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In this retrospective cohort study, we aimed to evaluate the incidence, risk factors and outcomes of amikacin-induced acute kidney injury (AKI) in critically ill patients with sepsis. A total of 311 patients were included in the study. Of them, 83 (26.7%) had amikacin-induced AKI. In model 1, the multivariable analysis demonstrated concurrent use of colistin (OR 25.51, 95%CI 6.99-93.05, p0.001), presence of septic shock during amikacin treatment (OR 4.22, 95%CI 1.76-10.11, p=0.001), and Charlson Comorbidity Index (OR 1.14, 95%CI 1.02-1.28, p=0.025) as factors independently associated with an increased risk of amikacin-induced AKI. In model 2, the multivariable analysis demonstrated concurrent use of at least one nephrotoxic agent (OR 1.95, 95%CI 1.10-3.45; p=0.022), presence of septic shock during amikacin treatment (OR 3.48, 95%CI 1.61-7.53; p=0.002), and Charlson Comorbidity Index (OR 1.12, 95%CI 1.01-1.26; p=0.037) as factors independently associated with an increased risk of amikacin-induced AKI. In conclusion, before amikacin administration, the risk of AKI should be considered, especially in patients with multiple complicated comorbid diseases, septic shock, and those receiving colistin therapy.

Rationale & Objective Data on kidney transplantation outcomes among patients with monoclonal gammopathy of renal significance (MGRS) are lacking. Study Design Case series of patients with MGRS, some of whom received clone-directed therapies before kidney transplantation. Setting & Participants 28 patients who underwent kidney transplantation from 1987 through 2016 after diagnosis with MGRS-associated lesions including light-chain deposition disease (LCDD), C3 glomerulopathy with monoclonal gammopathy (C3G-MG), and light-chain proximal tubulopathy (LCPT). Findings Of the 19 patients with LCDD, 10 were treated before kidney transplantation and 9 were treatment-naive. Among the treated patients with LCDD, 3 (30%) experienced histologic recurrence, 2 (20%) grafts failed, and 2 (20%) died during a median follow-up of 70 (range, 3-162) months after transplant. In the treatment-naive LCDD group, 8 (89%) had histologic recurrence, 6 (67%) grafts failed, and 4 (44%) patients died during a median follow-up of 60 (range, 35-117) months. Of the 5 patients who had a complete response before transplant, none died, and only 1 experienced graft failure, 162 months after transplant. Of 5 patients with C3G-MG, 3 were treatment-naive before transplant. Both patients who were treated before transplant had histologic recurrence, and 1 experienced graft failure and died. Among the 3 patients with treatment-naive C3G-MG, histologic recurrence occurred in all, and graft loss and death were observed in 2 and 1, respectively. In the LCPT group (n = 4), histologic recurrence was observed in all 3 patients who did not receive clone-directed therapies before transplant, and 2 of these patients died, 1 with a functioning kidney. The 1 patient with LCPT who received therapy before transplant did not have histologic recurrence or graft loss and survived. Limitations Small sample size, nonstandardized clinical management, retrospective design. Conclusions Recurrence is very common in all MGRS-associated lesions after kidney transplant. Achieving a complete hematologic response may reduce the risks of recurrence, graft loss, and death. More studies are needed to determine the effects of hematologic response on outcomes for each MGRS-associated lesion.

