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Calcineurin inhibitors are the cornerstone of immunosuppression following solid-organ transplant. However, hyperkalemia may occur by multiple mechanisms affecting potassium in the distal tubule. Hyperkalemia is commonly observed in renal transplant recipients, and it is dose-dependent. Here, we evaluated the impact of fludrocortisone in the management of calcineurin inhibitor-induced hyperkalemia after renal transplant.We evaluated newly transplanted patients who developed hyperkalemia or those with hyperkalemia who attended our outpatient renal transplant clinic (Hamed Al-Essa Organ Transplant Center, Kuwait). Clinical and laboratory parameters were collected before starting fludrocortisone (baseline values) and then at 1, 2, 4, and 8 weeks. Drug history was assessed, with any drugs that could induce hyperkalemia being discontinued (such as spironolactone); otherwise, essential drugs like prophylactic agents (sulfamethoxazole-trimethoprim) were maintained. Oral anti-hyperkalemic doses (bicarbonate, resonium calcium, fludrocortisone) were noted.Our study included 29 patients; most were men (aged 45.8 ± 15 years). Body weight did not significantly change after introduction of fludrocortisone (79.53 ± 24.31, 79.82 ± 23.85, 80.62 ± 24.24, 77.03 ± 20.7, and 79.21 ± 27.93 kg at baseline and at postdose week 1, 2, 4, and 8, respectively). Systolic and diastolic blood pressure levels were also similar at baseline versus postdose. Steroid doses (prednisolone) were significantly reduced over 1 month (15.7 ± 12.4, 14.1 ± 10.19, 12.6 ± 8.7, 9.5 ± 5.2, and 9.5 ± 5.2 mg/ day). Serum potassium levels significantly improved (5.18 ± 0.58, 4.9 ± 0.49, 4.8 ± 0.54, 4.8 ± 0.65, and 4.4 ± 0.72 mmol/L). Serum creatinine levels significantly improved by postdose week 8 (129.28 ± 48.9, 130.92 ± 52.2, 127.66 ± 50.9, 121.42 ± 41.7, and 124.1 ± 51.27 μmol/L). Serum bicarbonate levels remained similar.Fludrocortisone was a safe and effective option in management of calcineurin inhibitor-induced hyperkalemia among renal transplant recipients.

The first defense line of the battle, healthcare workers (HCWs), faces a significant challenge in managing the current COVID-19 pandemic.

OBJECTIVE: Millions of people suffer from sleep disturbances. In addition, the coronavirus disease 2019 (COVID-19) pandemic created several new challenges–particularly for frontline healthcare workers (HCWs). This study assessed the sleep quality (SQ) among HCWs. MATERIAL AND METHODS: A cross-sectional study was conducted using an English-language online survey. The participants were invited via a web link sent using social network platforms. It included sociodemographic- and profession-related characteristics. COVID-19-associated risks were assessed (e.g., being on the front line, doing swabs, satisfaction about protective equipment, and management protocols). Assessment of SQ was done using the Pittsburgh Sleep Quality Index (PSQI) and various medical errors were recorded. RESULTS: A total of 217 HCWs completed the survey with mean (±standard deviation) age of 35.8 (±7.3) years; 56.2% were male, 18.43% had comorbidities, and 61.75% experienced sleep difficulties before the COVID-19 crisis. This work reports a 78.8% prevalence of poor SQ, with the mean (standard deviation) global PSQI score of 9.36 (±4.4). HCWs with poor sleep experienced more positive comorbid profile (23.64% versus 6.52%, p=0.01). Working on the front lines of COVID-19 was associated with poor sleep (69.59% versus 47.83%, p=0.006). Among the participants, 77.42% performed medical errors, particularly not checking for drug allergies (17.97%), dispensing medication with incomplete instructions (20.74%), providing incorrect doses or overdosing (14.75%), incorrectly explaining the use of medication (9.22%), and prescribing a drug to the wrong patient (10.14%). CONCLUSION: This nationwide survey reported high prevalence of poor SQ among HCWs during the COVID-19 pandemic. Being an HCW on the front lines of COVID-19 and doing swabs with a positive comorbidity was associated with poor sleep.

The significance of pretransplant donor-specific antibodies (DSAs) despite negative complement-dependent lymphocytotoxicity crossmatch (CDC-XM) would be useful for clinical decision-making. Hence, we aimed to determine the impact of pretransplant DSA despite negative crossmatch on the outcome of kidney transplantation. One hundred and eleven kidney recipients were prospectively enrolled in this study after being transplanted at Hamed Al-Essa Organ Transplant Center of Kuwait between January 2011 and December 2013. Of them, 50 recipients with positive DSA at the time of transplant were subjected to desensitization (Group 1). Three local protocols were utilized; first included plasma exchange, high-dose intravenous immunoglobulin (IVIG), and rituximab; second included immunoadsorption plus RTX, and the third included high-dose IVIG and rituximab. The second group included 61 recipients with negative DSA. All recipients had negative CDC-XM and flow cytometry crossmatch at the time of transplant. Panel-reactive antibody (±DSA) levels with mean fluorescence intensity and graft function were monitored along the first 24 months for all patients. There were no statistically significant differences between the two groups regarding early posttransplant graft function, patient and graft survivals. Pretransplant DSA with negative CXM carries a minimal clinical risk with optimized immunosuppression.

