteinuric (n = 12, group 2) immunoglobulin A nephropathy. Both groups were matched for age and renal function at the time of biopsy. Proliferative glomerular changes were more commonly see in group 1. Both groups had similar numbers of intraglomerular and interstitial total leukocytes, monocytes/macrophages, and T cells (P = NS). However, glomerular LFA-1 alpha- and -beta-positive cells were significantly higher in group 1 (2.3 +/- 0.2 and 3.3 +/- 0.1 per glomerulus) than in group 2 (0.2 +/- 0.08 and 0.5 +/- 0.05 per glomerulus) (P < 0.005 and P < 0.01, respectively). Group 1 had much higher interstitial LFA-1 alpha- (109 +/- 20/mm(2)) and -beta-positive cells (157 +/- 40/mm(2)) in comparison with group 2 (29 +/- 12/mm(2) and 42 +/- 17/mm(2)). (P < 0.005 and P < 0.01, respectively). No association between glomerular and interstitial LFA-1-positive cells was seen. In addition, tubular HLA-DR expression was higher in group 1 (29 +/- 6/mm(2)) than in group 2 (9 +/- 2/mm(2)) (P < 0.005), but the interstitial HLA-DR-positive cells were similar in both groups. There was a significant association between interstitial LFA-1 alpha- and -beta-positive cells and tubular HLA-DR expression in group 1 (P < 0.01 and P < 0.005, respectively) but not in group 2. Interestingly, the extent of interstitial but not glomerular LFA-1-alpha and -beta expression was highly related to the degree of proteinuria in group 1 (P < 0.01 and P < 0.002, respectively). In conclusion, proteinuria in immunoglobulin A nephropathy is associated with increased LFA-1 expression by glomerular and interstitial infiltrating cells. However, interstitial but not glomerular LFA-1-positive cells are strongly related with the degree of urinary protein excretion. The exact link between LFA-1 expression and proteinuria needs further investigation.

Over the last 16 years the evolution of 24 pregnancies in 17 women with biopsy-proven glomerular disease was analyzed. The underlying renal histology was IgA nephropathy in 8 cases, lupus nephritis in 7, mesangiocapillary glomerulonephritis type I in 1, and focal segmental glomerulosclerosis in 1. All but 2 had normal renal function before conception and 3 were hypertensive. Fetal survival rate was 75%. There were 6 preterm deliveries (33.3%), 3 newborns small for gestational age (17%), 1 stillbirth, and 5 therapeutic abortions. The perinatal mortality was 5.5%. De novo hypertension occurred in 8 pregnancies (33.3%). In 11 pregnancies (46%) increased proteinuria was diagnosed and in 6 (25%) a decline in maternal renal function was recorded. Permanent impairment of renal function was seen in 2 women with renal insufficiency before conception. Maternal hypertension and renal function impairment were associated more frequently with obstetric complications. In conclusion, pregnancy is safe for normotensive mothers with glomerular diseases and normal renal function. Hypertension and impaired renal function at conception seem to carry increased risk for mothers and fetuses. Low-dose immunosuppressive treatment during pregnancy is not harmful for the fetus.

Objective: The aim of this study was to find out whether prosthetic mesh repair of recurrent and large abdominal hernias in continuous ambulatory peritoneal dialysis (CAPD) patients is effective in maintaining them on CAPD., Design: Retrospective analysis of case notes over a period of 5 years., Setting: Single renal unit of a university hospital., Patients: Forty-six of 217 CAPD patients (16%) had their hernias repaired. Among them, 5 women in whom hemodialysis was not possible had multiple or large hernias repaired with polypropylene (PP) mesh., Results: Radical repair was achieved by a modified operation consisting of a conventional hernioplasty complemented by a supporting prostetic overlay mesh, without discontinuation of CAPD. The patients continued CAPD for a mean period of 17.6 months without hernia recurrence. Two patients died in the twelfth and fifteenth post-operative month due to cardiac arrest and hepatic failure, respectively, and the remaining 3 are alive and have been doing well on CAPD for 13, 14, and 21 months., Conclusions: Prosthetic mesh repair of large recurrent hernias in CAPD patients with vascular access problems seems to be a valuable method to maintain them on this renal replacement therapy.

