Kidney Failure (kidney + failure)

Distribution by Scientific Domains

Selected Abstracts


Michael Nevins MD
No abstract is available for this article. [source]

Hepatitis C virus risk: a hepatitis C virus related syndrome

C. Mazzaro
Abstract. Mazzaro C, Panarello G, Tesio F, Santini G, Crovatto M, Mazzi G, Zorat F, Tulissi P, Pussini E, Baracetti S, Campanacci L, Pozzato G (Pordenone General Hospital, Pordenone; University of Trieste, School of Medicine, Trieste, Italy). Hepatitis C virus risk: a hepatitis C virus-related syndrome. J Intern Med 2000 247: 535,545. Background. The association between mixed cryoglobulinemia (MC) and hepatitis C virus (HCV) infection has been recently described in many reports. Objective. The aim of this study was to evaluate the long-term prognosis of hepatitis C virus-positive patients affected by mixed cryoglobulinemia with or without kidney involvement. Patients. At total of 119 hepatitis C virus-positive patients affected by mixed cryoglobulinemia were divided in two groups. Group A: mixed cryoglobulinemia without kidney involvement (103 cases); group B: mixed cryoglobulinemia with glomerulonephritis (GN) (16 cases). A further 37 patients affected by mesangio-proliferative glomerulonephritis (MPGN) were evaluated as controls (group C). Methods. Anti-hepatitis C virus antibodies were determined by commercial kits and hepatitis C virus-RNA was detected by polymerase chain reaction (PCR) amplification of the 5, untranslated region (5,UTR) of the virus. The hepatitis C virus genotype was determined according to Okamoto. Liver biopsy was performed in 62 patients, bone marrow biopsy in 65 patients, and kidney biopsy in all patients with proteinuria. Results. In group A, 46 patients (45%) were affected by chronic liver disease (CLD), 21 (20%) by low-grade non-Hodgkin's lymphoma (NHL) and 16 (15%) by both diseases. All patients of group B were affected by type I membrano-proliferative glomerulonephritis, 3 (19%) by chronic liver disease, 6 (37%) by low-grade non-Hodgkin's lymphoma, and 7 (44%) by both diseases. Several genotypes of hepatitis C virus were found, but Type 1b was prevalent. In group C, no patient showed chronic liver disease or non-Hodgkin's lymphoma. Younger age, higher mean blood pressure, lower C4 serum level, and poorer survival significantly distinguished group B from group A. Survival rates at 5 years were: 87.4% for group A, 89.5% for group C, and 50.0% for group B. None of the patients of group B developed kidney failure requiring dialysis, whilst infections were the leading cause of death. Conclusions. In hepatitis C virus-positive patients, the presence of mixed cryoglobulinemia associated with kidney involvement seems to indicate a new syndrome characterized by immune system impairment, lack of progression to kidney failure, and poor survival (hepatitis C virus-Risk syndrome). [source]

An ongoing process of inner negotiation , a Grounded Theory study of self-management among people living with chronic illness

Åsa Audulv RN
Aim., The aim of this study was to better understand the main concern of self-management processes among people with chronic illness. Background., One aspect of living with chronic illness is self-management that can reduce the illness impact on daily life and promote future health. Although factors that influence self-management have been identified in previous research, little attention has been brought to the process of making self-management decisions. In clinical settings, use of a theory could facilitate patient-empowering approaches. Method., The data collection for this Grounded Theory was mostly conducted in 2006. Data were collected by interviews with 26 adults with a variety of chronic illnesses, including rheumatoid arthritis, diabetes mellitus, inflammatory bowel syndrome, multiple sclerosis, ischaemic heart disease and chronic kidney failure. Results., Individuals are conflicted by competing preferences when taking decisions about self-management. Consequently, the decision-making process can be understood as an ongoing inner negotiation between different incompatible perspectives, e.g. social needs vs. medical needs. The process of negotiating self-management starts with the individual's considering beliefs about health and illness, which make the individual face illness threats and the need for self-management. Several aspects influence negotiating self-management namely, assessing effects of self-management; evaluating own capacity; perceiving normality or stigmatisation; and experiencing support and external resources. The process has been demonstrated in a model. Conclusions., The process of negotiating self-management is an ongoing inner debate rather than a one-time decision. This opens up new ways of understanding, and communicating with, patients. The described model also links behavioural theories and research findings in a comprehensive understanding. Relevance to clinical practice., This model could be applicable as a communication tool for health-care providers in identifying barriers to, and resources in, self-management behaviour among individuals with chronic illness. [source]

Prognostic factors for patients with cirrhosis and kidney dysfunction in the era of MELD: results of a prospective study