Patients undergoing maintenance hemodialysis have unique risk factors that render them prone to ischemia. To what extent coronavirus infectious disease 2019 (COVID-19) increases this risk is unknown.This retrospective cohort study included incident patients undergoing maintenance hemodialysis from one city in Turkey. A comparison was made between those who developed COVID-19 and those who did not for clinical variables. Independent predictors of acute ischemic complications in the total cohort were assessed using the logistic regression analysis.By the start of the pandemic in Turkey, 33 of 154 (21.4%) patients developed COVID-19. During the 15 months of median follow-up after the start of the pandemic, 16 (10.4%) patients developed acute ischemic complications. These included acute myocardial infarction (n = 10), acute ischemic stroke (n = 4), acute peripheral artery thrombosis (n = 1), and pulmonary thromboembolism (n = 1). Overall, acute ischemic events occurred more commonly in those who experienced COVID-19 (24.2% vs. 6.6%, p = 0.007). Ischemia-free survival was significantly shorter in the COVID-19 group (p = 0.001). In the eight patients with COVID-19, ischemic complications emerged at a median 185 (range 21-306) days after the diagnosis of COVID-19. While age, dialysis vintage, and experience of COVID-19 were found as factors significantly associated with the development of acute ischemic events in univariate analysis, the association between COVID-19 and acute ischemia remained significant in the multivariate regression model (odds ratio 3.99, 95% CI [1.3, 12.13], p = 0.016). During the pandemic, 23 (14.9%) patients died. Overall survival was significantly shorter among those who developed acute ischemic event (p 0.001). The hazard ratio of acute ischemic event for death was 6.76 (95% CI [2.92, 15.66], p 0.001).A considerable number of patients undergoing maintenance hemodialysis developed acute ischemic complications weeks to months after the resolution of COVID-19. Hemodialysis patients appear to require specific interventions in order to prevent subsequent acute ischemic events after the resolution of COVID-19.

Serious complications during hemodialysis (HD) are rarely observed in part owing to more sophisticated devices and experienced staff. However, such complications carry the risk of catastrophic consequences including death. This report highlights major emergencies in three cases that may occurred during HD treatments while alarm mechanisms did not work.

Purpose: Patients with chronic kidney disease (CKD) usually represent an aging population, and both older age and CKD are associated with a higher risk of falling. Studies on risk factors among subjects with CKD are lacking. Methods: Records of outpatients from one geriatric clinic in Turkey were retrospectively reviewed. A result of ≥ 13.5 s on the timed up and go (TUG) test was accepted as a high risk of falls. Independent predictors of an increased risk of falls among subjects with CKD (estimated glomerular filtration rate of < 60 mL/min/1.73 m2) were identified using logistic regression models. Results: Patients with CKD (n = 205), represented the 20.2% of the entire cohort and was identified as an independent predictor of increased fall risk (OR 2.59). Within the CKD cohort, serum folic acid levels and frailty were independent predictors of an increased risk of falls. The CKD/fall risk group was older, had a lower median years of education, lower vitamin D levels, and lower serum folic acid levels than the CKD/non-fall risk group. In addition to higher serum creatinine and potassium levels, the only significant difference between patients with CKD/fall risk and a matched non-CKD/fall risk was a lower median folic acid level in the former group. Conclusions: Frailty and low folic acid levels are independently associated with an increased risk of falls among elderly outpatients with CKD. Prevention of frailty may reduce the risk of falls in these subjects. Possible benefit of folic acid supplementation requires further studies. © 2021, The Author(s), under exclusive licence to Springer Nature B.V.

Geriatric syndromes are complex clinical manifestations and significant causes of mortality and morbidity. This study was aimed to determine the frequency and co-incidence of geriatric syndromes in older patients with chronic kidney disease (CKD).\ud Methods\ud Older patients were included in this cross-sectional retrospective study. All patients were questioned in terms of geriatric syndromes including dementia, polypharmacy, malnutrition, frailty, probable sarcopenia, urinary incontinence, falls, fear of falling, depression, insomnia, and excessive daytime sleepiness. Geriatric syndromes were evaluated according to Glomerular Filtration Rate (GFR) ≥ 60 ml/min/1.73 m2, 30–59 ml/min/1.73 m2 and

Background-\ud \ud Excessive daytime sleepiness (EDS) is prevalent in not only older adults, but also patients with chronic kidney disease (CKD), and is associated with higher risks of morbidity and mortality.\ud \ud Aims-\ud \ud The aim of the present study is to determine associations between EDS and nutritional status and serum nutrient levels in older patients with CKD.\ud \ud Methods-\ud \ud This cross-sectional study included 367 patients (aged ≥ 65 years) with CKD (eGFR 30 mg/day of albuminuria for > 3 months). EDS was recorded using the Epworth Sleepiness Scale (a score of ≥ 11). Malnutrition was diagnosed according to the Mini Nutritional Assessment (MNA) tool (a score of 0.05).\ud \ud Conclusions-\ud \ud EDS is associated with malnutrition in older patients with CKD. Therefore, EDS and nutritional status should be evaluated together in clinical practice. However, future studies are needed to determine the direction of the association between malnutrition and EDS and to evaluate if dietary intervention can improve EDS.

