Ahmed Fayed

BACKGROUND: Patients with Type 2 diabetes mellitus (T2DM) have decreased bone health. We aimed to investigate serum levels of bone turnover markers (BTMs) (markers of bone formation and bone resorption) and bone mineral density (BMD) at three sites (lumber, neck femur, and total femur) in middle-aged men with type 2 diabetes and to analyze the relationship between them. Also to evaluate serum osteoglycin as a novel marker and its relation to BTMs, BMD, and diabetic status.

METHODS: We recruited seventy-eight patients with T2DM and thirteen non-diabetic, male volunteers as a control group. BMD was measured using a DEXA scan. BTMs (carboxy-terminal crosslinking telopeptide of type 1 collagen [CTX] and procollagen type 1 N propeptide [P1NP]), osteoglycin, PTH, and vitamin D were estimated. Data was compared among subjects and statistical analysis was performed.

RESULTS: Most of the patients were having normal BMD with no significant difference between patients and the controls. BTMs and osteoglycin were significantly higher and vitamin D was significantly lower in the diabetic patients. Serum osteoglycin was positively correlated with DEXA Neck Femur (r = 0.233; p-value < 0.05).

CONCLUSION: Body mass index and Serum osteoglycin have a significant positive effect on BMD. Both markers of bone formation and bone resorption were increased indicating a state of increased bone turnover in T2DM.

BACKGROUND: Lupus nephritis (LN) is a common serious presentation of systemic lupus erythematosus. Cyclophosphamide (CYC) and mycophenolate mofetil (MMF) are listed as the first-line drugs in induction therapy for LN.

OBJECTIVE: This study aimed to compare high- and low-dose CYC in a cohort of Egyptian LN patients.

PATIENTS AND METHODS: The data of 547 patients with class III/IV active LN who received CYC as induction therapy were retrospectively analyzed. Whereas 399 patients received 6‑monthly 0.5-1 g/m CYC doses, 148 patients received six biweekly 500 mg CYC doses. Demographic data, laboratory test results, and disease activity index were recorded and compared at presentation and at 6, 12, 18, 24, and 48 months of follow-up.

RESULTS: After 48 months, the proportion of patients maintaining normal creatinine levels was higher in the group receiving induction therapy with high-dose CYC (67.9%, 60.4%, p = 0.029), and these patients also had higher proteinuria remission at 36 (26.6%, 14.8%, p = 0.014) and 48 months (24.3%, 12.8%, p = 0.006). Comparison of patient outcomes according to both induction and maintenance therapy showed the best results in patients who received high-dose CYC and continued MMF as maintenance therapy.

CONCLUSION: High- and low-dose CYC are comparable in early phases of treatment. However, after a longer duration of follow-up, high-dose CYC was associated with higher remission rates in the current cohort.

The kidney represents an important target of systemic inflammation. Its involvement in monogenic and multifactorial autoinflammatory diseases (AIDs) vary from peculiar and relatively frequent manifestations to some rare but severe features that may end up requiring transplantation. The pathogenetic background is also very heterogeneous ranging from amyloidosis to non-amyloid related damage rooted in inflammasome activation. Kidney involvement in monogenic and polygenic AIDs may present as renal amyloidosis, IgA nephropathy, and more rarely as various forms of glomerulonephritis (GN), namely segmental glomerulosclerosis, collapsing glomerulopathy, fibrillar, or membranoproliferative GN. Vascular disorders such as thrombosis or renal aneurysms and pseudoaneurysms may be encountered in patients with Behcet's disease. Patients with AIDs should be routinely assessed for renal involvement. Screening with urinalysis, serum creatinine, 24-h urinary protein, microhematuria, and imaging studies should be carried out for early diagnosis. Awareness of drug-induced nephrotoxicity, drug-drug interactions as well as addressing the issue of proper renal adjustment of drug doses deserve a special mention and should always be considered when dealing with patients affected by AIDs. Finally, we will explore the role of IL-1 inhibitors in AIDs patients with renal involvement. Targeting IL-1 may indeed have the potential to successfully manage kidney disease and improve long-term prognosis of AIDs patients.

BACKGROUND: Amelioration of proteinuria is one of main treatment targets in patients with glomerulonephritis, yet the remission rates are suboptimal.