Michael Schepke
Abstract: Background/Aim: Hepatorenal syndrome (HRS) is associated with a poor prognosis. The incidence and prognostic impact of kidney dysfunction due to other causes in cirrhotic patients are less well known. The current study prospectively evaluated the incidence and the prognostic relevance of different etiologies of kidney failure in cirrhotic patients. Methods: Eighty-eight consecutive patients with cirrhosis and serum creatinine ,1.5 mg/dl were enrolled. The etiologies of kidney dysfunction were analyzed, and prognostic factors including Model for End-Stage Liver Disease (MELD) score were evaluated in a multivariate Cox model. Results: HRS was present in 35 (40%) patients (15 HRS 1, 20 HRS 2), followed by renal parenchymal disease (23%), drug-induced kidney dysfunction (19%) and prerenal failure due to bleeding or infections (15%). HRS patients had a significantly higher MELD score and shorter survival. In addition to the MELD score, only HRS 1 was independently predictive for survival. HRS 2 patients had a similar outcome as patients with non-HRS kidney dysfunction. Conclusions: In patients with cirrhosis and renal failure, hepatorenal syndrome is associated with a worse prognosis than kidney dysfunction due to other conditions but only HRS type 1 has independent prognostic relevance in addition to the MELD score in these patients. [source]

Review Article: Review: Endothelial-myofibroblast transition, a new player in diabetic renal fibrosis

NEPHROLOGY, Issue 5 2010
ABSTRACT Diabetic nephropathy (DN) is the most common cause of chronic kidney failure and end-stage renal disease in the Western world. Studies from diabetic animal models and clinical trials have shown that inhibition of the renin-angiotensin system delays the progression of advanced DN. However, a recent large-scale clinical trial has revealed that inhibition of renin-angiotensin system in early phases of DN does not slow the decline of renal function or the development of morphological lesions, suggesting that different mechanism(s) may be involved in the different stages of DN. The role of epithelial-mesenchymal transition in renal fibrosis has been intensively investigated. Recently, endothelial-mesenchymal transition, or endothelial-myofibroblast transition (EndoMT) has emerged as another mechanism involved in both developmental and pathological processes. The essential role of EndoMT in cardiac development has been thoroughly studied. EndoMT also exists and contributes to the development and progression of cardiac fibrosis, lung fibrosis, liver fibrosis and corneal fibrosis. EndoMT is a specific form of epithelial-mesenchymal transition. During EndoMT, endothelial cells lose endothelial markers and obtain mesenchymal markers. Recent evidence from our laboratory and others suggests that EndoMT plays an important role in the development of renal fibrosis in several pathological settings, including experimental DN. This review considers the evidence supporting the occurrence of EndoMT in normal development and in pathology, as well as the latest findings suggesting EndoMT contributes to fibrosis in DN. Whether experimental findings of EndoMT will be reproduced in human studies remains to be determined. [source]

Novel renoprotective actions of erythropoietin: New uses for an old hormone (Review Article)

NEPHROLOGY, Issue 4 2006
SUMMARY: Erythropoietin (EPO) has been used widely for the treatment of anaemia associated with chronic kidney disease and cancer chemotherapy for nearly 20 years. More recently, EPO has been found to interact with its receptor (EPO-R) expressed in a large variety of non-haematopoietic tissues to induce a range of cytoprotective cellular responses, including mitogenesis, angiogenesis, inhibition of apoptosis and promotion of vascular repair through mobilization of endothelial progenitor cells from the bone marrow. Administration of EPO or its analogue, darbepoetin, promotes impressive renoprotection in experimental ischaemic and toxic acute renal failure, as evidenced by suppressed tubular epithelial apoptosis, enhanced tubular epithelial proliferation and hastened functional recovery. This effect is still apparent when administration is delayed up to 6 h after the onset of injury and can be dissociated from its haematological effects. Based on these highly encouraging results, at least one large randomized controlled trial of EPO therapy in ischaemic acute renal failure is currently underway. Preliminary experimental and clinical evidence also indicates that EPO may be renoprotective in chronic kidney disease. The purpose of the present article is to review the renoprotective benefits of different protocols of EPO therapy in the settings of acute and chronic kidney failure and the potential mechanisms underpinning these renoprotective actions. Gaining further insight into the pleiotropic actions of EPO will hopefully eventuate in much-needed, novel therapeutic strategies for patients with kidney disease. [source]