The use of immune checkpoint inhibitors has been increasing rapidly. Numerous untoward immune-related adverse events due to immune checkpoint inhibitors have been reported. Acute interstitial nephritis due to immune checkpoint inhibitors is one of these immune-related adverse events. Although gold standard, it is not always straightforward to perform a kidney biopsy in oncological patients. Helpful diagnostic methods are lacking. In this case report, we discuss the potential role of positron emission tomography–computed tomography on supporting the diagnosis of acute interstitial nephritis or ruling it out in the setting of acute kidney injury following treatment with immune checkpoint inhibitors. Studies are needed to assess the possible role of positron emission tomography–computed tomography for the diagnosis of acute interstitial nephritis in these subjects.

Background: Prevalence and characteristics of non-diabetic renal diseases (NDRD) in patients with type 2 diabetes mellitus is different between populations, and seems to be largely dependent on biopsy policies. Aim: To investigate clinical clues for NDRD in patients with type 2 diabetes mellitus and to analyse renal prognosis of patients based on pathological diagnosis. Methods: We retrospectively searched medical records of 115 patients with type 2 diabetes who underwent a renal biopsy between 2004 and 2018. Patients were divided into three groups as diabetic nephropathy (DN), NDRD + DN or NDRD based on histopathological examination. Results: Thirty-six (31.3%) patients had DN, 33 (28.7%) had DN + NDRD and 46 (40%) had NDRD. The absence of diabetic retinopathy, recent onset of diabetes, abnormal disease chronology, and blood haemoglobin was associated with the presence of NDRD in univariate analysis. Abnormal disease chronology which was defined as the presence of acute proteinuria and/or acute kidney injury that are unexpected to be related to evolution of diabetic nepropathy (odds ratio 4.65, 95% confidence interval 1.44-15.00; P = 0.010) and absence of diabetic retinopathy (odds ratio 3.44, 95% confidence interval 1.32-8.98; P = 0.012) were independently associated with the presence of NDRD in multivariate analysis. Focal segmental glomerulosclerosis was the most frequent type of NDRD. Diseases that affect tubulointerstitial area were more prevalent in the DN + NDRD group compared to the NDRD group (P = 0.001). Renal survival, which was defined as evolution to end-stage renal disease, was 59.5 +/- 14.4 months, 93.7 +/- 11.7 months and 87.2 +/- 2.6 months for DN, DN + NDRD and NDRD groups, respectively (P = 0.005). Conclusions: Renal biopsy is essential in certain clinical conditions as diagnosis of NDRD is vital for favourable renal survival. DN may facilitate superimposed tubular injury in the presence of toxic insults.

Data on kidney transplantation (KTx) outcomes of patients with multiple myeloma (MM) are very limited.We investigated the outcomes of patients with MM who underwent KTx between 1994 and 2019.A total of 12 transplants from 11 patients were included. At the time of KTx, 6 were classified as having stringent complete response (CR), 2 as CR, 2 as very good partial response (VGPR), and 2 as partial response (PR). With a median follow-up of 40 (minimum-maximum, 5-92) months after KTx, hematologic progression occurred in 9 transplants (75%). There were 3 grafts (25%) that failed, and 5 patients (45.5%) experienced death with functioning allografts. Graft survival at 1 and 5 years was 82.5% and 66%, respectively. Progression-free survival (PFS) rates of the cohort at 1, 3, and 5 years were 83.3%, 55.6%, and 44.4%, respectively. The estimated median PFS of patients who received bortezomib at any time (pre-KTx and/or post-KTx) was not reached, whereas it was 24 months for those who never received bortezomib (Kidney transplant outcomes of patients with myeloma who received bortezomib before or after KTx seem to be more favorable. Nevertheless, relapse after KTx in MM is still common. More studies are needed to better determine who benefits from a KTx.