AIM OF THE STUDY: To examine the effect of the sodium-glucose transporter 2 inhibitor (empagliflozin) on proteinuria and kidney function progression, in patients with glomerulonephritis not due to diabetic kidney diseases.

SUBJECTS AND METHODS: Fifty patients were recruited. The entry criteria were diagnosis of glomerulonephritis, and proteinuria (proteinuria ≥ 500 mg⁄g) in spite of the use of the maximal tolerated dose of RAAS blocking agents together with specific immunosuppression treatment regimens. Group 1 (Empagliflozin arm): 25 patients who received 25 mg of empagliflozin once daily for 3 months as add-on to their regular treatment protocol (RAAS blockers and immunosuppression). Group 2 (Placebo arm): 25 patients treated with RAAS blockers and immunosuppression. The primary efficacy endpoints were the change in creatinine eGFR, and proteinuria 3 months after starting treatment.

RESULTS: Progression of proteinuria was lower with empagliflozin as compared to placebo (odds ratio, 0.65; 95% CI, 0.55 to 0.72, p = 0.002). Decline in eGFR was lower with empagliflozin as compared to placebo; however, this was statistically not significant (odds ratio, 0.84; 95% CI, 0.82 to 1.2, p = .31). The percentage change in proteinuria was greater with empagliflozin as compared to placebo (median, - 77 (- 97-105) vs - 48 (- 80-117).

CONCLUSION: Empagliflozin has a favorable effect on amelioration of proteinuria in patients with glomerulonephritis. Empagliflozin has tendency to preserve kidney function in patients with glomerulonephritis as compared to placebo; however, longer term studies are required.

One of the most significant consequences of systemic lupus erythematosus (SLE) is lupus nephritis (LN). Visfatin, an adipokine that is significantly expressed in visceral fat and is a marker of endothelial dysfunction in chronic kidney disease, has multiple proinflammatory actions. We aimed to evaluate the state of serum visfatin in SLE patients and to detect its possible correlation with the disease's activity and effects on the kidney affection. Fifty patients with active LN, 50 patients with inactive lupus, and 50 healthy people had their serum visfatin levels tested. Chemical and immunological markers of SLE and LN were measured. The SLE Disease Activity Index (SLEDAI) was used to measure the disease's activity. Renal biopsies from the LN subgroup were collected and classified using the modified classification of the World Health Organization. The serum visfatin of patients with active LN was significantly greater than that of inactive lupus patients and the healthy controls (20.56 ± 1.07 ng/mL, 16.77 ± 1.02 ng/mL, and 9.96 ± 1.46 ng/mL, P <0.001). SLEDAI and serum visfatin levels were shown to be significantly correlated (P = 0.000057). Serum visfatin levels were likewise significantly correlated with the index of histological activity in the active group (P <0.00001). Serum visfatin was raised in individuals with active LN and was related to the SLEDAI and disease severity scores. Serum visfatin could be utilized as a noninvasive biomarker for evaluating the severity of LN and risk stratification of the risk.

BACKGROUND: Patients with diabetic kidney disease (DKD) are at increased risk to develop post-contrast acute kidney injury (AKI). Diabetic patients under dipeptidyl peptidase 4 inhibitors (DPP4Is) experience a lower propensity to develop AKI. We speculated that linagliptin as a single agent or in combination with allopurinol may reduce the incidence of post-contrast AKI in stage 3-5 chronic kidney disease (CKD) patients with underlying DKD.

METHODS: Out of 951 DKD patients eligible for this study, 800 accepted to sign informed consent. They were randomly allocated to 4 equal groups that received their prophylaxis for 2 days before and after radiocontrast. The first control group received N-acetyl cysteine and saline, the 2 received allopurinol, the 3 group received linagliptin, and the 4 received both allopurinol and linagliptin. Post-procedure follow-up for kidney functions was conducted for 2 weeks in all patients.

RESULTS: 20, 19, 14, and 8 patients developed post-contrast AKI in groups 1 through 4, respectively. Neither linagliptin nor allopurinol was superior to N-acetyl cysteine and saline alone. However, the combination of the two agents provided statistically significant renal protection: post-contrast AKI in group 4 was significantly lower than in groups 1 and 2 ( < 0.02 and <0.03, respectively). None of the post-contrast AKI cases required dialysis.

