scholarly journals Refractory ascites and graft dysfunction in early renal transplantation

2019 ◽  
Vol 41 (4) ◽  
pp. 570-574 ◽  
Author(s):  
Catarina Pereira Eusébio ◽  
Sofia Correia ◽  
Filipa Silva ◽  
Manuela Almeida ◽  
Sofia Pedroso ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Serum Albumin ◽  
De Novo ◽  
Varicose Veins ◽  
Portal Pressure ◽  
Graft Function ◽  
Refractory Ascites ◽  
Graft Dysfunction ◽  
Mild Anemia ◽  
Incomplete Septal Cirrhosis

Abstract The occurrence of ascites after Renal Transplant (RT) is infrequent, and may be a consequence of surgical or medical complications. Case report: 61 year-old, male, history of arterial hypertension, tongue carcinoma and alcoholic habits 12-20g/day. He had chronic kidney disease secondary to autosomal dominant polycystic kidney disease, without hepatic polycystic disease. He underwent cadaver donor RT in September 2017. He had delayed graft function by surgically corrected renal artery stenosis. He was admitted in January 2018 for ascites de novo, with no response to diuretics. HE had visible abdominal collateral circulation. Graft dysfunction, adequate tacrolinemia, Innocent urinary sediment, mild anemia, without thrombocytopenia. Serum albumin 4.0g / dL. Normal hepatic biochemistry. Peritoneal fluid with transudate characteristics and serum albumin gradient > 1.1. Ultrasound showed hepatomegaly, permeable vascular axes, without splenomegaly. Mycophenolate mofetil was suspended, with reduced remaining immunosuppression. He maintained refractory ascites: excluded infectious, metabolic, autoimmune and neoplastic etiologies. No nephrotic proteinuria and no heart failure. MRI: micronodules compatible with bile cysts. Upper Digestive Tract Endoscopy did not show gastroesophageal varicose veins. Normal abdominal lymphoscintigraphy. He underwent exploratory laparoscopy with liver biopsy: incomplete septal cirrhosis of probable vascular etiology some dilated bile ducts. He maintained progressive RT dysfunction and restarted hemodialysis. The proposed direct measurement of portal pressure was delayed by ascites resolution. There was further recovery of the graft function. Discussion: Incomplete septal cirrhosis is an uncommon cause of non-cirrhotic portal hypertension. Its definition is not well known, morphological and pathophysiological. We have not found published cases of post-RT ascites secondary to this pathology, described as possibly associated with drugs, immune alterations, infections, hypercoagulability and genetic predisposition.

CLINICAL ASPECTS OF RENAL TRANSPLANTATION

Vestnik ◽  
2021 ◽  
pp. 136-142
Author(s):  
Б.Г. Султанова ◽  
И.Б. Мансурова ◽  
С.Б. Бодесова ◽  
Н.С. Джуманов ◽  
Ш.А. Сарсенова ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Transplantation ◽  
Renal Transplantation ◽  
Kidney Disease ◽  
Immunosuppressive Therapy ◽  
Interdisciplinary Approach ◽  
Clinical Aspects ◽  
Graft Dysfunction ◽  
Donor Kidney ◽  
Donor Evaluation

В статье приведен литературный обзор, посвященный современным проблемам в трансплантологии почек. Нерешенными проблемами остаются оценка донора, низкая приверженность пациентов иммуносупрессивной терапии и развитие дисфункции трансплантата. Развивающиеся осложнения после трансплантации и иммуносупрессивной терапии требуют междисциплинарного подхода в лечении и наблюдении реципиентов донорской почки. Также необходимо широкое развитие трупного донорства для снижения числа потенциальных пациентов с хронической болезнью почек. The article presents a literature review of contemporary problems in kidney transplantation. Donor evaluation, low adherence of patients to immunosuppressive therapy and the development of graft dysfunction remain as unresolved problems. Developing complications after transplantation and immunosuppressive therapy require an interdisciplinary approach in the treatment and monitoring of recipients of donor kidney. It is also indispensable to the development of cadaveric donation to reduce the number of potential patients with chronic kidney disease.