Anemia is one of the common chronic renal failure (CRF) complications. Reduced renal erythropoietin (EPO) production and a shortened life span of erythrocytes due to uremic environment and iron deficiency are the main causes of anemia in patients with CRF. Correcting of iron deficiency constitutes the basis for the treatment of anemia in patients with CRF. Iron replacement can be done orally or intravenously. The seriousness of anemia and iron deficiency, tolerance of tablet use, response to previous treatments, and the presence of a ready vascular access determine the manner in which iron treatment is done. New generation parenteral iron preparations have complex carbohydrate structures that strongly bind to iron and reduce plasma free iron release. New generation iron molecules correct iron deficiency without causing an inflammatory process. The point that should be kept in mind is that new formulations may have a side effect profile that has not yet been experienced, in addition to various advantages. When using new iron molecules, precaution measures should be taken with regard to the development of arrhythmia, unstable angina, and hypophosphatemia.

Colistin methanesulfonate (CMS), a clinical form of colistin, is widely used as a last-line treatment for multidrug-resistant (MDR) gram-negative bacterial infections in critically ill patients presenting a considerably high mortality rate. However, nephrotoxicity is considered to be a critical adverse effect that limits CMS’s clinical use. Alpha-lipoic acid (ALA) is a strong antioxidant that is effective in preventing nephrotoxicity in many models. The aim of this study was to investigate ALA’s ability to protect against nephrotoxicity induced by colistin in rats. Male Wistar albino rats were randomly divided into four groups. Group 1 was the control group (Control; n = 6), in which isotonic saline was administered to the rats. Group 2 was the ALA group (ALA; n = 6) in which rats received 100 mg/kg ALA. Groups 3 was the CMS (CMS; n = 7) in which 450.000 IU/kg/day of CMS was administered to the rats. Groups 4 was the CMS + ALA group (n = 6), in which rats were injected with 100 mg/kg of ALA 30 min before administration of CMS. All injections were performed intraperitoneally at 1, 4, 7, and 10 days. Urine was collected by using a metabolic cage for 24 h after each administration. The rats were euthanized under ether anesthesia after 24 h of the last administration. Blood and kidney samples then were collected for histological and biochemical analysis. ALA pretreatment could reverse the effects of colistin-induced nephrotoxicity, partly through its suppressing effect on Nox4 and caspase-3, which in turn results in its antioxidant and antiapoptotic effect. Therefore, ALA may be an effective strategy for the management of colistin nephrotoxicity. © The Author(s) 2020.

The impact of mild hyponatremia on geriatric syndromes is not clear. Our aim was to determine associations between mild hyponatremia and results of comprehensive geriatric assessment tools in outpatient settings. We reviewed medical records of 1255 consecutive outpatient elderly subjects and compared results of comprehensive geriatric assessment measures among patients with mild hyponatremia (serum Na+ 130–135 mEq/L) versus normonatremia (serum Na+ 136–145 mEq/L). The comprehensive geriatric assessment measures included the Basic and Instrumental Activities of Daily Living, Mini Mental State Examination, Geriatric Depression Score, Tinetti Mobility Test, the Timed Up&Go Test, the Mini Nutritional Assessment, the handgrip test, the Insomnia Severity Index, polypharmacy, recurrent falls, urinary incontinence, orthostatic hypotension, and nocturia. Of the 1255 patients, 855 were female (68.1%), and the mean age was 73.7 ± 8.3 years. Mild hyponatremia was detected in 108 patients (8.6%). The median serum sodium was 140.5 [interquartile range (IQR) 138.4–141.8] versus 133.8 [IQR, 132.3–134.2] in normonatremia and mild hyponatremia groups, respectively (p