CONCLUSION: Linagliptin and allopurinol in combination may offer protection against post-contrast AKI in DKD exposed to radiocontrast. Further studies are needed to support this view.

TRIAL REGISTRATION CLINICALTRIALS.GOV: NCT03470454.

INTRODUCTION: Systemic lupus erythematosus is an autoimmune multisystem disease; renal affection is one of its most common manifestations. The effect of environmental factors on lupus nephritis flares is not fully understood.

METHODS: This is a retrospective study that included 200 patients with lupus nephritis flares. All patients had confirmed diagnosis of lupus nephritis on histopathological examination. Lupus nephritis flares were defined by either (1) nephritic flare: defined as increased proteinuria or serum creatinine concentration; abnormal urinary sediment or a reduction in creatinine clearance, or (2) proteinuria flare defined as persistent increase in proteinuria > 0.5-1.0 g/day after achieving complete remission; doubling to > 1 g/day after achieving partial remission. The time of renal flare (month of the year) was recorded to determine the effect of seasonal variation on lupus nephritis flares.

RESULTS: The median age for the patients was 33 years (IQR = 13); 92% of patients were females. The median duration of lupus was 7 years (IQR = 6). The median serum creatinine was 1.4 mg/dl, median serum urea level was 32, and median UPCR was 2.4 gm/dl. The highest incidence of flares occurred in June (14%) and July (12.5%) (p = 0.003).

CONCLUSION: Seasonal pattern of LN flare was observed in our study in Egyptian cohort of patients, with most flares observed during meteorological summertime. Larger studies are needed to confirm this seasonal pattern. Key Points • Flares of lupus nephritis are common in patients with systemic lupus erythromatosus. • A seasonal pattern of flares of lupus nephritis was observed in our study. This seasonal pattern has been observed by previous studies in variable ethnicities and variable climatic circumstances.

Endothelial dysfunction in patients with diabetic nephropathy is caused by nontraditional factors in addition to common risk factors (e.g., hypertension) in people with normal kidney function. These nontraditional factors include factors involved in mineral bone disease in these patients. One of these factors is fibroblast growth factor 23 (FGF-23). We aimed to evaluate the relationship between flow-mediated dilatation (FMD) as a measure of endothelial dysfunction and FGF-23. This was a cross-sectional observational study that was conducted on 100 diabetic patients (Group I: 50 patients with nephropathy; Group II: 50 patients without nephropathy) and 50 healthy volunteers (Group III). Serum levels of intact FGF-23, interleukin-6, intact parathyroid hormone, and 25-hydroxyvitamin D (25-(OH)Vit D); estimated insulin resistance; and FMD were evaluated. FGF-23 was significantly higher in Group I (median: 101 pg/mL) and Group II (median: 101 pg/mL) than in Group III (median: 4 pg/mL) (P <0.001), but FGF-23 was not significantly different between Groups I and II. A significant positive correlation was found between serum levels of FGF-23 and phosphorus in Group I. A significant negative correlation was found between serum levels of FGF-23 and 25-(OH)Vit D in Group II. However, FGF-23 failed to show a significant correlation with FMD in patients with diabetic nephropathy. Our data suggest another factor that rises earlier than FGF-23 in diabetic nephropathy and causes endothelial dysfunction.

AIM: Low skeletal muscle mass in ICU patients is associated with poor clinical outcome. Ultrasonography is a noninvasive method that can measure muscle thickness at the bedside. We aimed at studying the relation of the ultrasonography measured muscle layer thickness (MLT) at time of ICU admission with the patients' outcome namely mortality, duration of mechanical ventilation (MV) and ICU length of stay (LOS). In addition to define the best cut-off values that can predict mortality in medical ICU patients.

METHOD: this observational prospective study was conducted on 454 adult critically ill patients admitted to the medical ICU of a university hospital. At the time of admission, MLT of the anterior mid-arm and lower 1/3 thigh were assessed using ultrasonography with and without transducer compression. The clinical scores for assessment of disease severity; Acute Physiology and Chronic Health Evaluation score (APACHE-II) and Sequential Organ Failure Assessment score (SOFA) in addition to nutrition risk; modified Nutrition Risk in Critically ill score (mNUTRIC) were estimated for all patients. ICU LOS, duration on MV and mortality were reported.