Abstract 18139: Myocardial Fibrosis Quantified by Cardiovascular Magnetic Resonance is Associated with Histology and Graft Function After Pediatric Heart Transplantation

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Brian Feingold ◽  
Cláudia M Salgado ◽  
Miguel Reyes-Múgica ◽  
Stacey Drant ◽  
Susan A Miller ◽  
...  
Keyword(s):  
Cardiovascular Magnetic Resonance ◽  
Magnetic Resonance ◽  
Heart Transplantation ◽  
Myocardial Fibrosis ◽  
Graft Failure ◽  
Extracellular Volume ◽  
Graft Function ◽  
Automated Image Analysis ◽  
Graft Dysfunction ◽  
Pediatric Heart Transplantation

Background: Late survival after pediatric heart transplantation (HTx) remains poor. Many late deaths are due to “graft failure,” typically in the presence of vasculopathy and diffuse myocardial fibrosis (DMF) - a process associated with ventricular remodeling and heart failure (HF). Cardiovascular magnetic resonance (CMR)-derived extracellular volume (ECV) is a validated measure of DMF in the absence of edema or infiltrative disease, and predicts outcomes of HF and mortality in adults. We hypothesize that ECV is a meaningful biomarker of graft dysfunction following pediatric HTx. Objective: To test the association of ECV with histologic myocardial fibrosis after pediatric HTx. We also explored associations of ECV with hemodynamic, echocardiographic, and serum measures of graft function. Methods: We prospectively enrolled consecutive HTx recipients who were ≥13 years old and ≥9 months post HTx for ECV quantification at the time of surveillance endomyocardial biopsy (EMB). Fibrosis was quantified on EMB by automated image analysis after picrosirius staining and digital scanning. CMR measures of blood and myocardial T1 from basal and mid short axis slices, along with contemporaneous hematocrit, quantified ECV. Results: Nineteen pts (12 male) underwent CMR at a mean age of 18.4 ± 2.8 yrs (range 14.9 - 24.4 yrs) and a mean time after HTx of 10.4 ± 6.6 yrs (1.0 - 20.7 yrs). Four pts were excluded from analysis due to acute rejection (ISHLT grade ≥2R) on concurrent EMB (n=2) or poor quality imaging (n=2). Mean ECV was 27.1 ± 3.8 (20.9 - 32.1). Late gadolinium enhancement was observed in 1 pt. ECV showed moderate correlations with histologic myocardial fibrosis (r=0.61; p=0.02) and serum b-type natriuretic peptide (r=0.66; p=0.008). There was a trend to correlation with pulmonary capillary wedge pressure (r=0.51; p=0.06). We found no associations of ECV with systolic or diastolic function, time after HTx, or graft age. Conclusions: We demonstrate a novel association of ECV with histologic myocardial fibrosis and serum and hemodynamic markers of HF after pediatric HTx. Given prior observations of myocardial fibrosis in chronic graft failure, these findings suggest that ECV may be a relevant, noninvasive marker of graft dysfunction and a potential therapeutic target.

Association of Factor V Leiden Mutation with Delayed Graft Function, Acute Rejection Episodes and Long-term Graft Dysfunction in Kidney Transplant Recipients

2002 ◽  
Vol 87 (02) ◽  
pp. 194-198 ◽  
Author(s):  
Torsten Slowinski ◽  
Ingeborg Hauser ◽  
Birgit Vetter ◽  
Lutz Fritsche ◽  
Daniela Bachert ◽  
...  
Keyword(s):  
Acute Rejection ◽  
Kidney Transplant ◽  
Graft Function ◽  
Factor V Leiden ◽  
Factor V ◽  
Transplant Recipients ◽  
Graft Dysfunction ◽  
Kidney Transplant Recipients ◽  
Factor V Leiden Mutation

