MM, N., Issa HH, Maher AA, G. TA, and O. NA, "Cryoglobulinaemic vasculitis and glomerulonephritis associated with schistosomiasis: a case study", East Mediterr Health J., vol. 21, issue 5, pp. 354-8, 2015. 1_final_pub_emhj.pdf
MM, N., El-Shehaby AR, O. NA, Fayad T, Nassef A, N. A, and S. E. D. U. A. Salem MM, "The Association between Fibroblast Growth Factor-23 and Vascular Calcification Is Mitigated by Inflammation Markers.", Nephron extra., vol. 3, issue 1, pp. 106-112, 2013. 1-_final_publication.pdf
NA, O., Hassanein SM, Leil MM, and N. MM, "Complementary and Alternative Medicine Use Among Patients With Chronic Kidney Disease and Kidney Transplant Recipients", Journal of renal nutrition, vol. 25, issue 6, pp. 466-71, 2015.
MM, N., N. A, Elshaboni TH, Morise F, and O. NA, "Comparing different calcification scores to detect outcomes in chronic kidney disease patients with vascular calcification", International journal of cardiology. , vol. 220, pp. 884-9., 2016.
Nasrallah, M. M., and M. M. Kamal, "Polymorphisms of CCR5 A59029G Gene in Patients with TypeII Diabetes Mellitus and Their Association with Diabetic Nephropathy", Egyptian Journal of Internal Medicine, vol. 12, issue 3,4, 2009. Abstract

Background: Diabetic nephropathy is a serious complication in individuals with type II diabetes. Infiltration of renal tissue with monocytes secondary to activation by chemokines & their receptors have been implicated in the development of diabetic nephropathy. CCR5 is a chemokine whose signals may mediate monocyte infiltration, differentiation and activation in renal tissue.
Aims: The aim of this work is to determine the relative frequency of chemokine receptor CCR5 G59029A gene polymorphisms in Egyptian patients with type II diabetes and to investigate the possible association of these polymorphisms with diabetic nephropathy.
Methods: This study was conducted on 55 patients with type II DM of duration between 10-20 years. This included 15 patients with no evidence of diabetic nephropathy and 40 patients with diabetic nephropathy, including 30 patients with stage 3-4 chronic kidney disease and 10 with stage 5 chronic kidney disease. CCR5 59029 genotyping was performed using PCR followed by digestion with Bsp1286I restriction enzyme.
Results: We found that the genotype polymorphism frequency in the control group (diabetics without nephropathy) was as follows: GG in 3 out of 15 patients (20%), GA in 3 (20%) and AA in 9 patients (60%). In the pooled analysis of all patients with diabetic nephropathy, the genotype frequency was: GG in 11 out of 40 patients (27.5%), GA in 16 (40%) and AA in 13 (32.5%). The difference in frequencies between controls and nephropathic groups was not statistically significant, p=0.168. There was a trend towards an association between G+ve genotypes (GG and GA) in patients with diabetic nephropathy (67.5%) compared to controls (40%), odds ratio 3.1, p=0.06.
Conclusion: There is a trend towards a possible association between CCR5 G59029A gene polymorphisms and the development of diabetic nephropathy.
Keywords: chemokine receptor 5 (CCR5), type II diabetes, diabetic nephropathy, gene polymorphism

Nasralla, M. M., D. Belal, and M. M. Nasralla, "FACTORS INFLUENCING THE BODY-LEAD BURDEN IN CHRONIC RENAL FAILURE AND HYPERTENSION", ERA-EDTA, Stockholm, Sweden, 2008. Abstract

NTRODUCTION AND AIMS: Exposure to lead (Pb) has been a global health problem for decades. Renal effects of acute exposure to Pb as well as chronic high-level occupational exposure are well established. Controversy exists as to the role of low-level environmental exposure to Pb on the kidneys. Body-lead burden (BLB), is known to be elevated among renal failure patients and several explanations were proposed for this, though none is fully confirmed or uniformly accepted. These include: inadequate Pb excretion by the failing kidneys; cause-effect relation between Pb-exposure and renal failure of unknown cause; and an association with hypertension/hypertensive nephrosclerosis. A further proposed possibility is that increased bone-turnover due to 2ry hyperparathyroidism, in renal failure, releases Pb from its dormant stores in bone. We tried to test these various hypotheses head-on, for the first time, in this study

METHODS: We included 84 subjects divided to 2 main groups.Group1: 50 with pre-ESRD (CKD2-4) divided into 3 subgroups: 1a:19 with CKD of known cause; 1b:15 with hypertensive nephrosclerosis; 1c:16 with CKD of unknown cause. Group2: 34 matched controls with normal kidney functions including 18 normtensive and 16 with essential hypertension

All subjects were evaluated by inquiry about sources of environmental exposure to Pb, symptoms/signs suggestive of Pb toxicity, assessment of BLB by EDTA lead-mobilisation test, measurement of serum parathormone (PTH), calcium, phosphorus, alkaline phosphatase, urea, creatinine, uric acid.