Cystinosis is the most frequent cause of the inherited renal Fanconi syndrome and is also potentially treatable. In this study, we have reported our single-center experience of the longterm outcomes of kidney transplant in patients with cystinosis.Pediatric patients with cystinosis (n = 17) were compared with a matched control group without cystinosis (n = 126). The 2 groups were compared with regard to demographic data, posttransplant complications, and graft and patient outcomes.Most patients with cystinosis were male teenagers (52.9%) with comparable mean age (12.4 ± 4.1 vs 14 ± 3.1 years) versus the group without cystinosis. The 2 study groups were comparable with regard to type of dialysis, type of donor, blood group, and pretransplant comorbidities (P.05). Patients with cystinosis received significantly more potent induction therapy (P0.05), but both groups were maintained on comparable immunosuppressive regimens (mostly tacrolimus based) (P.05). Most grafts in both groups displayed immediate graft function. The percentage of patients with cystinosis with primary graft function was significantly higher than the percentage of those patients without cystinosis who had primary graft function (P = .024); this was associated with a relatively lower baseline creatinine level, although this was not significant (P.05). Posttransplant complications, especially posttransplant diabetes, cytomegalovirus viremia, or BK nephropathy, were comparable (P.05). Moreover, patient and graft survival rates were similar in the 2 groups (P.05).Under standard immunosuppression, renal transplant and cysteamine therapy were safe with good long-term outcomes in patients with cystinosis. Studies that can include more patients and that have longer follow-up are needed to better understand the nature of this genetic disease and to discover the best treatment options.

Diabetes knowledge among kidney transplant recipients with posttransplant diabetes has not been exhaustively assessed. Here, we evaluated the effects of structured diabetes education on development of diabetic micro- and macroangiopathies in kidney transplant patients with posttransplant diabetes.This prospective randomized controlled study categorized 210 renal transplant patients with posttransplant diabetes mellitus into 2:1 groups according to type of diabetes education. Group 1 (n = 140) received structured education, and group 2 (n = 70) received conventional education. Patient data were collected through patient identification and metabolic control parameter forms.Most patients in groups 1 and 2, respectively, were Kuwaiti (60.7% vs 58.6%), men (57.9% vs 68.6%), and had high school-level education (43.6% vs 48.6%). Chronic glomerulonephritis was the original disease in 36.4% versus 35.4% of patients. Most patients (72.8% vs 78.6% in group 1 vs 2) received pretransplant hemodialysis. At study start, the rate of patients with diabetic neuropathy was comparable between groups (32.4% vs 27.9%). Moreover, after completion of 24 months of education, neurological evaluation by electromyograph and nerve conduction studies did not show any significant differences between the groups (P.05). Similarly, the number of patients with fundus imaging showing retinopathy was comparable between groups at start and end of study (P.05). Although macroangiopathic events were higher in group 1, this finding was not significant (P.05). However, although the percentage of patients with nephropathy was comparable in both groups at start of study, the percentage decreased significantly in group 1 at 24 months after completion of education compared with group 2 and baseline value (P = .016).Structured diabetes education was associated with reduced diabetic nephropathy but had no significant effects on other micro- or macroangiopathies. However, we recommend education for all kidney transplant recipients with diabetes.

Atherosclerotic renal artery stenosis is one of the risk factors for cardiovascular death and can lead to the ischemic nephropathy. In this report, we describe the successful management of ischemic nephropathy that developed in a kidney transplant recipient with graft artery stenosis. The 52-year-old male patient had diabetes and hypertension and was a nonsmoker with hypothyroidism on replacement therapy. He had a history of recurrent urinary tract infection due to vesicoureteric reflux before starting hemodialysis in July 2009. In November 2020, he received a deceased donor renal allograft and showed slow graft function. He received thymoglobulin as induction and steroid, tacrolimus, and mycophenolate mofetil as maintenance therapy. He was discharged with nadir creatinine around 130 μmol/L. His diabetes was controlled by intensive insulin regimen. Later, he presented with graft dysfunction with partially controlled hypertension and suspected graft artery stenosis by Doppler ultrasonography but no evidence of obstruction. His tacrolimus level was adequate, and his echocardiography was unremarkable. He received empirical pulse steroid. A graft biopsy showed severe acute tubular necrosis, suspicious T-cell-mediated rejection, and negative C4d and positive SV40 stain, suggesting BK nephropathy. His BK viremia (500 copies/mL) and viruria (885 billion copies/mL) improved after immunosuppression minimization, although he remained dependent on dialysis. A repeated Doppler ultrasonogram showed flattening of the systolic wave. Computed tomographic angiography revealed diffusely attenuated graft arteries. The patient received graft artery angioplasty and stenting of the 2 arteries. The patient showed good response, with same-day urine production and Doppler showing good systolic wave. His graft function started to improve, and he was discharged with stable graft function. His immunosuppressive regimen was subsequently tailored to steroid and low-dose tacrolimus. In conclusion, we found that ischemic nephropathy could be reversed if properly managed, even in presence of other comorbidities.

Nocardiosis is a life-threatening infection in immunocompromised patients. The prevalence of the disease ranges from 2.3% to 5% in renal allograft recipients. Here, we describe a case of BK nephropathy associating with nocardiosis with successful recovery. The 54-year-old male patient had end-stage kidney disease due to diabetic nephropathy associated with diabetic retinopathy, hypertension, and dyslipidemia. He started hemodialysis in October 2017; 2 years later, he underwent a deceased donor kidney transplant with 2 HLA mismatches and high panel reactive antibodies. He received desensitization with intravenous immunoglobulin and rituximab, received thymoglobulin as induction, and was maintained on prednisolone, mycophenolate mofetil, and tacrolimus. His serum creatinine decreased to a nadir of 90 μmol/L. He developed graft dysfunction, which was proven to be due to BK nephropathy. Therefore, mycophenolate mofetil was replaced with leflunomide in addition to intravenous immunoglobulin therapy. Ten months later, he had an accidental fall and sought an orthopedic evaluation. Magnetic resonance imaging of the lumbar spine and pelvis revealed lumbar spondylosis, avascular necrosis of the femoral head, and obturator muscle abscess. He was explored surgically, but the surgeon found no abscess or avascular hip necrosis. The patient's blood grew Nocardia, and he was readmitted and started imipenem and linezolid empirically. Brain and chest computed tomography scans ruled out any central nervous system or pulmonary involvement, but a bone scan revealed osteomyelitis of the right superior pubic ramus and prepubic swelling, which was confirmed by computed tomography to be an abscess in both obturator externus and internus. He continued the same antibiotics for 6 months based on culture and sensitivity. At follow-up, the patient has shown stable graft function (creatinine 155 μmol/L) with improved BK viremia with immunosuppression minimization. In renal transplant recipients, successful management of combined BK nephropathy and nocardiosis was feasible with minimization of immunosuppression and proper antimicrobial therapy.