RESULTS: The mean age of our patients was 51 years ± 19. The ICU mortality rate was 36.56%. The baseline MLT was negatively associated with APACHE-II, SOFA and NUTRIC scores but not with duration of MV or ICU-LOS. The non-survivors had lower values of baseline MLT. A cut-off value of 0.895 cm (AUC: 0.649, 95% CI of 0.595-0.703) using the mid-arms as a reference point with maximum probe compression showed the highest sensitivity (90%) to predict mortality compared to other techniques however with low specificity (22%).

CONCLUSION: the baseline ultrasonography measured mid-arm MLT is a sensitive risk assessment tool that can reflect disease severity and predict ICU mortality.

Endothelial dysfunction is evident in systemic lupus erythematosus (SLE). Pro-inflammatory adipokines are involved in endothelial derangement and premature atherosclerosis, particularly in lupus nephritis (LN). This study aimed to investigate the impact of LN on endothelial function by estimating the serum levels of adiponectin, leptin, visfatin, and homeostatic model assessment-insulin resistance (HOMA-IR) and calculating the flow-mediated dilatation (FMD) of the brachial artery. This is a case-control study in which 190 systemic lupus patients who were fulfilling the American College of Rheumatology revised classification were enrolled. The patients were divided into 100 LN patients and 90 lupus non-nephritis patients. Demographic data, clinical parameters, and SLE activity were reported. Serum adiponectin, leptin, visfatin, and HOMA-IR were measured. The endothelial dysfunction was assessed by calculating the FMD of the brachial artery. The mean age of participants was 25.62 ± 5.81 years. Elevated levels of adiponectin, leptin, visfatin, and HOMA-IR were observed in LN cases (12.2 ± 0.3, 20.1 ± 0.5, 16.8 ± 0.1, and 12.0 ± 3.8, respectively) compared to non-nephritis cases (12.2 ± 0.3, 8.5 ± 0.5, 16.8 ± 0.5, and 9.0 ± 3.8, respectively) with a more reduced FMD percentage in LN cases with a statistical significance. Brachial artery FMD is negatively correlated with lipid profile, adipokines, and HOMA. Visfatin has better sensitivity (82.1%) and specificity (81%) with the area under a curve of 0.893, compared to other biomarkers. LN patients are characterized by impaired endothelial function. Elevated serum adiponectin, visfatin, and HOMA-IR were significantly correlated with poor FMD of the brachial artery. Visfatin has a better performance in detecting atherosclerosis.

INTRODUCTION: Direct-acting antiviral agents (DAAs) have modified the management of chronic hepatitis C virus (HCV) infection, including HCV-related cryoglobulinemic vasculitis (CryoVas). However, patients might experience vasculitis relapse, and no reliable predictors of CryoVas relapse after sustained virologic response (SVR) have been established. We aimed to describe HCV-CryoVas relapse rates and factors associated with it.

METHODS: An international multicenter cohort where patients with HCV-CryoVas from Egypt, France, and Italy treated with DAA were analyzed retrospectively. Factors associated with relapse-free survival were evaluated in a multivariate-adjusted model.

RESULTS: Of 913 patients, 911 (99.8%) obtained SVR. After 35 months of the median follow-up, 798 patients (87.4%) had sustained remission of vasculitis, while 115 (12.6%) experienced CryoVas relapse. By the time of relapse, skin involvement was present in 100%, renal involvement in 85.2%, and peripheral neuropathy in 81.7%. Relapses were treated with glucocorticoids in 90.9%, associated with plasma exchange, cyclophosphamide, or rituximab in 50%, 37.3%, and 6.4%, respectively. The cumulative incidence of CryoVas relapse was 0.7% (95% CI 0.3-1.4), 12.3% (95% CI 10.2-14.6), and 13.1% (95% CI 11.0-15.5) at 12, 24, and 36 months after DAA treatment, respectively. Independent baseline risk factors associated with CryoVas relapse were male sex, skin ulcers, kidney involvement at baseline, and peripheral neuropathy at the end of DAA treatment. Death occurred in 11 relapsers, mainly due to infections.

DISCUSSION: A substantial proportion of patients with CryoVas experience relapse after DAA-induced SVR. Relapses are moderate-to-severe and affect survival after 24 months, mainly due to infections. Independent risk factors for relapse or death were found.

