Consequences of Nephrotic Proteinuria and Nephrotic Syndrome after Kidney Transplant.

Proteinuria is the main predictor of kidney graft loss. However, there is little information regarding the consequences of nephrotic proteinuria (NP) and nephrotic syndrome (NS) after a kidney transplant. We aimed to describe the clinical and histopathological characteristics of kidney recipients with nephrotic-range proteinuria and compare the graft surveillance between those who developed NS and those who did not. A total of 204 patients (18.6% of kidney transplants in the study period) developed NP, and 68.1% of them had NS. Of the 110 patients who underwent a graft biopsy, 47.3% exhibited ABMR, 21.8% the recurrence of glomerulonephritis, 9.1% IFTA, and 7.3% de novo glomerulonephritis. After a median follow-up of 97.5 months, 64.1% experienced graft loss. The graft survival after the onset of NP declined from 75.8% at 12 months to 38% at 5 years, without significant differences between those with and those without NS. Patients who developed NS fewer than 3 months after the onset of NP exhibited a significantly higher risk of death-censored graft loss (HR: 1.711, 95% CI: 1.147-2.553) than those without NS or those with late NS. In conclusion, NP and NS are frequent conditions after a kidney transplant, and they imply extremely poor graft outcomes. The time from the onset of NP to the development of NS is related to graft survival.

Primary intraarterial occlusive lipoma.

Lipomas are the most frequent soft tissue tumors. Intravenous lipomas are very uncommon, but even more unusual are intraarterial lipomas. A 68-year-old heavy smoker man, with chronic alcoholism, retinopathy, dyslipidemia, and a history of type 2 diabetes mellitus of more than 10 years of evolution was hospitalized in a state of dependency. He presented ulcers on both heels and right foot sole extending to the fifth metatarsal base and bedsores in the iliac and sacral regions. Ulcer cultures showed growth of Klebsiella pneumoniae OXA34. A computed tomography angiography scan revealed that the right posterior tibial artery showed several segments with signs of obstruction or sub-occlusive stenosis along its entire length, but especially in the distal two-thirds. The patient underwent supracondylar amputation of the right lower limb. Histopathological sections of the amputated leg showed calcific atherosclerosis obliterans of the posterior tibial artery and complete occlusion in the middle portion of this artery. The occlusion was due to a well-differentiated, white adipose tissue with lipid vacuoles of uniform size. To our knowledge, this case is the first known report of a primary intraarterial lipoma in a peripheral artery. The proliferating adipose tissue within the arterial lumen contributed to distal limb ischemic necrosis. Although an intraarterial lipoma is rare, it should be considered in the differential diagnosis of the causes of peripheral arterial occlusion.

Urinary CXCL10 specifically relates to HLA-DQ eplet mismatch load in kidney transplant recipients.

BACKGROUND: Urinary CXCL10 (uCXCL10) is associated with graft inflammation and graft survival, but the factors related to its excretion are not well known. HLA molecular matching at epitope level allow estimating the "dissimilarity" between donor and recipient HLA more precisely, being better related to further transplant outcomes. The relationship between uCXCL10 and HLA molecular mismatch has not been previously explored. METHODS: HLA class I and class II typing of some 65 recipients and their donors was retrospectively performed by high resolution sequence-specific-primer (Life Technologies, Brown Deer, WI). The HLA-Matchmaker 3.1 software was used to assess eplet matching. Urine samples collected on the day of the 1-year surveillance biopsy were available of these 65 patients. uCXCL10 was measured using a commercial enzyme-linked immunoassay kit. RESULTS: 1-year uCXCL10 was independently associated with HLA-DQB1 eplet mismatch load (ß 0.300, 95%CI 0.010-0.058, p = 0.006). Kidney transplant recipients with a HLA-DQB1 eplet mismatch load >3 showed higher values of uCXCL10 at 1-year (p = 0.018) than those with ≤3. Patients with a HLA-DQB1 eplet mismatch load >3 with subclinical AbMR had significantly higher levels of the logarithm of 1-year uCXCL10 (No AbMR 0.88, IQR 0.37; AbMR 1.38, IQR 0.34, p = 0.002) than those without AbMR. CONCLUSIONS: uCXCL10 specifically relates to HLA-DQ eplet mismatch load. This relationship can partly explain the previously reported association between uCXCL10 excretion and graft inflammation. An adequate evaluation of any potential non-invasive biomarker, such as uCXCL10, must take into account the HLA molecular mismatch.

Controlled Donation After Circulatory Death Using Normothermic Regional Perfusion Does Not Increase Graft Fibrosis in the First Year Posttransplant Surveillance Biopsy.