Severe anemia requiring multiple blood transfusions in the posttransplant period can trigger rejection. The evaluation of anemia among transplant recipients is a challenging task. Awareness should be continued for tacrolimus to manage pure red cell aplasia, but further evidence is needed to prove whether tacrolimus is a real cause of posttransplant anemia. Our case patient, a 66-year-old male patient with end-stage renal disease due to diabetic nephropathy, underwent a preemptive living donor renal transplant in September 2018. He had received a coronary artery bypass graft with transcatheter aortic valve implantation 3 years before renal transplant. Initially, he was maintained on prednisolone, mycophenolate mofetil, and tacrolimus after basiliximab induction. One month later, he presented with low cardiac output symptoms. His complete blood count showed normocytic normochromic anemia with reticulocytopenia (his hemoglobin level dropped from 112 to 69 g/L), which necessitated regular blood transfusions. His iron profile, serum folate, and vitamin B12 were within normal limits, and he had negative hemolytic and autoimmune screening tests. A bone marrow biopsy revealed acquired pure red cell aplasia, which was most likely drug induced as viral profiles were negative for parvovirus B19, cytomegalovirus, and Epstein-Barr virus. The patient was managed by discontinuing mycophenolate mofetil, and the steroid dose was increased up to 20 mg/day but without improvement. With tacrolimus then considered, 3 weeks after presentation, we replaced tacrolimus with cyclosporine. Complete blood count follow-up showed improvement without any need for further blood transfusions. After 1 month of cyclosporine maintenance, mycophenolate mofetil was resumed with a steady increase of hemoglobin up to 150 g/L and serum creatinine of 122 μmol/L. Pure red cell aplasia is a rare disorder among renal transplant recipients, which could be induced by maintenance tacrolimus therapy.

Background The lungs are commonly involved after renal transplantation, with many complications, either infectious or noninfectious. The infectious complications significantly increased morbidity and mortality. Several risk factors were involved, such as old age, smoking status, comorbid diseases, pretransplant peritoneal dialysis, cadaveric renal transplantation, heavy immunosuppression, and treatment of graft rejection. Aim To study the predisposing risk factors, etiologic factors, and the timeline of pulmonary complications within the first year after renal transplantation (either infectious or noninfectious complications). Patients and methods We conducted this prospective observational study in the Organ Transplant Center in Kuwait from March 2016 to October 2019. The kidney recipients were followed up for 1 year after transplantation. For suspected infectious pulmonary complications, the patients were subjected to blood, sputum, and or bronchoalveolar lavage within the first 24 h after admission; all samples were subjected to microbiological and serological examinations. Results We had 60 patients who developed postrenal transplant pulmonary complications. A total of 42 patients developed infectious pulmonary complications and 54 patients developed noninfectious complications. The most common infectious pulmonary complications were bacterial pneumonia (42 patients), opportunistic fungal infection (47 patients), and viral pneumonia (37 patients). The most common noninfectious pulmonary complications were pulmonary congestion (51 patients), pleural effusion (29 patients), and pulmonary embolism (16 patients). In the first 6 months, surgery-related complications and opportunistic fungal infection predominated owing to heavy immunosuppression. After 6 months, infections were due to community-acquired pathogens. The mortality rate was 38%. Bacterial pneumonia was the main cause of death (39%) followed by viral pneumonia (26%) and Pneumocystis jiroveci pneumonia (13%). Septic shock and respiratory failure were the leading causes of death. Conclusion Renal transplant was associated with infectious and noninfectious pulmonary complications. Infections were highly prevalent in the first year after transplantation. Old age, smoking status, comorbid diseases, pretransplant peritoneal dialysis, cadaveric renal transplantation, heavy immunosuppression, and treatment of graft rejection were the main risk factors for posttransplant pulmonary complications. Sepsis and respiratory failure represented the commonest causes of death.

Background Osteoporosis and osteopenia occur frequently in renal transplant recipients due to long-term use of immune-suppressants including corticosteroids. Previous treatment options like bisphosphonates had acceptable but rather unsatisfactory results after transplant. The aim of the current study is to directly compare the efficacy of denosumab and oral ibandronate in late RTR with low bone mineral density. Results The study was conducted Iin Hamed Al-Essa Kidney transplant center, Kuwait, in 2020. The data of 52 denosumab and 48 ibandronate patients were collected at the baseline and after one year of treatment. Spine and hip T-score readings, side effects, and other laboratory results were analyzed to evaluate the use of both medications. The mean number of months after transplant was 25 (± 13.9) months. After one year of treatment, denosumab alleviated both spinal osteoporosis and osteopenia T-score values from −3.13 to −2.4 (p = 0.008) and from −1.9 to −1.5 (p = 0.015), respectively. Besides, it reduced hip osteoporosis and osteopenia insignificantly from −3.45 to −3.1 and from −1.5 to −1.3, respectively (p > 0.05). Ibandronate improved spinal osteopenia from −1.6 to −1.55 (p = 0.97) and failed to show any positive impact on other sites; the spinal osteoporosis changed from −2.8 to −3 and hip osteoporosis and osteopenia changed from −3.1 to −3.12 and from −1.4 to −1.45, respectively (p > 0.05). The use of ibandronate was more associated with gastrointestinal tract (GIT) side effects, while hypocalcemia episodes were significantly higher in the denosumab group. Conclusion Denosumab improved both spinal and hip T-score values in comparison with ibandronate in RTR. Close monitoring is required for denosumab patients to prevent the associated hypocalcemia. Graphical Abstract

