الفهرس 
chronic kidney diseaseOnly 14 pages are availabe for public view
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Abstract
Chronic kidney disease (CKD) is a worldwide public health alarming problem. All patients with evidence of persisting kidney damage for more than 90 days, are defined as having chronic kidney disease. renal impairment should be assessed by measuring albuminuria, mainly by the urinary albumin/creatinine ratio (ACR), and renal function assessment by estimating the glomerular filtration rate (GFR), using serum creatinine values in one of several available equations.
Although both heart and kidneys are separated by a quite distance within the body and they perform varied functions, there are close physiological relationship between them. The diseases in the kidneys can trigger a disease in the heart and vice versa.
High blood pressure is the most significant risk factor for the development and progression of chronic kidney disease (CKD). Lowering blood pressure is a goal to prevent CKD progress.
CKD shares many common risk factors with CVD and type 2diabetes, such as overweight and obesity, physical inactivity, poor diet, tobacco smoking, and high blood pressure, all of which are potentially preventable.
Lowering blood pressure (BP) is a major treatment goal to prevent both CKD progression and CVD among people with CKD.
Most common causes of renal impairment in cardiac patient:
1. Hypertension.
2. Cardiorenal syndrome
3. Pharmacotherapies used in the management of heart failure
4. Contrast induced nephropathy.
High BP is an important risk factor for the development of CKD and a major leading cause of kidney failure after diabetes
Chronic abnormalities in cardiac function (e.g., chronic congestive heart failure) causing p Congestive heart failure, chronic kidney disease and anemia appear to act together in a vicious circle in which each condition causes or exacerbates the other progressive chronic kidney disease.
Elevated serum creatinine on admission to hospital with ADHF and worsening renal function during admission for ADHF have both been shown to predict prolonged hospitalization, increased need for intensive care facilities, and increased mortality
Renin-angiotensin system blocking agents have been reported to decrease proteinuria more than non–renin angiotensin system blocking therapies (including α-blockers, β-blockers, CCBs, centrally acting drugs, and diuretics) and slow renal failure progression in patients with both diabetic and non-diabetic nephropathies with proteinuria, even with advanced renal insufficiency.
SUMMARY
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It should be remembered that ACE inhibitors do not damage the kidney but rather modify intrarenal hemodynamics and reduce filtration fraction. They protect the kidney by reducing pathological hyperfiltration.
Renal insufficiency can be induced or worsened by the administration of diuretics. It is unknown if a relation exists between diuretic-induced worsening renal function and clinical outcomes. In addition, the cardio-renal syndrome is increasingly recognized as an important component of HF pathophysiology.
Early detection of high BP and its effective management to levels that are as close to target as possible makes a difference in the prevention of CKD progression and control of the CKD health burden, hypertension can cause kidney disease and kidney disease can cause hypertension. However, hypertension may cause progressive kidney disease only in genetically susceptible individuals.