OBJECTIVES: The number of kidney transplants obtained from controlled donations after circulatory death is increasing, with long-term outcomes similar to those obtained with donations after brain death. Extraction using normothermic regional perfusion can improve results with controlled donors after circulatory death; however, information on the histological impact and extraction procedure is scarce. MATERIALS AND METHODS: We retrospectively investigated all kidney transplants performed from October 2014 to December 2019, in which a follow-up kidney biopsy had been performed at 1-year follow-up, comparing controlled procedures with donors after circulatory death and normothermic regional perfusion versus donors after brain death. Interstitial fibrosis/tubular atrophy was assessed by adding the values of interstitial fibrosis and tubular atrophy, according to the Banff classification of renal allograft pathology. RESULTS: When we compared histological data from 66 transplants with donations after brain death versus 24 transplants with donations after circulatory death and normothermic regional perfusion, no differences were found in the degree of fibrosis in the 1-year follow-up biopsy (1.7 ± 1.3 vs 1.7 ± 1.1; P = .971) or in the ratio of patients with increased fibrosis calculated as interstitial fibrosis/tubular atrophy >2 (18% vs 13%; P = .522). In our multivariate analysis, which included acute rejection, expanded criteria donation, and the type of donation, no variable was independently related to an increased risk of interstitial fibrosis/tubular atrophy >2. CONCLUSIONS: The outcomes of kidney grafts procured in our center using controlled procedures with donors after circulatory death and normothermic regional perfusion were indistinguishable from those obtained from donors after brain death, showing the same degree of fibrosis in the 1-year posttransplant surveillance biopsy. Our data support the conclusion that normothermic regional perfusion should be the method of choice for extraction in donors after circulatory death.

Urinary C-X-C Motif Chemokine 10 Is Related to Acute Graft Lesions Secondary to T Cell- and Antibody-Mediated Damage.

BACKGROUND Non-invasive biomarkers of graft rejection are needed to optimize the management and outcomes of kidney transplant recipients. Urinary excretion of IFN-g-related chemokine CXCL10 is clearly associated with clinical and subclinical T cell-mediated graft inflammation, but its relationship with antibody-mediated damage has not been fully addressed. Further, the variables influencing levels of urinary CXCL10 excretion are unknown. MATERIAL AND METHODS A total of 151 kidney graft biopsies (92 surveillance and 59 indication biopsies) and 151 matched urine samples obtained before biopsy were prospectively analyzed. T cell-mediated rejection (TCMR) and antibody-mediated rejection (AbMR) were defined according to the 2017 Banff classification criteria. Urinary CXCL10 levels were measured by ELISA and corrected by urinary creatinine. RESULTS Banff scores 't', 'i', 'g', and 'ptc' were significantly related to urinary CXCL10 levels. Multivariate analysis showed that 't' (ß=0.107, P=0.001) and 'ptc' (ß=0.093, P=0.002) were significantly associated with urinary CXCL10. Donor-specific antibodies (DSAs) were related to the high excretion of urinary CXCL10 at 1 year after transplantation (odds ratio [OR] 17.817, P=0.003). Urinary CXCL10 showed good discrimination ability for AbMR (AUC-ROC 0.760, P=0.001). The third tertile of urinary CXCL10 remained significantly associated with AbMR (OR 4.577, 95% confidence interval 1.799-11.646, P=0.001) after multivariate regression analysis. CONCLUSIONS DSA was the only variable clearly related to high urinary CXCL10 levels. Urinary CXCL10 is a good non-invasive candidate biomarker of AbMR and TCMR, supplying information independent of renal function and other variables normally used to monitor kidney transplants.

[Idiopathic progressive bilateral ureteral stenosis]. / Estenosis ureteral bilateral progresiva e idiopática.

OBJECTIVE: To report one case of progressive bilateral ureteral stenosis without demonstrable etiologic cause. METHODS: We diagnosed and treated a 73-year-old female patient who developed progressive bilateral distal ureteral stenosis without a demonstrable cause. RESULTS: Surgery was carried out and the pathologic study showed a bilateral ureteral stenosis secondary to fibrosis and chronic unspecific inflammation. CONCLUSIONS: Idiopathic ureteral stenosis is a rare clinical picture, more if progressive and bilateral.

Estenosis ureteral bilateral progresiva e idiopática / Idiopathic progressive bilateral ureteral stenosis

OBJETIVOS: Presentar un caso de estenosis ureteral bilateral de evolución progresiva sin constatar causa etiológica responsable del cuadro. METODOS: Se diagnostica y trata una paciente de 73 años de edad que desarrolla de forma progresiva una estenosis bilateral distal de ambos uréteres, sin objetivarse la causa responsable. RESULTADOS: Intervenida quirúrgicamente la paciente, el estudio anátomo-patológico puso de manifiesto una estrechez ureteral bilateral debido a una fibrosis e inflamación crónicas e inespecíficas. CONCLUSIONES: La estenosis ureteral idiopática es un cuadro raro, más si cabe si su evolución es progresiva y con afectación bilateral (AU)

OBJECTIVE: To report one case of progressive bilateral ureteral stenosis without demonstrable etiologic cause. METHODS: We diagnosed and treated a 73-year-old female patient who developed progressive bilateral distal ureteral stenosis without a demonstrable cause. RESULTS: Surgery was carried out and the pathologic study showed a bilateral ureteral stenosis secondary to fibrosis and chronic unspecific inflammation. CONCLUSIONS: Idiopathic ureteral stenosis is a rare clinical picture, more if progressive and bilateral