BACKGROUND: Many of the mineral metabolite abnormalities encountered in chronic kidney disease (CKD) patients were found also associated with acute kidney injury (AKI). In the last decade, sclerostin was found to intimately affect bone mineral metabolism in CKD patients. Nothing is known about sclerostin in AKI.

OBJECTIVE: We looked for serum level of sclerostin in AKI patients in comparison to normal control subjects and if there is an impact on metabolic derangement, endothelial function or clinical outcome.

CASES AND METHODS: This is a cross sectional case control observational study of 219 AKI cases (group I) beside 219 age matched normal control subjects (group II). All cases of group I were in the intensive care because of sepsis; 86 had acute on CKD (group Ib), while 133 had de novo AKI (group Ia). All studied subjects underwent estimation of serum sclerostin, parathyroid hormone (PTH), 25 hydroxy vitamin D (25 OH vit D), fibroblast growth factor 23 (FGF23), C-reactive protein (CRP), interleukin 6 (IL6), Homeostatic Model Assessment for Insulin Resistance (Homa IR), beside the routine CBC, kidney and liver function tests, serum calcium, and phosphorus, and flow mediated vasodilation of brachial artery (FMD). Follow-up of group I cases was done till they recovered or passed away.

RESULTS: Serum sclerostin, PTH, FGF23, phosphorus, CRP, IL6, HOMA IR, creatinine, urea, uric acid, ALT, AST and white blood cell count (WBC) were significantly higher while serum calcium, 25 OH vit D, hemoglobin, platelet count and FMD were significantly lower in group I compared to group II (P<0.001 in all). On the other hand, there was no significant difference in serum sclerostin, PTH, FGfF23, 25 OH vit D, CRP, IL6, Homa IR and FMD between group Ia and Ib. Survivors were younger in age (median 55.5 vs. 60 years, P<0.04), had lower AST (30.5 vs. 58 units, P<0.001), had higher platelet count (206 vs 162×10/L, P<0.001), otherwise, there was no significant difference in any of the other parameters between survivors and patients that were lost. Serum sclerostin had strong correlation with FGF23 in group I (r=0.99, P<0.001) and group II (r=1, P<0.001). Homa IR had positive correlation with serum sclerostin (r=0.148, P=0.014) and serum FGF23 (r=0.142, P=0.018) in group I.

CONCLUSION: Sclerostin is intimately related to FGF23. Sclerostin level increases in AKI patients. Both sclerostin and FGF23 might increase insulin resistance but have no impact on FMD. Neither sclerostin nor FGF23 interfere with AKI outcome.

OBJECTIVES: Several biological markers have been studied for the differentiation of infection from disease activity in systemic lupus erythematosus (SLE) patients with discrepant results. We aimed to evaluate the role of serum presepsin, hs-CRP, procalcitonin (PCT), and copeptin (CPP) in differentiating bacterial infections from disease activity in SLE patients.

METHODS: This study is a cross-sectional observational study in which 94 Egyptian patients were recruited from June 2017 to January 2018. Our patients were divided into two groups: group (1) included 48 patients with active SLE hospitalized with any sort of lupus activity and group (2) included 46 patients with active SLE admitted with a proven bacterial infection. Hs-CRP, presepsin, PCT, and CPP were measured using enzyme-linked immune sorbent assay technique.

RESULTS: Hs-CRP, presepsin, PCT, and CPP were highly significantly higher among group (2) patients compared to group (1) patients (p < 0.001). Serum presepsin expressed higher specificity than hs-CRP (87.5% vs 60.4%) but the same sensitivity (80.4%) in the detection of bacterial infection in SLE patients. Serum PCT expressed higher specificity than hs-CRP (100% vs 60.4%) but lower sensitivity (73.9% vs 80.4%). Serum CPP expressed higher specificity than hs-CRP (65.9% vs 60.4%) but lower sensitivity (65.9% vs 80.4%).

CONCLUSION: Our study suggests that increased serum levels of hs-CRP, presepsin and PCT levels are useful in differentiating bacterial infections from disease activity in SLE patients. Serum CPP could be used as an adjunct with more specific inflammatory biomarkers in making better diagnostic judgments.

