الفهرس | Only 14 pages are availabe for public view |
Abstract Chronic kidney disease (CKD) is a multifactorial disorder affected by various environmental and genetic factors. A genetic predisposition for renal failure is demonstrated by the 3 - 9 times higher probability of ESRD in patients with a family history of CKD, compared to the general population. In clinical practice, renal damage is usually diagnosed on the basis of proteinuria/albuminuria in urinalysis or quantitative measurement of creatinine concentration and the calculation of e-GFR. However, these methods are non-specific and do not always provide accurate information on the risk of progression. A good biomarker of CKD should accurately predict an individual’s risk of CKD progression or developing hard renal end points (e.g., ESKD or death), identify additional risk factors for CKD, indicate and quantify a pathological process within the kidney and finally it should act as an indicator of treatment response. Therefore, there is a need for alternative biomarkers of renal damage enabling early and more accurate disease assessment. The term hypertensive nephrosclerosis is usually used for kidney disease which complicates arterial hypertension. Its causal relation with essential hypertension is still a subject of debate, as still it is not clear that how a well-treated AHT can lead to end-stage CKD. Renal function can remain stable for years if hypertension is well controlled. However, in a few cases the disease progresses to end-stage CKD. The lack of correlation between the degree of hypertension control and the prevention of disease progression suggests that this process may be an intrinsic and early renal disease. For many years, genetic markers have been sought that could explain the onset and progression of the disease. The failure of blood pressure control to halt nephropathy progression in some patients strongly suggested that the underlying causes of nondiabetic nephropathy attributed to hypertension differed between the races provided a major clue to the existence of an overarching nephropathy susceptibility gene. To our knowledge, no data are available about the association between APOL1 gene variation and the occurrence of nephroscelerosis among Egyptian hypertensive patients so the aim of this work was to study the influence of the APOL1 gene variants on the hypertensive induced kidney disease among Egyptian Patients. This study included 88 adult patients (≥ 18 years old ) of both sexes with essential hypertension for ≥ 5 years and classified into two groups: group 1: Fifty-three patients with essential hypertension (Bl.Pr. ≥ 140/90) who have normal kidney function. group 2: Thirty-five patients with essential hypertension (Bl.Pr. ≥ 140/90) who have impaired kidney function mostly attributed to hypertension. We excluded cases with other Causes than hypertension for renal impairment e.g.: Diabetic patients, Obstructive uropathy….etc. and patients with secondary hypertension. Essential hypertension was diagnosed if the patient gave history of hypertension, with antihypertensive medications or if Bl.Pr. ≥ 140/90 at the time of examination without definite cause. All patients were subjected to thorough medical history taking, physical examination, and investigations including plasma lipid profile (Total cholesterol, Triglycerides, HDL- cholesterol and LDL-cholesterol), complete blood count, kidney function tests, liver function tests and APOL1 gene study using Polymerase Chain Reaction (PCR). |