Addressing the epidemic of chronic kidney disease in Australia

NEPHROLOGY, Issue 2004
Timothy MATHEW
SUMMARY: The Australia Diabetes, Obesity and Lifestyle Study (AUSDIAB) study provided, for the first time in Australia, a snapshot of the prevalence of kidney damage, reduced kidney function, hypertension and diabetes in the adult population. With this information, and the Australia and New Zealand Dialysis and Transplant Registry (ANZDATA) registry, that has recorded kidney failure statistics for many years, the extent of the chronic kidney disease burden in Australia is being better defined. This burden is even more pronounced in the Indigenous population where the incidence of kidney disease and kidney failure is increased several-fold. Diabetes is the second most common cause of kidney failure among Australians. The number of patients with diabetes accepted to dialysis has doubled in the last 7 years, the mean body weight of patients commencing dialysis has increased 7 kg in the past decade and the mean age at acceptance to dialysis is rising in a linear fashion (presently 60 years). These facts, together with a static transplant rate, all point to the prevalence of dialysis likely staying at or increasing beyond the present yearly growth rate of 6,7%. The evidence shows that a large proportion of chronic kidney disease patients are dying of cardiovascular risk factors before they reach dialysis or transplantation. There are many gaps in delivering appropriate preventative treatment to these patients. A relatively small reduction in the rise in dialysis numbers that might flow from an effective prevention of progression program, could make a significant impact on the spiralling numbers and associated cost of kidney failure treatment in Australia. We now need to develop and implement a national kidney disease strategy designed to address the whole continuum of chronic kidney disease from its earliest stage right through to dialysis and transplantation. [source]

Vitamin E as a protective antioxidant in progressive renal failure

NEPHROLOGY, Issue 1-2 2000
Michael J Fryer
SUMMARY: Progression to renal failure is significantly worsened by oxidative stress in chronic inflammatory kidney disease (IgA nephropathy, antiglomerular basement membrane nephritis, focal segmental glomerulosclerosis), rhabdomyolysis (myoglobinic acute renal failure), diabetic nephropathy and in poisoning by nephrotoxic compounds such as transition metals, paraquat and drugs such as cyclosporine A and cisplatin. The membrane antioxidant vitamin E (,-tocopherol) is examined as a potential therapeutic intervention that may help to slow the rate of decline of kidney function in such conditions. An impaired plasma antioxidant defence system is characteristic of chronic renal failure and the uremic state. Vitamin E therapy is also considered as a means of correcting plasma antioxidant status and attenuating the cardiovascular disease that accompanies kidney failure. [source]

Long-term effect of the complement inhibitor eculizumab on kidney function in patients with paroxysmal nocturnal hemoglobinuria,,

Peter Hillmen
Paroxysmal nocturnal hemoglobinuria (PNH) is a debilitating and life-threatening disease in which lysis of PNH red blood cells frequently manifests with chronic hemolysis, anemia, and thrombosis. Renal damage in PNH is associated with chronic hemosiderosis and/or microvascular thrombosis. We determined the incidence of renal dysfunction or damage, defined by stages of chronic kidney disease (CKD), in a large cohort of PNH patients and evaluated the safety and efficacy of the complement inhibitor eculizumab in altering its progression. Renal dysfunction or damage was observed in 65% of the study population at baseline with 21% of patients with later stage CKD or kidney failure (glomerular filtration rate [GFR] ,60 ml/min/1.73 m2; Stage 3, 4, or 5). Eculizumab treatment was safe and well-tolerated in patients with renal dysfunction or damage and resulted in the likelihood of improvement as defined as categorical reduction in CKD stage (P < 0.001) compared with baseline and to placebo (P = 0.04). Improvement in renal function was more commonly seen in patients with baseline CKD Stages 1,2 (67.1% improvement, P < 0.001) although improvement was also observed in patients with CKD Stages 3,4 (P = 0.05). Improvements occurred quickly and were sustained for at least 18 months of treatment. Patients categorized at CKD Stages 3,5 did not worsen during treatment with eculizumab. Overall, 40 (21%) of 195 patients who demonstrated renal dysfunction or damage at baseline were no longer classified as such after 18 months of treatment. Administration of eculizumab to patients with renal dysfunction or damage was well tolerated and was usually associated with clinical improvement. Am. J. Hematol. 85:553,559, 2010. © 2010 Wiley-Liss, Inc. [source]

Renal Failure Five Years After Lung Transplantation Due to Polyomavirus BK-Associated Nephropathy