The clinical characteristics of 118 patients (60 male) with acute renal failure (ARF) admitted between 1980 and 1991, were retrospectively analyzed and compared with our earlier series of the 1960s. The mean age was 53 years (16-82 years). There was a marked decline in the hypotension-related cases (43% vs. 17%, p < 0.01) and a concomitant increase in the nephrotoxic cases (5% vs. 17%, p < 0.005) in recent years. The number of ARF cases significantly decreased after 1986 (31%) compared to the pre-1986 era (69%, p < 0.001). A complete (35%) or partial recovery (55%) was the rule in the majority of the patients. The overall mortality was 27%, virtually unchanged in comparison to the 1960s (30%). However, a tendency toward lower mortality was seen after 1986 (17%) in comparison to before (32%, p < 0.05). Sepsis and cardiovascular complications were the leading causes of death. Fewer deaths were observed among younger patients (< 30 years, 12.5%) compared to middle-aged patients (30-59 years, 34%, p < 0.05) and to these older than 60s (53.5%, p < 0.002). Also, deaths were rare in patients with only renal involvement (6%), increasing to 30% when 2 vital organ systems were affected (p < 0.005) and to 67% in cases with multiple organ failure (p < 0.001). Early institution of dialysis and the nonoliguric forms of the syndrome seem to be associated with better prognosis. In conclusion, the incidence of ARF has declined in recent years, with a concomitant tendency towards lower mortality. Death rate is mainly determined by the age and the number of organ involvement. Early dialysis seems to contribute to the lower mortality seen in recent cases.

Thirty-six patients with idiopathic membranous nephropathy were retrospectively studied. The mean age was 47 years and the male to female ratio 25 to 11. Twenty-eight patients (77.8%) had nephrotic syndrome at first investigation. Nineteen patients received corticosteroids alone (group A) and 17 received corticosteroids combined with cyclophosphamide (group B). The mean period of follow-up was 58.9 months (range, 12 to 156 months). The two groups did not differ in clinical or laboratory features at the time of biopsy or at the start of treatment. In the entire series a complete remission of proteinuria occurred in 13 of 36 patients (36.1%) and a partial remission occurred in 13 (36.1%); 10 patients (27.8%) had no response. Optimal remission of proteinuria was usually recorded 6 to 12 months after the start of treatment. The two groups showed no statistical differences regarding the rate of complete (seven v six patients; P = not significant) or partial (six v seven patients; P = not significant) remissions. Two patients (one from each group) entered end stage renal failure during follow-up. At last assessment, the number of patients with complete remission (four v three patients; P = not significant), nonnephrotic proteinuria (nine v nine patients; P = not significant), or nephrotic syndrome (five v four patients; P = not significant) was similar in both groups. In addition, final plasma creatinine did not differ significantly between the two groups (1.8 +/- 2.3 mg/dL v 2.6 +/- 2.6 mg/dL; P = not significant).(ABSTRACT TRUNCATED AT 250 WORDS)

Between 1982 and 1992, 18 cases of pregnancy-related acute renal failure (PR-ARF) were observed (9% of the total number of ARF). Mean age of the women was 32 years (22-40 years). Uterine hemorrhage and preeclampsia/eclampsia were the major causes of ARF, accounting for 61% of the cases. Patchy renal cortical necrosis was suspected in 2 cases whereas signs of disseminated intravascular coagulation (DIC) or microangiopathic hemolytic anemia were present in 6 (33%) and 9 (50%) cases, respectively. Ten women required hemodialysis; and 6 of them, additional plasma exchange sessions. Five patients (28%) died during the acute phase of the illness, mainly due to brain damage, hepatic failure, and sepsis. Among the survivors, a complete (61.5%) or partial recovery (23.1%) was usually seen, but irreversible renal failure was recorded in 2 cases with postpartum hemolytic uremic syndrome (HUS). Short-lasting oligoanuria (< 3 days) represents a good prognostic index. However, the presence of vascular injury (cortical necrosis, HUS) seems to carry a poor prognosis. In conclusion, PR-ARF is still a critical occurrence, associated with serious prognosis for both women and kidneys. So far, the most effective measures remain the careful prevention and the aggressive management of the obstetric complications.

The differentiation between cyclosporine nephrotoxicity (CyN) and acute rejection (AR) still remains a matter of intensive research. In a retrospective study over the last 2 years, we assessed the clinical and histopathological data of 43 episodes of renal dysfunction in 39 renal transplant recipients immunosuppressed with cyclosporine (CyA). Ten episodes (23.2%) were identified as AR and 10 (23.2%) as acute CyN; in six cases (13.9%), signs of both AR and CyN were found. Fever (80%), oliguria (50%), and edema (50%) were prominent features in AR, but not in CyN. Renal blood flow was higher in the nephrotoxicity group and for corresponding degree of renal dysfunction. Significant hyperuricemia (greater than 8 mg/dL) was a prominent finding in CyN (80%) and to a lesser extent in AR (20%). The helper to suppressor cell ratio in the peripheral blood remained stable or slightly decreased in all cases with CyN, but increased in 70% of the cases with AR. CyN was associated with significantly higher whole blood CyA levels (P less than 0.005) and there was a positive correlation between plasma creatinine and CyA levels during the nephrotoxicity episodes (P less than 0.02). Diffuse mononuclear cell infiltrate was observed in 90% of the biopsies with AR and only in 20% with CyN (P less than 0.005). Concerning the extent of the tubular lesions, no significant differences were observed between the two groups. In contrast, vascular lesions such as arterial endothelial proliferation (P less than 0.05), hyalinosis (P less than 0.05), and glomerular capillary thrombi (P less than 0.05) were more commonly seen in nephrotoxicity biopsies.(ABSTRACT TRUNCATED AT 250 WORDS)