Those with occupational exposure to Pb, acute renal failure, malignant hypertension or renal replacement therapy were excluded

RESULTS: 34 CKD patients (68%) vs 1 control (2%) had a positive Pb mobilisation test (>600ug).Only 9 recalled a source of exposure to Pb, those had higher BLB (p0.038) and 3 had symptoms suggestive of Pb toxicity

BLB was higher in CKD patients compared to controls (<0.0001), there was no difference in BLB between different subgroups of CKD patients nor between normo- and hyper-tensive controls. PTH was higher among CKD patients than controls (p 0.001) with no differences between CKD subgroups. PTH was higher in hyper- than normo-tensive controls (p 0.012)

In CKD patients, BLB correlated positively with serum PTH (r 0.7, p 0.0001). This was true for all subgroups (1a: r 0.84, p <0.0001; 1b: r 0.56, p 0.04; 1c: r 0.7, p 0.02). Regarding the other studied parameters, BLB only correlated posititively with serum creatinine (r 0.4, p .007).

In controls, BLB did not correlate with any studied parameter

CONCLUSIONS: We conclude that: a)BLB is elevated in CKD irrespective of the cause of renal failure b)BLB in CKD is related to hyperparathyroidism c) Higher serum creatinine was associated with higher BLB (ie more Pb excretion in urine) (probably due to higher PTH) d) absence of symptoms of Pb toxicity or failure to recall exposure to Pb donot exclude elevated BLB in renal patients.

These results support the hypothesis that elevated PTH releases Pb from its bone stores which may explain several manifestations of and modify treatment for hyperparathyroidism and the uremic syndrome

TA, G., E. - F. HS, N. MM, and H. H, "Insulin resistance and metabolic syndrome in primary gout: relation to punched-out erosions", Int J Rheum Dis, vol. 15, issue 6, pp. 521-5, 2012. Abstract

OBJECTIVES:

To verify the relation of gout to insulin resistance (IR) and metabolic syndrome (MetS) and find any association of metatarsophalangeal (MTP) joint erosions to the features of MetS and IR.

METHODS:

Forty-six primary gout male patients with a mean age of 41.96 ± 5.77 years were grouped according to the presence of MetS. Twenty-seven age and sex matched healthy volunteers served as controls. Insulin sensitivity was estimated using the homeostatic model assessment index (HOMA-B) for beta cell function and HOMA-IR for peripheral tissue IR.

RESULTS:

Gout patients had significantly higher HOMA-IR and HOMA-B compared to controls. Those with MetS (n = 27) had significantly higher serum uric acid (SUA) than those without (n = 19; 11.51 ± 3.72 mg/dL vs. 9.15 ± 2.34 mg/dL; P = 0.012). Gout patients with MTP erosions had notable higher insulin levels and more IR as shown by the higher levels of HOMA-IR and HOMA-B compared to those without. HOMA-IR and HOMA-B significantly correlated with the presence of erosions. Moreover, the presence of erosions significantly correlated with SUA (r = 0.64, P < 0.0001).

CONCLUSIONS:

The level of SUA is closely related to IR in patients with and without MetS. There is an association of the severity of gout and presence of MTP erosions to IR. Metabolic syndrome forms an important marker for those who develop more punched-out erosions.

TA, G., R. HA, S. S, E. - F. H, N. MM, and A. - R. E, "Metabolic syndrome and insulin resistance comorbidity in systemic lupus erythematosus. Effect on carotid intima-media thickness", Z Rheumatol, vol. 72, issue 2, pp. 172-7, 2013. Abstract

OBJECTIVE:
The aim of the present study was to assess the effect of metabolic syndrome (MetS) and insulin resistance comorbidity on the carotid intima-media thickness (IMT) in systemic lupus erythematosus (SLE) patients and their relationship to clinical manifestations, disease activity, and damage.
METHODS:
The study included 92 SLE patients (mean age 30.18 ± 8.27 years) and 30 matched controls. Disease activity and damage were assessed by the SLEDAI and SLICC indices, respectively. The Health Assessment Questionnaire II (HAQII) and Quality of Life (QoL) index were evaluated in the patients. Levels of insulin, glucose, and creatinine and the lipid profile were measured in patients and controls. Insulin sensitivity was estimated using the homeostatic model assessment index (HOMA-B) for beta cell function and (HOMA-IR) for peripheral tissue insulin resistance. The carotid IMT was measured by ultrasonography.
RESULTS:
The SLE patients had high HOMA-IR and HOMA-B. The IMT was significantly increased (0.82± 0.29 mm) compared to the controls (0.45± 0.2 mm).The HOMA-IR, SLEDAI, SLICC, HAQII, and IMT were significantly higher and the QoL lower in those with MetS (n = 34) compared to those without (n = 58), while the HOMAB was comparable. There was a significant correlation between the IMT and the SLEDAI, SLICC, and WHR.
CONCLUSION:
Insulin sensitivity and IMT are altered in SLE patients, especially those with MetS comorbidity with an associated increase in disease activity and damage. Effective management of MetS would help control SLE activity, damage, and the future development of cardiovascular events especially in the absence of symptoms of cardiovascular disease.