Background and Aims The outcome of Plasma cell-rich acute rejection (PCAR) in kidney transplant is reported to be poor. However, PCAR which can be associated with any type of rejection, may not be considered as independent morphological prognostic feature. Different treatment modalities were prescribed with variable responses. We report here four cases of PCAR and describe their presentations, type of rejection, associated conditions and treatment outcome. Method Out of 1920 kidney transplant recipients under follow up in our centre from 1996 till 2019, four patients were reported to have PCAR according to 2007 Banff classification. They were re-evaluated based on 2015 Banff classification. The treatment protocol was tailored according to the type of rejection and associated conditions. Results The four patients, aged 28, 44, 46 and 54 years, had live unrelated renal transplant done somewhere abroad with no data about donor HLA typing. Two of them were females. One had high PRA and she was positive for HBsAg. One patient received induction immunosuppression with basiliximab. They all received prednisolone, mycophenolate and cyclosporine as the maintenance immunosuppression and had immediate graft function. Rejection happened between 23 to 180 months post-transplant. Two patients had acute T-cell mediated Banff 1A rejections with features consistent with early membranous nephropathy. One had acute T-cell mediated rejection Banff 1B and the fourth had borderline T-cell mediated rejection with morphological changes suggestive of chronic active antibody mediated rejection (AMR). Plasma cells constituted 10 to 30% of the interstitial infiltration. All patients received solumedrol pulse. Both patients with features of membranous nephropathy received rituximab and one of them had additionally IVIG. The patient with AMR received plasma exchange and IVIG. However, she did not receive rituximab as she was positive for HBsAg. All patients responded well to treatment and the mean improvement in eGFR was 12.8%, 24.9%, 40.3% and 39.1% at 1-, 3-, 6- and 12-months post treatment. Repeat kidney biopsy at 3 to 12 weeks post treatment showed resolution of plasma cell infiltration in all patients. Conclusion Outcome of PCAR management was favourable among our patients irrespective of the type of rejection and associated conditions.

Introduction and aim: New onset diabetes after transplantation (NODAT) is a serious metabolic complication following kidney transplantation. Although beta-cell dysfunction is considered the main contributing factor in the development of this complication, its exact etiology is yet to be identified. We aimed to investigate NODAT among kidney transplant cohort in Kuwait with special stress on correlation between its risk factors and interferon gamma genotyping. Materials and methods: We surveyed 309 kidney transplant recipients from Hamed Al Essa Transplantation Centre, Kuwait. The participants were categorized into cohorts according to the development of NODAT diagnosed based on the American Diabetes Association guidelines. Statistical analyses were performed using SPSS software. We genotyped interferon gamma as the leading immunosignature for T lymphocyte. Results: No relationship between ethnicity and the development of NODAT was identified. However, there was a significant difference in age between cohorts. Younger patients demonstrated a lower rate of NODAT while, NODAT reached its maximum in 40-60-year age group. IFNG TT genotype was significantly associated with NODAT (p=0.005), while IFNG AA was considerably higher in the non-NODAT group. Conclusion: Beside the conventional contributing factors of NODAT, our results might represent a suitable platform for a larger cytokine and chemokine spectrum genotyping.

Diabetes knowledge among kidney transplant recipients with posttransplant diabetes has not been exhaustively assessed. We evaluated levels of diabetes knowledge among our kidney transplant patients using a 35-item diabetes self-care management questionnaire.The study comprised renal transplant patients with posttransplant diabetes mellitus who were referred from Hamed Al-Essa Organ Transplant Center of Kuwait to the Dasman Diabetes Institute. Patient data were collected through patient identification forms, metabolic control parameters forms, and diabetes self-care scale questionnaires (with score from 0-7).Of 356 (25.6%) kidney transplant recipients with posttransplant diabetes, 210 patients were enrolled in this study. Most were Kuwaiti (60%), men (48.8%), and with high school education level (43.8%). Some were smokers (11.9%), and the original kidney disease was glomerulonephritis in 37.6% of patients. Most patients (71.9%) received hemodialysis pretransplant. Most patients (88%) reported low mean score of healthy diet (0-3), with93% reporting low mean score of practicing exercise (0-3),62% not checking blood sugar at home, 85% not following the recommended frequency, and72% not caring for their feet (except washing in 86.7%). Moreover, most patients lacked information about sharp disposal, diet regimen, using logbooks, hypoglycemia and hyperglycemia, sick day management, and the importance of hemoglobin A1c and regular fundus examination. Mean score of practicing exercise was significantly higher in men (especially non-Kuwaiti; P.05); otherwise, other mean scores were comparable between sexes and different nationalities (P.05).Diabetes knowledge is deficient in patients with posttransplant diabetes. Seminars, counseling sessions, and workshops should be arranged periodically for renal transplant recipients to improve their low level of diabetes knowledge. This is a preliminary report of our randomized controlled study evaluating the impact of structured diabetes education on self-care activities and metabolic control variables.

Objectives The prevalence of BK-induced nephritis in renal transplant recipients is estimated to be 1% to 10%; the rate of graft loss within 1 year is 30% to 65%. We conducted this study to evaluate screening of BK virus in blood and/or urine among renal transplant recipients and to assess the effects of different therapeutic modalities in renal transplant recipients with BK nephropathy. Materials and methods Kidney transplant recipients were screened at the time of transplant and then at 1, 2, 3, 6, 9, 12, 18, and 24 months posttransplant. Fiftynine patients were diagnosed with BK virus viremia. Patients were divided into 2 groups according to treatment: group 1 (n = 29) received an active treatment and group 2 (n = 30) received minimized immunosuppression. Results Most patients required graft biopsies to confirm diagnosis (86.2% in group 1 vs 50% in group 2; P = .03). Both groups were comparable regarding demographic data. Initial posttransplant graft function was significantly better in group 1 (P = .017); ultimately, there was no significant difference between both groups regarding graft survival (P= .51). Fifty percent of patients had biopsy-proven acute T-cell-mediated rejection before BK virus-associated nephropathy diagnosis (significantly higher in group 1). Serum creatinine levels were significantly better in group 2 at 3, 4, and 5 years after BK nephropathy (P = .001, .017, and .003, respectively). Conclusions The prevalence of BK nephropathy in our renal transplant recipients was 5.9% with a rate of graft loss ranging from 43% to 51%. Regular screening, less intensive immunosuppressive therapy, and early intervention by reduction of immunosuppressive medications are advisable to obtain early diagnosis and to have better outcomes of BK virus-associated nephropathy with antiviral agents.