KEY POINTS: • The increased serum levels of hs-CRP, presepsin and PCT levels are useful in differentiating bacterial infections from disease activity in SLE patients. • Serum Presepsin expressed higher specificity than hs-CRP but the same sensitivity in the detection of bacterial infection in SLE patients. • Serum CPP expressed higher specificity than hs-CRP but lower sensitivity.

AIM: Lupus nephritis (LN) is one of the most serious complications of SLE. Tregs (Regulatory T lymphocytes) are thought to play a part in the pathogenesis of SLE. According to recent research, Foxp3, a Treg identification marker, plays a significant role in the pathogenesis of SLE. This study aimed to compare the urinary Foxp3 mRNA levels of patients with active and inactive forms of LN and healthy control subjects to see whether it played a role in disease activity.

METHODS: We measured FOXP3 messenger RNA (mRNA) expression in the urine of 50 people with active LN, 50 people with inactive lupus, and 50 healthy people.

RESULTS: We found that the expression level of FOXP3 was significantly higher in urine from patients with active LN than from subjects with inactive lupus and healthy controls (22.93 ± 4.13 vs 5.66 ± 0.47 vs 0.57 ± 0.15copy; P < 0.001).Urinary FOXP3 mRNA level significantly correlated with SLEDAI (0.000057) In the active group, urinary FOXP3 mRNA level also significantly correlated with histological activity index (< 0.00001).

CONCLUSION: We concluded that urinary FOXP3 mRNA is elevated in patients with active LN and that it is linked to the SLEDAI and the severity of the disease. FOXP3 mRNA in urine sediment may be used as a non-invasive biomarker for evaluating the severity of LN and risk stratification.

Systemic lupus erythematosus (SLE) is a multisystem chronic autoimmune disease characterized by tissue inflammation. There is increased cardiovascular mortality in cases with SLE. Endothelial dysfunction is an early stage of atherosclerosis, which can be reversed early. We aimed to study noninvasive assessment of endothelial dysfunction in Egyptian patients with SLE. Three hundred individuals were recruited; 100 SLE patients with lupus nephritis (LN), 100 SLE patients free of LN as well as 100 healthy volunteers. The vascular endothelial function was evaluated through ultrasonographic assessment of brachial artery diameter to determine the flow-mediated dilation (FMD) as well as a blood endothelial marker called platelet endothelial cell adhesion molecule-1, also known as cluster of differentiation 31 (CD31), was measured. CD31 is abnormal in 93% of cases with LN and 79% in cases without nephritis. There was a significant higher level in CD31 in cases of LN compared with lupus without nephritis with P = 0.016. FMD is impaired in all cases with LN, 95% in cases without nephritis, and in 20% of the controls. There was a significant lower FMD in cases of LN compared with lupus without nephritis with P <0.001. Multiple regression analysis showed that FMD of the brachial artery (P <0.001) is an independent factor to predict LN. Endothelial dysfunction is increased in cases with SLE especially those with nephritis. CD31 and FMD can be used as noninvasive methods for early detection of endothelial dysfunction.

BACKGROUND: The incidence of subdural hematoma (SDH) in chronic maintenance hemodialysis (CMH) patients may change over time, along with the evolving characteristics of the underlying populations.

METHODS: We conducted a retrospective, single-center study at Cairo University hospitals, assessing the incidence, associated risk factors, and outcomes of nontraumatic SDH in CMH patients between January 2006 and January 2019.

RESULTS: Out of 1217 CMH patients, nontraumatic SDH was diagnosed in 41 (3.37%) during the study, increasing with the enrollees' age but stable over the observation period and translating into an annual incidence rate of 28 per 1000 patients per year. SDH patients were likely to use central venous catheters, reported pruritis and history of bone fractures, and had higher phosphorus, parathyroid hormone, and alkaline phosphatase values ( < 0.001); however, there was no association with atrial fibrillation or use of anticoagulants. In the SDH cohort ( = 41), six patients did not need surgical intervention and 13 patients died before becoming surgically fit for intervention; mortality correlated with ischemic heart disease ( = 0.033) and the presence of atrial fibrillation or chronic anticoagulation with warfarin ( < 0.0001 for both), among others. Twenty-two patients received surgical operations and of these 2 died postoperatively; overall patient mortality was 12/41 (29.27%) at 30 days and 15/41 (36.59%) at 1 year.