Aim: Although mild hypomagnesemia is frequently asymptomatic, given it’s widespread physiological roles through the body system hypomagnesemia may be associated with crucial patient outcomes in elderly, whose body systems are more prone to disease states. In this study, we have evaluated association of hypomagnesemia with geriatric syndromes and mortality among subjects with an age of 65 years or more.Material and Methods: Electronic medical records of subjects who were evaluated in geriatrics clinic were reviewed retrospectively. A serum magnesium level of, Amaç: Hafif hipomagnezemi sıklıkla asemptomatik olmasına rağmen vücutta önemli olan çok sayıda sistem üzerindeki kofaktör rolü nedeniyle bu sistemleri daha duyarlı yaşlı bireylerde hipomagnezemi ciddi hasta sonlanımlarıyla birlikte olabilir. Ayaktan geriatri polikliniğinde değerlendirilen 65 yaş ve üzeri bireylerde hipomagnezeminin geriatrik sendromlar ve mortalite ile ilişkisini değerlendirmeyi hedefledik.Gereç ve Yöntemler: Geriatri polikliniğinde değerlendirilen tüm bireylerin (≥65 yaş) elektronik tıbbi kayıtları geriye dönük incelendi. Serum magnezyum düzeyi

Iron has been implicated in oxidative tissue injury owing to its ability to generate reactive oxygen species (ROS). We investigated the reno-protective effects of alpha lipoic acid (ALA) by investigating its effects on the kidney isoform of NADPH oxidase (Nox4) and the specific signaling pathways, p38 MAPK and PI3K/Akt, which participate in apoptosis and survival, respectively. We established four groups of seven rats: control, 100 mg/kg ALA, 80 mg/kg iron sucrose (IS) and IS + ALA. IS and ALA were injected intravenously and rats were sacrificied after 6 h. The mRNA expression of the subunits of NADPH oxidase, Nox4 and p22phox; tumor necrosis factor-alpha (TNF-α); and kidney injury molecule-1 (KIM-1) were measured using quantitative real time polymerase chain reaction (qRT-PCR). Active caspase-3 protein expression was evaluated by immunostaining. Also, p38 MAPK and PI3K/Akt signaling pathways were analyzed using western blot. ALA suppressed the mRNA expression of Nox4, p22phox, TNF-α and KIM-1. Active caspase-3 protein expression induced by IS was decreased by ALA. ALA also suppressed p38 MAPK and activated the PI3K/Akt signaling pathway following IS administration. We found that ALA may be an effective strategy for preventing oxidative acute kidney injury caused by IS. © 2020 The Biological Stain Commission.

Nephrotoxicity following colistin administration is common and factors alleviating nephrotoxicity are yet to be determined. We retrospectively evaluated outcomes of subjects who were treated with colistin (n = 133) and with antibiotics other than colistin (control, n = 133) in intensive care units. Acute kidney injury (AKI) occurred in 69.2% and 29.3% of patients in colistin and control groups, respectively (p < 0.001). In the colistin group, glucocorticoid exposure was more common in subjects who did not develop AKI (p < 0.001). This was not the case in the control group. In the colistin cohort, older age (per 10 years, odds ratio [OR] 1.41, 95% CI 1.05-1.91; p = 0.025), PPI use (OR 3.30, 95% CI 1.18-9.23; p = 0.023) and furosemide treatment (OR 2.66, 95% CI 1.01-6.98; p = 0.047) were independently associated with the development of AKI while glucocorticoid treatment (OR 0.23, 95% CI 0.10-0.53; p = 0.001) was independently associated with reduced risk of AKI. Mortality was observed in 74 patients in the colistin cohort (55.6%). A higher APACHE-II score (OR 1.17, 95% CI 1.08-1.26; p < 0.001) was independently associated with mortality while a higher serum albumin level (per 1 g/dL increase, OR 0.20, 95% CI 0.070-0.60; p = 0.004) was associated with a lower risk of mortality. In conclusion, glucocorticoid exposure is associated with a lower risk of AKI caused by colistin therapy in critically-ill patients. Prospective studies are needed to confirm these findings and determine the optimal type, dose and duration of glucocorticoid therapy.