SummaryWe analysed whether the factor V Leiden mutation – the most common hereditary predisposing factor for venous thrombosis – is associated with early and long-term graft dysfunction after kidney transplantation in 394 Caucasian kidney transplant recipients. The presence of factor V Leiden mutation was identified by allele specific PCR. The prevalence of the factor V Leiden mutation was compared to 32216 unselected neonates. The prevalence of the factor V Leiden mutation (GA genotype) was similar in 394 kidney transplant recipients and 32216 neonates. The frequency of known factors predicting long-term graft function were similar in patients with the GA genotype and with the normal factor V gene (GG genotype). The GA genotype was associated with the occurrence of no primary graft function (risk: 2.87; 95% confidence interval: 1.01-8.26; p < 0.05), the number of dialysis after transplantation in patients with no primary graft function until graft function (7.5 ± 2.06 dialysis in GA patients; 4.2 ± 0.36 dialyses in GG patients; p < 0.05), and the risk for at least one acute rejection episode (risk: 3.83; 95% confidence interval: 1.38-10.59; p < 0.02). The slope of 1/creatinine per year was significantly lower in patients with the GA genotype (GA patients: – 0.0204 ± 0.008 dl/mg per year; GG patients: 0.0104 ± 0.004 dl/mg per year; p < 0.02). The annual enhancement of the daily protein excretion rate was elevated in patients with the GA genotype (GA patients: 38.5 ± 16.6 mg/24 h per year; GG patients: 4.9 ± 4.4 mg/24 h per year; p < 0.02). Our study showed that the factor V Leiden mutation is associated with the occurrence of delayed graft function, acute rejection episodes and chronic graft dysfunction after kidney transplantation.

1856 ASSOCIATION OF RISE IN C-REACTIVE PROTEIN WITH DE NOVO CHRONIC KIDNEY DISEASE AFTER PARTIAL NEPHRECTOMY

2012 ◽  
Vol 187 (4S) ◽  
Author(s):  
Seth A. Cohen ◽  
Kerrin L. Palazzi ◽  
Ryan P. Kopp ◽  
Reza Mehrazin ◽  
Samuel K. Park ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Partial Nephrectomy ◽  
De Novo ◽  
C Reactive Protein ◽  
Reactive Protein

MO609PREVALENCE OF MALNUTRITION AND INFLAMMATION IN NONDIALYZED PATIENTS WITH CHRONIC KIDNEY DISEASE: A CLINICAL STUDY

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Manzoor Parry ◽  
Hamad Jeelani
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Serum Albumin ◽  
Serum Ferritin ◽  
Chronic Glomerulonephritis ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
North East ◽  
Inflammatory Status ◽  
Initiation Of Dialysis

Abstract Background and Aims The prevalence of chronic kidney disease (CKD) in India varies from 0.16–0.78%. The reported incidence of malnutrition in CKD patients is 37–84%. There is a paucity of data on the quantification of malnutrition and inflammation in undialyzed patients of CKD from north east of India. This study analyzed the prevalence and causes of malnutrition and inflammation in patients with CKD before the initiation of dialysis treatment. Method This study was conducted from May 2017 to May 2019 in the department of nephrology Guahati medical college hospital. Assessment of nutritional and inflammatory status was carried out in patients with CKD before initiation of dialysis. Serum albumin; body mass index (BMI); triceps skin fold thickness (TST); mid-arm muscle circumference (MAMC); and subjective global assessment (SGA) scoring were used for assessment of nutritional parameters. Serum C-reactive protein; serum albumin and serum ferritin level were used to assess the inflammatory status in these patients. Results A total of 528 (male:female= 359:169) patients with CKD participated in this study. Diabetic Nephropathy (35%) was the most common; followed by; hypertension (23%) and chronic glomerulonephritis (20 %). The evidence of malnutrition was noted in 344 (65%). The mean age of patients with malnutrition was 52.8±12.45 years with a male predominance (68%). On the basis of SGA score; malnutrition was noted in 344 patients (mild moderate [36%]; severe; [30%]); remaining (34%) were well nourished. Thus; evidence of Malnutrition was noted in 65% of patients with CKD.). Serum total protein & albumin were higher in the non-malnourished patients in comparison to malnourished (5.83±1.0 vs 5.31±1.12 p&lt;0.05; 3.65±0.7 vs 2.62±0.74) The inflammatory markers (serum ferritin & C reactive protein) were elevated significantly in patients with malnutrition in comparison to those without malnutrition (308.15±60.18 mg/dL vs. 251.64±63.14 mg/dL; p &lt; 0.001; 77% vs. 50%; p &lt; 0.01). Conclusion Malnutrition and inflammation are common in patients with CKD before the commencement of dialysis. This indicates that an emphasis should be placed on the assessment and prevention or correction of malnutrition and inflammatory burden in these patients with CKD.