To determine the role of the renin-angiotensin-aldosterone system in the maintenance of hypertension in patients with end stage renal disease, twenty four hypertensive patients were studied on regular haemodialysis treatment (RDT) and after successful kidney transplantation. The first group consisted of nine patients on RDT with their own kidneys in situ, and the second group consisted of nine kidney transplants. All 18 patients were given spironolactone 300 mg daily for three weeks following a control period of the same duration. In addition, three anephric patients on RDT were studied with the above protocol and three other patients on RDT were given the same dose for only six days. Blood pressure (BP), body weight, plasma K-Na, aldosterone and renin activity in all patients, and Na and aldosterone in urine in the second group were measured. In the first group of patients on RDT plasma potassium and renin activity increased significantly but BP remained unchanged. In the second group of transplanted patients plasma potassium, renin activity, and aldosterone were increased and BP diminished significantly. In the group of three anephric patients plasma potassium increased but plasma renin activity remained very low. Finally, in the patients on dialysis who received spironolactone for only six days there was a parallel increase of serum potassium and plasma renin activity. These findings suggest that in patients on RDT spironolactone stimulates renin secretion and potassium retention possibly by an effect on the remaining nephrons and/or the intestinal wall. On the contrary, in the transplanted patients the effect of spironolactone on the renal tubule is capable of producing sodium depletion and fall in BP.

The incidence of cutaneous malignancies and non-Hodgkin lymphomas is higher in transplant recipients than in the general population. From 1968 to 1984, 200 kidney grafts were transplanted to 180 patients with end-stage renal disease. All patients were on azathioprine (Aza) and prednisolone. In selected cases ALG and/or small doses of CsA were added. Six patients developed malignant tumors (two Kaposi sarcoma, one squamous cell and one squamous plus basal cell skin cancers, one reticulosarcoma, and one glioma). Mean age of patients was 43 years (range 35-53 years), and mean time of appearance of the tumor after transplantation was 62 months (range 24-98 months). Treatment consisted of reduction of the dosage of Aza, surgical removal or local irradiation of the tumor, and chemotherapy in case of systemic involvement (two cases). Three patients died (one Kaposi sarcoma, one reticulosarcoma, and one glioma) 3 to 6 months after diagnosis, and all three had previously been on high doses of Aza. The remaining three cases (one Kaposi) were cured by stopping or decreasing Aza, by excision, and/or local irradiation of the tumor. It seems that late diagnosis and Aza in high dosage are the main factors leading to the rapid dissemination of the initially localized tumor.

From 1980 to 1983, 69 patients (36 male) with end-stage renal disease underwent kidney transplantation (11 from cadaveric donors). Twenty-six out of 69 (17 male) with a mean age of 37 years (range 16-50 years) developed 69 UTI episodes. The standard immunosuppressive regimen consisted of prednisolone and azathioprine and, in selected cases, antilymphocyte globulin or cyclosporin A were given for a short period of time. Thirty-five episodes (50%) occurred within two months of the operation. The most commonly isolated bacteria were E. coli (28 cases), Ps. aeruginosa (16) and Proteus mirabilis (9). Kidney graft dysfunction, diabetes mellitus, urological complications and antirejection treatment were the main predisposal factors. Recurrence or reinfections were finally diagnosed in 19/26 patients (73%). Thirteen patients presented with asymptomatic bacteriuria (55% of episodes). Aminoglycosides, ureidopenicillins and third-generation cephalosporins were found to be very effective for treating severely ill, febrile patients. In addition, trimethoprim/sulphamethoxazole and mecillinam were useful for patients on long-term chemotherapy. There were no deaths or impairment of the renal graft function directly attributable to the urinary infection. In conclusion, UTIs are a very common cause of morbidity in kidney graft recipients, with the highest incidence in the early post-transplant period. Recurrences or reinfections occur often and asymptomatic bacteriuria is a common finding which needs not be treated aggressively in the absence of symptoms or obstructive uropathy. Patient and graft survival in the long term remain unaffected by the presence of the urinary infection.