Hemophagocytic syndrome combines febrile hepatosplenomegaly, pancytopenia, hypofibrinemia, and hepatic dysfunction. It is characterized by bone marrow and organ infiltration of activated, nonmalignant macrophages that phagocytize blood cells. It is rare among renal transplant recipients. Here, we present the successful management of late-onset cytomegalovirusinduced hemophagocytic lymphohistiocytosis in a kidney transplant recipient after coronary artery bypass graft surgery. In 2012, our patient had end-stage kidney disease due to diabetic nephropathy and underwent related living-donor renal transplant. He was also hypertensive and hyperuricemic and had heart ischemia for which percutaneous coronary intervention for triple vessel disease was performed before transplant. In March 2017, he underwent successful aortic valve replacement and coronary artery bypass graft surgery; however, the patient had persistent thrombocytopenia. Heparin-induced thrombocytopenia was negative. His bone marrow showed hemophagocytosis possibly due to cytomegalovirus. Moreover, antiglycoprotein IIb/IIIA autoantibodies were positive. A positron emission tomography scan was negative for malignancy. He started treatment for cytomegalovirus with modifi cation of his immunosuppressive regimen (pulse steroid). Antiplatelet therapy was held and only resu med if platelet count exceeded 30000/L. Moreover, he received intravenous immunoglobulin and romiplostim treatment with partial response. Throughout treatment, he had stable kidney graft function with improving platelet count. A multi disciplinary approach is needed to treat patients with hemophagocytic syndrome, especially renal transplant recipients. Late-onset cytomegalovirus is an important cause for this syndrome.

The number of renal transplants in elderly patients is increasing as age per se does not constitute a contraindication to transplant. We compared renal transplant outcomes in elderly recipients versus a group of middle-aged patients.Our retrospective casecontrolled study compared elderly transplant recipients (n = 252;60 y old) with a matched cohort of younger adult recipients (n = 710; between 40 and 60 years old) who underwent renal transplant at the Hamed Al-Essa Organ Transplant Center of Kuwait between 2000 and 2014. Demographic characteristics, comorbidities, complications after transplant, and graft and patient outcomes were compared between groups.There were 252 elderly kidney transplant recipients (mean age of 65.5 ± 4.8 y; 59.52% males) and 710 younger adult patients (mean age of 49.3 ± 5.5 years; 61.4% males). Most donors were males in their thirties. Deceased donors predominated in the younger adult group, whereas living unrelated donors predominated in the elderly group (P.05). Diabetes represented the most common cause of endstage kidney disease. Younger patients tended to receive heavier induction therapy but comparable maint enance immunosuppression. Posttransplant diabetes was higher in younger patients; however, there were more elderly patients with micro- and macroangiopathies (P.05). No significant differences were shown between groups with regard to patient or graft survival (P.05). This could be attributed to a significantly higher number of patients with cardiovascular risks, less rejection episodes, and higher number of malignancies in the elderly group (P.05).Due to relatively less potent immunosuppression, elderly patients experienced lower rejection rates and better graft survival; however, patient survival was lower due to higher cardiovascular risk factors. Older patients should not be discouraged from living-donor renal transplant. Targeted research studies on protocols for the elderly are needed.

Objectives Data on the management of chronic antibody-mediated rejection after kidney transplantation are limited. We aimed to assess the impact of treatment of biopsy-proven chronic active antibodymediated rejection with combined plasma exchange, intravenous immunoglobulin, and rituximab treatment versus intravenous immunoglobulin alone or conservative management on the evolution of renal function in renal transplant recipients. Materials and methods In this retrospective study, we compared patients diagnosed with chronic active antibody-mediated rejection who were treated with standard of care steroids, intravenous immunoglobulin, plasma exchange, and rituximab (n = 40) at our center versus those who received intravenous immunoglobulin only or just intensified maintenance immunosuppression (n = 28). All patients were followed for 12 months clinically and by laboratory tests for graft and patient outcomes. Results The two groups were matched regarding mean recipient age (41.9 ± 15.4 vs 37.8 ± 15.5 y in patients with conservative versus combined treatment), recipient sex, mean body weight, and the cause of end-stage kidney disease. Most patients and their donors were males. Glomerulonephritis represented the most common cause of end-stage kidney disease in both groups followed by diabetic nephropathy. The type of induction and pretransplant comorbidities were not different between groups (P > .05) except for the significantly higher number of chronic hepatitis C infections in patients who received conservative treatment (P = .007). Mean serum creatinine values before and after treatment of chronic active antibodymediated rejection were comparable between groups (P > .05). Active treatment with heavier immunosuppression (rituximab and plasma exchange) was associated with posttreatment viral (cytomegalovirus and BK virus) and bacterial infections that necessitated more hospitalization (P > .05). However, graft and patient outcomes were significantly better in the active treatment group than in patients with conservative treatment (P = .002 and .028, respectively). Conclusions Combined treatment of chronic active antibody-mediated rejection with plasma exchange, intravenous immunoglobulin, and rituximab can significantly improve outcomes after renal transplant.

