الفهرس 
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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).