Transplant-associated thrombotic microangiopathy (TA-TMA) has a wide range of presentations after hematopoietic stem-cell transplantation (HSCT). We retrospectively studied the risk factors and outcomes of patients with early (≤day 100) and late (>day 100) TA-TMA. Among the 1451 HSCT recipients, early TA-TMA occurred in 45 (3.1%) patients at a median of 27 (3-91) days, and late TA-TMA in 39 (2.7%) patients at a median of 303 (122-2595) days. Patients with early TA-TMA were more likely to have high blood calcineurin-inhibitor levels (P < .001) and acute graph-vs-host disease (GVHD, P < .001), while late TMA patients were more likely to have chronic GVHD (P < .001). The estimated median overall survival after onset of TMA for the entire cohort was 6 months. The estimated median overall survival was not reached in patients with an improvement of TMA vs 2 months in patients with no improvement (P < .001). In the early TMA group, older age (for every 10 years, HR 1.40; 95% CI 1.00-1.94; P = .049) and bacterial infection (HR 2.42; 95% CI 0.98-6.00; P = .056) were positively associated with mortality. Switching to MMF treatment (HR 0.40; 95% CI 0.16-0.99; P = .047) and improvement of TMA (HR 0.08; 95% CI 0.03-0.25; P < .001) were negatively associated with mortality in the multivariate analysis. In the late TMA group, the improvement of TMA was the only independent predictor associated with a lower risk of death (HR 0.05; 95% CI 0.02-0.19; P < .001). Mortality rates in both early and late TMA remain unacceptably high. Future studies are needed for early diagnosis, trigger identifications, and use of targeted treatments.

Objective: The goal of this study was to identify risk factors among donor characteristics that affect delayed graft function (DGF) in paired kidney transplants.

We aimed to investigate the protective effect of alpha lipoic acid (ALA), a powerful antioxidant, against oxidative kidney damage induced by iron overload in rats. Male Wistar albino rats were separated into groups: control (n = 7), ALA (100 mg/kg (n = 7), iron sucrose (IS) (40 mg/kg) (n = 7), and IS + ALA (40 mg/kg IS administration followed by 100 mg/kg ALA) (n = 7). IS and ALA were injected weekly for 4 weeks via the tail vein. Blood and kidneys were collected at sacrification on day 29. Serum creatinine and iron levels were analyzed. Tubular injury and iron deposits were evaluated histopathologically. Additionally, iron, malondialdehyde (MDA), superoxide dismutase (SOD), catalase, and glutathione (GSH) levels and mRNA expressions of the subunits of NADPH oxidase, known as NOX4 and p22(phox), tumor necrosis factor (TNF)-alpha, kidney injury molecule-1 (KIM-1), and also p38 MAPK signaling in the kidneys, were evaluated biochemically. In the IS group, serum creatinine and iron level, tubular dilation, and loss of brush border in the kidneys were significantly higher than those of the control. Although those changes were reduced by ALA, the differences were not statistically significant. However, ALA reduced significantly MDA level and increased SOD activity in the kidney during IS administration. ALA also significantly reduced mRNA expressions of NOX4 and p22(phox) induced by IS, which was parallel to significant decreases of TNF-alpha and KIM-1 mRNA expressions. Moreover, ALA could suppress the activation of p38 MAPK during IS administration. In conclusion, ALA may be an effective strategy to attenuate in IS-induced oxidative kidney injury.

BackgroundGlomerular immunoglobulin G deposition in patients with immunoglobulin A nephropathy (IgAN) has been shown to be associated with adverse renal outcomes. Clinical significance of mesangial immunoglobulin M (IgM) deposition in these patients remains to be proven.MethodsOne hundred patients who had a diagnosis of IgAN between 2001 and 2017 were enrolled. Patients were divided into two groups based on mesangial IgM deposition status. Groups were compared for demographic, clinical, and pathologic variables at baseline and in follow-up. Cox regression analysis was performed to evaluate the effect of mesangial IgM positivity on renal survival.ResultsIgM-positive group included 51% of participants. Baseline demographic and clinical parameters were not significantly different between groups. Mesangial IgM deposition was significantly associated with a higher segmental sclerosis score (p=0.008). At last visit, median serum creatinine was higher (p=0.021) and eGFR was lower (p=0.006) in IgM-positive group. Nineteen (19%) of all patients reached the combined primary outcome which includes doubling in serum creatinine or evolution to ESRD. Cumulative renal survival was lower (p=0.001) and resistant disease was more frequent in IgM-positive group (p=0.026). Renal survival at 15years was 94.2% and 59.7% in IgM-negative and IgM-positive groups, respectively (p=0.006). Time-averaged proteinuria (HR 2.9; 95% CI 1.9-4.5; p