CONCLUSION: Our study demonstrated a striking enrichment for underlying comorbidities in those patients developing SDH and a high risk of immediate mortality. The benefit of chronic anticoagulation therapy should be carefully weighed against the risk of CNS bleed in MHD patients.

Diabetic nephropathy (DN) is the most common cause of end-stage renal disease. Urinary pigment epithelium-derived factor (PEDF) has also been shown to suppress the expression of fibrogenic, pro-inflammatory, and angiogenic factors, thus contributing to pathological changes in early DN. We aimed to study the role of urinary PEDF as a biomarker for the detection of chronic kidney disease progression in patients with type 2 diabetes mellitus (T2DM). Sixty patients with T2DM were recruited in addition to 20 nondiabetic healthy volunteers. Urinary PEDF using enzyme-linked immunoassay technique was performed to all subjects, and correlations between it and different clinical parameters were examined. Our study showed a statistically significant correlation between urinary PEDF level and duration of DM (P <0.001), glycosylated hemoglobin (P <0.001), serum creatinine (P <0.001), urinary albumin-to-creatinine ratio (P <0.001), and stage of diabetic retinopathy by fundus examination (P <0.001). Urinary PEDF is a good indicator of progression of DN and microvascular damage (as a complication of diabetes) in general. It was also increased in case of poor diabetic control.

BACKGROUND: The impact of hepatitis virus infection on arterial calcification (AC) was not studied.

OBJECTIVE: To study the prevalence, severity and distribution of AC in incident hemodialysis patients with hepatitis B and C viral infection.

CASES AND METHODS: 172 stage 5 CKD adults (98 male and 74 female) were included; 58 of them were seronegative for both hepatitis B and C (SN group), 48 were positive for hepatitis B virus infection (HBV group) and 66 were hepatitis C virus positive (HCV group). Beside histopathology of the obtained arterial samples, all these cases were examined for body mass index (BMI), serum calcium (Ca), phosphorus (P), alkaline phosphatase (AP), serum albumin, uric acid (UA), alanine transaminase (ALT), parathormone (PTH), fibroblast growth factor 23(FGF23), interleukin 6 (IL6), and 25 hydroxy vitamin D (25 (OH) vit D), hemoglobin concentration, and serum ferritin.

RESULTS: 86 (50%) of the cases had AC; 11 of them were in SN group (19%), 9 in HBV group (18.8%) and all the 66 HCV group (100%). In SN group, 4 had intimal calcification, 5 had medial calcification, and 2 had both intimal and medial calcification. In HBV group, 9 had intimal calcification, while no cases were encountered with either medial or both site calcifications. In HCV group, 16 had intimal calcification, 31 had medial calcification, and 19 had both intimal and medial calcification. Calcification was in the form of spots in one case in SN group, and 6 cases in HBV group, a single plaque of calcification in 5 cases of SN group, 3 cases of HBV group, and 16 cases of HCV group, multiple plaques were detected in 4 cases in SN group, and 31 cases in HCV group, and diffuse calcification in one case in SN group, and 19 cases in HCV group. In HBV group, calcification was only detected in patients with high viremia, while all patients with low or moderate viremia were devoid of calcification. In HCV group, all patients with low viremia had intimal solitary plaque of calcification, all patients with moderate viremia had multiple plaques of medial calcification, while all patients with high viremia had diffuse intimal and medial calcification. Both groups of viral hepatitis were significantly different in comparison to SN group in either distribution or calcification score (P<0.001 in all). HBV group had significantly lower serum P, CaxP and PTH in comparison to SN group (4.6±0.66 vs. 5.45±0.77mg/dL, 36.4±7.2 vs. 44.1±8.69, and 348±65.4 vs. 405.9±83.2pg/mL, P<0.001, <0.001, and 0.035 respectively). On the other hand, HCV group did not show any significant difference in any of the studied parameters compared to SN group.

CONCLUSION: HCV positive patients are more prone to develop AC that is more extensive. HBV positive patients were less likely to have arterial medial calcification, probably related to lower serum phosphorus, CaxP product and PTH. HCV infection should be added as risk factor for AC among CKD patients. Further studies are needed to confirm these findings.