Introduction COVID‐19 is an ongoing pandemic with high morbidity and mortality and with a reported high risk of severe disease in kidney transplant recipients (KTR). Aim We aimed to report the largest number of COVID‐19‐positive cases in KTR in a single center and to discuss their demographics, management, and evolution. Methods We enrolled all the two thousand KTR followed up in our center in Kuwait and collected the data of all COVID‐19‐positive KTR (104) from the start of the outbreak till the end of July 2020 and have reported the clinical features, management details, and both patient and graft outcomes. Results Out of the one hundred and four cases reported, most of them were males aged 49.3 ± 14.7 years. Eighty‐two of them needed hospitalization, of which thirty‐one were managed in the intensive care unit (ICU). Main comorbidities among these patients were hypertension in 64.4%, diabetes in 51%, and ischemic heart disease in 20.2%. Management strategies included anticoagulation in 56.7%, withdrawal of antimetabolites in 54.8%, calcineurin inhibitor (CNI) withdrawal in 33.7%, the addition of antibiotics in 57.7%, Tocilizumab in 8.7%, and antivirals in 16.3%. During a follow‐up of 30 days, the reported number of acute kidney injury (AKI) was 28.7%, respiratory failure requiring oxygen therapy 46.2%, and overall mortality rate was 10.6% with hospital mortality of 13.4% including an ICU mortality rate of 35.5%. Conclusion Better outcome of COVID‐19‐positive KTR in our cohort during this unremitting stage could be due to the younger age of patients and early optimized management of anticoagulation, modification of immunosuppression, and prompt treatment of secondary bacterial infections. Mild cases can successfully be managed at home without any change in immunosuppression.

New Onset Diabetes After Transplantation (NODAT) is a serious metabolic complication. While β-cell dysfunction is considered the main contributing factor in the development of NODAT, the precise pathogenesis is not well understood. Cytokines are thought to be involved in the inflammation of islet β-cells in diabetes; however, few studies have investigated this hypothesis in NODAT. A total of 309 kidney transplant recipients (KTRs) were included in this study. An association between kidney transplants, and the development of diabetes after transplant (NODAT) was investigated. Comparison was made between KTRs who develop diabetes (NODAT cases) or did not develop diabetes (control), using key cytokines, IL-6 G (− 174)C, macrophage mediator; IL-4 C (− 490)T, T helper (Th)-2 cytokine profile initiator; Th-1 cytokine profile initiator interferon-γ T (+ 874) A gene and TGF β1 C (+ 869) T gene polymorphisms were investigated. The genes were amplified using well-established polymerase chain reaction (PCR) techniques in our laboratory. Compared to the AA and AT genotypes of interferon gamma (IFNG), there was a strong association between the TT genotype of IFNG and NODAT kidney transplant recipients (KTRs) versus non-NODAT KTRs (p = 0.005). The AA genotype of IFNG was found to be predominant in the control group (p = 0.004). Also, significant variations of IL6 G (− 174) C, IL-4 C (− 590) T, interferon-γ T (+ 874) A gene and transforming growth factor β1 C (+ 869) T may contribute to NODAT. Our data is consistent with theTh-1/T-reg pathway of immunity. Further larger pan Arab studies are required to confirm our findings.

Delayed graft function (DGF) is a form of acute renal failure which results in increased post-transplantation allograft immunogenicity and risk of acute rejection episodes in addition to decreased long-term survival. Its incidence and risk factors have been extensively studied, especially after deceased donation. Until now, only few data has been published on DGF in living donor kidney transplant recipients. The present study was performed to investigate the frequency and risk factors of DGF among living- kidney transplant recipients. In this retrospective study, data had been collected from existing local hospital registries in three countries (Iran, Kingdom of Saudi Arabia (KSA) , and Kuwait ).

Organ transplant in patients with congenital bleeding disorders is a challenge requiring an integrated approach of various specialists. Inherited factor VII deficiency is the most common of the rare bleeding disorders, with a wide set of hemorrhagic features. Although a kidney allograft is the most frequent type of solid-organ transplant, it is rarely performed in individuals with congenital hemorrhagic disorders. Here, we highlight the course of a patient with coagulation factor VII deficiency who underwent successful kidney transplant without significant coagulopathy. Our patient was a 19-year-old man with end-stage kidney disease and congenital coagulation factor VII deficiency. Perioperative bleeding was successfully prevented by administration of recombinant factor VII, confirming its safety in solid-organ transplants. Success requires evaluation of doses and therapeutic schedules, as well as a multidisciplinary approach.

Rhinocladiella mackenziei is a rare fungal pathogen which belongs to a large group of pigmented fungi causing phaeohyphomycosis. R. mackenziei primarily infects the brain and leads to high fatality rates among both immunocompetent and immunocompromised individuals. Among solid organ transplant recipients, the infection may disseminate to extra-neuronal sites, necessitating comprehensive radiologic imaging. Here we describe a new case of R. mackenziei infection in a renal transplant patient involving the brain and renal allograft. She received liposomal amphotericin B and voriconazole but no surgical intervention. Ultimately, the patient died after two months of hospital stay. A review of all reported cases of transplant patients infected with R. mackenziei is also presented.

Diabetic nephropathy is one of the main long-term diabetic microangiopathies that can complicate type 1 and 2 and other secondary forms of diabetes mellitus, including posttransplant diabetes mellitus. Posttransplant diabetes mellitus was initially reported in the 1960s, with case reports of recurrent and de novo diabetic nephropathy after kidney transplant reported in the early 2000s, mostly as a result of same-risk and precipitating factors of diabetic nephropathy as in native kidneys. The disease may appear early in view of the hyperfiltration risk of being a single grafted kidney. Here, we discuss risk factors, early serologic and genetic biomarkers for early detection, and strategies to avoid and delay the progression of diabetic nephropathy after posttransplant diabetes mellitus. In this overview of published literatures, we searched PubMed and MEDLINE for all articles published in English language between January 1994 and July 2018. Included studies reported on the prevalence, incidence, or determinants of post-transplant diabetes among renal transplant recipients and studies reporting diabetic nephropathy in their cohorts. Our review showed that avoidance or good control of posttransplant diabetes is the cornerstone in management of posttransplant diabetes mellitus and hence diabetic nephropathy. Control and avoidance can be commenced in the preparatory stage before transplant using validated genetic markers that can predict posttransplant diabetes mellitus. The use of well-matched donors with tailored immunosuppression (using less diabetogenic agents and possibly steroid-free regimens) and lifestyle modifications are the best preventative strategies. Tight glycemic control, early introduction of angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers, and possibly conversion to less diabetogenic regimens can help to delay progression of diabetic nephropathy.

