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Early allograft dysfunction (EAD) after liver transplantation (LT) is related to ischemia–reperfusion injury and may lead to a systemic inflammatory response and extrahepatic organ dysfunction. We evaluated the effect of EAD on new‐onset acute kidney injury (AKI) requiring renal replacement therapy within the first month and end‐stage renal disease (ESRD) within the first year post‐LT in 1325 primary LT recipients. EAD developed in 358 (27%) of recipients. Seventy‐one (5.6%) recipients developed AKI and 38 (2.9%) developed ESRD. Compared with those without EAD, recipients with EAD had a higher risk of AKI and ESRD (4% vs. 9% and 2% vs. 6%, respectively, p < 0.001 for both). Multivariate logistic regression analysis showed an independent relationship between EAD and AKI as well as ESRD (odds ratio 3.5, 95% confidence interval 1.9–6.4, and odds ratio 3.1, 95% confidence interval 11.9–91.2, respectively). Patients who experienced both EAD and AKI had inferior 1‐, 3‐, 5‐, and 10‐year patient and graft survival compared with those with either EAD or AKI alone, while those who had neither AKI nor EAD had the best outcomes (p < 0.001). Post‐LT EAD is a risk factor for both AKI and ESRD and should be considered a target for future intervention to reduce post‐LT short‐ and long‐term renal dysfunction. In this study of 1325 primary liver transplant recipients, the authors identify a link between early liver allograft dysfunction and new onset acute kidney injury within one month and end‐stage renal disease at one year after liver transplantation.

Early allograft dysfunction (EAD) after liver transplantation (LT) is related to ischemia–reperfusion injury and may lead to a systemic inflammatory response and extrahepatic organ dysfunction. We evaluated the effect of EAD on new-onset acute kidney injury (AKI) requiring renal replacement therapy within the first month and end-stage renal disease (ESRD) within the first year post-LT in 1325 primary LT recipients. EAD developed in 358 (27%) of recipients. Seventy-one (5.6%) recipients developed AKI and 38 (2.9%) developed ESRD. Compared with those without EAD, recipients with EAD had a higher risk of AKI and ESRD (4% vs. 9% and 2% vs. 6%, respectively, p < 0.001 for both). Multivariate logistic regression analysis showed an independent relationship between EAD and AKI as well as ESRD (odds ratio 3.5, 95% confidence interval 1.9–6.4, and odds ratio 3.1, 95% confidence interval 11.9–91.2, respectively). Patients who experienced both EAD and AKI had inferior 1-, 3-, 5-, and 10-year patient and graft survival compared with those with either EAD or AKI alone, while those who had neither AKI nor EAD had the best outcomes (p < 0.001). Post-LT EAD is a risk factor for both AKI and ESRD and should be considered a target for future intervention to reduce post-LT short- and long-term renal dysfunction.

Background/Aim:Heparin has been shown to be renoprotective in a number of experimental nephropathies. The inflammatory component in the early phase of Adriamycin (ADR) induced nephropathy has been established. A microdose of low molecular weight heparin (Fragmin; F) has been noted to exert immunomodulatory effects independent of its anticoagulant activity. We assessed the effects of microdoses of F on daily proteinuria and glomerular production of tumor necrosis factor alpha (TNF-α) and prostaglandins 8 and 15 days after induction of ADR nephropathy. Methods:Following intravenous injection of ADR (7 mg/kg) to Wistar rats weighing 200 ± 20 g, F 20 µg/day/rat s.c. was administered for 8 and 15 days (groups F8 and F15). The respective control groups (C8 and C15) received normal saline subcutaneously. Proteinuria, serum albumin, and creatinine clearance were evaluated on days 8 and 15. The production of TNF-α and prostaglandins from glomerular supernatants was measured by radioimmunoassay on days 8 and 15. Results:F significantly reduced proteinuria (mg/day) on day 8: 13.6 ± 1.2 in F8 versus 40.3 ± 2.7 in C8 (p = 0.008). The glomerular production of TNF-α (pi/ml) was significantly lower on day 8 in rats treated with F: 356 ± 33 in F8 versus 764 ± 81 in C8 (p = 0.006). A decrease in the prostaglandin E2/thromboxane B2 ratio was noted in the F group between 8 and 15 days (1.1 in F8 vs. 0.9 in F15, p = 0.005) which principally reflects an increase of thromboxane B2. The antiproteinuric effect of F shown after 8 days was no longer present after 15 days (354 ± 91 mg/day in F15 vs. 499 ± 69 mg/day in C15, p = 0.33). The same trend was seen for the glomerular production of TNF-α. Light microscopy and immunohistochemistry for interstitial and glomerular macrophages were negative. Conclusion:The lowering effect of microdoses of F on the proteinuria seen during the early phase of ADR nephropathy may be mediated by a decreased production of glomerular TNF-α, supporting the anti-inflammatory action of low molecular weight heparin.

Haemodialyzed (HD) patients have been found to have an increased bile cholesterol level and an increased saturation index in bile. These changes were markedly enhanced in the presence of a low-protein diet. To evaluate whether such changes influence the prevalence of cholelithiasis in patients with end-stage renal failure, real-time sonography was performed to detect the presence of gallstones (GS) in 54 HD (28 males, 26 females, mean age 52.4 ± 15.4 years) and 39 continuous ambulatory peritoneal dialysis (CAPD; 22 males, 17 females, mean age 59.1 ± 14.9 years) patients. No patient had diabetes. The patients’ charts were reviewed for the following data: age, sex, primary renal disease, obesity (20% above ideal weight), history suggestive of gallbladder disease or previous cholecystectomy, duration of dialysis, and serum cholesterol levels. Overall, cholelithiasis was documented in 12 of 93 (12.9%) patients, 7 HD and 5 CAPD. When comparing the factors outlined above, no significant difference was found between HD and CAPD patient groups, either with or without cholelithiasis. Gallbladder disease was asymptomatic in all except 1 patient who required cholecystectomy. Using a healthy control group consisting of local age- and sex-matched inhabitants, GS were found in 8 of 134 (6%) of them (p > 0.05). We conclude that the prevalence rate of GS in our dialysis population (HD and CAPD) is similar to that of a local general population following a western-style diet, irrespective of dialysis mode.

The prevalence of complement deficiency was studied among 111 survivors of sporadic menin-gococcal disease located through the medical records of 10 Israeli hospitals. There were 11 patients with CH50=0: one with systemic lupus erythematosus and 10 with hereditary terminal complement deficiency (four with homozygous C7 and six with C8 deficiency). There was no hereditary complement deficiency among 39 Ashkenazi subjects as against 18 per cent among 38 Sephardi subjects and 40 per cent among 15 of Moroccan ancestry (p<0.05). The age at first presentation of meningococcal disease in complement deficient patients was 14.7+7.6, years compared with 8.1+10.9 in the non-deficient patients (p<0.25). None of the complement deficient patients had meningitis below the age of 5 years vs. 49 per cent of non-deficient subjects. Recurrent meningitis was observed in 40 vs. 4 per cent (p<0.01) and meningitis in siblings in 40 vs. 2 percent respectively (p<0.001). In addition to the 10 propositi, 11 non-propositus siblings were identified with severe complement deficiency (six with homozygous C7 and five with C8 deficiency). Seven of the non-propositi had no history at all of meningitis or any other serious systemic disease, underlining the relatively favourable prognosis of terminal complement deficiency. With increasing familiarity with the clinical features of this hereditary disease, it is possible now to identify on clinical grounds patients with meningococcal disease with a high likelihood of terminal complement deficiency.