Colistin is an old antibiotic, which is abandoned decades ago because of high nephrotoxicity rates. However, it is reintroduced to clinical medicine due to lack of newly discovered antibiotics and is still widely used for the treatment of resistant gram-negative infections. Discovering mechanisms to reduce nephrotoxicity risk is of significant importance since exposed patients may have many other factors that alter kidney functions. Several agents were evaluated in animal models of colistin nephrotoxicity as a means to prevent kidney injury. Considerable heterogeneity exists in terms of reporting colistin dosing and experimental designs. This issue leads clinicians to face difficulties in designing studies and sometimes may lead to report dosing strategies inadequately. Here, we present a review according to animal models of colistin nephrotoxicity using data gathered from previous experiments to draw attention on possible complexities that researchers may encounter.

Objectives Reported graft and patient survival rates in amyloidosis after renal transplant differ considerably between studies. Materials and methods Group 1 included 24 patients who had end-stage renal disease secondary to amyloidosis. Group 2 (the control group) included 24 consecutive patients who had kidney disease secondary to various causes other than amyloidosis. Comparisons between groups were made for kidney and patient survival rates and other complications following kidney transplant. We also compared survival rates of patients in group 1 versus another control group that included patients with amyloidosis who were treated with hemodialysis (group 3; n = 25). Results Mean follow-up was 109.5 ± 79.8 months. Biopsy-proven acute rejection and graft failure rates were not significantly different between groups. In group 1 versus group 2, the cumulative 10-year and 20-year patient survival rates were 68.2% versus 86.1% and 36.9% versus 60.3%, respectively (P = .041). Survival was not significantly different in group 1 compared with group 2 and group 3, although patients in group 3 had significantly shorter duration of time to death after the start of renal replacement therapy. Conclusions Patient survival may be lower in kidney transplant recipients with amyloidosis compared with patients with end-stage renal disease due to other causes. However, graft failure and acute rejection rates seem to be similar.

Background : P-glycoprotein (P-gp) transports many chemicals that vary greatly in their structure and function. It is normally expressed in renal proximal tubular cells. We hypothesized that P-gp expression influences light chain excretion. Therefore, we investigated whether renal tubular P-gp expression is altered in patients with plasma cell disorders. Methods : We evaluated renal biopsy specimens from patients with plasma cell disorders (n = 16) and primary focal segmental glomerulosclerosis (the control group, n = 17). Biopsies were stained with an anti-P-gp antibody. Loss of P-gp expression was determined semi-quantitatively. Groups were compared for loss of P-gp expression, and clinical variables. Results : P-gp expression loss was more severe in patients with plasma cell disorders than it was in those with glomerulonephritis (P = 0.021). In contrast, clinical and histological parameters including serum creatinine, level of urinary protein excretion, and interstitial fibrosis/tubular atrophy grade were not significantly different between the groups. P-gp expression loss increased with age in patients with plasma cell disorders (P = 0.071). This expression loss was not associated with serum creatinine, the level of urinary protein excretion or the interstitial fibrosis/tubular atrophy grade. There was no significant association between the severity of P-gp expression loss with the types and serum levels of light chains, isotypes and serum immunoglobulin levels. Conclusion : Renal tubular P-gp expression is significantly down-regulated in patients with plasma cell disorders characterized by nephrotic range proteinuria. Additional studies are needed to determine whether reintroduction of renal tubular P-gp expression would mitigate the proximal tubular injury that is caused by free-light chains.

C4d deposition is defined as the footprint of immune injury and it is associated with unfavorable renal outcomes in patients with IgA nephropathy. We searched whether mesangial C4d deposition is associated with poor renal survival in patients with primary focal segmental glomerulosclerosis (FSGS). Biopsy specimens were stained with anti-C4d antibody. Patients were classified based on mesangial C4d deposition as C4d-negative and C4d-positive. Groups were compared according to baseline and follow-up clinical variables. Factors that predict renal progression and treatment failure were determined using Cox-regression and multivariate logistic regression models, respectively. Forty-one FSGS patients were followed for a mean of 67.7 ± 40.8 months. C4d-positive group included 18 patients while remaining 23 patients were C4d-negative. Urinary protein excretion and serum creatinine levels at baseline were comparable between groups. Fifteen patients reached the composite primary endpoint which included serum creatinine increasing > 30% from the baseline and reaching > 1.5 mg/dl, and/or evolution to end-stage renal disease (36.6%). In multivariate regression analysis, baseline eGFR (OR 0.71, 95% CI 0.53–0.94; p = 0.016) and mesangial C4d deposition (OR 10.5, 95% CI 1.51–73.18; p = 0.018) were independently associated with treatment failure rates. Mesangial C4d deposition was independently associated with the progression to the primary endpoint (HR 6.54, 95% CI 1.49–28.7, p = 0.013). We showed for the first time that mesangial C4d deposition is an independent predictor of disease progression and treatment failure in patients with primary FSGS.