Although chronic kidney disease decreases fertility, kidney transplantation provides restoration of fertility in women, enabling them to get pregnant. Data available from registries have shown that pregnancy is feasible in solid-organ transplant recipients without significant impact on long-term graft function. Despite these reassuring data, some studies have reported that one-third of female transplant recipients are still actively being counseled against pregnancy. Here, we present a patient who received a simultaneous deceased-donor kidney and pancreas transplant and who had a favorably evolved pregnancy. The 36-yearold kidney-pancreas transplant recipient conceived 5 months after her marriage. The patient was closely followed during pregnancy by a multidisciplinary team that included a nephrologist, gynecologist, and endocrinologist. Renal function and blood glucose levels remained within normal limits. She delivered her baby normally at 31 weeks of pregnancy (1.3-kg male baby). Currently, both mother and baby are doing well. Pregnancy in combined kidney and pancreas transplant recipients with stable graft functions is feasible but remains risky. Proper planning, modification of immunosuppressive drugs, and close monitoring are the keys to optimized maternal, fetal, and graft outcomes.

To avoid graft rejection during pregnancy, frequent monitoring of serum drug levels is recommended. Pregnancy induces hyperfiltration in transplanted kidneys, as in native kidneys; therefore, detection of rejection can be difficult when monitoring by serum creatinine. If rejection is suspected, ultrasonographguided graft biopsy can be done; once proven, it can be treated with pulse steroids, but data are scarce regarding other agents. Here, we present a 28-year-old pregnant female patient with resistant acute rejection but with successful pregnancy outcome. Our patient had end-stage kidney disease secondary to lupus nephropathy and underwent living-donor renal transplant in May 2013 after hemodialysis support for 1 year. She received thymoglobulin as induction therapy and was maintained on prednisolone, mycophenolate mofetil, and tacrolimus. She had normal renal graft function without proteinuria. After she received counseling, she became pregnant in February 2015. In June 2015, she presented with acute graft dysfunction with serum creatinine level of 365 μmol/L. Her abdominal ultrasonography showed mild hydronephrosis and viable fetus. She received empirical pulse steroids with partial response, and her graft biopsy showed acute T-cell-mediated rejection and negative C4d. Intravenous immunoglobulins and minipulse steroids were administered but without response. After gynecologic counseling and informed consent, she received 5 doses of thymoglobulin. She was dialysis dependent until premature vaginal labor, which resulted in birth of a viable 2-kg boy. We suggest that successful pregnancy outcomes could occur with close monitoring and daily dialysis in female kidney transplant patients with resistant rejection.

Objectives Pregnancy after kidney transplant has a high risk for maternal and fetal complications; however, it can be successful if patients are properly selected. Here, we studied outcomes and complications of pregnancies in kidney transplant recipients who received calcineurin inhibitor-based immunosuppression. Materials and methods In this case control study, we reviewed patients who became pregnant between 2004 and 2017. For this analysis, each pregnancy was considered an event. We divided pregnancies into 2 groups according to calcineurin inhibitor-based maintenance immunosuppression: group 1 (49 pregnancies) received cyclosporine, and group 2 (33 pregnancies) received tacrolimus. Patients also received steroids and azathioprine. Patients had regular antenatal follow-up at the Hamed Alessa Organ Transplant Center (Kuwait) and in the maternity hospital (monthly until month 7 and then weekly until delivery). Results Of 750 female kidney transplant recipients within childbearing potential, there were 82 pregnancies (10.9%) in 49 recipients (6.5%). Seventy-eight pregnancies were planned, and 4 pregnancies occurred while women were using contraception. There was 1 triple pregnancy, 5 double, and 76 single pregnancies. Two women had preeclampsia as maternal complication, 2 had uncontrolled hypertension, and 7 developed graft dysfunction. Forty-seven women (57.3%) had caesarean section, and the remaining had vaginal deliveries. Of 89 babies, 86 were viable (1 intrauterine fetal death and 2 abortions). Eight babies were delivered prematurely with low birth weight, and 2 needed incubators. Mean serum creatinine levels were 97.9 ± 24, 109 ± 38, 100 ± 39, 120 ± 46, and 115 ± 57 μmol/L at baseline, first, second, and third trimesters, and postpartum, respectively. Twelve patients showed high panel reactive antibodies but without donor-specific antibodies. Conclusions Posttransplant pregnancy can be successful in most renal allograft recipients, but the increased risk of fetal and maternal complications, including low birth weight, spontaneous abortus, and preeclampsia, should be considered.

Posttransplant diabetes is a common complication of solid-organ transplantation. We present the possible role of diabetes education in improvement of posttransplant diabetes in a 36-year-old bodybuilder who was a kidney transplant recipient. The patient had been abusing some medications to help in bodybuilding. He underwent living unrelated-donor renal transplant with thymoglobulin induction and was maintained on steroids, tacrolimus, and mycophenolate mofetil. Posttransplant diabetes was confirmed by blood tests. His blood sugar was partially controlled by 3 oral agents. The patient participated in our structured diabetes education program. This program was created to cover different items related to diabetes control, including diet, proper exercise, blood sugar monitoring, sick day management, and pathophysiologic roles of diabetes medications. Within 4 months of participation in this program, the patient's blood sugar became well controlled and his diabetes medications started to be minimized. He presently has stable graft function with hemoglobin A1c level around 5.6% on only diet management. Bodybuilders are at risk of deterioration of their kidney function. A proper diabetes education program is recommended to help renal transplant recipients with early posttransplant diabetes mellitus to control their disease. Success requires close evaluation and a multidisciplinary approach.