Much evidence highlighted the role of interferon alpha (IFN-α) in systemic lupus erythematosus (SLE) and suggested its possible role in assessing disease activity. We measured serum IFN-α in Egyptian SLE patients in order to determine a cutoff value that can be used to distinguish patients from healthy controls and explored its clinical value in monitoring disease activity and different aspects of the disease, in particular lupus nephritis. This cross-sectional, case-control study was conducted on 59 SLE patients and 30 healthy controls. Serum IFN-α was measured in all participants using sensitive enzyme-linked immunosorbent assay (ELISA). SLE patients underwent assessment of disease activity using the SLE disease activity index-2000 (SLEDAI-2K) as well as an evaluation of proteinuria, complement C3 and C4, and serology. Patients with evidence of renal involvement underwent renal biopsy. The median serum IFN-α was 81.8 pg/mL (interquartile range [IQR] 63.4:102.4), which was significantly higher than in healthy controls (median 10.3 pg/mL [IQR 7.3:11.6]) (p<0.001). At serum level of 14.7 pg/mL, IFN-α has high sensitivity and specificity to discriminate SLE patients from controls, with high positive and negative predictive values. Serum IFN-α was not associated with markers of disease activity, clinical features and anti-double stranded DNA. Furthermore, it was not associated with markers of renal activity, including proteinuria, C3 and C4 complement factors and histopathology renal classes. Despite elevated levels of serum IFN-α in SLE patients, it is not possible to use it as a biomarker for disease activity.

Systemic lupus erythematosus (SLE) is an inflammatory autoimmune disease characterized by production of a number of antinuclear antibodies. Podocyte injury is an important feature and can be detected by several markers including podocalyxin. We aimed to evaluate the impact of SLE on urinary levels of podocalyxin and to determine its relationship to renal biopsy, proteinuria, and disease activity in lupus nephritis (LN) patients. Sixty individuals were recruited; 30 SLE patients with LN as well as 30 healthy volunteers and they were subjected to full history, clinical examination, kidney function, protein/creatinine ratio, urinary podocalyxin, and kidney biopsy. Patients with LN had higher level of urinary podocalyxin (3.96 ± 2.24) than the other group (0 ± 0), (P <0.001). Class IV LN was the most common class found among LN patients [18 cases (60%)]. There was a statistically significant positive correlation between SLE disease activity index score, protein/creatinine ratio, and urinary podocalyxin (P <0.001, r = 0.98) (P <0.001, r = 0.765). There was a statistically significant negative correlation between serum albumin, serum calcium, and urinary podocalyxin (P = 0.001, r = -0.589) (P = 0.025, r = -0.407). Urinary podocalyxin level significantly predicts the pathological impact of SLE on the kidney and could be used as a noninvasive marker for such effect and its progression.

BACKGROUND: Women with chronic kidney disease commonly have menstrual irregularities and fertility abnormalities. Antimüllerian hormone (AMH) and antral follicle count (AFC) are well-recognized indicators of ovarian reserve.

AIMS: To assess AMH level and total AFC in women who are on hemodialysis and after successful kidney transplantation (KTx).

METHODS: Sixty women with end-stage kidney disease (ESKD) on regular hemodialysis were included in this study with 20 patients of them were going to have renal transplant. Fifty age-matched healthy females were enrolled as control. Serum AMH level was measured in all participants once and in transplant patients four times (before surgery, and at 1, 6, and 12 months after surgery). AFC was evaluated once in all subjects and in transplant patients twice (before and 1 year after surgery).

RESULTS: ESKD patients had significantly lower AMH concentration and AFC than healthy controls (1.8 ± 1.2 vs. 3.5 ± 1.7 ng/ml, p < 0.001) and (12 ± 4.6 vs. 17.4 ± 4.3, p < 0.001), respectively. In the subgroup transplant patients, AMH level decreased significantly from (1.7 ± 1.3 ng/ml) before Ktx to (1.5 ± 1.2 ng/ml, p = 0.001) at 1 month, (1.1 ± 0.9 ng/ml, p < 0.001) at 6 months, (0.9 ± 0.8 ng/ml, p < 0.001) at 1 year after Ktx. Also, total AFC declined in transplant females from (11.1 ± 4.5) before KTx to (6.6 ± 3.4) after KTx (p < 0.001).

CONCLUSIONS: Women with ESKD who are on hemodialysis have lower ovarian reserve than healthy females. Moreover, renal transplantation was associated with reduction in AMH level and AFC.