Systolic time intervals (STI) and echocardiograms (Echo) were performed before and 30 min after hemodialysis (H) in 19 stable patients (pts) with chronic renal failure undergoing maintenance H. The % shortening of the internal diameter (% delta D), the mean velocity of circumferential fiber shortening (VCF), and the ratio of the pre-ejection period to the left ventricular (LV) ejection time (PEP/LVET) were used as indices of LV performance; the electromechanical systole corrected for heart rate (QS2I) was used as an index of adrenergic activity. After hemodialysis, LV function was improved in 9 pts, Group (GI) and decreased in 10 pts (GII). Changes due to H are shown. The % delta D and VCF before H were normal in GI but abnormal in GII (31.6 +/- 1.4 vs 24.5 +/- 1.4 and 1.07 +/- 0.06 vs 0.88 +/- 0.04, respectively). Systolic blood pressure remained unchanged in GI but decreased in GII (-9.5 +/- 4 mm Hg, p less than 0.01). Body weight decreased significantly (p less than 0.05) and equally in both Gs (-1.2 +/- 0.03 in GI and -1.6 +/- 0.03 in GII). Serum electrolytes, creatinine, and hemoglobin were identical in both Gs before and after H. LV performance improved in pts with LV dysfunction before H, but decreased in pts with normal LV function before H. The decreased afterload in GII and the different effect of alterations in preload and afterload in the failing and normal LV most likely account for these changes. STI and Echo provide simple techniques to assess changes in LV function due to H and one is complementary to the other.

Changes in the haemoglobin-oxygen dissociation curve (Hb-O2) and the factors which influence its position were studied before and after dialysis in 7 patients on regular haemodialysis during 20 dialyses. Seven normal subjects were used as controls. Haemoglobin showed a lower than normal affinity for O2 in uraemic patients before haemodialysis (p50in vivo = 33.09 +/- 0.92 mmHg and p507.4 = 31.51 +/- 0.73 mmHg, P less than 0.001), and this could be considered as a protection against tissue anoxia. After dialysis Hb-O2 affinity at the patient's pH (p50 in vivo = 27.97 +/- 0.57 mmHg, P less than 0.001). This probably eliminates the benefits of the predialysis balance of tissue oxygenation, producing a degree of hypoxia, and may play a role in the genesis of post-dialysis symptoms. Measures should be taken to improve oxygenation of high risk patients with latent heart failure or respiratory disturbances during and after dialysis.

The changes in left ventricular anatomy in 30 patients with end-stage renal disease and stable cardiac function, undergoing regular haemodialysis (10 patients), continuous ambulatory peritoneal dialysis (10 patients) and after successful renal transplantation (10 patients) were evaluated by M-mode echocardiography. Initially all had evidence of left ventricular hypertrophy and dilatation. Reevaluation after a mean follow-up of 22 months on each mode of treatment showed that in the haemodialysis group the left ventricular mass and volume were increased, while in continuous ambulatory peritoneal dialysis (CAPD) and, especially renal transplantation, the hypertrophy and dilatation were reversed. This improvement was probably due to a reduction of cardiac workload.

Two out of four patients who had severe ischaemic E.C.G. changes when first accepted on to the dialysis programme showed much improvement after six months. From an analysis of 40 electrocardiograms (20 before and 20 after dialysis) of a further 17 patients it was found that the height of the T wave is a good index of the plasma potassium level. The tolerance of higher plasma potassium levels by these patients compared with patients with acute renal failure may be explained by the fact that the former do not have a hypercatabolic process and have a lesser degree of acidosis.

Total white cell, neutrophil, and lymphocyte counts were compared in patients with chronic renal failure treated successively by conservative means (low-protein diet), regular haemodialysis, and renal allotransplantation. The lowest total white cell and neutrophil counts and the highest lymphocyte counts were found in patients on regular haemodialysis. A rapid fall in neutrophil count during the first half-hour of dialysis and a more gradual fall between the first and sixth hours were observed. Adherence of neutrophils and mononuclear cells to the cuprophane (PT 150) dialysis membrane has been shown.

A 5-megacycle Doppler flow meter, calibrated in-vitro, was found to give a linear response to blood flow in the ranges commonly encountered in haemodialysis. With this, blood flow through artificial kidneys could be measured simply and with a clinically acceptable error. The method is safe, as blood lines do not have to be punctured or disconnected and hence there is no risk of introducing infection. Besides its value as a research tool the flow meter is useful in evaluating new artificial kidneys. Suitably modified it could form the basis of an arterial flow alarm system.

Episodes of clotting that occurred in 22 patients on regular haemodialysis were studied over a six-month period. The venous pressure during dialysis and the radiology of the Teflon-Silastic arteriovenous shunt were found to be satisfactory guides for the management of the shunt. The failure of the shunt during the early stage was mainly due to technical reasons. Histological study of the excised vessels in removed long-term shunts showed that these had failed because of rigidity and thickening of the vessel wall due to calcium and iron deposits or chronic inflammation, or both.