Objectives In a previous study, we evaluated 1-year outcomes of using low-dose valganciclovir prophylaxis for cytomegalovirus infection in intermediate-risk kidney transplant recipients. Whether this effect persists in the long term is unknown. We aimed to evaluate the 2-year follow up of such adopted prophylaxis. Materials and methods We randomized 2 matched groups of kidney transplant recipients (1:1) to receive valganciclovir as 450 mg daily (group 1) or 900 mg daily (group 2) for the first 6 months after kidney transplant. The final analysis included 196 patients as intermediate-risk patients (98 in each treatment group) after exclusion of 5 high-risk patients. Serologically, all patients were at moderate risk for cytomegalovirus infection. Long-term outcomes including cytomegalovirus disease, acute rejection, new-onset diabetes after transplant, graft loss, and patient survival were assessed. Results Through year 2 of follow-up, cytomegalovirus infection was reported in only 1 patient in group 1 (at month 13) and 1 patient in group 2 (at month 19) (not significant). Biopsy-proven acute rejection episodes were not statistically different between the groups (2 episodes in group 1 and 6 in group 2; P = .431). New-onset diabetes posttransplant was reported in 8.1% in group 1 and 13.2% in group 2 (P = .535). Graft failure was equal in both groups (1 in each group) at 2 years of follow up (not significant). Patient survival was comparable in both groups (100% in group 1 versus 97.9% in group 2; P = .661). The total number of cytomegalovirus infections at 2 years was numerically less in group 1 (P = .128). Conclusions Low-dose valganciclovir prophylaxis for 6 months was associated with sustained reduction of cytomegalovirus infection up to 2 years after kidney transplant without significant impact on the acute rejection, new-onset diabetes posttransplant, or patient and graft outcomes.

Background It has been reported that the long-term survival of second transplants may be similar to that of primary transplants. Reports of retransplantation outcomes are scarce, especially in the middle east region. We aimed to present our experience with second renal transplant in Kuwait and compare the donor source among our retransplant recipients. Patients and methods Data of kidney retransplants, under follow-up at the Hamed Al-essa Organ Transplant Center of Kuwait, between 1980 and 2019 were retrospectively analyzed. Out of 3038 kidney transplants, 198 (6.51%) were kidney retransplants. The number of kidney transplants from living donors was 150; from deceased donors, 48 and third transplants represented 15 cases. We compared living donor group 1 with deceased donor group 2 in terms of demographics, posttransplant complications and outcome. Results We observed that episodes of acute antibody-mediated rejection (nine cases, 18.7%, in group 1 vs. eight cases, 16.6%, in group 2, respectively) and T-cell-mediated rejection (14 cases, 9.33%, in group 1 vs.15 cases, 10%, in group 2, respectively) were more frequent among patients in group 2, but this did not reach statistical significance. In terms of the second graft outcome, we observed that the percentage of patients with failed grafts was higher among group 2 patients, but this did not reach statistical significance during their last follow-up, while the two groups were comparable in terms of patient outcome. Conclusion Both living donor and cadaveric renal allotransplants carry the same risk for graft rejection, either AMR or ACR. Meanwhile retransplants who received their kidneys from either living or deceased donors had experienced similar graft and patients’ outcomes. Therefore, retransplant either from living or deceased donor is considered a good option after first renal allograft loss.

Thalassemia minor has a good prognosis, whereas thalassemia major (TM) is a severe disease, and the long-term prognosis depends on the treatment adherence to transfusion and iron chelation therapies. To our knowledge, there are no reported thalassemia cases that underwent kidney transplant. We aimed to highlight a successful kidney transplant in a patient with TM with stable graft function after 16 months of follow-up. In our case, repeated blood transfusions were inevitably associated with iron overload despite iron chelating agents. Moreover, she developed anti-HLA antibodies, but fortunately, there were no donor-specific antibodies, which facilitated the procedure of renal transplant that was performed on 17/3/2019. After 6 weeks of transplant, she started follow-up in the clinic and resumed iron chelation using deferasirox along with much less frequent blood transfusion. After more than 20 months of follow-up, she is enjoying stable graft function, hemoglobin around 9.2 g/dl, and with occasional trace proteinuria. This is a case report showing a β-TM case can undergo renal transplant with no contraindications under special circumstances, and it is the first case in the literature.

Diabetic kidney disease – which is defined by elevated urine albumin excretion or reduced glomerular filtration rate (GFR) or both – is a serious complication that occurs in 20% to 40% of all diabetics. In this review we try to highlight the prevalence of diabetic nephropathy which is not uncommon complication of diabetes all over the world. The prevalence of diabetes worldwide has extended epidemic magnitudes and is expected to affect more than 350 million people by the year 2035. There is marked racial/ethnic besides international difference in the epidemiology of diabetic kidney disease which could be explained by the differences in economic viability and governmental infrastructures. Approximately one-third of diabetic patients showed microalbuminuria after 15 years of disease duration and less than half develop real nephropathy. Diabetic kidney disease (DKD) is more frequent in African-Americans, Asian-Americans, and Native Americans. Progressive kidney disease is more frequent in Caucasians patients with type 1 than type 2 diabetes mellitus (DM), although its overall prevalence in the diabetic population is higher in patients with type 2 DM while this type of DM is more prevalent. Hyperglycemia is well known risk factor for in addition to other risk factors like male sex, obesity, hypertension, chronic inflammation, resistance to insulin, hypovitaminosis D, and dyslipidemia and some genetic loci and polymorphisms in specific genes. Management of its modifiable risk factors might help in reducing its incidence in the nearby future.