Objective: Helicobacter pylori (HP) is a bacterial pathogen that leads to gastroduodenal inflammation, gastric and duodenal ulcer and atrophic gastritis. Colonization of bacteria can be shown by using rapid-urease test during endoscopy. There are conflicting data about the route of transmission and reservoir. It’s thought to be transmitted primarily by oral route. Many studies showed results supporting that the presence of bacteria in dental plaques has effects on gastric colonization and eradication. There are data about the potential inhibitory effect of oral flora on HP. We aimed to analyze the association of simplified oral hygiene index -a possible representation of a healthy oral flora- with HP positivity. Methods: Patients undergoing upper gastrointestinal system endoscopy for symptoms of dyspepsia were assessed by a dentist for the simplified oral hygiene index (OHI). Patients were classified as good, poor and bad groups based on oral hygiene index scale. Pre-pyloric biopsy materials were assessed using rapid-urease test. Oral hygiene indexes were analyzed retrospectively, groups were compared for HP positivity. Results: 66 patients (30 females, 45.5%) were included. Mean age of patients was 34.17±14.7 years. 11 (16.7%), 29 (43.9%) and 26 (39.4%) patients were classified as in good, poor and bad hygiene index groups, respectively. In patients with good OHI gastric HP positivity was less frequent. Conclusion: Decreased frequency in gastric HP may be observed with maintaining an ideal oral hygiene. Key words: Endoscopy, helicobacter pylori, oral hygiene index

Background: In patients with IgA nephropathy (IgAN) lectin and alternative pathways of the complement can be activated. Our aim was to analyze the association of glomerular and extraglomerular C4d stainingthe representative of lectin pathwaywith demographic, clinical and histopathological findings in primary IgAN patients. Design: Seventy-three patients were enrolled and after re-evaluation 37 of them were included in this study. Biopsies were analyzed for staining with anti-C4d primary monoclonal antibody by immunohistochemistry. Patients were classified as positive and negative groups based on their glomerular C4d deposition. Groups were compared for their baseline clinical and histopathological findings. Results: Sixteen (43.2%) of 37 patients were C4d-positive. Glomerular C4d-staining was associated with more severe proteinuria (2906mg/day vs. 1091mg/day; p=0.002), lower GFR (54.87mL/min vs. 95mL/min; p=0.023), higher blood pressure (p=0.022), more severe endocapillary hypercellularity (p

A 39-year-old female presented with malaise, weight loss, and generalized joint pain. Symptoms started 6 months prior to presentation and progressed over time. Laboratory tests revealed increased C-reactive protein (43.4 mg/L) and lactate dehydrogenase (330 U/L). Chest imaging showed mediastinal lymphadenopathy and nodular infiltration in the parenchyma of both lungs. Due to the subtle loss of weight and results of other imaging studies, positron emission tomography (PET) with fluorodeoxyglucose (FDG) was performed. Pathological FDG uptakes were observed in the cervical, hilar, and intraabdominal lymph nodes, lung parenchyma, liver, humerus, and ilium (Figure 1A). The patient was diagnosed as sarcoidosis according to the histopathological examination of a mediastinal lymph node. Corticosteroid and azathioprine were prescribed. Four months after treatment, a control PET scan was performed (Figure 1B). There was dramatic improvement in all anatomical sites compared with the first scan, correlating with symptom relief. In conclusion, PET scan may be a useful tool for monitoring disease activity in widespread sarcoidosis.