Incidence And Risk Factors Of Contrast Nephropathy After Tace In Patients With Liver Cancer And Chronic Kidney Disease

2021 ◽  
Vol 44 (3) ◽  
pp. E19-24
Author(s):  
Kun-Kun Cao ◽  
Ning Ding ◽  
Xiao-We Li ◽  
Jia-Ming Zhong ◽  
Jian Zhai ◽  
...  
Keyword(s):  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Liver Cancer ◽  
Serum Albumin ◽  
Multivariate Logistic Regression Analysis ◽  
Arterial Embolization ◽  
Solitary Kidney ◽  
Kidney Volume ◽  
Iodized Oil

Purpose: Incidence of contrast induced nephropathy (CIN) and related risk factors in patients with liver cancer and chronic kidney disease after trans-catheter arterial chemoembolization (TACE) is higher. The purpose of this study was to investigate the feasibility and safety of TACE therapy in such patients. Methods: A retrospective analysis was performed on 103 patients with liver cancer and chronic kidney disease who underwent TACE treatments. TACE was performed according to Seldinger’s technique of arterial embolization with minor modifications. Based on CIN diagnostic criteria, patients were divided into non-CIN (n=89) and CIN (n=14) groups. Multiple clinical parameters were assessed for the two groups after TACE. Serum creatinine levels were measured 48-72 h after TACE. Results: Tumor size (>5 cm), TACE frequency, contrast agent dosage, solitary kidney, volume of iodized oil used in the TACE (ml) and urea levels were significantly higher in CIN group in comparison with the non-CIN group, while serum albumin and haemoglobin levels were significantly lower. Multivariate logistic regression analysis confirmed that the volume of iodized oil and TACE frequency were significantly positively correlated, and serum albumin level was negatively correlated in the CIN group. Conclusion: Volume of iodized oil, TACE frequency and low serum albumin levels were found to be independent risk factors for CIN after TACE. Thus, it is safe and feasible for hepatocellular carcinoma patients with chronic kidney disease to receive TACE treatment, but adverse events management after TACE needs to be addressed.

scholarly journals Antibody-mediated rejection with detection of de novo donor-specific anti-human leucocyte antigen Class II antibodies 3 years after heart transplantation: a case report

2020 ◽  
Vol 4 (1) ◽  
pp. 1-4
Author(s):  
Bernd Ludwig ◽  
Johanna Schneider ◽  
Daniela Föll ◽  
Qian Zhou
Keyword(s):  
Heart Transplantation ◽  
De Novo ◽  
Survival Rates ◽  
Graft Function ◽  
Left Ventricular ◽  
Cardiac Allograft ◽  
Left Ventricular Ejection ◽  
High Dose ◽  
Ventricular Ejection Fraction ◽  
Antibody Mediated Rejection

Abstract Background Antibody-mediated rejection (AMR) in cardiac transplantation may manifest early within the first weeks after transplantation but also late after months to years following transplantation resulting in mild heart failure to cardiogenic shock. While patients with early cardiac AMR are less affected and seem to have survival rates comparable to transplant recipients without AMR, late cardiac AMR is frequently associated with graft dysfunction, fulminant forms of cardiac allograft vasculopathy, and a high mortality rate. Nevertheless, AMR of cardiac allografts remains difficult to diagnose and to treat. Case summary We report the case of a 47-year-old male patient with late AMR of the cardiac allograft 3 years after heart transplantation. Antibody-mediated rejection was confirmed by endomyocardial biopsy and the presence of donor-specific antibodies (DSA). The patient was treated with high dose of prednisolone, plasmapheresis, intravenous Gamma Globulin, rituximab, immunoadsorption, and bortezomib. Under this treatment regimen left ventricular ejection fraction and pro B-type natriuretic peptide recovered, and the patient improved to New York Heart Association Class I. Currently, 3 years after the diagnosis of cardiac AMR, graft function continues to be nearly normal, and there is no evidence for transplant vasculopathy. Discussion This case illustrates that AMR can occur at any time after transplantation. Although graft function fully recovered after treatment in our patient, the level of DSA remained high, suggesting that DSA may not be a reliable parameter to determine the intensity and duration of the therapy.