A. Egli
Polyomavirus-associated nephropathy (PyVAN) is rare in nonrenal solid organ transplantation and only limited information is available from single cases. We describe a 67-year-old female presenting with hypertension and progressive kidney failure due to PyVAN 60 months after lung transplantation. Plasma BK virus (BKV) loads were 4.85 log10 copies/mL at diagnosis and cleared slowly over 14 months after switching from tacrolimus, mycophenolate and prednisone to low-dose tacrolimus, sirolimus and leflunomide, the latter being discontinued for anemia and diarrhea. BKV- and JC virus-specific immunoglobulins were detectable prior to transplantation. Only BKV-specific IgG and IgM increased during follow-up. BKV-specific T cells were detectable in blood following in vitro expansion, but cleared with reincreased sirolimus, yet BKV viremia remained undetectable. We identified eight other cases of PyVAN in nonrenal solid organ transplantation including lung (n = 1), heart (n = 6) and pancreas (n = 1). Overall, diagnosis was later than commonly seen in kidney transplants (median 18 months, interquartile range 10,29). Seven patients were male, five received triple immunosuppression consisting of tacrolimus, mycophenolate, prednisone. Immunosuppression was reduced in four cases and cidofovir and/or leflunomide administered in five and two cases, respectively. Renal function deteriorated in five requiring hemodialysis in four. We discuss mTOR inhibitors versus cidofovir and leflunomide as potential PyVAN rescue therapy. [source]

Unrecognized Acute Phosphate Nephropathy in a Kidney Donor with Consequent Poor Allograft Outcome

N. Agrawal
Acute phosphate nephropathy following a large phosphate load is a potentially irreversible cause of kidney failure. Here, we report on the unfavorable graft outcome in two recipients of deceased donor kidneys from a donor who had evolving acute phosphate nephropathy at the time of organ procurement. The donor, a 30-year-old with cerebral infarction, developed hypophosphatemia associated with diabetic ketoacidosis and was treated with intravenous phosphate resulting in a rise in serum phosphorus from 0.9 to 6.1 mg/dL. Renal biopsies performed on both recipients for suboptimal kidney function revealed acute tubular injury and diffuse calcium phosphate microcrystal deposits in the tubules, which were persistent in subsequent biopsies. A retrospective review of preimplantation biopsies performed on both kidneys revealed similar findings. Even though initial renal histology in both recipients was negative for BK virus, they eventually developed BK viremia with nephropathy but both had a substantive virologic response with therapy. The first patient returned to dialysis at 6 months, while the other has an estimated glomerular filtration rate of 12 mL/min, 17 months following his transplant. We conclude that unrecognized acute phosphate nephropathy in a deceased donor contributed substantially to poor graft outcome in the two recipients. [source]

End-stage kidney failure in Indigenous Australians

John Mathews
No abstract is available for this article. [source]

Acute non-oliguric kidney failure and cholestatic hepatitis induced by ibuprofen and acetaminophen: a case report

Marco Zaffanello
Abstract The combined use of acetaminophen with ibuprofen has long been in clinical use because the target of action of each drug is different and they do not interfere with each other. Appropriate dosing and managing of these drugs do not likely lead to organ toxicity. However, both acetaminophen and ibuprofen can induce liver problems and acute kidney failure, respectively, if administered at high doses. We report the case of a female child, in treatment with both acetaminophen and ibuprofen, administered at therapeutic antipyretic doses in condition of volume depletion, who suffered acute kidney and liver failure. Conclusion: The combined ibuprofen and acetaminophen treatment, even if administered at therapeutic dosages and in a reduced number of doses, may be dangerous in conditions of volume depletion. [source]

Antibody-Mediated Microcirculation Injury Is the Major Cause of Late Kidney Transplant Failure

G. Einecke
We studied the phenotype of late kidney graft failure in a prospective study of unselected kidney transplant biopsies taken for clinical indications. We analyzed histopathology, HLA antibodies and death-censored graft survival in 234 consecutive biopsies from 173 patients, taken 6 days to 31 years posttransplant. Patients with late biopsies (>1 year) frequently displayed donor-specific HLA antibody (particularly class II) and microcirculation changes, including glomerulitis, glomerulopathy, capillaritis, capillary multilayering and C4d staining. Grafts biopsied early rarely failed (1/68), whereas grafts biopsied late often progressed to failure (27/105) within 3 years. T-cell-mediated rejection and its lesions were not associated with an increased risk of failure after biopsy. In multivariable analysis, graft failure correlated with microcirculation inflammation and scarring, but C4d staining was not significant. When microcirculation changes and HLA antibody were used to define antibody-mediated rejection, 17/27 (63%) of late kidney failures after biopsy were attributable to antibody-mediated rejection, but many were C4d negative and missed by current diagnostic criteria. Glomerulonephritis accounted for 6/27 late losses, whereas T-cell-mediated rejection, drug toxicity and unexplained scarring were uncommon. The major cause of late kidney transplant failure is antibody-mediated microcirculation injury, but detection of this phenotype requires new diagnostic criteria. [source]