scholarly journals P0057ADPKD: COMPLEX GENOTYPES MAY EXPLAIN SEVERE PHENOTYPE AND INTRAFAMILIAL PHENOTYPIC VARIABILITY

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Claudia Izzi ◽  
Elisa Delbarba ◽  
Laura Econimo ◽  
Chiara Dordoni ◽  
Gianfranco Savoldi ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Early Onset ◽  
Mutant Allele ◽  
De Novo ◽  
Phenotypic Variability ◽  
Family Members ◽  
Cystic Kidney Disease ◽  
Cystic Kidney ◽  
Polycystic Kidney

Abstract Background and Aims Discordant affected relative-pairs are seen in ∼10% of families with Autosomal Dominant Polycystic Kidney Disease (ADPKD); &lt;1% of patients exhibit very early onset (VEO) disease. Complex genotypes may result in renal disease variability beyond that predicted by the sole effect of a single PKD mutant allele, leading to the discovery of biallelic or digenic disease. Here we illustrate such complexity in 6 ADPKD pedigrees. Method Among our single-center ADPKD cohort (186 index patients), we selected pedigrees (P) in which marked familial phenotypic variability or severe and early onset disease was investigated by NGS and MLPA analysis of PKD1 and PKD2 genes and NGS analysis of other cystogenes. Segregation analysis by Sanger sequencing of PKD variants was performed in available affected and unaffected family members. Results In P1 and P2, the index cases (IC), presented with very early onset (VEO) disease characterized by prenatal/neonatal enlarged and hyperechogenic kidneys mimicking autosomal recessive polycystic kidney disease (ARPKD). In P1, with neonatal onset, the ADPKD affected father transmitted a PKD1 PT variant p.Gln4231*, whereas the mother, without renal cystic phenotype, transmitted a PKD1 hypomorphic variant p.Asp1332Asn. In P2, the ADPKD-PKD2 mother’s pregnancy was complicated by Potter sequence. Parent’s PKHD1 gene analysis was negative. Two missense NT variants in PKD1/PKD2 genes were detected in the healthy father, respectively p.Gly1944Arg and p.Thr203Ile. Therefore, a complex PKD inheritance was supposed in the fetus. Fetus DNA was not available. In P3 early onset (EO) ADPKD in two monozygous twins was underpinned by a PKD1 NT variant (p.Arg1951Gln) inherited by the ADPKD mild affected father and worsened by a de novo PKD1 truncating variant p.Arg2402*. In P4 and P5 a digenic ADPKD (PKD1 +PKD2 and PKD1 +PKHD1) was diagnosed in severe ADPKD IC. In P4 the two most severely affected siblings carried a PKD2 T variant (p.Ala365fs) and a PKD1 NT variant p-Cys259Tyr. In P5 the IC presented with EO ADPKD, a de novo splicing variant c.2097 + 5_+6insT in PKD1 gene was discovered but the phenotype was probably worsened by the presence of biallelic variant in a second cystogene PKHD1: one paternally inherited: p.Gly1712Arg and one maternally inherited: p.Asp3088Asn . Elderly parents in P6 had mild ADPKD with bilateral few kidney cysts and preserved eGFR, whereas IC showed moderate/severe CKD due to ADPKD biallelic variants. The IC carried a homozygous PKD1 NT variant (p.Arg4154Cys): each mutant allele inherited from the mild ADPKD affected parents. Conclusion Our study illustrates the genetic complexity in an otherwise “simple” Mendelian disorder, providing insights into the genetic basis of severity of ADPKD cases and into ADPKD intrafamilial disease variability. In our pedigree all cases with more severe clinical picture in the family presented at least two PKD variants. In P5 we found for the first time an EO ADPKD due to both PKD1 and PKHD1 variants. PKD1 and PKD2 sequence analysis together with cystic kidney disease gene panel analysis is recommended in those patients with discordant phenotype compared to family members. Molecular study of PKD patients is expected to be a good prognostic tool together with clinical and renal imaging data to better manage disease therapy, follow-up and reproductive issues.

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